Acute Coronary Syndrome: An Overview For Nurses: How To Receive Credit

_________________________________________
Course #3091 — 15 CONTACT HOURS

#3091 Acute Coronary Syndrome: An Overview for Nurses
Release Date: 02/01/10 Expiration Date: 01/31/13
Acute Coronary Syndrome:

An Overview for Nurses
earned a Master’s degree in professional and technical
HOW TO RECEIVE CREDIT writing, with a concentration in medical writing, at
Northeastern University, Boston, has completed the
• Read the enclosed course. AMWA core and advanced certificate programs, and is
• Complete the questions at the end of the course. certified by the Board of Editors in the Life Sciences.
• Return your completed Evaluation to CME
Resource by mail or fax, or complete online at
Faculty Disclosure
www.NetCE.com. (If you are a Florida nurse or a Contributing faculty, Karen Majorowicz, RN, ARNP,
behavioral health professional, please return the has disclosed no relevant financial relationship with any
included Answer Sheet.) Your postmark or facsimile product manufacturer or service provider mentioned.
date will be used as your completion date.
Contributing faculty, Lori L. Alexander, MTPW, ELS,
• Receive your Certificate(s) of Completion by mail, has disclosed no relevant financial relationship with any
fax, or email. product manufacturer or service provider mentioned.
Division Planners
Jane Norman, RN, MSN, CNE, PhD
Faculty
Sharon Cannon, RN, EdD, ANEF
Karen Majorowicz, RN, ARNP, is currently employed
in the Cardiac Intermediate Care Unit at Shands Division Planners Disclosure
Healthcare, UF-Gainesville, Florida. She received her The division planners have disclosed no relevant
masters in Medical-Surgical Nursing in 1978 from the financial relationship with any product manufacturer
University of Maryland. Karen has created numerous or service provider mentioned.
instructional manuals on Medicare and conducted edu- Audience
cational programs on cardiovascular assessment and was This course is designed for nurses practicing in primary
curriculum and instructional design consultant to the care, inpatient, outpatient, and home care settings
Institute for Child Health Policy, University of Florida to enhance their knowledge of the evidence-based
for a self-paced instructional module of SSI Disability guidelines related to the assessment, management, and
for children. secondary prevention of acute coronary syndrome.
Lori L. Alexander, MTPW, ELS, is President of Edito- Accreditation
rial Rx, Inc., which provides medical writing and editing CME Resource is accredited as a provider of continu-
services on a wide variety of clinical topics and in a range ing nursing education by the American Nurses Cre
of media. A medical writer and editor for nearly 25 years, dentialing Center’s Commission on Accreditation.
Ms. Alexander has written for both professional and lay
audiences, with a focus on continuing education materi- Designation of Credit
als, medical meeting coverage, peer-review articles and CME Resource designates this continuing education
guidelines for healthcare professionals, and educational activity for 15 ANCC contact hours.
materials for patients. She is the Editor of the American CME Resource designates this continuing education
Medical Writers Association (AMWA) Journal, providing activity for 18 hours for Alabama nurses.
oversight for all aspects of this quarterly peer-review
CME Resource designates this continuing education
journal that represents the largest association of medical
activity for 3.5 pharmacology contact hours.
communicators in the United States. Ms. Alexander
AACN Synergy CERP Category A.
Copyright © 2010 CME Resource

A complete Works Cited list begins on page 63. Mention of commercial products does not indicate endorsement.
CME Resource • Sacramento, California Phone: 800 / 232-4238 • FAX: 916 / 783-6067 1
#3091 Acute Coronary Syndrome: An Overview for Nurses__________________________________________
Individual State Nursing Approvals 5. Identify key elements that should be included
In addition to states that accept ANCC, CME Resource in the history and physical examination of
is approved as a provider of continuing education patients with suspected ACS, including the
in nursing by: Alabama, ABNP0353 (valid through role of stress tests.
December 12, 2013); California, CEP9784; California 6. Review key recommendations for the medical
BVNPT Provider #V10662; Florida Provider #50-2405; and nursing management of patients with
Iowa, #295; Kentucky, 7-0054, Kentucky Board of UA/STEMI, including initial treatment,
Nursing approval of an individual nursing continuing early inpatient care, and recommended
education provider does not constitute endorsement of pharmacotherapy.
program content; Texas, ANCC/Type I Provider. 7. Describe “early invasive” and “early
About the Sponsor conservative” strategies related to the
The purpose of CME Resource is to provide challeng- management of patients with UA/STEMI.
ing curricula to assist healthcare professionals to raise 8. Discuss key components of medical and
their levels of expertise while fulfilling their continuing nursing management of patients with
education requirements, thereby improving the quality variant angina and cocaine-induced ACS.
of healthcare. 9. Explain the role of PCI in the management
Our contributing faculty members have taken care to of STEMI, including the issues of timing,
ensure that the information and recommendations are stent selection, supporting pharmacological
accurate and compatible with the standards generally therapy, risks and possible complications.
accepted at the time of publication. The publisher dis- 10. Outline the use of fibrinolytic therapy as a
claims any liability, loss or damage incurred as a conse- reperfusion therapy in the management of
quence, directly or indirectly, of the use and application STEMI, including the issues of indications,
of any of the contents. Participants are cautioned about contraindications, supporting pharmacological
the potential risk of using limited knowledge when therapy, and risks.
integrating new techniques into practice. 11. List key measures used to prevent reocclusion
in coronary circulation following reperfusion
Disclosure Statement
with PCI or fibrinolytic therapy.
It is the policy of CME Resource not to accept com-
mercial support. 12. Identify critical components of discharge
planning for patients following recovery
Course Objective from ACS.
The pace at which these guidelines are updated make 13. Discuss the role of smoking cessation in
it challenging for clinicians to remain current with reducing the risk of recurrent ACS and
the recommendations that lead to improved outcomes tools for helping patients quit smoking.
for this substantial patient population. The purpose of
14. Describe other measures patients may take
this course is to reduce the widening gap between care
to reduce risk of recurrent ACS and on-going
according to guidelines and actual care delivered by
CAD from hypertension, dyslipidemia, and
providing nurses with knowledge necessary to imple-
other modifiable risk factors.
ment the most appropriate approach to diagnosis and
treatment. 15. Explain factors that impact on patient’s
adherence to prescribed therapy and measures
Learning Objectives to reduce risk of recurrent coronary disease.
Upon completion of this course, you should be able to:
1. Explain the pathophysiology of ACS, including
the role of plaque formation and rupture. Sections marked with this symbol include
2. Discuss key aspects of screening for evidence-based practice recommendations.
The level of evidence and/or strength
atherosclerotic plaque and CAD.
of recommendation, as provided by the
3. List key elements to include in chest pain evidence-based source, are also included
assessment for a patient with possible ACS. so you may determine the validity or relevance of the
4. Outline the role of 12-lead ECG and information. These sections may be used in conjunc-
cardiac biomarkers in the diagnosis and tion with the course material for better application to
risk stratification of ACS. your daily practice.
2 CME Resource • March 4, 2011 www.NetCE.com

_________________________________________ #3091 Acute Coronary Syndrome: An Overview for Nurses
• Lack of systems within current healthcare
Introduction models for effectively implementing
practice guidelines
Acute coronary syndrome (ACS) is an umbrella
term for any condition characterized by symptoms • Disparities in assessment, treatment, and
of acute myocardial ischemia caused by an abrupt outcomes across subgroups according to
reduction in blood flow to the heart. Three related age, gender, race/ethnicity, risk level, type
but distinct clinical entities fall under the category of MI, and practice setting
of ACS: unstable angina (UA), non-ST-segment Although physicians are responsible for directing
elevation myocardial infarction (NSTEMI), and prescribing care, nurses play a vital role in pro-
and ST-segment elevation myocardial infarction moting adherence to practice guidelines. Several
(STEMI) [73]. quality improvement initiatives developed to help
Advances in the understanding of the pathophysi- improve adherence to established ACS guidelines
ology of ACS have led to the identification of UA/ have met with success [52]. These initiatives
NSTEMI and STEMI as distinct clinical entities, include Can Rapid Risk Stratification of Unstable
with differences in etiology, clinical features, treat- Angina Patients Suppress Adverse Outcomes with
ment, and outcomes [7; 8; 9; 10]. In addition, the Early Implementation? (CRUSADE), Guidelines
development and evaluation of pharmacologic Applied in Practice, and Get With the Guidelines
therapies and reperfusion procedures in a mul- [36; 52; 53]. Studies have indicated that physi-
titude of large-scale trials over the past 20 years cians and nurses as well as healthcare systems can
have resulted in a redefinition of the diagnosis and improve the quality of care they provide to their
treatment of acute myocardial infarction (MI). The patients by implementing a combination of best
results of these trials have formed the evidence practices, including participation in continuing
base for clinical practice guidelines developed by education and in quality management efforts [21;
the American College of Cardiology (ACC), the 36].
American Heart Association (AHA), and other The purpose of this course is to provide nurses
specialty organizations [11; 12; 13; 14; 15; 16; 17; practicing in primary care, inpatient, outpatient, or
18; 19; 20]. Use of evidence-based guidelines has home care settings, as well as those who practice in
been associated with better patient outcomes and emergency rooms or in cardiovascular specialty set-
decreased risk for subsequent cardiac events such tings, with current information about the evidence-
as recurrent ischemia/infarct. Although they have based guidelines for the management of patients
been widely published and disseminated, studies with ACS. The program begins with an overview
have shown that adherence to evidence-based of the scope of the problem and its economic
guidelines has been less than optimal [21; 22; 23; impact on health care in the United States. An
24; 25; 26; 27; 28; 29; 30; 31; 32; 33; 34; 35; 36; overview of the pathophysiology of ACS and its
37; 38; 39]. Reasons for low compliance to these underlying disease process, coronary artery disease
guidelines include [5; 27; 28; 35; 37; 40; 41; 42; (CAD), will be presented to provide background
43; 44; 45; 46; 47]: for understanding specific practice recommenda-
• Lack of knowledge of the current tions. Clinical signs and symptoms, diagnosis, and
recommendations by healthcare providers management of UA, NSTEMI, and STEMI will
be discussed and illustrated through the use of
• Need for frequent changes in practice simulated clinical scenarios. Emergent assessment,
due to the rapid pace of research diagnostic measures, and initial treatment options
• Lack of acceptance/understanding of will be explored, followed by a discussion of follow-
the concept of evidence-based practice up care and preparation for discharge. Key points
of secondary prevention, including smoking cessa- Each of these individuals has ACS.
tion, treatment of dyslipidemia, and modification CAD, which encompasses angina pectoris (stable
of other risk factors, will be outlined. angina), coronary insufficiency (UA), MI, and
CAD-related death, affects approximately 15 mil-
lion people in the United States [1; 2]. Preliminary
scope of the problem
data for 2005 indicate that CAD caused approxi-
A man presents to the emergency room with complaints mately one in every 2.8 deaths [2]. The World
of chest pain and shortness of breath. He describes the Health Organization has predicted that CAD-
chest pain as “crushing.” When asked to identify the related deaths will increase by 120% for women
location of the pain, he points to the left substernal and 137% for men over the next two decades [3].
area of his chest. He denies previous episodes of chest As a chronic disease, CAD has a significant impact
pain. His initial electrocardiogram (ECG) shows on quality of life, negatively affecting physical,
non-specific ST wave changes, and his initial cardiac psychologic, and social well-being [4]. CAD also
biomarkers are within normal limits. He is admitted to carries a tremendous economic burden, with a total
the cardiology unit with an initial diagnosis of unstable amount of $71.2 billion spent on inpatient hospital
angina. costs, an amount that accounts for one-quarter of
the total cost of hospital care [2].
An elderly man collapses at home. Unable to arouse
him, his family calls emergency services. When the Atherosclerosis, the underlying condition of CAD,
paramedics arrive they find him to be in ventricular is progressive, with periods of stable and nonstable
fibrillation and promptly defibrillate, restoring normal disease. Periods of instability can cause the occur-
rhythm. An ECG obtained en route shows ST wave rence of ACS, a spectrum of life-threatening
changes indicative of an MI. Emergency medical ser- disorders that includes UA, NSTEMI, STEMI.
vices (EMS) notifies the emergency department that More than 1.4 million hospitalizations in 2005
they have a probable ST elevation MI patient en route were associated with a first or secondary discharge
and call for a STEMI alert. diagnosis of ACS, and 35% of all deaths among
individuals 65 years of age or older were attribut-
A young woman presents to the emergency department
able to ACS [2; 5]. It is estimated that in 2008,
with complaints of severe chest pain. She is tachycardic
770,000 individuals had a new episode of ACS and
with an elevated blood pressure. She has no history
430,000 had a recurrent episode [2]. In addition,
of cardiac disease. Her cardiac enzymes are positive
approximately 190,000 silent MIs occurred [2].
for MI, but her 12-lead ECGs show no ST-wave
As with CAD, the financial cost associated with
changes. She is admitted to the hospital with diagnosis
ACS is high; in a 2005 study, the total first-year
of NSTEMI.
direct cost of ACS in a managed care setting was
A woman presents to her primary care physician with $309 million [6].
complaints of increasing episodes of chest pain. Her
The prevalence of ischemic heart disease increases
physician notes that she was diagnosed with stable
with age [51]. It has been well-documented that
angina approximately 3 years earlier. Her “typical”
women tend to be substantially older than men at
angina attack was precipitated by exertion (walking
the time of a first cardiac event, with women being
more than 5 blocks or climbing a flight of stairs). Now,
an average of 6 to 10 years older in most studies
the patient reports that her angina attacks are occur-
and registries [44; 62; 63; 64; 65]. The average age
ring at rest and occasionally awaken her at night. A
of women at the time of the first event has been
12-lead ECG in the physician’s office shows no char-
reported to be 72 years, compared with 62 years
acteristic ST wave changes. The patient is sent to the
for men [64].
local emergency department with a tentative diagnosis
of ACS/UA.

The reported prevalence of CAD is consistent
among some racial/ethnic groups, with a 6.6% Pathophysiology of acs
rate in the white population, a 6.2% rate in the
black population, and a 5.9% rate in the Hispanic/ The underlying cause of ACS is a form of athero-
Latino population [2]. The rates are lower for Asian sclerosis known as CAD. In CAD, lipids, calcium,
Americans (3.8%) and American Indian/Alaska fibrin, and other cellular substances/cellular debris
Natives (2.5%) [2]. are deposited in the lining of the arteries, forming
an atherosclerotic plaque.
In community surveillance studies, STEMI
accounts for 29% to 38% of MIs documented in Although the exact mechanisms are not com-
various registries [2; 27; 48]. Among women, UA pletely understood, most researchers agree that
and NSTEMI are more common than STEMI; injury to the inner (endothelial) layer of the
however, among men, STEMI is more common artery initiates a series of biochemical events that
than UA/NSTEMI [51; 63]. NSTEMI is more com- result in the formation of atherosclerotic plaque.
mon in older men than in younger men [65]. Cigarette smoking, high levels of low-density lipo-
protein (LDL), hypertension, and diabetes have
The predominance of UA and NSTEMI is con- been identified as major risk factors for endothe-
sistent across racial/ethnic populations. In the lial injury. When the endothelium is injured, an
National Cardiovascular Data Registry, UA was inflammatory response is triggered at the site of
the most common ACS clinical entity, account- the injury. Circulating monocytes respond to the
ing for more than half of all ACS events in black, site and become macrophages. These cells act as
Hispanic, Native American, Asian, and white scavengers, taking up the LDL cholesterol that has
(non-Hispanic) populations [66]. NSTEMI was penetrated the vessel wall and forming the char-
more common than STEMI in each population; acteristic cell seen in early atherosclerosis. Fatty
the lowest rate of STEMI was found among black streaks, the earliest atherosclerotic lesion, may be
individuals and the highest among Native Ameri- observed in many individuals by 20 years of age.
can and Asian populations [66]. Through complicated mechanisms that include
The long-term morbidity and mortality associ- proliferation of smooth muscle cells in the arterial
ated with ACS is high. The likelihood of illness wall and the deposit of extracellular connective
and death for individuals who have had an MI is tissue, a complex atherosclerotic plaque develops
1.5 to 15 times greater than that for the general consisting of a fibrous cap overlying a rich lipid
population [2]. Pooled data from the Framingham core. The fibrous cap may be thick, providing a
Heart Study, the Atherosclerotic Risk in Com- dense barrier between the circulating blood and
munities Study, and the Cardiovascular Health the lipid core; this type of lesion is referred to as
Study indicate that among individuals 40 years “stable” and is less likely to be injured by substances
of age and older, 18% of men and 23% of women circulating in the blood stream. On some plaques,
will die within 1 year after the first MI; 33% of the fibrous cap is thin and more susceptible to
men and 43% of women will die within 5 years [2]. injury; referred to as “vulnerable” plaque, this type
Improvements in adherence to secondary preven- of lesion is more at risk to rupture or erode, causing
tion strategies can help to reduce these rates. thrombus formation and disruption of blood flow
[71; 73; 80; 87].
Growth of plaque narrows the lumen of the affected When the lipid-rich core of the plaque is exposed
vessel(s); this disrupts normal blood flow, reduces to circulating blood, an inflammatory response is
the blood and oxygen available to the tissue sup- triggered. This response increases platelet aggrega-
plied by the vessel, and creates increased turbulent tion and activates the coagulation pathway, result-
blood flow at the site of the plaque. Initially, the ing in the formation of a thrombus in the lumen
coronary artery responds to the growth of the of the vessel. The extent to which blood flow and
plaque/narrowing of the vessel lumen through oxygen supply are compromised by the thrombus
a process of vascular remodeling. In vascular depends on whether the thrombus occludes the
remodeling, the artery enlarges to compensate for lumen completely or only partially [84]. Clini-
the narrowing lumen. However, as the atheroscle- cally, partial occlusion is associated with UA and
rotic process continues, the vessel lumen becomes NSTEMI while complete occlusion usually results
stenosed, unable to dilate or constrict in response in the development of a STEMI [71; 73; 80; 87].
to metabolic demands [71; 73; 80; 87]. When a thrombus occludes a coronary artery,
At one time, it was thought that plaque simply oxygen supply to the area of the heart supplied by
continued to grow larger and larger until the that vessel is reduced. When the supply becomes
lumen of the affected vessel was totally occluded, insufficient to meet the tissue’s metabolic demands,
disrupting the blood flow and oxygen supply to part the myocardial cells become ischemic; ischemia
of the myocardium. However, today it is acknowl- can develop within 10 seconds. After 1 minute of
edged that the process is much more complex [81]. inadequate oxygen supply, the heart’s function is
Research has shown that the precipitating cause of affected. Irreversible tissue death and damage will
acute myocardial ischemia is not the plaque itself. occur after 20 minutes of ischemia [87].
Instead, acute ischemia occurs when a thrombus
forms in the area of plaque, partially or totally Other Causes of MI
occluding the vessel lumen [71; 73; 80; 87]. While thrombus formation is the most com-
mon cause, several other etiologies may cause
Thrombus Development ACS. These include cocaine toxicity and variant
Formation of a thrombus occurs when the fibrous angina.
cap of an atherosclerotic lesion erodes or rup-
tures, exposing the rich lipid core to circulating Cocaine-Induced ACS
blood. It is thought that the same stimuli that are A 2008 AHA position statement notes that the
responsible for the initial injury to the vessel wall acute effects of use of cocaine include coronary
are also responsible for causing erosion or rupture artery vasoconstriction, thrombus formation, and
of vulnerable plaque. Cigarette smoking and high increased myocardial oxygen demand. Cocaine
levels of circulating LDL head the list of injurious toxicity creates a setting in which oxygen demand
agents along with hypertension and diabetes [71; is increased and supply is reduced, leading to
73; 80; 87]. ischemia and increased potential for infarction.
Patients with cocaine toxicity present with a
Plaque rupture generally begins at its junction with clinical picture that is almost identical to that of
the arterial wall, mechanically the weakest point. non-cocaine-related ACS. The “typical” patient
Rupture does not occur throughout the coronary who presents with cocaine-induced ACS is a
artery tree but rather in three vulnerable sites: the male younger than 40 years of age, is a smoker,
proximal portion of the left anterior descending has used cocaine within several hours before the
coronary artery, near the origin of the marginal onset of symptoms, and has few risk factors for
branch on the right coronary artery, and near the CAD. Research has found that long-term effects
origin of the first obtuse marginal branch on the of cocaine use include the development of prema-
left circumflex coronary artery [72]. ture atherosclerosis and hypertrophy of the left
ventricle [75; 77; 87].

Variant Angina supply. Anaerobic metabolism of glycogen occurs,
Also known as vasospastic or Prinzmetal’s angina, and less ATP is produced. Without adequate oxy-
variant angina is caused by vasospasm of the gen and ATP, the sodium-potassium and calcium
coronary arteries. With vasospasm, the affected pumps in the myocardium begin to fail. Hydrogen
artery tightens and narrows. Blood flow through ions and lactate accumulate, resulting in acidosis.
the artery is significantly decreased, reducing the The heart’s ability to conduct electrical impulses
amount of oxygen reaching the tissue. Vasospasm and to contract becomes impaired. Cardiac output
may occur spontaneously or may be precipitated drops, and arrhythmias can develop. If the damage
by a stress factor such as exercise, hyperventila- to the myocardium is severe, cardiogenic shock
tion, or cold. Smoking increases the risk that a will develop [73].
person may develop variant angina. Variant angina When the body senses the drop in cardiac output
may be characterized by transient, intermittent and blood pressure that occur in the acute phase
chest pain; the chest pain may occur at rest. With of myocardial ischemia, compensatory mecha-
severe spasm that produces almost total occlusion nisms activate in an attempt to maintain adequate
of a vessel, ST-segment elevation may be seen on circulation to vital organs. The sympathetic
ECG. This elevation resolves when the spasm is nervous system (SNS) stimulates the release of
relieved. Variant angina can occur in the absence the hormones epinephrine and norepinephrine;
of atherosclerotic disease but may occur in the area as a result, heart rate and blood pressure increase
of plaque in persons with CAD [75; 87]. [73]. Instead of helping the heart compensate for
Impact on the myocardium reduced blood flow and oxygen demands, these
mechanisms increase myocardial workload and
For the myocardium to conduct electrical impulses, increase myocardial oxygen demands. In addition,
contract, and pump blood effectively, it requires the drop in cardiac output triggers the release of
both oxygen and adenosine 5B-triphosphate renin and angiotensin by the kidney, causing vaso-
(ATP) (Table 1). When blood flow is interrupted, constriction and retention of sodium and water in
cells are immediately deprived of their oxygen an attempt to compensate for reduced output. The
OVERVIEW OF CORONARY CIRCULATION
The vessels that supply the myocardium with oxygen and nutrients are called the coronary arteries. Because these arteries
lie on the surface of the myocardium, they are sometimes referred to as epicardial coronary arteries. Two main arteries,
known as the right coronary artery and the left coronary artery, emerge from the aorta, very near the top of the heart.
The right coronary artery supplies blood to the posterior part of the left ventricle, as well as to the right atrium and
right ventricle. Occlusions of the right coronary artery can cause ischemia, injury, or infarction of the right atrium, right
ventricle, and the back (or posterior) wall of the left ventricle.
The left coronary artery consists of three main segments. Together, the three segments supply a large part of the myocardium
with blood. The initial segment arising from the aorta is called the left main coronary (or colloquially just the left main).
The left main coronary quickly branches into two arteries known as the left anterior descending coronary artery and the
left circumflex coronary artery. The left anterior descending artery supplies blood to the anterior wall of the left ventricle,
the interventricular septum, the right bundle branch, and part of the left bundle branch. The left circumflex circles
around the left side of the heart, supplying the lateral wall of the left ventricle, the left atrium, and a posterior part of
the left bundle branch. Occlusions of the left main coronary artery are extremely dangerous because obstruction at that
level disrupts blood flow through both the left anterior descending artery and the circumflex, causing ischemia, injury, or
infarct of a large part of the heart muscle.
Source: [73; 87] Table 1
amount of blood volume in the ventricles at the facing the area of infarct in the heart, in pericardi-
end of diastole increases, again increasing myo- tis, ST segments throughout all 12 leads may be
cardial workload and myocardial oxygen demand. elevated. Nonsteroidal anti-inflammatory drugs
Because the oxygen supply to the myocardium (NSAIDs) should not be used to treat pericarditis
is already inadequate, increasing the demands in the immediate post-infarction period.
accelerates the ischemic process. Ischemic tissue When infarction damages the full thickness of the
can become necrotic, resulting in irreversible dam- myocardium, the area of damage initially thins.
age [73]. If more than 40% of the myocardium is The damaged area loses the ability to conduct elec-
damaged, circulatory collapse and cardiogenic trical impulses or to contract. In the initial period
shock can result. There is also an increased risk following acute MI, this tissue is very weak and
of life-threatening arrhythmias developing during may rupture. As scar tissue forms in the area, the
ischemia and infarction [71; 73; 80; 87]. damaged tissue is strengthened but is still unable
The impact of MI on the heart’s ability to maintain to conduct electrical impulses or contract. If the
adequate cardiac output depends on whether the area is large enough, an aneurysm can result. This
damage to the myocardium is reversible ischemia aneurysm is not at risk to rupture, but its presence
or permanent necrosis and the extent and location severely impairs the ability of the left ventricle to
of the ischemia/infarction [71; 73; 80; 87]. Ischemia contract and maintain cardiac output. Conges-
causes an immediate impairment of pumping func- tive heart failure can result. In some cases, the
tion in the affected tissue; if blood flow is restored, aneurysm can be surgically resected; removal of
this loss is temporary. If necrosis occurs, the ability the inert, non-contractile tissue has been found
of the affected tissue to conduct electrical impulses to improve overall pumping of the left ventricle.
and contract normally is permanently impaired. In Left ventricular aneurysm formation is associated
terms of location and extent, factors include the with infarctions of the anterior and lateral walls
coronary artery or branch involved and where the of the left ventricular.
occlusion is located in the vessel. Lesions in the
proximal part of a vessel can result in more damage Forms of ACS
than lesions in the very distal portion. The part of As discussed, three distinct clinical entities fall
the heart muscle supplied by the affected artery is under the general umbrella of ACS: UA, NSTEMI,
also important. and STEMI.
Other complications can occur after acute MI, Unstable Angina
including pericarditis and left ventricular aneurysm UA occurs when a thrombus partially or intermit-
[87]. Pericarditis is inflammation of the pericardial tently blocks blood flow through a coronary artery.
sac surrounding the heart. This condition may It is characterized by the development of chest
develop within days of an infarction, or it may pain that may or may not radiate. The chest pain
not develop until several weeks later. A common may be accompanied by additional symptoms such
symptom is chest pain that is described as sharp as dyspnea, diaphoresis, nausea, lightheadedness,
and severe; it often worsens with inspiration and elevated heart rate, hypo- or hypertension, and
may be relieved when the individual sits up and arrhythmias. Chest pain occurs at rest or with exer-
leans forward. A pericardial friction rub may be tion; the pain and associated symptoms are severe
auscultated. ST-segment elevations may be seen on enough to limit the patient’s activity. A 12-lead
12-lead ECG. Unlike the ST-segment elevations ECG may show transient/temporary ST-segment
seen in STEMI that occur in the specific leads depression or T-wave inversion [73].

Chest pain that occurs with minimal exertion or and arrhythmias. Also like UA and NSTEMI, this
requires an increasing dose of sublingual nitro- pain may occur at rest or with exertion and is severe
glycerin to obtain relief is defined as UA. UA also enough to limit the person’s activity. Qualitatively,
includes prolonged episodes of chest pain at rest, pain is longer in duration and more severe than
any chest pain that increases in severity, or any chest pain in UA. Definitive diagnosis of STEMI is
chest pain that is very severe upon first presenta- made on the basis of 12-lead ECG changes indica-
tion [73; 87]. tive of MI. Serum cardiac biomarkers are elevated
[73; 75; 87].
NSTEMI
NSTEMI also occurs when a thrombus partially
or intermittently blocks blood flow through a Screening for
coronary artery. On initial presentation, it may be Atherosclerotic
difficult to differentiate between UA and NSTEMI. Plaque and CAD
Like UA, it is characterized by chest pain that may
or may not radiate to the arm, neck, back, or epigas- Primary prevention remains the best intervention
tric region. The chest pain may be accompanied by for the reduction of morbidity and mortality associ-
additional symptoms such as dyspnea, diaphoresis, ated with CAD and ACS. Routine screening for
nausea, light-headedness, elevated rate, hypo- or the presence of CAD risk factors, including routine
hypertension, arrhythmias, and a drop in oxygen screening for hypertension and dyslipidemia, is
saturation. Like the chest pain associated with UA, an important part of preventive care along with
this chest pain occurs at rest or with exertion; the counseling for smoking cessation and chemopre-
pain and associated symptoms are severe enough to vention with aspirin (Table 2) [123; 124; 125;
limit the patient’s activity. Compared to the chest 126]. The ACC/AHA guidelines for UA/NSTEMI
pain of UA, however, chest pain in NSTEMI lasts and STEMI confirm the need for screening, noting
longer and is more severe. A 12-lead ECG may that primary care clinicians should evaluate the
show signs indicative of myocardial ischemia: ST- presence and control of these risk factors at regular
segment depression or T wave inversion. Diagnosis intervals (every 3 to 5 years) [11; 12]. The guide-
of NSTEMI is made on the basis of elevated cardiac lines also recommend that the 10-year risk of CAD
biomarkers [73; 87]. be determined for patients who have two or more
STEMI
STEMI occurs when a thrombus fully occludes RISK FACTORS FOR
a coronary artery, resulting in necrosis of part of CORONARY ARTERY DISEASE
the myocardium. Development of an acute MI is Traditional Risk Factors
characterized by a central necrotic area surrounded Increasing age (especially older than 65 years)
by zone of injury. Tissue in the zone of injury can Male gender
Family history
recover if blood flow is restored quickly enough; if Cigarette smoking
it is not, the area of injury will become necrotic. Hyperlipidemia
The zone of injury, in turn, is surrounded by outer Hypertension
zone of reversible ischemia. Obesity and overweight
Sedentary lifestyle
Like other forms of ACS, STEMI is characterized Diabetes
by chest pain that may or may not radiate to the Emerging Risk Factors
arm, neck, back, or epigastric region. Accompany- Systemic lupus erythematosus
ing symptoms may include dyspnea, diaphoresis, Rheumatoid arthritis
nausea, light-headedness, tachycardia, tachypnea, HIV infection
hypo- or hypertension, a drop in oxygen saturation, Source: [129] Table 2
risk factors [11; 12]. A risk assessment algorithm, techniques, such as multidetector computerized
such as that from the Framingham Heart Study, tomography (CT), electron-beam CT, resting ECG
can be used to project a short-term or intermediate- and exercise stress test, magnetic resonance imag-
term 10-year absolute risk. This risk assessment ing (MRI) or angiography (MRA), and biochemi-
tool can be accessed online at http://hp2010. cal markers [82]. These tests, which are primarily
nhlbihin.net/atpiii/calculator.asp?usertype=prof. performed and interpreted by cardiologists, are in
The Framingham risk score includes factors for age, varying stages of development as screening and/
total cholesterol, high-density lipoprotein (HDL) or diagnostic tools; some tests have been used for
cholesterol, systolic blood pressure, treatment for many years, and others are still years away from
hypertension, and cigarette smoking to provide routine use in clinical practice.
a risk level estimate for “hard CAD,” which is
defined as MI or CAD-related death. Coronary Angiography
Coronary angiography is the most widely used
Primary prevention interventions should be imple- imaging tool to evaluate luminal obstructive
mented when a patient has a single risk factor, and disease in coronary arteries. However, coronary
the benefit of prevention increases as the number angiography is not an optimal tool for identifying
of risk factors increases [11]. The National Choles-
plaque. [82]. First, most atherosclerotic lesions
terol Education Program (NCEP) guidelines and
are undetectable on angiography [70]. Second,
the Seventh Report of the Joint National Com- plaque composition cannot be assessed because
mittee on Prevention, Detection, Evaluation, and only a luminal view of a lesion is possible [82].
Treatment of High Blood Pressure (JNC7) should The use of contrast medium creates radiographic
be used to identify individuals who would benefit silhouettes that can help classify lesions as stable
from lipid-lowering and antihypertensive therapy, or unstable, and these findings have correlated
respectively [127; 128]. The AHA has developed well with histopathologic findings [97]. The use
evidence-based guidelines for the primary preven- of intracoronary acetylcholine can help to detect
tion of CAD, and the ACC has established pre- endothelial dysfunction, which is considered to be
vention guidelines targeted to the unique needs of an early stage of atherosclerosis and has been inde-
women [129; 130]. pendently associated with cardiovascular events
To facilitate determination of risk and enhance [98]. Although coronary angiography is not the
prevention of CAD and ACS, research is explor- optimal modality to identify plaque, it can detect
ing clinical tools that could effectively screen changes in the diameter of arteries and reliably
healthy individuals for evidence of sub-clinical identify stenosis.
atherosclerotic disease. Much research has focused
on how to use imaging techniques to identify and Coronary Angioscopy
assess plaque, particularly that which is prone to A direct view of plaque is possible with coronary
rupture, by visualizing indicators of vulnerable angioscopy; a cross-sectional view is not. With this
plaque, such as inflammation, a thin cap, positive technique, fibrous plaques are white and lipid-rich
remodeling, or endothelial erosion or fissuring with plaques are yellow, often with an irregular surface
thrombus [82]. In addition, researchers continue [72; 82]. Studies have shown that yellow plaques,
to explore techniques to better identify thrombosis especially glistening ones, are more likely to
and stenosis. rupture [99]. Angioscopy has several drawbacks,
including the need to occlude the coronary artery
Among the modalities being studied to identify (for a saline flush to enhance the quality of the
and evaluate plaque and stenosis are invasive image), the inability to visualize the first 2 cm of
techniques, such as coronary angiography, coronary the coronary arteries (the location of many culprit
angioscopy, intravascular ultrasound, and optical lesions), and the inability to pass a high-grade
coherence tomography, as well as noninvasive stenosis [100].

Intravascular Ultrasound In the early 2000s, the ACC, AHA, American
Intravascular ultrasound is the gold standard for College of Physicians (ACP), and U.S. Preventive
evaluating coronary plaque and determining the Services Task Force (USPSTF) all recommended
dimensions of the lumen and vessel walls [82]. against coronary artery calcification screening with
Compared with coronary angioscopy and histopa- electron-beam CT because of insufficient evidence,
thology, intravascular ultrasound has a high sensi- most notably limited clinical outcomes data and
tivity and specificity in identifying characteristics lack of established independent prognostic value
of a vulnerable plaque [101; 102]. Intravascular [17; 110; 111]. Since that time, however, several
ultrasound has begun to fulfill the criteria of an studies have demonstrated the prognostic value
effective screening tool, but it has not been recom- of coronary artery calcification in large series of
mended as a screening tool for any population to patients [112; 113; 114; 115; 116]. The results of
date [82; 106]. these studies led the American College of Cardiol-
ogy Foundation and the AHA to publish a revised
Optical Coherence Tomography consensus document in 2007. In that document,
Optical coherence tomography usually uses pulses the expert panel noted that it “may be reason-
of near-infrared light that are split with a beam able to consider” determining the coronary artery
splitter; half of the light is directed at the sample calcification score for asymptomatic patients with
and the other half at a moving mirror. This imag- intermediate risk for CAD (10-year risk of 10%
ing can provide accurate information on tissue to 20%) [96].
characteristics, identifying intimal hyperplasia
and lipid/necrotic cores that are not evident on Other Tests
intravascular ultrasound [107]. Optical coherence The ACC, AHA, ACP, and USPSTF have all
tomography can also provide a measurement of recommended against routine screening with
the thickness of an atherosclerotic lesion’s fibrous resting ECG and exercise stress test for low-risk
cap. Optical coherence tomography currently has individuals because the potential harms outweigh
several limitations that make it unlikely to be used the potential benefits [17; 110; 111]. Specifically,
in routine clinical practice. [107]. the USPSTF noted that testing in this population
commonly yields false-positive results, especially in
Electron-Beam CT women, and as such, the tests are likely to cause
Electron-beam CT is an imaging tool with known harm through overtreatment and unnecessary
benefit, and its use in measuring coronary artery invasive procedures [111]. With regard to patients
calcification is now recommended for screening at high risk for CAD events, the ACC/AHA and
patients at intermediate risk of CAD [96]. Coronary USPSTF stated there was insufficient evidence to
artery calcification occurs only in atherosclerotic recommend for or against routine screening with
vessels, with small amounts in early lesions and ECG or exercise stress test as it was not clear that
larger amounts in advanced lesions [96]. Patients such screening would lead to interventions that
who have calcified plaque are more likely to have would improve health outcomes [17; 111].
noncalcified plaque, which is prone to rupture. Several biochemical markers of CAD have been
The occurrence of both types of plaque is factored studied as screening tools among asymptomatic
into the estimation of risk for an acute coronary patients. C-reactive protein, an inflammatory
event [109]. The coronary artery calcification score marker, has been associated with both nonfatal
can be used to carry out global risk assessment, and fatal CAD [118; 119]. A meta-analysis showed
but electron-beam CT cannot identify stenosis or that the odds ratio for CAD among asymptomatic
vulnerable plaque [96]. individuals with a C-reactive protein level in the
top one-third of the distribution of levels was 1.45
to 2.0 compared with individuals with a level in
the bottom one-third [120; 121]. However, other Patient I walked into the triage area of the local emer-
inflammatory markers, such as tumor necrosis gency department. He stated that his primary care
factor-alpha (TNF-α) and interleukin-6, have not physician instructed him to come to the emergency
been associated with the development of clini- department because his angina attacks were “getting
cally apparent disease [107]. An increased level of worse.” He stated that his physician instructed him to
plasma natriuretic peptide may help in the early come in an ambulance, but he drove himself. The tri-
detection of CAD. age nurse noted that the patient was diaphoretic and in
distress. When asked, the patient admitted that he was
currently experiencing “some discomfort” in his chest
triage and diagnosis that started when he walked into the hospital from the
remote parking area. An ECG showed characteristic
If a person is outside of a healthcare facility when
ST-segment elevation indicative of an anterior wall
he or she develops signs of ACS, the following
MI.
actions should be taken [11]:
Patient Q was admitted to outpatient surgery for an
• 911 should be called to transport the patient
elective procedure. Her preoperative work-up the day
to the hospital via EMS. Friends or family
prior to admission showed normal laboratory values and
should not drive the patient to the hospital.
ECG. Her admitting vital signs on the day of surgery
• Persons out of the hospital setting who were within normal limits. While Patient Q was in
develop symptoms of ACS and who the preoperative holding area, she told the nurse that
already have a prescription for sublingual she was experiencing “some weirdness” in her chest.
nitroglycerin should take no more than With questioning, she described the sensation as burn-
1 dose of nitroglycerin. If chest pain is ing and the location as “my chest; no, I can’t point to
not relieved within 5 minutes, the person one place, but it hurts a lot.” The nurse noted that
should call EMS before taking any more Patient Q looked anxious and in distress; her respira-
nitroglycerin. tory rate increased to 24 breaths per minute, her blood
• During transport to the hospital, EMS should pressure rose to 180/94 mm Hg, and her telemetry
give the patient 162–325 mg of aspirin monitor showed that she was having isolated premature
(chewed or crushed, not swallowed whole). ventricular contractions (PVCs). Patient Q’s initial
When a patient presents with clinical signs suspi- ECG was negative for indications of ischemia, but her
cious for MI, immediate medical intervention is initial set of cardiac biomarkers come back positive for
directed at confirming a diagnosis and stratifying myocardial damage.
the person’s risk for adverse events such as cardiac Patient J, a man 82 years of age, was admitted to
arrest and severe/significant damage to the myo- an inpatient medical-surgical unit with a diagnosis of
cardium [11]. community-acquired pneumonia. He was treated with
Although a large percentage of individuals with antibiotics and nebulizer treatments, but he developed a
suspected ACS will be seen initially in emergency productive cough and complained intermittently about
departments, patients in any healthcare setting, pain in his ribs from coughing. Three or four days after
regardless of other diagnoses, may abruptly develop admission, Patient J called to tell the nurse saying, “I
chest pain suspicious for ACS. think my pneumonia is getting worse. I have this ter-
rible pain in my chest, and I’m not coughing anything
Consider these simulated clinical situations: up.” When asked, Patient J described the pain as severe
discomfort located on the left side of his chest. A check
of vital signs showed that Patient J’s heart rate was 110
beats per minute and his oxygen saturation on room
air was 88%. He was diaphoretic but denied nausea.

“I’m just tired, really tired,” he reported. “I haven’t DIFFERENTIAL DIAGNOSIS OF CHEST PAIN
felt this bad before. I thought I was getting better.” An Life-Threatening Causes
initial 12-lead ECG showed changes suspicious for Aortic dissection
myocardial ischemia. Pulmonary embolism
Tension pneumothorax
When a patient complains of symptoms suspi-
Esophageal rupture
cious for ACS, AHA/ACC guidelines recommend
Other Causes
[11]:
Pneumonia
• Early risk stratification (for risk of death Pleurisy
or re-infarct) should be done for any person Pericarditis
who presents with chest discomfort or Myocarditis
Hypertrophic cardiomyopathy
other ischemic symptoms. Costochondritis
• Risk stratification includes patient history, Cervical disc or neuropathic pain
assessment of chest pain, physical findings, Peptic ulcer disease
ECG findings, and cardiac biomarkers. Gastroesophageal reflux and spasm
Biliary or pancreatic pain
Chest Pain Panic attack
Source: [12; 62; 133; 137; 159] Table 3
Chest pain is the most commonly reported symp-
tom in all patients with ACS, regardless of age,
gender, race/ethnicity, or the presence of comorbid The effects of the medications on the patient’s vital
conditions [5; 155; 156]. So-called “classic” ACS- signs and other symptoms should also be noted.
related chest pain has been described as diffuse In the past, it was thought that cardiac pain could
pain or pressure in the substernal or epigastric be distinguished from some types of noncardiac
area that frequently radiates to the neck, jaw, and pain by assessing the relief of chest pain with use
left arm [57; 62; 134; 160]. Chest pain related to of specific drugs, such as nitroglycerin or antacids.
ACS usually begins abruptly and lasts at least 15 However, relief of chest pain after administration
to 20 minutes; however, the duration of pain var- of either of these drugs should not be used to dis-
ies among patients [56; 57; 62]. Pain that lasts for tinguish pain as cardiac or noncardiac in nature.
longer than 20 minutes is associated with increased Studies have shown that nitroglycerin may relieve
short-term risk of MI (nonfatal or fatal) [74]. The both cardiac and noncardiac chest pain [170; 171;
intensity of “classic” ACS chest pain increases 172]. Similarly, a gastrointestinal cause of pain
over time, reaching maximal intensity after a few should not be assumed if the chest pain is relieved
minutes [62; 159]. Pain is usually worse with activ- by antacids, as some patients with ACS have
ity and improves with rest [62]. reported relief after use of such a drug [137; 173].
Chest pain assessment should begin with an assess-
ment of the patient’s current chest pain and associ- Typical ACS Symptoms
ated symptoms. Data important to collect include “Typical” ACS-related chest pain is often described
time of onset of the pain, description of the pain or as: tightness, sensation of pressure, heaviness,
discomfort, location of the pain, intensity/severity crushing, vise-like, aching [62; 161]. Pain features
of the pain, radiation to any other body part, any that are not generally characteristic of ACS-related
associated symptoms, how long the pain lasts, and pain include: sharp, stabbing pain; pain reproduced
what relieves the pain (Table 3) [73; 75; 83; 87]. with movement or palpation of the chest wall
or arms; pain of several hours’ duration; fleeting
When medications such as nitroglycerin or mor- pain (episodes lasting for a few seconds or less);
phine are administered, their effectiveness in lump in the throat; or band-like sensation [11; 62;
reducing or relieving chest pain should be noted. 133; 137; 159]. The classic presentation of ACS
includes some symptoms in addition to chest pain, Chest pain in women is an area of emphasis in
primarily dyspnea, diaphoresis, nausea, or syncope current research. Findings have shown that women
[5; 12; 57]. Again, there is wide variation in the may experience symptoms similar to men but also
symptoms reported by patients with ACS, as well may experience different symptoms, including
as differences in subgroups of patients. Patients complaints of epigastric discomfort or complaints
with STEMI more commonly report nausea, cold of dyspnea. Some sources recommend that any
sweats, and vomiting [135]. Several studies have woman presenting with symptoms of discomfort
demonstrated an increased prevalence of diapho- from the nose to the navel be evaluated for the
resis among men with ACS compared with women presence of CAD. Nonspecific symptoms are more
[65; 155; 166; 174; 175]. likely to occur in women than in men with ACS;
higher rates of fatigue, nausea and/or vomiting,
indigestion, palpitations, dyspnea, dizziness, and
Patients with symptoms of ACS (chest
discomfort with or without radiation to lightheadedness have been reported [64; 65; 87;
the arm, back, neck, jaw, or epigastrium; 135; 155; 160; 166; 167; 174; 175; 176; 177].
shortness of breath; weakness; diaphoresis;
The elderly, because of age-related physiological
nausea; lightheadedness) should be
instructed to call 911 and should be changes and multiple co-morbidities, may present
transported to the hospital by ambulance rather than with more generalized symptoms including weak-
by friends or relatives. ness, dyspnea, and confusion. Among older indi-
(http://www.guidelines.gov/summary/summary. viduals, dyspnea and fatigue have been noted to be
aspx?doc_id=11333. Last accessed October 21, 2010.) the most common symptoms and diaphoresis has
Strength of Recommendation/Level of Evidence: been reported less often [5; 87; 133; 137; 160].
IB (Procedure should be performed based on the
evaluation of limited population risk strata.) It is also important to note that some people with
ACS will not experience chest pain. This so-called
“silent ischemia” is more likely to occur in persons
Atypical ACS Symptoms with diabetes, women, older adults, and persons
with heart failure [73; 87].
A significant number of patients with ACS may
present with what are commonly referred to as 12-Lead Electrocardiogram (ECG)
“atypical” signs of ACS. Failure to recognize Electrocardiography has historically been used to
atypical symptoms of ACS has been found to delay assess myocardial ischemia, and it continues to be
diagnosis and/or result in the use of less aggressive an essential diagnostic tool [188]. A 12-lead ECG
treatment. It has been estimated that more than can be used to [73; 75; 80; 87]:
40% of patients with angina have one or more
“atypical” elements in their chest pain descrip- • Confirm the diagnosis of acute STEMI
tion [83; 130]. Atypical symptoms that have been • Differentiate between UA/NSTEMI and
found to be associated with ACS include shortness STEMI
of breath, fatigue, lethargy, indigestion, anxiety, • Identify the affected part of the myocardium
tingling in upper extremities, palpitations, loss of • Diagnose arrhythmias and conduction
appetite, and flushing. Words commonly used to abnormalities that may occur during
describe “atypical” chest pain associated with ACS ischemia and infarct
include numbness, tingling, burning, stabbing, or
pricking. Atypical chest pain location includes
any area other than substernal or left sided, such
as the back, area between shoulder blades, upper
abdomen, shoulders, elbows, axillae, and ears [83;
130].

Overview of Basic ECG Principles ECG Changes Indicative of MI
To understand how 12-lead ECGs can provide Three classic ECG characteristics are used in
information about myocardial ischemia, injury, the diagnosis of STEMI: ST-segment elevation,
or infarct, an understanding of the basic electro- T-wave inversion, and Q-wave formation. During
cardiography principles is necessary. A thorough MI, these ECG changes can evolve over minutes
discussion of 12-lead ECG interpretation in the to hours. They reflect the impact of the infarction
diagnosis, evaluation, and management of MI on the functioning of affected myocardial tissue.
exceeds the scope of this program; the information In STEMI, the damage generally involves the
presented below is intended as an introduction and full width of the myocardial wall (from the inner
overview only. endocardium through the upper epicardium); the
term “transmural” is used to designate this type of
The standard 12-lead ECG is a representation
full-wall thickness damage. The associated ECG
of the heart’s electrical activity recorded from
changes in STEMI mirror the spread of the damage
electrodes on the body surface. In a traditional
as it begins in the endocardium and travels outward
12-lead ECG, 10 recording electrodes are placed
through the heart wall until the epicardium of the
in designated positions on the patient’s arms, left
wall is also damaged [73; 75; 87].
leg, and the left side of the chest. Twelve different
recordings of the patient’s heart rhythm are taken The earliest ECG hint of an acute STEMI is an
simultaneously; each records the electrical signals increase in the height of the T wave. Referred to as
from the heart using a particular combination of “hyperacute,” these T-wave changes are transient.
the recording electrodes. Each combination of They are not considered a definitive diagnostic sign
electrodes is referred to as a “lead.” Each lead is but should be taken as highly suspicious for possible
given a designation that reflects its location and acute MI in a patient with clinical symptoms of
its view of the heart [75]. ACS [73; 75; 87].
Some leads look at the bottom (inferior) section The first of the three classic signs is ST-segment
of heart, others monitor what occurs in the ante- elevation. It may be followed by T-wave inversion
rior wall, and still others monitor the lateral wall. and pathologic Q-wave formation. This sequence
Because of the way the heart is positioned in the of changes is called the electrocardiographic evolu-
thorax, none of the surface leads in a standard ECG tion of an infarction. Because these changes hap-
directly look at the very back of the heart. How- pen over a period of time, a series of 12-lead ECG
ever, the placement of some leads can be modified tracings may be required for accurate diagnosis. In
to provide more direct information [75]. the very early stages of infarct, clear patterns may
not be immediately revealed on ECG. As always,
In normal conduction, the ST segment begins
ECG findings should be correlated with clinical
at the end of the QRS complex and stops at the
signs and symptoms. Over a period of months to
beginning of the T wave. In the cardiac cycle, this
days, ST-segment elevation and T-wave changes
segment corresponds to mechanical systole. On
will resolve and no longer be present on 12-lead
ECG, the ST segment normally appears flat and
ECG recordings. Pathologic Q waves, on the other
lies along the baseline.
hand, frequently remain permanently. Presence of
The T wave represents the period of ventricular a pathologic Q wave on 12-lead ECG with no evi-
repolarization. In appearance, the T wave looks dence of ST-segment elevation or T-wave changes
asymmetrically rounded. Normally, the T wave is usually indicates that the person has had an infarct
upright in leads I, II, and V [75]. Changes in the ST in the past [73; 75; 87].
segment and the T wave can indicate the presence
of acute myocardial ischemia and acute MI. The
ECG leads in which these changes occur provide
information about the part of the heart involved.
ECG CHANGES AND DIAGNOSIS OF STEMI

Leads Showing Changes Location of Infarction Location of Occlusion
II, III, aVF Inferior wall Right coronary artery
I, aVL, V5-6 Lateral wall Circumflex artery
V1-4 Anterior wall Left anterior descending
Reciprocal changes only in V1-2, Suspect posterior wall of the heart Right coronary artery
sometimes V4
ST elevation in inferior leads and Suspect right ventricular wall Right coronary artery
lead V1
The ST segment in a normal ECG complex runs presence of necrotic tissue. Although a pathologic
along the baseline of ECG. In STEMI, the ST Q wave can be seen in either STEMI or NTSEMI,
segment lifts upward off the baseline on the ECG it is more common in STEMI. Unlike ST-segment
tracing, reflecting the movement of injury in the elevation and T-wave inversion, formation of a
myocardium. ST-segment elevation will be noted pathological Q wave is permanent [75; 87].
in the ECG leads that are facing the affected area It is possible for an acute infarction to occur that
of the heart wall. These changes are referred to as causes ST-segment elevation but does not extend
changes indicative of infarct. To confirm a diag- damage through the full thickness of the myo-
nosis of STEMI, characteristic ECG changes must cardial wall. This type of infarction is sometimes
be present in two adjacent (contiguous) leads [73; referred to as a subendocardial infarction. It will
75; 87]. cause ST-segment changes (elevation initially,
As an acute MI continues to evolve, the elevated then resolving) and T-wave inversion but will not
ST-segment will begin to drop. As it drops, the T have a Q wave during the acute episode or after-
wave begins to come down to baseline and eventu- wards. The diagnosis of non-Q wave MI is based on
ally inverts. When a 12-lead ECG shows evidence ST-wave changes and T-wave changes. The leads
of the ST-segment elevation resolving and the T in which the classic signs of STEMI are seen give
wave inverting, it indicates that the infarction is an indication what vessel and what wall of heart
well along in evolution [75]. are involved (Table 4).
When an infarct damages the full thickness of Identification of right ventricular acute MI can
affected wall, the myocardial tissue loses its ability be difficult because standard ECG lead place-
to depolarize and conduct electrical impulses. The ment does not provide a good direct view of the
tissue becomes electrically inert and generates no right ventricle. If a right ventricular acute MI is
electrical activity. When a 12-lead ECG is per- suspected, a modified 12-lead ECG may be done
formed, the area of infarction acts like “window” in which V leads are placed on right side of chest
that allows ECG monitoring leads to look through (instead of the left) in corresponding positions. An
the infarct to the opposite wall of heart. This results “R” is added to the lead designation to indicate the
in characteristic changes in the recorded ECG change in position [73; 75; 87].
pattern. One of these changes is referred to as a True posterior acute MI may be caused by dam-
pathologic Q wave. Pathologic Q waves are seen age to the posterior wall of the left ventricle. The
in the leads that reflect the infarction. In a normal traditional 12-lead ECG may also be modified to
ECG recording, a Q wave may be present as the provide additional diagnostic information through
first negative deflection of the QRS complex. How- use of additional leads (V7-V9) positioned at set
ever, when the Q wave is significantly over-sized, points on the patient’s back [73; 75; 87].
it reflects a change in depolarization due to the

ECG Changes in NSTEMI Cardiac Biomarkers
An NSTEMI may be characterized by ST-segment Cardiac biomarkers are another major physiologi-
depression and T-wave abnormalities. ST-segment cal indicator used in diagnosis and risk stratification
elevation does not occur [75]. in ACS (Table 5). The ACC/AHA 2007 guideline
recommends the following Class I recommenda-
During myocardial ischemia, blood flow to the
tions [11]:
endocardium is reduced first; blood flow to the
outer layer of heart (epicardium) remains adequate. • Cardiac biomarkers should be measured
As a result, the endocardium experiences signifi- on all persons who present with chest
cant metabolic changes associated with ischemia discomfort indicative of ACS.
while the epicardium does not. These changes alter • The preferred choice of biomarker
the electrical potential and current flow through is cardiac troponin.
the myocardium. A 12-lead ECG records these • If initial biomarkers are negative for
changes as ST-segment depression. Measured from myocardial damage, levels should be
the isoelectric line, an ST depression of 1 mm or remeasured within 8 to 12 hours after
more below baseline can indicate ischemia. It is
onset of patient’s symptoms.
important to note, however, that when ST-segment
depression is seen in some leads along with ST- When myocardial cells are damaged, the cells
segment elevation in other leads, the ST-depression release proteins and enzymes into the blood
is a reciprocal ECG change associated with STEMI. stream; these are collectively referred to as “cardiac
As always, it is important to place ECG findings biomarkers.” The specific biomarkers used in the
within the full context of the patient’s symptoms. diagnosis of MI have evolved over time. The mark-
Because it reflects the changing balance of oxygen ers that have been found to be the most specific
supply and demand in the affected coronary artery, indicators for myocardial damage are the cardiac
ST-segment depression may be present during troponins [11; 73].
the period of ischemia only to disappear when
the ischemia is relieved. Ischemia can also cause
T-wave abnormalities such as T-wave inversion.
In NSTEMI, these changes can be difficult to
interpret [75].
COMPARISON OF PRIMARY CARDIAC BIOMARKERS

Biomarker Time to Peak Duration Primary Advantages Disadvantages
Initial Elevation of Elevation
Elevation after MI
CK-MB 3 to 12 hrs 24 hrs 2 to 3 days Early detection; rapid Low specificity for
testing; cost-efficient myocardial damage
Myoglobin 1 to 4 hrs 6 to 7 hrs 24 hrs Most useful for ruling Low specificity for
out MI; earliest marker myocardial damage
of myocardial damage
Cardiac Troponins
Troponin I 3 to 12 hrs 24 hrs 5 to 10 days Highest sensitivity Low sensitivity
Troponin T 3 to 12 hrs 12 to 48 hrs 5 to 14 days and specificity during 6 hrs or less
after symptom onset
MI = myocardial infarction; CK-MB = cardiac-specific isoenzyme of creatine kinase.

Source: [11; 12; 57; 207] Table 5
Cardiac Troponins shock), myocardial contusion, ischemia due to
Cardiac troponins include troponin T and troponin myocardial bridging, coronary spasm, cardiac
I and are derived from heart-specific genes [11]. toxins, and cardiac infiltrative disorders [11; 207;
Elevated serum levels of troponin T or troponin 210; 212; 213]. In addition, elevated levels have
I give a good indication of the presence and the been associated with many noncardiac conditions,
extent of myocardial damage. Elevated troponin including gastrointestinal bleeding, sepsis, stroke,
levels are very sensitive indicators and can be hypertensive emergency, pulmonary embolus, aor-
used to identify even small amounts of myocardial tic dissection, diabetic ketoacidosis, exacerbation
damage. of chronic obstructive pulmonary disease, severe
pulmonary infections, rhabdomyolysis, and end-
The cardiac troponins can be detected in the stage renal disease [11; 207; 210; 212; 213].
bloodstream starting 2 to 4 hours after the onset
of ACS-related symptoms, but an elevated level Creatine Kinase
may not occur for 8 to 12 hours [11]. The levels Serial measurements of creatine kinase (CK) at
of troponins also remain elevated for a prolonged 6 and 12 hours after admission were once the
period of time after myocardial necrosis (4 to 7 standard. Now, the cardiac troponins and the
days for troponin I, 10 to 14 days for troponin T) cardiac-specific isoenzyme of CK (CK-MB) have
[11; 87]. This long period of elevation makes the primarily replaced CK because of its low specific-
biomarkers helpful in identifying myocardial dam- ity and sensitivity for cardiac damage. Although
age in a patient who may not be evaluated until the level of CK becomes elevated within 3 to 4
several days after the onset of symptoms [11]. The hours after the onset of an ischemic injury, it is
exact ranges for “normal” vary among laboratories. not cardiac-specific. It has significant distribution
Standards require that any level interpreted as posi- in skeletal muscle, and low levels are present in
tive for infarction must be elevated more than 99% healthy individuals [57; 58]. CK-MB levels are the
of the agreed upon reference group [87]. best alternative if cardiac troponin assays are not
The ACC/AHA guidelines recommend that when available [11; 57].
the initial cardiac biomarker level (within 6 hours CK-MB levels differ from troponin levels in that
after the onset of symptoms) is not elevated, a they are elevated earlier after myocardial necrosis
repeat level should be measured again 8 to 12 hours and return to normal within 48 to 72 hours [58].
after the onset of symptoms [11]. The guidelines When CK-MB is used as the biomarker, a level
note that clinicians should consider several factors should be determined at the time of admission and
when establishing the exact time of biomarker again 6 to 9 hours later. As with cardiac troponins,
measurement, including the uncertainty of the an increased CK-MB level is defined as a measure-
onset of symptoms and the sensitivity of the assays ment above the 99th percentile of a normal refer-
being used [11]. A sequential change in cardiac ence population [57]. If the clinical presentation is
troponin levels within the first 24 hours after onset highly suggestive of MI but CK-MB levels have not
suggests new myocardial damage; levels that remain been elevated, another level should be measured
the same are more likely to be associated with a at 12 and 24 hours [57].
chronic disease state [11].
The ACC/AHA guidelines also note that it is
Elevated troponin levels may also occur as a result reasonable to consider a newer diagnostic approach
of other cardiac conditions, including severe tachy- that allows for earlier risk stratification of patients.
cardia, atrial fibrillation, pericarditis, myocarditis, Rather than evaluating serial measurements of
severe aortic stenosis, ventricular hypertrophy, biomarkers over 6 to 8 hours, changes in levels
severe congestive heart failure, electrical trauma of CK-MB and troponin (delta levels) may be
(automatic internal cardioverter-defibrillator evaluated over a shorter amount of time (2 hours)

[11]. This approach enables clinicians to identify Other Markers
higher risk patients earlier for more aggressive Several other biomarkers continue to be evalu-
anti-ischemic therapy, such as glycoprotein IIb/ ated for their usefulness in providing diagnostic
IIIa inhibitors [11]. or prognostic information in ACS. Most require
The results of biomarkers are often delayed beyond further study and validation before they can be used
the recommended 30 to 60 minutes. Review of in the clinical setting. B-type natriuretic peptide
data on 1,340 patients indicated that the mean (BNP) and N-terminal proBNP have shown the
time from arrival in the emergency department most promise in providing prognostic information.
to notification of the treating physician with These markers have demonstrated strong predic-
biomarker results was 115.7 minutes [31]. Bedside tive value for short-term and long-term mortality
testing with point-of-care biomarker assays offer for patients with UA/NSTEMI and patients with
time advantages, but such systems have not been STEMI [215; 216]. On the basis of these findings,
widely accepted [11; 31]. The disadvantages of the ACC/AHA guidelines note that it is reason-
point-of-care systems include the need for stringent able to consider the use of BNP or N-terminal
quality control, higher costs, need for training of proBNP to aid in assessing risk [11].
emergency department staff in the use of the sys- patient History
tems, and the lack of capability for quantitative
results [11]. Initiatives to improve the laboratory In addition to chest pain assessment and immediate
turnaround time are needed to help ensure more diagnostic testing with ECG and serum biomarkers,
timely delivery of results. the ACC/AHA practice guidelines recommend a
carefully taken history and physical examination
Myoglobin [11].
Myoglobin is a low-molecular-weight protein found A carefully taken patient history is essential to
in cardiac and skeletal muscle. Increased levels of elicit the details needed to make an accurate
myoglobin can be detected as early as 1 to 4 hours diagnosis. The medical history should focus not
after myocardial damage, earlier than either the only on the type of pain the individual is having
cardiac troponins or CK-MB. Myoglobin has been but also on risk factors that may predispose the
shown to have a significantly better negative pre- patient to ACS. Information to obtain includes
dictive value within the first 6 hours after symptom [11; 12; 87; 145]:
onset than either CK-MB or troponin T [214]. If
the myoglobin level is normal within this time- • Time symptoms began
frame, an acute MI can be ruled out [214]. How- • Identification of contraindications
ever, if the initial level is elevated and the ECG to potential treatment measures
is nondiagnostic, an MI should not be assumed; a • Medications the patient is currently taking
more cardiac-specific biomarker should be mea- • Allergies
sured [11]. Serial determinations of myoglobin are
• Risk factors for CAD
not useful for diagnosing MI, as the level returns
to normal after less than 24 hours [11]. • History of previous admissions for chest
pain or ACS
The ACC/AHA guidelines state that it is reason-
• Past history of intervention for CAD/
able to use myoglobin in conjunction with another
ACS, including percutaneous coronary
marker, such as CK-MB or troponin, to rule out
intervention (PCI) and coronary artery
MI earlier in patients who are evaluated within 6
bypass graft (CABG) surgery
hours after the onset of symptoms [11].
• Known cerebral vascular or peripheral
vascular disease
Research has shown that a history of traditional Considerations for Non-
cardiac risk factors varies among some subgroups. English Proficient Patients
Women with ACS are more likely than men to Given the importance of the patient’s history in
have a history of diabetes, hypertension, or hyper- determining a diagnosis of ACS, accurate com-
lipidemia [44; 62; 64; 181]. It has been suggested munication between the patient and healthcare
that this is due to the fact that women tend to providers is essential. However, language and cul-
develop ACS at a older age. [181]. Women are less tural barriers between patient/patient’s family and
likely to be smokers, to have a history of angina or healthcare team can make effective communica-
MI, and to have had PCI or CABG, regardless of tion difficult. Results of a London study identified
the cardiac history [44; 65; 182]. Data on the preva- significant obstacles to communication for most
lence of risk factors across racial/ethnic subgroups patients with ACS who were of Afro-Caribbean or
with ACS was reported in 2008 (Table 6) [66]. South East Asian descent [146]. The three primary
The five most important history-related factors communication-related barriers to appropriate
that relate to the likelihood of ischemia due to care were leading questions to define chest pain,
CAD are (in order of importance) [183; 184; 185; patient-clinician conflict related to poor commu-
186; 187]: nication, and frank miscommunication as a result
of language barriers and translational difficulties
• Nature of the chest pain [146].
• History of CAD
According to the U.S. Census Bureau, more than
• Sex/gender 34 million Americans are foreign-born and 23 mil-
• Age lion of these Americans have limited English pro-
• Number of traditional risk factors ficiency [147]. It has been suggested that patients
should be asked what language is spoken at home
Among patients who have no pre-existing CAD,
and if they speak English “very well” [148]. In addi-
older age seems to be the most important factor
tion, patients should also be asked what language
related to a diagnosis of ACS. An age of older than
they prefer for their medical care information, as
55 years for men or older than 65 years for women
some patients prefer their native language even
has been shown to be more important than all
though they can understand and discuss symptoms
other factors [186; 187].
in English [148].
RISK FACTORS FOR CORONARY ARTERY DISEASE (CAD) ACCORDING TO

RACE/ETHNICITY AMONG PATIENTS WITH ACUTE CORONARY SYNDROME
Patient White Black Hispanic Native Asian
Characteristics American
Average age 63.9 years ±13 59.4 years ±13 61.3 years ±13 58.7 years ±12 63.7 years ±12
Female gender 38% 50.2% 39.1% 37.6% 39.4%
Risk Factors
Family history of CAD 42.2% 37.8% 37.3% 41.6% 28.2%
Hypertension 68.6% 81.3% 71.0% 70.2% 74.9%
Diabetes 27.7% 40.1% 44.1% 53.7% 37.2%
Current smoker 25.8% 30.7% 21.8% 38.2% 16.1%
Source: [66] Table 6

Many studies have demonstrated that the lack of an • Neurologic evaluation
interpreter for patients with limited English profi- • Evaluation for signs of cardiogenic shock
ciency compromises the quality of care [149; 150]. (hypotension and organ hypoperfusion)
In addition, the use of professional interpreters is • Identification of contraindications
associated with improvements in communication to antiplatelet or fibrinolytic therapy
(errors and comprehension), healthcare utilization,
clinical outcomes, and patient satisfaction with The presence of bruits or pulse deficits (which
care [149; 151]. “Ad hoc” interpreters (untrained would suggest extracardiac vascular disease) is
staff members, family members, friends, or strang- associated with a higher likelihood of significant
ers in the hospital) are often used instead of CAD [11]. Similarly, significant CAD is more likely
professional interpreters for a variety of reasons, in a patient who has an S3 or S4 gallop, a new
including convenience and cost. However, clinical mitral insufficiency murmur, or signs of congestive
consequences are more likely with ad hoc inter- heart failure (pulmonary rales and elevated jugu-
preters than with professional interpreters [153]. A lar venous pressures) [133]. Cardiogenic shock is
systematic review of the literature has shown that associated more often with STEMI than NSTEMI,
the use of professional interpreters provides better and mortality rates are high [11]. Contraindications
clinical care than the use of ad hoc interpreters, to antiplatelet or fibrinolytic therapy include any
with the former improving the quality of care for prior intracranial hemorrhage, known malignant
patients with limited English language skills to a intracranial neoplasm, suspected aortic dissection,
level equal to that for patients with no language active bleeding or bleeding diathesis (excluding
barriers [151]. In addition, individuals with limited menses), or significant closed-head or facial trauma
English language skills have indicated a preference within the previous 3 months [12].
for professional interpreters rather than family
Imaging Studies
members [154].
Imaging studies are emerging as an important com-
Physical Examination ponent of evaluation of patients with chest pain.
Most often, the physical examination is normal for
Chest X-Ray
patients being evaluated for possible ACS. Thus,
for these patients the physical examination is A portable chest x-ray is a class I recommendation
important not to establish a diagnosis of ACS but in the ACC/AHA guidelines for the diagnosis of
rather to rule out an alternate diagnosis, identify UA/NSTEMI [11]. Chest x-ray is used primar-
any comorbidities that may have an impact on ily to rule out other causes of chest pain, such as
treatment decisions, and add prognostic informa- pulmonary embolus, aortic dissection, and cardio-
tion [11; 12; 159]. Ruling out a noncardiac cause myopathy [57; 159].
of chest pain is especially important given the Echocardiography
severity of other possible causes of chest pain [12;
In the ACC/AHA/American Society of Echocar-
62; 133; 137; 159].
diography guidelines, echocardiography is a class I
The physical examination should include [11]: recommendation for patients with chest pain and
• Evaluation of vital signs suspected ACS when the baseline ECG and bio-
markers are nondiagnostic [19]. The guidelines sug-
• Determination of the presence of stroke,
gest that the test be done while the patient is hav-
pulses, and jugular venous distention
ing pain or within minutes after pain has subsided.
• Pulmonary auscultation for rales [159]. The strengths of echocardiography are its
• Cardiac auscultation for murmurs ability to assess myocardial thickness, thickening,
and gallops and motion at rest, and it can aid in risk stratifica-
tion of patients with suspected UA/NSTEMI [57].
Transient segmental wall motion abnormalities Because patients must be physically able to walk
that normalize with treatment support a diagnosis on the treadmill, this test is contraindicated for
of UA [19]. Persistent wall motion abnormalities anyone who cannot do so. Chemical stress tests
indicate more severe, chronic ischemia and a may be used instead. Consumption of caffeine or
higher risk of adverse events [217]. Echocardiog- cigarette smoking is contraindicated for several
raphy is also useful for assessing left ventricular hours prior to the test. Patients should be instructed
function before angiography [217]. The ACC/ to wear comfortable clothes and shoes appropriate
AHA guidelines for STEMI note that it is reason- for walking on a treadmill; female patients should
able to use portable echocardiography to clarify a be directed to wear a bra that provides adequate
diagnosis of STEMI and to aid in risk stratification support. Echocardiogram imaging may be added
[12]. The disadvantages of echocardiography are its to an exercise stress test to provide information
inability to distinguish between acute and chronic about the presence or absence of heart wall abnor-
abnormalities and the need for skilled technicians malities. If echocardiography is included, a baseline
and interpreters of results [159]. test will be performed prior to the exercise part of
the test. Immediately following the conclusion of
Cardiac MRI the treadmill portion, the echocardiogram will be
Cardiac MRI has been validated for assessing repeated [85; 86; 87].
myocardial function and has a similar capability to
Diagnostic findings from an exercise stress include
echocardiography in the diagnosis of MI [159]. The
[85; 86; 87]:
usefulness of MRI in this setting was studied in 161
consecutive patients who had 30 minutes of chest • Negative: The patient achieves the target
pain and ECG findings that were nondiagnostic heart rate with no symptoms of ischemia.
of acute MI. MRI that included perfusion, left No evidence of new heart wall motion
ventricular function, and gadolinium-enhanced abnormalities are noted on echocardiogram.
MI detection was shown to have a sensitivity • Positive: The patient develops symptoms
and specificity of 84% and 85%, respectively, for of ischemia during the test. New heart
diagnosing ACS [218]. MRI is not generally used wall motion abnormalities are evident in
in the acute setting because of the inconvenience the echocardiogram completed after the
of its use [57]. treadmill portion of the test. Follow-up
testing, usually cardiac catheterization,
Stress Tests
is indicated.
Exercise Stress Test • Equivocal: The patient develops symptoms
Used to evaluate the effects of stress on the heart during the test that are not directly linked
muscle and coronary blood flow, an exercise stress to myocardial ischemia, or the patient is
test involves some type of physical exercise. Walk- unable to achieve the target heart rate but
ing on a treadmill is a common method. Following has no symptoms of ischemia. Additional
a predetermined protocol, the speed of the tread- testing is indicated.
mill and its angle are increased at set intervals. The
patient’s ECG and blood pressure are monitored. Adenosine Thallium Test
The test is terminated when a target heart rate is Combining a chemical stress test with radionuclide
achieved or the patient develops symptoms such imaging, an adenosine thallium test evaluates the
as chest pain, hypotension, bradycardia, severe blood supply to the myocardium. This test may be
hypertension, or ST-segment changes on ECG. performed in two parts. The patient is kept NPO for
4 to 6 hours prior to the start of the test. Adenos-
ine is injected to increase heart rate, myocardial

contractility, and myocardial oxygen demand. • The Thrombolysis in Myocardial
Radioactive thallium is injected, and a series of Infarction (TIMI) risk score
images are taken to assess the adequacy of blood • The GRACE risk model
flow to the myocardium. Several hours later, the • The Platelet Glycoprotein IIb/IIIa in
patient is again scanned to evaluate blood flow to Unstable Angina: Receptor Suppression
the myocardium at rest. Adenosine thallium scans Using Integrilin Therapy (PURSUIT)
may identify site(s) of old infarctions, areas of par- model
tial obstruction of blood flow to the myocardium,
and areas where blood flow (perfusion) decreases The TIMI risk score is based on seven independent
during exercise [85; 86; 87]. risk factors [221]:
Dobutamine Stress Echocardiogram (DSE) • Advanced age (65 years or older)

A DSE test may be utilized to evaluate the heart’s • At least three risk factors for CAD
response to stress in patients who are unable to • Previous coronary artery stenosis
physically perform a treadmill exercise test. This of 50% or more
test uses IV dobutamine to “stress” the heart by • ST-segment deviation on initial ECG
increasing myocardial contractility and heart • At least two episodes of angina in the
rate, which in turn increases myocardial oxygen past 24 hours
demands. Echocardiogram imaging is done when
• Use of aspirin in the past 7 days
the patient is at rest and after the dobutamine has
been injected to look for wall motion abnormali- • Elevated levels of cardiac biomarkers
ties [85; 86; 87]. Briefly, a TIMI score is calculated by assigning
Results may be: points for each variable and adding up the score.
The higher the score, the greater the risk of death,
• Negative: The patient’s heart rate reaches reinfarction, or recurrence of severe ischemia
the target rate, and the patient shows no requiring urgent revascularization. The TIMI
symptoms of ischemia. Echocardiogram risk score has been validated in several studies,
imaging shows no new heart wall motion including one involving an unselected population
abnormalities. of patients with chest pain seen in the emergency
• Positive: The patient develops symptoms department [11]. A TIMI risk calculator can be
before reaching the target heart rate and/ accessed online at http://www.timi.org.
or new heart wall motion abnormalities are
Additionally, risk scores may be used in determin-
seen on Echocardiogram. Follow-up testing,
ing the prognosis for patients with STEMI to help
usually a cardiac catheterization, is indicated.
clinicians assess the possible harm and benefit of
Comprehensive Risk potential therapies. Risk assessment is discussed
Score and Prognosis in the ACC/AHA guidelines for the management
Risk stratification is an integral component of diag- of STEMI but without a stated recommendation
nosis, especially for patients with UA/NSTEMI. [12]. The TIMI risk score has been validated in a
The risk of cardiac death and ischemic events population of patients with STEMI.
varies widely in the UA/NSTEMI population, and
prognosis can help inform decision making regard-
ing treatment [11]. The ACC/AHA guidelines for
UA/NSTEMI recommend risk stratification and
note three risk prediction models [11]:
Final Diagnosis Patients who are considered to be at intermediate
Four diagnoses are possible after complete evalua- or high risk for adverse outcomes should be admit-
tion for possible ACS [11]: ted to a coronary care or intensive care unit.
• Noncardiac diagnosis
• Chronic stable angina Treatment of UA/NSTEMI
• Possible ACS
In 2007, ACC/AHA published the third update of
• Definite ACS their guidelines for UA/NSTEMI treatment [234;
ACC/AHA guidelines recommend that patients 235; 236]. According to data from several studies
with chronic stable angina should be treated and quality improvement initiatives, adherence to
according to the ACC/AHA guidelines [11; 233]. ACC/AHA guidelines for the treatment of UA/
Patients with possible ACS should be transferred NSTEMI has been suboptimal, with the use of
to a chest pain or similar type unit where they can recommended acute drugs ranging from 20% to
continue to be evaluated with serial monitoring 96% [21; 22; 23; 27; 29; 30; 32; 33; 34; 36; 38; 203].
of biomarker levels and ECG. Critical pathways However, adherence has increased since the early
or protocols are used to aid in decision making 2000s [30; 36]. While these increases are promising,
regarding the diagnosis, and it is recommended the overall rates of adherence indicate that con-
that a decision be made in 6 to 12 hours [11]. If a tinued improvement is needed [30]. Studies have
patient has no recurrent pain and biomarkers and also shown that adherence rates vary according to
ECG findings continue to be nondiagnostic, a diagnosis, age, gender, race, and clinical setting,
stress study may be done [11]. The patient should with lower rates for UA/NSTEMI (compared with
be admitted to the hospital for further treatment STEMI), low-risk patients (compared with high-
if the findings are positive and may be discharged risk patients), older patients, women, and racial/
if they are negative. Patients who are discharged ethnic minority populations [5; 27; 37; 41; 42; 43;
from the emergency department should be told to 44; 45; 46].
see their primary care physician as soon as possible, The need for better adherence to guidelines is
preferably within 72 hours [11]. The results of all emphasized by the finding that outcomes are better
diagnostic testing in the emergency department for patients treated at hospitals with high scores
should be sent to the primary care physician to for providing guideline-based treatment. Review of
ensure continuity of care [11]. data on more than 250,000 patients demonstrated
Patients with definite ACS should be treated that the inpatient mortality for hospitals in the
according to the type of MI. Patients with STEMI leading quartile for guideline-based treatment
should be evaluated for immediate reperfusion (82% adherence) was significantly lower than the
therapy and treated according to the ACC/AHA mortality for hospitals in the lowest quartile (63%
guidelines [12; 13]. Among patients with a diagno- adherence) [33].
sis of confirmed (or suspected) UA/NSTEMI, triage As noted, efforts throughout the healthcare deliv-
is based on the individual patient’s risk. Patients ery system are needed to help improve adherence
with a low likelihood of having ACS should remain to guidelines. Closer coordination of care between
under observation, either in the emergency depart- emergency departments, pharmacy, nursing depart-
ment or in a chest pain unit. Patients with possible ments, imaging facilities, and cardiac catheteriza-
ACS or with definite ACS but nondiagnostic ECG tion laboratory would allow for the development
findings and normal initial cardiac marker levels of institution-specific algorithms and processes.
should be admitted to the hospital with continuous Administrative support, with the commitment of
telemetry monitoring, usually in a stepdown unit. adequate resources, is essential [31]. Standardized

(preprinted) order sheets based on ACC/AHA for patients at risk of hypoxemia. Continuous ECG
guidelines also may be helpful, as they have been monitoring should also be carried out, not only to
shown to lead to a greater number of patients detect ECG changes that may provide additional
treated with appropriate medications in a timely diagnostic and prognostic information but also
fashion [238]. Storing resources such as order sheets because sudden, unexpected ventricular fibrillation
and clinical pathways online offers staff ease of is the primary preventable cause of death during
access [239]. National quality improvement ini- this initial period [11]. Continuous 12-lead ECG
tiatives will help to enhance guideline adherence monitoring is preferred. When available monitor-
by providing feedback on performance, and data ing equipment only permits continuous monitor-
from registries are also providing valuable insight ing of 2 or 3 leads, it is important to monitor the
into guideline-driven treatment and patient out- specific leads most likely to reflect ST-segment
comes. changes for the individual patient [73; 75].
The 2007 ACC/AHA guidelines reflect the Analgesic and
research advances made in ACS since publication Anti-ischemic Therapy
of the previous document in 2002. Many more The goal of immediate treatment for patients
treatment options are now available, and clini-
with UA/NSTEMI is to provide relief of ischemia
cians should be familiar with the choices in order
and to prevent recurrent adverse ischemic events
to select a strategy on the basis of an individual’s [11]. This is initially achieved through anti-isch-
status and preference [240]. The most substantial emic, antiplatelet, and anticoagulant therapies
changes in the updated guidelines relate to the (Table 7).
following issues [240]:
Analgesic and anti-ischemic therapy for UA/
• More aggressive anticoagulant/ NSTEMI involves the use of nitroglycerin, mor-
antiplatelet therapy phine, beta blockers, calcium-channel blockers,
• Selection of a therapeutic strategy and angiotensin-converting enzyme (ACE) inhibi-
(initial invasive or initial conservative) tors. These agents will help alleviate pain through
• Early hospital care related to an initial their mechanisms of action. If patients are taking
conservative strategy cyclo-oxygenase-2 (COX-2) inhibitors or NSAIDs
• Discharge planning and secondary at the time they are evaluated, it is recommended
prevention that these drugs be discontinued immediately due
to the documented increased risk of cardiovascular
General care measures events [11].
The general care of patients with UA/NSTEMI
Nitroglycerin
is directed at the severity of symptoms. Bedrest is
recommended while patients have ischemic pain. Nitroglycerin is a vasodilator that relieves isch-
After symptoms have subsided, patients may move emia-related pain by reducing myocardial oxygen
to a chair. Although there is no evidence to support demand and enhancing oxygen delivery. Nitro-
the use of supplemental oxygen, the guidelines note glycerin can be given as either sublingual tablets
that it is reasonable to provide routine supplemen- or buccal spray every 5 minutes for three doses.
tal oxygen while the patient is stabilizing [11]. Fin- Nitroglycerin is contraindicated in patients who
ger pulse oximetry is not necessary but can be useful have taken sildenafil (Viagra) within the last 24
hours.
ADJUNCTIVE TREATMENT FOR PATIENTS WITH UNSTABLE ANGINA/

NON-ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (UA/NSTEMI) OR STEMI
Adjunctive UA/NSTEMI STEMI Comments
Therapy Indication Dose Indication Dose
Analgesia
Nitroglycerin All patients 0.4 mg sublingual All patients Same as for Contraindicated
(class IC) or buccal spray, (class IC) NSTEMI for patients with
every 5 min (X 3) hypotension or who
All patients 10 µg/min IV, All patients Same as for have used sildenafil
(class IB) increased by 10 µg/ (class IC) NSTEMI or tadalafil within
min every 3 to 5 previous 24 or 48
min until relief hr, respectively
Morphine Reasonable for 1–5 mg IV every Patients who 2–4 mg IV; may be --
patients who 5 to 30 min; may have chest pain increased 2–8 mg
have chest pain be repeated every unrelieved by IV at 5 to 15 min
unrelieved by 5 to 30 min nitroglycerin
nitroglycerin (class IC)
(class IIa)
Anti-ischemia Therapy
Beta blocker All patients, unless Propranolol: 20–80 All patients, unless Same as for Contraindicated
(propranolol, contraindicated mg PO, twice daily contraindicated NSTEMI for patients with
metoprolol, (class IB) Metoprolol: 50–200 (class IB) signs of heart
atenolol) mg PO, twice daily failure, evidence of
Atenolol: 50–200 low-output state,
mg PO, twice daily or increased risk of
cardiogenic shock
Angiotensin- Patients intolerant Captopril: 6.2 mg Patients intolerant Same as for Contraindicated
converting of beta blockers; PO, with dose of beta blockers; NSTEMI for patients with
enzyme (ACE) patients with increased steadily patients with hypotension
inhibitor pulmonary to full dose pulmonary (systolic blood
(captopril, congestion or left (50 mg twice daily) congestion or left pressure of <100
enalapril, ventricular ejection within 24 to 48 hr ventricular ejection mm Hg or <30 mm
lisinopril) fraction 0.40 fraction 0.40 Hg below baseline).
(class IC) (class IA) An angiotensin
receptor blocker
should be used for
patients intolerant
of ACE inhibitors.
Calcium- Patients intolerant Verapamil: 80–160 Reasonable for -- --
channel of adequate doses of mg 3 times daily patients in whom
blocker nitroglycerin and/ (immediate release) beta blockers are
(verapamil, or beta blockers; or 120–480 mg ineffective or
diltiazem) patients in whom daily (slow release) contraindicated
beta blockers are Diltiazem: 30–90 (verapamil
contraindicated mg 4 times daily or diltiazem)
(class IB) (immediate release) (class IIa C)
or 120–360 mg
daily (slow release)
Table 7 continues on next page.


NON-ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (UA/NSTEMI) OR STEMI (Continued)
Antiplatelet Therapy
Aspirin All patients 162–325 mg All patients Same as for Should be given as
(class IA) PO, followed by (class IA) NSTEMI soon as possible at
75–162 mg PO time of evaluation.
daily, continued Contraindicated for
indefinitely patients who have
aspirin allergy or
active bleeding.
Clopidogrel All patients Clopidogrel: All patients (in Same as for Should be
(class IA) loading dose of addition to aspirin), NSTEMI, withheld for 5 days
300 mg PO, regardless of with daily dose (preferably 7 days)
followed by 75 mg reperfusion strategy continued for at in patients
daily, continued for (class IA) least 14 days to have CABG
at least 1 mos and (class IB), up to
preferably up to 1 yr 1 yr (class IIa C)
Glycoprotein Patients selected Abciximab: 0.25 Reasonable for -- The rate of
IIb/IIIa inhibitor for early invasive mg/kg IV, followed patients to have IV infusion of
(abciximab, treatment, given by 0.125 µg/kg/min abciximab before eptifibatide or
eptifibatide, before diagnostic Eptifibatide: loading primary PCI tirofiban should
tirofiban) angiography dose of 180 µg/kg (class IIa B); be reduced by 50%
(class IA); IV bolus, followed eptifibatide or for patients with
eptifibatide or by 2.0 µg/kg/min tirofiban may also estimated creatinine
tirofiban is the as IV infusion be considered clearance
preferred agent, Tirofiban: loading before primary <50 mL/min
with abciximab dose of 0.4 µg/kg/ PCI (class IIb C);
used only if min as IV infusion abciximab may
there is no over 30 min, be considered for
appreciable delay followed by 0.1 patients who have
to angiography µg/kg/min IV fibrinolytic therapy
and PCI is likely infusion (class IIb A)
to be performed
(class IB); may
be considered for
patients selected
for conservative
treatment
(class IIb B)
Anticoagulant Therapy
Unfractionated Option for patients Loading dose: Option for patients Same as for The UFH dose
heparin (UFH) selected for early 60 U/kg (max: selected for primary NSTEMI; given should be reduced
invasive treatment 4,000 U) IV bolus, PCI (class IC) or for minimum of 48 when a glycoprotein
(class IA) and followed by 12 U/ fibrinolytic therapy hr, preferably for IIb/IIIa inhibitor is
early conservative kg/hr (max: 1,000 (class IC) duration of index also given
treatment U/hr) to maintain hospitalization
(class IA) activated partial
thromboplastin
time at 1.5 to
2.0 times control
(approximately 50
to 70 sec), usually
given for 2 to 5 days
Table 7 continues on next page.

NON-ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (UA/NSTEMI) OR STEMI (Continued)
Anticoagulant Therapy (Continued)
Low-molecular- Option for patients Loading dose Option for patients 30 mg IV bolus, --
weight heparin selected for early (30 mg IV bolus) selected for followed by 1 mg/kg
(LMWH) invasive treatment may be given, fibrinolytic therapy SC every 12 hr for
(enoxaparin) (class IA) and followed by 1 mg/kg (class IA) duration of index
early conservative SC every 12 hr hospitalization
treatment (up to 8 days)
(class IA);
preferred agent
for conservative
approach
(class IIa B)
Direct thrombin Option for patients 0.1 mg/kg IV Reasonable as -- --
inhibitor selected for early bolus, followed by an alternative
(bivalirudin) invasive treatment 0.25 mg/kg/hr IV to heparin for
(class IB) infusion patients with
known heparin-
induced thrombo-
cytopenia
(class IIa B)
Factor Xa Option for patients 2.5 mg SC daily Option for patients 2.5 mg IV, Avoid for creatinine
inhibitor selected for early selected for followed by 2.5 clearance less
(fondaparinux) invasive treatment fibrinolytic therapy mg SC daily for than 30 mL/min
(class IB) and (class IB) duration of index
early conservative hospitalization
treatment (IB); (up to 8 days)
preferred agent
for conservative
approach
(class IIa B)
Source: [11; 12; 13] Table 7
SIZE OF TREATMENT EFFECT FOR RECOMMENDED INTERVENTIONS

Class Predicted Treatment Effect
I Benefit >>> Risk
Procedure/treatment should be performed/ administered.
IIa Benefit >> Risk (Additional studies with focused objectives needed)
It is reasonable to perform procedure/ administer treatment.
IIb Benefit > Risk (Additional studies with broad objectives needed; additional registry data would be helpful)
Procedure/treatment may be considered.
III Risk > Benefit
Procedure/treatment should not be performed/ administered since it is not helpful and may be harmful.
LEVEL OF EVIDENCE
Level Supporting Evidence
A Multiple randomized trials or meta-analyses
B Single randomized trial or nonrandomized studies
C Expert opinion, case studies, or standard-of-care

Patient A was admitted from the emergency department After a single nitroglycerin tablet, Patient A reported
to an inpatient telemetry/stepdown unit with a diagnosis that his chest pain has dropped to 4 on a scale of 10,
of ACS. Both the patient’s initial cardiac biomarkers and his blood pressure remained slightly elevated.
and initial ECGs were negative for indications of MI. Ongoing chest pain indicates continuing ischemia.
However, because his initial symptoms (increased If the patient’s blood pressure has not dropped
severity of chest pain, chest pain at rest) coupled with significantly, a second nitroglycerin tablet should
his history of PCI 6 months ago for an occlusion in his be given. If the patient becomes hypotensive from
right coronary artery are highly suspicious for ACS, the the first dose, no additional doses should be given
physician admitted him for on-going observation and and the physician should be notified. Morphine,
monitoring. A few hours after admission to the inpa- if ordered, may be given as another drug of choice
tient unit, Patient A experienced a chest pain attack at to relieve chest pain. If the patient’s chest pain
rest. He described the pain simply as “bad,” 10/10 on drops to 0 after the second nitroglycerin tablet,
the pain scale, and located in the left substernal area no additional tablets are indicated. However, if
of his chest. His admitting medical orders included the patient’s pain persists (even at a low level)
nitroglycerin, 1 tab sublingually every 5 minutes for and blood pressure remains stable, a third tablet
chest pain, which may be repeated every 5 minutes to should be given.
a total of 3 doses as needed. The nurse obtained an
ECG and notified the physician. Per physician orders, an ECG should be obtained if
Patient A has chest pain. Ideally, the ECG would
In this case example, the patient’s chest pain is be taken while the patient is still having chest
characteristic of ischemic chest pain: its intensity pain. Clinically significant signs of myocardial
is “severe,” it is located in the left substernal area ischemia, such as ST depression and T-wave inver-
of his chest, and it occurred at rest. The immedi- sion, may be seen on 12-lead ECG during chest
ate response should be to check Patient A’s vital pain episodes.
signs and to administer sublingual nitroglycerin
as ordered. A major side effect of nitroglycerin is severe head-
ache. Orders for acetaminophen may be effective
Administering Nitroglycerin in reducing the patient’s headache. However, some
Prior to administering sublingual nitroglycerin, patients will decline further nitroglycerin therapy
the patient’s blood pressure should be checked. If due to the discomfort of the associated headache.
the patient is hypotensive, sublingual nitroglycerin The patient’s physician should be notified if the
should not be administered and the physician patient is having chest pain and refusing nitro-
should be notified. Intravenous morphine may be glycerin.
ordered for pain relief instead. If the patient’s blood
After administration of two sublingual nitroglycerin
pressure is normal or elevated, sublingual nitroglyc- tablets, Patient A’s chest pain was relieved. He reported
erin may administered as follows [73; 87; 88]: that he was chest pain free. One hour later, he again
• Obtain an initial pain rating for the developed chest pain and required a third sublingual
patient’s chest pain. nitroglycerin tablet for relief. His blood pressure was
• Administer 1 sublingual nitroglycerin elevated during this attack; when his pain was relieved,
tablet. The tablet should produce a mild his blood pressure returned to his baseline normal. Less
burning sensation under the tongue. than one hour later, Patient A developed a third bout of
chest pain. He rated the pain as 10/10, and his blood
• Wait 5 minutes, then recheck the patient’s
pressure increased to 190/120 mm Hg. Three sublin-
vital signs and chest pain intensity.
gual nitroglycerin tablets again reduced his chest pain to
• Carefully document the episode, including 0 and his blood pressure decreased to baseline. Because
pain ratings, vital signs, and medications the chest pain episodes are increasing in frequency and
administered, in the appropriate part of intensity, the physician decided to initiate a continuous
the patient’s medical record. nitroglycerin drip.
The AHA/ACC guidelines note that if pain is not relieve symptoms. If morphine is used in conjunc-
relieved, continuous intravenous nitroglycerin may tion with intravenous nitroglycerin, the patient’s
be started. If ischemia recurs, the rate of infusion blood pressure should be closely monitored, as
may be increased until symptoms are relieved. hypotension is a potential adverse effect, especially
The administration of intravenous nitroglycerin for patients who have volume depletion. Caution
should be discontinued within 24 hours after the should be used when administering morphine to
patient’s condition has stabilized, at which point elderly persons or persons with impaired renal
oral nitroglycerin can be given. Discontinuation of function [88].
intravenous nitroglycerin should be gradual, as the
abrupt cessation has been associated with exacerba- Beta Blockers
tion of ischemic changes on ECG [11]. The inhibition of beta-1 adrenergic receptors by
beta blockers acts to decrease cardiac work and
Depending on the hospital’s policy and proce- myocardial oxygen demand. Beta blockers also
dure, nitroglycerin may be ordered in micrograms slow the heart rate, which helps enhance coronary
per minute or as a weight-based calculation (i.e., blood flow. A beta blocker should be given orally to
micrograms per kg per minute). The physician’s all ACS patients (unless contraindicated) within
order should specify the starting dose and rate, the
24 hours of presentation [11]. Use of beta blockers
maximum dose and rate, and whether or not the
in general is contraindicated in persons who have
infusion can be increased until the patient is chest heart failure, low-output state, increased risk of
pain free, the maximum dose has been achieved, or cardiogenic shock, or other relative contraindica-
the patient becomes hypotensive. Nursing respon- tions to beta blockade. Metoprolol, propranolol,
sibilities include [73; 87; 88]. or atenolol have been the typical choices as initial
• Monitoring the patient’s blood pressure therapy [11]. A beta blocker can be given intrave-
frequently while increasing/titrating the nously for patients who have ongoing chest pain,
infusion especially if hypertension or tachycardia is present
• Maintaining the patient on continuous [11].
ECG monitoring Patient A continued to experience severe chest pain;
• Monitoring the effect of the nitroglycerin initiation and titration of the nitroglycerin infusion to
on the patient’s chest pain higher doses did not relieve his pain. ECG showed ST
• Notifying the physician if the patient depression in the inferior leads, and his most recent
becomes hypotensive cardiac biomarkers indicated that his CK-MB levels
were positive for myocardial damage. The troponin
• Notifying the physician if the maximum
level remained within normal limits. The physician
specified dose is reached and the
was notified and ordered morphine 2 mg. Patient A
patient continues to have chest pain
remained hypertensive, and his chest pain persisted at
Morphine a lower intensity (5/10). The physician ordered 5 mg
The strength of the recommendation for the use of IV of metoprolol to be administered immediately and
morphine for chest pain relief was downgraded in 25 mg metoprolol to be taken by mouth twice a day.
the ACC/AHA guidelines after review of data indi- Nursing responsibilities in the administration of
cated a higher adjusted risk of in-hospital mortality IV metoprolol include maintaining the patient on
[241]. The updated guidelines state that morphine continuous ECG monitoring; monitoring blood
is reasonable for patients who do not have relief pressure before, during, and after administration;
of ischemia-related symptoms after three doses of and monitoring heart rate and rhythm before, dur-
nitroglycerin or for patients who have recurrence of ing, and after administration. Contraindications to
symptoms during anti-ischemic therapy. Morphine metoprolol (or other beta blocker) administration
can be given every 5 to 30 minutes as needed to include bradycardia and hypotension [88].

Calcium-Channel Blockers ACE Inhibitors
Calcium-channel blockers act to inhibit contrac- The 2007 ACC/AHA guidelines for the manage-
tion of myocardial and smooth muscle and cause ment of UA/NSTEMI include new recommenda-
vasodilation, although the agents in this drug class tions for the use of ACE inhibitors. According
vary in the degree of vasodilation and myocardial to the guidelines, an ACE inhibitor should be
contractility they produce [11]. Their ability to administered orally within the first 24 hours to
relieve (or prevent) signs and symptoms of isch- patients who have pulmonary congestion or a
emia has been found to be similar to that of beta left ventricular ejection fraction of 0.40 or less,
blockers [11]. provided that the patient does not have hypoten-
sion (systolic blood pressure less than 100 mm Hg
The strongest evidence for a benefit of calcium-
or more than 30 mm Hg below baseline) or any
channel blockers in the setting of UA/NSTEMI
known contraindications to this class of agents
primarily relates to symptom control [11]. Calcium-
[11]. The guidelines also note that an angiotensin-
channel blockers are indicated in UA/NSTEMI
receptor blocker (ARB) should be given to patients
patients with [11]:
who cannot tolerate an ACE inhibitor and have
• Ongoing or recurring ischemia-related either clinical or radiographic signs of heart fail-
symptoms despite adequate doses ure or left ventricular ejection fraction of 0.40 or
of nitroglycerin and beta blockers less. The benefits of ACE inhibitors have been
• Intolerance of adequate doses demonstrated primarily in the long-term setting
of nitroglycerin or beta blockers after MI, with significant reductions in adverse
• Variant angina outcomes, including mortality and hospitalizations
[244; 245]. Examples of ACE inhibitors include
The four agents used most commonly are nife- lisinopril and ramipril.
dipine, amlodipine, verapamil, and diltiazem.
Although there are limited data on comparisons When administering ACE inhibitors, the following
of these four drugs, verapamil and diltiazem are nursing actions should be taken [88]:
recommended because of their heart-rate-lowering • Monitor blood pressure for hypotension.
effects [11]. However, because of that effect, they Be alert for orthostatic hypotension
should not be used for patients who have severe and syncope.
left ventricular dysfunction or pulmonary edema • Implement fall precautions as indicated
[11]. by patient status.
Nursing responsibilities when administering cal- • Monitor serum potassium levels and
cium-channel blockers include monitoring heart renal function studies; elevated serum
rate and blood pressure prior to administering the potassium levels or increasing signs of renal
medication. In some patients, calcium-channel insufficiency/failure can be an indication
blockers may cause hypotension and bradycardia. that the medication should be discontinued.
Special caution should be taken if the patient is • Monitor for the development of intolerable
taking other medications, such as ACE inhibi- side effects. A common and often fatiguing
tors, that can lower blood pressure. Especially in side effect is a dry, nagging cough.
the elderly, use of multiple medications will have
an additive effect and will be more likely to cause ARBs such as valsartan and candesarten may
hypotension, orthostatic hypotension, and an be prescribed for persons who cannot tolerate
increased risk of falls [88]. ACE inhibitors [55]. When administering ARBs,
the nurse should monitor serum electrolytes,
renal function studies, and vital signs, especially
blood pressure [88]. Hypotension and orthostatic
hypotension may result.
Antiplatelet Therapy Clopidogrel
Aspirin continues to be a key element in the Clopidogrel inhibits platelet activation. Its mecha-
treatment of patients with UA/NSTEMI as part nism of action is different from that of aspirin,
of overall antithrombotic therapy. Antiplatelet and its effects are not manifested for several days
therapy reduces platelet formation and aggregation, when a loading dose is not given. Clopidogrel was
integral components in the formation of a throm- approved by the U.S. Food and Drug Administra-
bus after plaque disruption. Antiplatelet therapy tion (FDA) in 2002 on the basis of the findings
includes the use of aspirin and a thienopyridine of the Clopidogrel in Unstable Angina to Pre-
(clopidogrel or ticlopidine). vent Recurrent Events (CURE) trial, in which
12,562 patients with UA/NSTEMI were randomly
Aspirin assigned to treatment with aspirin with or without
The ACC/AHA guidelines recommend that clopidogrel (loading dose of 300 mg followed by
aspirin be given as soon as possible after a patient 75 mg daily) and followed up for 3 to 12 months,
arrives in the emergency department if he or she regardless of the treatment strategy used [251]. The
has not taken aspirin before arrival [11]. Aspirin risk of cardiovascular-related death, MI, or stroke
is contraindicated for patients who are allergic to was significantly lower for patients who received
the drug or who have active bleeding; clopidogrel clopidogrel. The results were similar in many sub-
is recommended for patients who cannot tolerate groups of patients.
aspirin. In several studies in the late 1980s and
Clopidogrel has also been found to offer benefit to
early 1990s, aspirin (at an initial dose of 62–325
patients who will have an early invasive strategy.
mg followed by a daily dose of 81–162 mg) led to
A substudy of the CURE trial showed that clopi-
a 70% reduction in the risk of MI during the acute
dogrel with aspirin led to a relative risk reduction
phase and a 50% to 60% reduction at 3 months to
(compared with aspirin alone) of 30% in a com-
3 years [246; 247; 248; 249].
posite endpoint of cardiovascular-related death
and nonfatal MI for patients who had PCI [252].
Aspirin should be administered to UA/ Similarly, in the Clopidogrel for the Reduction
NSTEMI patients as soon as possible of Events During Observation (CREDO) trial,
after hospital presentation and continued
the risk of a composite endpoint (death, MI, or
indefinitely in patients not known to be
intolerant of that medication. stroke) at 1 year after PCI was significantly lower
(http://www.guidelines.gov/
for patients who received clopidogrel before the
summary/summary.aspx?doc_id=11333. procedure, with a relative risk reduction of 26.9%
Last accessed October 21, 2010.) compared to aspirin alone [169].
Strength of Recommendation/Level of Evidence: Some questions about clopidogrel in the acute care
IA (Treatment should be administered based on the
evaluation of multiple population risk strata.)
setting remain unanswered. The optimal load-
ing dose has not been firmly established, but the
approved loading dose (300 mg) is the one most
often used [11]. Higher doses (600 mg) are under
Adherence to the recommended use of aspirin
study. The optimal timing of clopidogrel before PCI
has been better than for other drug therapies for
has not been established, nor has the duration of
patients with UA/NSTEMI, with approximately
treatment after PCI been determined [243]. In the
85% to 96% of patients receiving aspirin within
CREDO study, the timing of clopidogrel before PCI
24 hours after presentation [5; 24; 27; 30; 31; 37;
varied widely (from 3 to 24 hours) [169]. Although
44; 45]. Most patients (67.4%) who receive aspirin
the use of clopidogrel has increased over the past
are given an initial dose of 325 mg [34].
few years, the drug is still given to only slightly
more than half of patients [5; 24; 27; 30; 31; 37;
44; 45].

The decision to give clopidogrel may also be influ- Glycoprotein IIb/IIIa Inhibitors
enced by anticipated management of the patient’s Potent inhibitors of platelet aggregation, glyco-
coronary disease. If coronary artery bypass surgery protein IIb/IIIa inhibitors may also be used in the
is planned, clopidogrel should be withheld for at treatment of UA/NSTEMI. Three intravenous
least 5 days (7 days preferred) prior to the surgery glycoprotein IIb/IIIa inhibitors have been approved
unless the need for urgent revascularization out- for clinical use: abciximab, eptifibatide, and tiro-
weighs the risks of excess bleeding [12]. However, fiban [11]. In general, major contraindications
clopidogrel, if ordered, should not be discontinued to the use of any glycoprotein IIb/IIIa Inhibitor
unless approved by the prescribing cardiologist. include [67; 68; 69; 88]:
Patient D was scheduled to go to the cardiac cath- • History of bleeding within previous 30 days
eterization laboratory for a left heart catheterization • Severe hypertension (systolic blood
and probable PCI with stent to treat an obstruction in pressure >200 mm Hg or diastolic blood
the circumflex branch of his left coronary artery. The pressure >110 mm Hg) not adequately
cardiac catheterization laboratory physician’s orders controlled on antihypertensive therapy
specified that Patient D should receive a loading dose
of 300 mg of clopidogrel on call to the catheterization • Major surgery in preceding 6 weeks
laboratory. When the nurse brought the patient the • History of stroke within 30 days or
medication as ordered, he commented, “I know that any history of hemorrhagic stroke
one. They wanted me to take it last year after my last • Current or planned administration
heart attack and stent. But I couldn’t afford it. That of another parenteral glycoprotein
stuff is expensive!” IIb-IIIa inhibitor
In today’s economic climate, the cost of medica- • Known hypersensitivity to any
tions can pose a serious problem for the patient. product component
Patients who are uninsured or underinsured can
Abciximab
find it difficult to afford medications such as clopi-
dogrel. Even patients with “good” insurance can According to the manufacturer’s guidelines and
find co-pay charges too high to manage on their prescribing information, abciximab has been
current budget. Variations in Medicare Part D plans approved for use as adjunct therapy with PCI to
can create confusion and obstacles. Some drug prevent ischemic complications. It is specifically
companies may offer assistance; local hospitals may indicated for patients undergoing PCI and for
also provide assistance through resources such as patients with UA unresponsive to other medical
charity pharmacies. Nurses are in a position to ini- therapies who will undergo PCI within 24 hours
tiate discussion with the patient and family about of the initiation of the infusion. Abciximab is
how they plan to obtain medications after discharge designed to be used in combination with heparin
and can tactfully ask if the patient has any financial and aspirin. Risk of bleeding can be increased with
issues related to obtaining prescribed medications. the use of abciximab, particularly when the patient
If the patient or family indicates a need, a case is also receiving heparin, other anticoagulants, or
manager, discharge planner, or social worker can thrombolytic therapy. Recommendations to reduce
assess financial issues and assist patients/families to the risk of bleeding complications include: use of a
identify available resources. If a patient is unable low-dose, weight-based heparin regimen; discon-
to afford (or is unlikely to adhere to) taking clopi- tinuing heparin when PCI is complete; removal of
dogrel following PCI with stent placement, the the arterial sheath within 6 hours; careful manage-
physician may choose to implant bare-metal stents ment of the vascular access site; and careful patient
(as opposed to drug-eluting stents). The different management and assessment [69].
types of stents will be discussed in detail in a later
section of this course.
Eptifibatide After a bolus dose, an intravenous infusion of
According to the manufacturer’s guidelines and heparin is administered to maintain a targeted
prescribing information, eptifibatide is indicated level of anticoagulation [58]. In the past, the “gold
for patients with UA/NSTEMI who will be man- standard” for monitoring the effectiveness of hepa-
aged medically or who will undergo PCI, including rin was the activated partial thromboplastin time.
those undergoing intracoronary stenting. Risk of However, the use of a new monitoring parameter
bleeding complications is increased with use of known as the anti-factor Xa heparin assay has
eptifibatide [68]. arisen as a possible new standard of care in moni-
toring infusions of unfractionated heparin.
Tirofiban
When glycoprotein IIb/IIIa inhibitors are given
Tirofiban is indicated, in combination with hepa- in combination with heparin, a lower dose of
rin, for the treatment of ACS, including patients heparin is usually prescribed. The optimum dura-
who are to be managed medically and those tion of treatment with unfractionated heparin has
undergoing PCI. Like other glycoprotein IIb/IIIa not been defined, but it is usually given for 2 to 5
inhibitors, there is an increased risk of bleeding, days.
particularly at the arterial puncture site [67].
Low-Molecular-Weight Heparin
Anticoagulant Therapy
Low-molecular-weight heparin offers many phar-
One of the most important updates in the 2007 macologic advantages compared with unfraction-
ACC/AHA guidelines is a recommendation for ated heparin, including [58]:
more aggressive antiplatelet/anticoagulant therapy,
regardless of whether an early invasive or early • More predictable anticoagulant effect
conservative strategy is selected. In this setting, • Lower incidence of heparin-induced
anticoagulant therapy with enoxaparin, unfrac- thrombocytopenia
tionated heparin, bivalirudin, or fondaparinux • Easier to administer
should be initiated as soon as possible after pre-
• Given as a fixed-weight base dose
sentation, with clopidogrel or a glycoprotein IIb/
IIIa given before angiography [11]. For patients Two low-molecular-weight heparins—enoxaparin
who will be treated with an early conservative and dalteparin—are approved by the FDA for the
approach, anticoagulant therapy with enoxaparin, treatment of UA/NSTEMI. Enoxaparin has been
unfractionated heparin, or fondaparinux should be studied the most, and it has been shown to offer
added to antiplatelet therapy as soon as possible the most clinical benefit and cost savings as well
after presentation [11]. [232]. It is the only low-molecular-weight heparin
to be recommended in the ACC/AHA guidelines,
Unfractionated Heparin and it is noted as a choice for initial anticoagulant
Unfractionated heparin has been used in the ACS therapy for patients who are to have either an ini-
setting since the early 1960s. Heparin prevents tial invasive or conservative treatment [11].
the formation of thrombi by accelerating the
Enoxaparin acts by preventing the conversion
action of the proteolytic enzyme antithrombin
of fibrinogen to fibrin and the conversion of
that inactivates factors IIa, IXa, and Xa [58]. The
prothrombin to thrombin. Enoxaparin should be
findings of several small trials have demonstrated
administered as a subcutaneous injection; it should
that unfractionated heparin plus aspirin is more
never be given as an intramuscular injection.
beneficial than aspirin alone [11]. A meta-analysis
Bleeding complications may result from use. The
of six randomized trials (1,353 patients with UA)
manufacturer’s prescribing guidelines note that if
confirmed those findings, as unfractionated heparin
enoxaparin is to be given following PCI, the dose
plus aspirin reduced the risk for death or MI by 33%
should be given no sooner than 6 to 8 hours after
compared with aspirin alone [242].
the arterial catheter sheath is removed. Thrombo-

cytopenia has occurred with the administration of with unfractionated heparin; thus, unfractionated
this medication [61]. heparin is preferred for patients who are likely to
have CABG within 24 hours [11].
Dalteparin is indicated for prophylaxis of ischemic
complications in UA (when accompanied by ECG Choice of Treatment Strategy
changes) and non-Q wave MI when concurrently As stated, risk stratification is essential to determine
administered with aspirin therapy. Contraindica- the level of treatment: an early invasive or an early
tions to this medication include active major bleed- conservative strategy. An early invasive approach
ing; known hypersensitivity to the drug, heparin, involves coronary angiography and a revascular-
or pork products; or presence of thrombocytopenia ization procedure, typically done within 12 to 48
associated with a positive antiplatelet antibody hours after patient arrival in the emergency depart-
test. Like enoxparin, its use increases the risk of ment, unless there are contraindications to such
bleeding complications [60]. a procedure. With an early conservative approach
Direct Thrombin Inhibitors (also referred to as selective invasive approach or
medical management), noninvasive testing is done
Three direct thrombin inhibitors have been
and angiography is performed only when testing
approved by the FDA for clinical use, but only
demonstrates evidence of ischemia.
one—bivalirudin—is approved for use in the
ACS setting [11; 59]. The use of bivalirudin is An early invasive strategy was recommended
recommended as a choice of anticoagulant agent for high-risk patients in the 2002 ACC/AHA
for patients to have early invasive treatment [11]. guidelines, but the question of which approach
Bivalirudin is a synthetic analog of hirudin, a provides optimal outcomes has been evaluated
thrombin inhibitor that has shown little benefit extensively, with some conflicting data [26; 220;
in lowering the risk of adverse outcomes compared 222; 223; 224; 225; 226; 227; 228; 229; 230].
with unfractionated heparin [231]. Because of The recommendation was upheld, and the 2007
its shorter half-life, bivalirudin has the potential guidelines recommend an early invasive strategy
advantage of minimizing the risk of bleeding for patients who are at high risk for a clinical event
[58]. (Table 8), provided that they do not have serious
comorbidities or contraindications to a revascular-
Fondaparinux ization procedure [11].
Fondaparinux is another recommended anticoagu-
lant therapy option for patients who are to have
an early invasive procedure [11]. This synthetic CRITERIA FOR IDENTIFYING HIGH
RISK PATIENTS WITH UA/NSTEMI
polysaccharide factor Xa inhibitor is also recom-
mended as a choice for patients who are to have Recurrent angina/ischemia at rest or with
conservative treatment [11]. low-level activity
Elevated levels of cardiac biomarkers
Fondaparinux was compared with enoxaparin in
New ST-segment depression
one trial in which patients with UA/NSTEMI
Signs or symptoms of heart failure or new/worsening
were randomly assigned to receive one of these two
mitral valve regurgitation
agents. Among the 6,238 patients who had PCI,
High-risk findings from noninvasive testing
the rate of ischemic events at 9 days was similar
Hemodynamic instability
for both drugs, but the rate of major bleeding was
Sustained ventricular tachycardia
significantly lower for fondaparinux, yielding a
PCI within six months previously
significant net clinical benefit. Fondaparinux was
High risk score (TIMI, GRACE, PURSUIT)
also associated with significantly fewer adverse
events at 30 and 180 days. The anticoagulant effect Left ventricular ejection fraction of less than 0.40
of fondaparinux is not as easily reversed compared Source: [1] Table 8
Research has shown that many factors other than be taken to make sure that the patient understands
risk influence the use of an early invasive strategy. the treatment discussion and a professional inter-
An early invasive strategy is used more often, preter should be used when necessary.
regardless of patients’ risk, when a cardiac catheter- The 2007 ACC/AHA guidelines state that physi-
ization laboratory is available or the treating physician and patient preferences may be considered
cian is a cardiologist [37; 39; 219]. Demographic in a decision to choose an initial conservative
characteristics, such as age, race, and gender, are strategy [11]. Most patients wish to participate in
also factors. Data from trials indicate that older decision making, according to the findings of a
patients are treated with an invasive strategy less small study in the United Kingdom. Nearly one-
frequently than younger patients, with the likeli- half of a convenience sample of 53 patients wished
hood of an invasive strategy decreasing 20% for to share the decision-making responsibility with
each 10 years of advancing age [26; 144]. Data also their physician, with only 4% wishing to leave
show that black patients are 20% to 40% less likely the decision entirely to the physician [209]. Most
than white patients to have an early invasive inter- of the patients chose a treatment strategy based
vention [45]. Across all racial/ethnic populations, on the extent of the benefit and said they would
revascularization procedures are done more often “accept any treatment, no matter how extreme, to
on men than women [2; 26; 39; 44; 66]. return to health” [209]. The preferred treatment
Some findings have suggested that women do not was angioplasty for 80% of the patients and CABG
gain the same benefit from an invasive approach for 19%. Medications were the least preferred and
compared with men [211; 225]. However, when least acceptable options to patients [209].
women have high-risk features, such as elevated
troponin levels, an early invasive approach does Early Invasive Strategy
lead to better outcomes; women at low risk Use of an early invasive strategy can provide
have better outcomes from an early conserva- important details about the coronary vessels and
tive approach [51; 63; 230]. Based on this, an the location and extent of atherosclerotic obstruc-
early conservative approach for low-risk women tion. Studies have shown that approximately 20%
is a recommendation in the 2007 ACC/AHA of ACS patients will have three-vessel disease with
guidelines [11]. The findings of a study published left ventricular dysfunction or left main CAD [11].
in 2008 support this recommendation. Research- Disease of this extent is associated with a high
ers found that among women who did not have risk of adverse outcomes, and a revascularization
elevated biomarker levels, there was no reduction procedure offers survival benefit [11]. Angiography
in composite endpoint of death, nonfatal MI, or also identifies patients with insignificant CAD for
rehospitalization for ACS [222]. whom revascularization is not necessary, as the risk
for adverse outcomes is low [11; 208; 222].
The availability of treatment options for UA/
NSTEMI, along with lingering questions about the Multivessel disease is found on angiography for
superiority of one strategy over the other, provides most patients with UA/NSTEMI (40% to 50%),
an opportunity for patients to participate in select- and insignificant disease is found in 10% to 20%
ing treatment. Patients who are in stable condition [11]. However, the findings for men and women
should be involved in a discussion of the treatment differ significantly. For example, studies have
choices and the associated risks and benefits, and shown that three-vessel disease is more common in
patient preferences and values should be consid- men (35%) than women (23%). Most commonly,
ered [11; 220]. When a patient does not speak the women (32%) have one-vessel disease [222].
same language as the healthcare team, care should

CABG surgery was once the procedure of choice Imaging modalities, such as cardiac radionuclide
for revascularization. However, advances in less imaging and stress echocardiography, may be use-
invasive techniques have led to an increase in the ful for some patients [19; 206]. Some evidence
use of PCI, from 32.4% in 1999 to 63.5% in 2005 suggests that imaging studies are more accurate
[48]. The increase in invasive interventions has than exercise testing in evaluating women, in
been associated with significant decreases in in- part because of the lower likelihood of significant
hospital mortality, heart failure, cardiogenic shock, CAD [11; 51]. Stress echocardiography has been
and reinfarction [48]. noted to be the most accurate provocative test for
women, with higher sensitivity and specificity than
The ACC/AHA/Society for Cardiovascular
exercise testing [51]. These findings prompted the
Angiography and Interventions (SCAI) 2005
AHA to develop a consensus statement on the role
guideline update for PCI noted that an early
of noninvasive testing in women with suspected
invasive PCI is indicated for patients with UA/
ACS [205]. In addition, the ACC/AHA guidelines
NSTEMI who have no serious comorbidity, occlu-
for the treatment of UA/NSTEMI note that stress
sions that are likely to improve with PCI, and one
echocardiography is an accurate and cost-effective
of a number of symptoms that place them at high
risk for reinfarction and death. High-risk factors technique for detecting CAD in women [11].
include, but are not limited to, recurrent ischemia Angiography should be done after discharge in
despite the use of intensive optimal anti-ischemic patients who have recurrent ischemia. It should
therapy, elevated troponin level, evidence of new be used for severe chronic stable angina after
ST-segment depression on ECG, congestive heart initial management with a conservative strategy
failure symptoms, previous PCI within the last 6 if the patient is a candidate for a revascularization
months, previous CABG surgery, sustained ven- procedure [11].
tricular tachycardia, and hemodynamic instability
[14; 15].
Management of
Early Conservative Strategy Variant Angina
ACC/AHA guideline recommendations note that
the objective of an early conservative strategy is Patient V, a woman 45 years of age, was admitted
to avoid unnecessary treatment (and associated to a general medical-surgical unit with a diagnosis of
costs) for patients at low risk for significant CAD. possible upper gastrointestinal bleeding. She stated that
Normal ECG findings and biomarker levels are the she had no known cardiac history; however, she had
primary indicators of low risk, and it is appropriate risk factors for CAD, including a current history of 1
to defer invasive procedures for patients with these to 2 pack per day smoking history and dyslipidemia for
features and to carry out stress testing to determine which she takes simvastatin.
the presence of ischemic disease and identify Two days following admission, Patient V called the
patients at risk for adverse outcomes [11]. The nurse complaining of extreme, severe chest pain that
ACC/AHA guidelines recommend that a stress started while she was in the bathroom. The physician
test be done within 12 to 24 hours after evaluation was notified and ordered cardiac biomarkers and a
in the emergency department for low-risk patients 12-lead ECG. Sublingual nitroglycerin tablets were
or after 12 to 24 hours of being asymptomatic for administered and effectively relieved the acute chest
intermediate-risk patients [11]. An exercise stress pain. The patient’s biomarkers returned negative for
test is the easiest, most cost-effective test and MI; however, her ECG during the chest pain episode
should be the choice unless the patient is unable showed ST-segment elevation. A follow-up ECG,
to exercise or has abnormal findings on a resting taken when the pain had resolved, showed resolution
ECG. In the latter case, a pharmacologic stress test of ST-segment elevation and no electrocardiographic
should be done [11]. indications of an evolving or resolving MI.
After careful assessment and evaluation of serial labo- The 2008 AHA statement contains several recom-
ratory test, serial ECGs, physical exam findings, and mendations for the management of patients with
other diagnostic tests, the physician determined that cocaine-associated chest pain and MI [77]. Because
Patient V had variant (Prinzmetal’s or vasospastic) cocaine use may impact treatment, patients (espe-
angina. Diltiazem was ordered to prevent coronary cially younger patients) who present with signs of
vasospasm and recurrent chest pain attacks. possible ACS should be asked about cocaine use.
The primary medical therapy for management Establishing that a patient does use cocaine should
of variant or vasospastic angina involves nitrates depend primarily upon self-reporting. However,
and calcium-channel blockers. Within minutes of a urine toxicology screen that measures cocaine
administration, nitroglycerin has been found to metabolites (as well as other drug metabolites)
effectively treat episodes of angina and myocardial may be indicated in patients who are young, have
ischemia caused by vasospasm. Long-acting nitrates a history of illicit drug use, or who are unable to
can reduce the frequency of recurrent episodes of communicate with the healthcare team [77].
chest pain. Calcium-channel blockers, specifically Evaluation of possible cocaine-induced chest pain
nifedipine, amlodipine, verapamil, and diltiazem, in the emergency department should follow the
are prescribed to prevent coronary vasospasm and same guidelines as the evaluation for ACS without
the subsequent ischemia that can result. In this cocaine use. Cardiac biomarkers should be moni-
patient population, calcium-channel blockers are tored. Because cocaine can cause a breakdown of
preferred over beta blockers [54]. muscle fibers resulting in the release of myoglobin
into the bloodstream, elevated myoglobulin and
total creatine kinase levels may be present that are
Management of not indicative of myocardial ischemia or infarct.
Cocaine-Induced ACS Cardiac troponins are the biomarkers of choice to
assess for a diagnosis of infarction [77].
Patient C presented to the emergency department with
a complaint of severe substernal chest pain, radiating Patients with cocaine-induced chest pain who show
from the left side of his chest down his left arm. He ECG and biomarker evidence of ischemia or infarct
stated that he was “very nauseated” and that his symp- should be admitted for monitoring, observation,
toms came on suddenly. The patient is 19 years of age; and further treatment as indicated. General medi-
when questioned, he admitted that he smoked 1 to 2 cal therapies, similar to those used in management
packs per day but denied all other risk factors for CAD. of non-cocaine related ACS, should be employed.
He had no previous history of ACS or interventions for In addition, the use of IV benzodiazepines as part
CAD, such as PCI. He appeared “jittery” and anxious of the early management of these patients may be
and asked to leave the emergency department to smoke. indicated. In patients who use cocaine, benzodi-
His initial 12-lead ECG showed sinus tachycardia but azepines help to relieve chest pain and manage
no evidence of myocardial ischemia or infarct. His ini- neuropsychiatric manifestations [77].
tial biomarkers showed slightly elevated CK-MB levels If the presence of STEMI is confirmed, use of
with a troponin I within normal limits. Upon careful timely PCI is recommended. Due to concerns about
questioning by the emergency department physician, adherence with long-term antiplatelet therapy, the
Patient C admitted that he used cocaine approximately guidelines recommend that use of a bare-metal
one hour before the development of his symptoms. stent (as opposed to a drug-eluting stent) should
be strongly considered for persons with ongoing
cocaine abuse. Discharge management and second-
ary prevention should focus heavily on cessation
of cocaine use [77].

better outcomes than fibrinolytic therapy [12; 25;
Treatment of STEMI 145; 198; 199; 200]. In a meta-analysis of 23 ran-
domized controlled trials involving 7,739 patients
Patient K, a man 59 years of age, was admitted to
with STEMI who were eligible for fibrinolytic
the hospital with a diagnosis of possible H1N1 flu. He
therapy, PCI was associated with better outcomes
was treated with appropriate medical therapy, and his
with respect to lower rates of short-term mortality,
condition improved. On the day before his expected
nonfatal reinfarction, and stroke [199].
discharge, he called the nurse and complained of a
severe, stabbing pain in his chest. He was diaphoretic PCI encompasses a variety of procedures that may
and complained of feeling nauseated. His blood pres- be used to restore blood flow through an occluded
sure was elevated to 170/90 mm Hg, and his heart artery. These procedures include percutaneous
rate was 100–110 beats per minute. He rated his pain transluminal coronary angioplasty, or balloon
10 out of 10 and stated the pain was located in his left angioplasty, and angioplasty with placement of
chest, left arm, and back. An ECG was completed, one or more intracoronary stents. In PCI, a slen-
and blood for cardiac biomarkers was obtained. The der balloon-tipped catheter is inserted through an
12-lead ECG showed non-specific ST-wave changes. artery in the groin to the area of blockage in the
A serial 12-lead ECG taken 30 minutes later, however, coronary artery. Once in position, the balloon is
showed ST elevation in the anterior leads. Cardiology inflated, compressing the plaque and dilating the
confirmed a diagnosis of STEMI. narrowed coronary artery so that blood can flow
more easily [80; 87].
When an ECG demonstrates ST-segment eleva-
tion indicative of MI, the goal of treatment is to To maintain patency in the newly re-opened
immediately restore normal coronary perfusion artery, intracoronary stents may be deployed. Best
through the occluded infarct-related artery, thus described as a wire metal-mesh tube, an intracoro-
decreasing ischemic time. Re-establishing blood nary stent is carried by a balloon catheter to the
flow through the occluded artery is crucial for area of the blockage. When the balloon is inflated,
limiting the size of the infarct, minimizing myocar- the stent expands and locks in place against the
dial damage, preserving left ventricular function, vessel wall, keeping the lumen of the vessel open.
decreasing morbidity, and improving survival [12; Blood flow to the affected area of the heart is
145; 200; 201; 202]. Options for re-establishing restored, and myocardial ischemia is relieved. The
normal coronary blood flow through an occluded stent stays in the artery permanently. Within a few
artery include: weeks of the time a stent is placed, the endothelium
of the artery grows over the metal surface of the
• PCI with or without placement
stent [80; 87].
of intracoronary stents
• Fibrinolytic therapy Following stent placement, occlusions may develop
in a stent or near the junction between the end
• Combination PCI and fibrinolytic
of a stent and the native vessel. To combat this
therapy
issue, researchers developed a new type of stent
• CABG surgery called a drug-eluting stent; these stents are coated
Percutaneous with medications that reduce inflammation and
Coronary Intervention thrombus formation, thereby reducing the risk of
restenosis at the site of the stent. Stents not coated
PCI is an invasive procedure performed in the with drugs are called bare-metal stents. Not all
cardiac catheterization laboratory by a highly occlusions or all vessels are amenable to balloon
skilled, trained team. In the treatment of STEMI, dilatation or deployment of stents. In some cases,
the goal of PCI is to open the occlusion in the the degree of coronary occlusion is too great to be
infarct-related vessel, restoring blood flow and oxy- re-opened through percutaneous means. Coronary
gen supply. Studies have shown that PCI achieves
artery bypass surgery may be indicated in these
Patients with STEMI who have
cases. PCI also cannot be performed on smaller contraindications to fibrinolytic therapy
vessels that branch off from the major arteries; the should be brought immediately or
lumens in these vessels are too small to permit safe secondarily transferred promptly
passage of the catheter [80; 87]. (i.e., primary receiving hospital door-
to-departure time less than 30 minutes)
Categories of PCI to facilities capable of cardiac catheterization and
rapid revascularization (PCI or CABG).
PCI for STEMI can be categorized according to
(http://www.guidelines.gov/summary/
when the procedure is performed and whether summary.aspx?doc_id=12192.
or not it occurs in conjunction with fibrinolytic Last accessed October 21, 2010.)
therapy. Primary PCI refers to a procedure that is Strength of Recommendation/Level of Evidence:
done alone as primary treatment after diagnostic IB (Procedure should be performed based on the
angiography [12]. Primary PCI is preferred because evaluation of limited population risk strata.)
of the many advantages it offers compared with
fibrinolytic therapy, including wider eligibility, bet-
ter rates of reperfusion, lower risks, and improved Facilitated PCI involves a combination of fibrin-
outcomes (Table 9) [12; 25; 145; 198; 199; 200]. olytic therapy and PCI. Fibrinolytic therapy is
PCI is especially preferred for high-risk patients, given first to open the artery lumen before PCI is
specifically patients 75 years of age and older, attempted. This strategy is designed to capitalize on
patients with an unclear diagnosis, and patients the advantages of both approaches: the timeliness
with cardiogenic shock, congestive heart failure, or of pharmacologic reperfusion and the superior out-
ventricular arrhythmias [12]. However, analysis of comes associated with PCI. Various pharmacologic
data has shown that PCI is done less often among regimens have been evaluated in facilitated PCI,
patients at high risk (41%) than among patients at including a glycoprotein IIb/IIIa inhibitor alone,
low risk (60%) or intermediate risk (54%) [37]. fibrinolytic therapy (at full or reduced dose), fibrin-
olytic therapy (at half or full dose) with a glycopro-
tein IIb/IIIa inhibitor, and high-dose heparin [12;
13]. ACC/AHA guidelines state that facilitated
PCI might be considered if [13]:
COMPARISON OF FIBRINOLYTIC THERAPY AND PCI

Factors PCI Fibrinolytic Therapy
Recommended timing (from first medical contact) <90 min <30 min
Patient eligibility 90% 67%
Reperfusion rate (TIMI grade 3) 70% to 95% 30% to 60%*
Adverse Events
Death, reinfarction, or stroke 8% 14%
Short-term mortality 7% 9%
Nonfatal reinfarction 3% 7%
Stroke 1% 2%
Intracranial hemorrhage 0.05% 1%
*Achievement of TIMI grade 3 blood flow of 30% to 40% with streptokinase and 50% to 60% with a fibrin-specific agent.
TIMI = Thrombolysis in Myocardial Infarction.
Source: [12; 145; 198; 199; 200] Table 9

• PCI is not available within 90 minutes, Aspirin should be given to all patients with sus-
noting that the pharmacologic reperfusion pected STEMI as early as possible. Aspirin alone
should not be full-dose fibrinolytic therapy has reduced the risk of 35-day mortality when used
• The patient is at high risk for severe to treat an evolving acute MI and leads to greater
myocardial damage or death risk reductions in mortality as well as decreases in
reocclusion and recurrent ischemic events when
• The patient has a low risk of bleeding
given in combination with fibrinolytic therapy
complications
[12]. The initial dose should be 162–325 mg (to
The guidelines also include a recommendation that be chewed) [12]. Most of the evidence supports the
a planned reperfusion strategy involving full-dose lower of these two doses because of similar efficacy
fibrinolytic therapy followed by immediate PCI and a better safety profile [12]. Formulations with
may be harmful [13]. no enteric coating are preferred because of their
Rescue PCI is performed within 12 hours after fail- more rapid absorption [12].
ure of pharmacologic reperfusion. Early assessment The drug of choice to manage the pain associated
of reperfusion is essential to determine whether with STEMI is intravenous morphine, which can
additional treatment, such as rescue PCI, is needed. be given in increasing amounts at intervals of 5
The ACC/AHA guidelines for STEMI suggest to 15 minutes [12]. When giving morphine, the
that it is reasonable to monitor clinical symptoms, patient’s blood pressure, respirations, and oxygen
the pattern of ST-segment elevation, and cardiac saturation levels should be monitored; morphine
rhythm over the 60 to 180 minutes after the start can cause hypotension and respiratory depression
of fibrinolytic therapy [12]. The ACC/AHA [87].
guidelines recommend that 90 minutes is the best
Sublingual nitroglycerin may be given to patients
point at which to evaluate the need for rescue PCI
with STEMI for persistent or recurrent ischemic
[13]. The benefit of rescue PCI should be balanced
discomfort [12]. Intravenous nitroglycerin is
against the increased risk of stroke and bleeding
indicated to relieve ongoing ischemic discom-
complications after the combination of fibrinolytic
fort, control hypertension, or manage pulmonary
therapy and rescue PCI [13]. Hospitals that do not
congestion [12]. As noted, nitroglycerin is contra-
have the capacity for PCI should establish transfer
indicated in patients who have taken sildenafil
protocols to help ensure timely transfer for rescue
within the last 24 hours [87].
PCI [13].
Upon further questioning, Patient K reported a history
Adjuvant Therapies of CAD with stent placement 5 years previously and
The ACC/AHA guidelines for STEMI state that CABG surgery 10 years previously. The medical team
it is reasonable to begin treatment with abcix- determined that primary PCI was indicated to open the
imab as early as possible before primary PCI (with occluded, infarct-related vessel. While awaiting the
or without stenting) [12]. The precise timing of start of the procedure, Patient K received aspirin 325
administration has not been defined [145]. Treat- mg and 600 mg of clopidogrel. He also received a bolus
ment with tirofiban or eptifibatide may also be of abciximab, and a continuous infusion was started.
considered before primary PCI [12]. The guidelines
note that when a glycoprotein IIb/IIIa inhibitor Post-PCI Assessment and Monitoring
is used, the bolus dose of unfractionated heparin Monitoring the patient closely for complications
should be decreased to 50 to 70 units/kg to achieve and signs of recurrent ischemia is particularly
a target activated partial thromboplastin time of important in the 24-hour period following rep-
200 seconds [12]. erfusion with PCI. Complications may include
bleeding, formation of clot or obstruction, drop
in platelet count, reocclusion, renal failure, and
cerebrovascular accident [14; 87].
Bleeding may occur from the arterial puncture site. initial chest pain. ECG changes indicative of acute
Initial indications include frank bleeding from the ischemia or infarct may appear. Cardiac biomark-
puncture site and/or development of a hematoma ers may trend upward. The treatment of choice is
in the area surrounding the site. A retroperitoneal an emergent return to the cardiac catheterization
bleed may also occur; an early sign is a complaint laboratory for direct visualization of the vessels
of severe flank pain. To reduce the likelihood of and possible removal of a thrombus in or near the
bleeding, the patient should be maintained on newly placed stent. Cardiac biomarkers should be
bedrest as specified by physician orders. The length monitored post-PCI. CK-MB and troponin levels
of time bedrest is indicated depends on the method that fall from previously high levels are indicative
used to close the arterial puncture site. The arte- of restored perfusion; levels that initially drop, then
rial puncture site, often the femoral artery, must trend upward again are concerning for possible
be monitored frequently for signs of bleeding or recurrent damage. Continuous ECG monitoring
hematoma formation [14; 87]. should also be maintained. If only 2 or 3 leads can
be monitored continuously, the leads selected for
Formation of a clot at the puncture site reduces
monitoring should be the ones most likely to reflect
distal arterial blood flow and can result in signs
of peripheral ischemia below the site. Indications any recurrent ST-segment changes [14; 87].
include loss of or decrease in the peripheral pulse Renal failure can develop from the kidneys’
distal to the arterial puncture site and change response to the dye load administered during
in color or temperature of the distal extremity. cardiac catheterization. Postprocedure orders
The peripheral pulse distant to the site should be may include administration of IV fluids to help
checked frequently with vital signs and arterial site to “flush” the dye through the kidneys. Adequate
checks [14; 87]. intake of fluids should be provided as well. Moni-
toring intake and output and renal function studies
A significant drop in platelet count may be caused
is indicated postprocedure [14; 87].
by an allergy or intolerance to infusing glycoprotein
IIb/IIIa inhibitors. With a drop in platelet count, During PCI, it is possible for parts of plaque to
the patient’s risk of bleeding increases. Patients break off and travel, lodging in cerebral circulation.
receiving glycoprotein IIb/IIIa inhibitors should Patients should be monitored for any change in
have a complete blood count checked at desig- mental status or abrupt development of any tran-
nated intervals to make sure that platelet counts sient ischemic attack-like symptoms [14; 87].
are not dropping. Parameters should include orders Patient K underwent successful PCI to a branch of
to notify the physician if the platelet count drops his circumflex artery, with placement of a drug-eluting
below a specified level. If a patient develops a stent. Following the procedure, he was transferred to
significant drop in platelet count, the infusion of the coronary care unit for observation and monitoring.
the glycoprotein IIb/IIIa inhibitor is discontinued He was placed on continuous ECG monitoring, which
and the patient is placed on bleeding precautions assessed ST-segment changes in the most appropriate
and observed carefully for any signs of bleeding leads. Vital signs were checked frequently, and the right
[14; 87]. femoral site and right pedal pulse were assessed for
Abrupt reocclusion of the infarct-related artery bleeding, signs of hematoma, or disrupted circulation.
can occur within hours of the original procedure. The patient remained on bedrest per orders. Labora-
A thrombus may form in the newly placed stent, tory tests were sent at prescribed intervals to monitor
occluding blood flow and causing symptoms of cardiac biomarkers and complete blood count. Patient
myocardial ischemia or infarct. Clinical indications K was also monitored for signs of recurrent ischemia,
include the recurrence of severe chest pain. This including recurrent chest pain and recurrent or new
chest pain may be similar or worse than the patient’s ST-wave changes.

Patient K recovered from the PCI. During the postpro- less than 30 minutes from the time of first
cedure period, it was noted that his groin site was dry, medical contact (known as the door-to-
with no evidence of bleeding or hematoma. His pedal needle time).
pulse remained strong and readily palpable. His vital
Barriers to meeting the 90 minute door-to-balloon
signs were stable. The blood pressure measurement
time include [196; 201]:
remained around 130 mm Hg systolic, and the patient
remained chest pain free. ECG showed no further • The time it takes to transfer the patient
ischemic changes. His initial post-PCI complete blood from one hospital to another hospital.
count showed a slight drop in platelet count, and the Many hospitals do not have a cardiac
initial post-PCI biomarkers showed his elevated levels catheterization laboratory and a skilled
starting to trend down. The follow-up laboratory results PCI team readily available.
8 hours later showed his platelet count unchanged and • Hospitals with a cardiac catheterization
his biomarkers continuing to trend downward. Patient laboratory and a skilled PCI team may
K was discharged uneventfully 24 hours later. lack 24-hour coverage. Studies have
shown delays of 13 to 21 minutes between
The Issue of Timing
midnight and 7:59 a.m.
A familiar adage associated with STEMI is “time is
• Patient’s delay in seeking help. Research
muscle,” and every effort should be made to shorten
has shown that the length of time from
the ischemic time as much as possible. The timing
the patient’s onset of symptoms to arrival
of reperfusion therapy is a complex issue involv-
at the hospital can range from 1.5 to 6
ing the time from the onset of symptoms and the
hours in the United States. It is estimated
time from presentation to treatment. Despite the
that approximately half of patients with
clear benefit of PCI, it is a challenge for it to be
symptoms of ACS wait more than 4 hours
performed as recommended. Achieving an optimal
before seeking treatment.
outcome from PCI depends on many factors; the
most significant factor is timing [12; 201]. The find- • Delays resulting from the time it takes to
ings from data registries, clinical trials, and quality triage and evaluate patients, to perform
improvement initiatives have shown that fewer diagnostic testing, to verify the diagnosis,
than 40% of patients are treated with primary PCI and to obtain informed consent.
within the recommended 90-minute window [145; Strategies to Improve Timing of Therapy
203]. An additional 40% are treated with PCI at 2
Timely reperfusion therapy can be enhanced
hours or more after hospital arrival [145].
through the implementation of strategies at several
The AHA/ACC practice guidelines make the fol- points along the continuum of care, from prehos-
lowing recommendations [12; 13]: pital evaluation to treatment delivery. Strategies
• PCI is preferred over fibrinolytic therapy that are being explored include [198; 204]:
for restoration of blood flow for patients • EMS use of prehospital ECGs and enhanced
with STEMI. communication with the receiving hospital
• PCI must be done within less than 90 • Implementation of standardized protocols
minutes after the patient’s first medical and integrated systems of transfer to
contact (known as the door-to-balloon significantly reduce delays related to
time). Increases in the door-to-balloon transferring patient to another facility
time have correlated with higher rates • Use of institution-specific protocols that
of short-term and long-term mortality. have been developed in collaboration with
• When PCI cannot be done within 90 cardiologists, interventional cardiologists,
minutes, fibrinolytic therapy should be primary care physicians, nurses, and other
initiated as the reperfusion strategy within staff, as appropriate
The ACC and AHA have launched initiatives to fibrinolytic therapy. One report indicated that only
help improve the healthcare system response for 20% of the patients who had fibrinolytic therapy
treatment of STEMI. The AHA Mission Lifeline received it within the recommended window of
program is a community-based, national initia- 30 minutes [197]. However, door-to-needle times
tive to enhance the quality of care and outcomes have improved over the last few decades, from 60
for patients with STEMI. Another campaign, the minutes in the 1990s to 32 minutes in the mid-
Door-to-Balloon: An Alliance for Quality (http:// 2000s [25].
www.d2balliance.org), launched by the ACC (in Four fibrinolytic agents have been evaluated and
partnership with the AHA and other organiza- approved in the STEMI setting: streptokinase,
tions), is committed to improving the timeliness alteplase (tPA), reteplase, and tenecteplase
of primary PCI. The goal of these programs is to (Table 10) [145; 198]. Each is associated with
increase the percentage of patients treated with risks and benefits, and the choice of drug is based
timely PCI (within 90 minutes) to 75%, the per- on several factors, including preferences in the
centage recommended in the ACC/AHA guide- hospital formulary, cost, ease of administration, and
lines [13]. the possibility of subsequent PCI [145]. Although
FIBRINOLYTIC THERAPY streptokinase is the least expensive agent, it is
rarely used in the United States because it has
Sometimes referred to as “clot-busting drugs,”
been shown to be less effective than the other
fibrinolytic agents have the potential to open
three drugs [145].
an infarct-related vessel by dissolving exist-
ing thrombi. Fibrinolytic agents degrade fibrin The most common complication of fibrinolytic
clots by converting plasminogen to plasmin. therapy is major bleeding [201]. In addition, fibrin-
Re-establishment of coronary blood flow within the olytic therapy is less effective than primary PCI;
first 30 minutes after occlusion can abort infarc- approximately 30% to 60% of patients do not have
tion [192]. Reperfusion within 30 minutes to 2 early and complete restoration of coronary blood
hours can salvage myocardial tissue substantially flow [145]. Adverse outcomes after fibrinolytic
[191]. Fibrinolytic therapy will be the treatment of therapy are generally more common among women
choice for some patients who present with STEMI. and older patients [189; 190]. In cases of failed
As with PCI, there are barriers to meeting the 30 fibrinolytic therapy, rescue PCI is the preferred
minute door-to-needle time for administration of strategy [13; 193; 194].
COMPARISON OF FIBRINOLYTIC AGENTS FOR TREATMENT

OF ST-SEGMENT MYOCARDIAL INFARCTION (STEMI)
Characteristic Streptokinase Alteplase Reteplase Tenectoplase
Dose 1.5 MU Up to 100 mg Two doses of 10 U 30-50 mg
(over 30-60 min) (over 90 min) (over 2 min)
30 min apart
Administration Infusion Infusion and bolus Bolus (two) Bolus
Weight-based dosing No Yes No Yes
Allergic reactions Yes No No No
Patency rate* (approx.) 50% to 55% 75% 80% to 83% 75% to 83%
Cost per recommended $562.50 $3,404.78 $2,872.50 $2,917.48
dose (for 50 mg)
*Grade 2 or 3 TIMI blood flow.
TIMI = Thrombolysis in Myocardial Infarction.

Contraindications to Fibrinolytic Therapy Nursing Assessment and Monitoring
Absolute contraindications for fibrinolytic therapy Immediately following reperfusion with fibrinolyt-
include patients with [73; 76; 87]: ics, the patient is at risk to develop serious bleeding
episodes or to reocclude the infarct-related vessel
• High risk for bleeding complications
[76; 87]. Nursing assessment during this period is
• History of intracranial hemorrhage crucial and should include [87]:
within last 3 months
• Continuous ECG monitoring for rate,
• History of substantial closed head
rhythm, or reoccurrence of signs of acute
or facial trauma within last 3 months
ischemia, development of life-threatening
• Suspected aortic dissection or active bleeding arrhythmias
Possible contraindications to fibrinolytic therapy • Assessment for reoccurrence of chest
include: pain or other symptoms associated
• History of poorly controlled hypertension with an acute ischemic episode
• Recent internal bleeding • Frequent vital sign monitoring for
hypotension, drop in oxygen saturation,
• Diagnosis of STEMI not clearly confirmed
or other signs indicative of developing
heart failure
As a systems goal, STEMI patients • Assessment for any changes in level
presenting to a hospital with PCI capability
of consciousness
should be treated with primary PCI within
90 minutes of first medical contact. • Assessment for indications of bleeding
(http://www.guidelines.gov/ In addition, explanations about the patient’s care
summary/summary.aspx?doc_id=12192.
Last accessed October 21, 2010.)
and progress should be provided to the patient and
the patient’s family.
Strength of Recommendation/Level of Evidence:
IA (Treatment should be administered based on the Ancillary Therapy Following
evaluation of multiple population risk strata.)
Thrombolytic Therapy
Glycoprotein IIb/IIIa Inhibitor
Unlike PCI, the effects of fibrinolytic therapy on A glycoprotein IIb/IIIa inhibitor may be consid-
the vessel occlusion cannot be directly monitored ered as an ancillary agent for patients who receive
or measured. Indications that the therapy has fibrinolytic therapy. The ACC/AHA guidelines for
been successful in re-opening an occluded vessel STEMI note that the use of abciximab may be con-
include [76]: sidered to prevent reinfarction and other complica-
• Patient’s chest pain symptoms are relieved. tions of STEMI in selected patients [12]. Studies
have shown that the benefit of this combination
• Repeat ECG shows that the ST-segment
therapy is confined to patients who are younger
elevation initially seen has been reduced
than 75 years of age (primarily because of the risk
by one-half.
of intracranial hemorrhage), have an anterior MI,
• Vital signs are stable. and have no risk factors for bleeding [12]. When
• ECG shows stable rhythm. With reperfusion, abciximab is used, the dose of the fibrinolytic agent
arrhythmias often occur (such as accelerated should be decreased by half [12].
idioventricular rhythm). If reperfusion
is successful, these arrhythmias should
be transient and should not result in an
unstable rhythm.
Heparin or Fondaparinux and hospital stay, but the long-term outcomes,
Anticoagulant therapy is associated with bleeding including survival, have been similar for the two
complications, so care must be taken in select- procedures [16].
ing an appropriate agent, with attention paid to
NO REPERFUSION
the patient’s renal function status, the time to
an invasive procedure, and overall bleeding risk Despite the clear benefit of reperfusion, some
[180]. Unfractionated heparin, enoxaparin, and patients with STEMI do not receive reperfusion
fondaparinux are the recommended anticoagulant therapy [25; 48; 197; 201]. Women are less likely
agents [13; 178; 180]. The 2007 focused update of to receive reperfusion therapy as are patients who
the ACC/AHA guidelines include three new rec- are older than 65 years of age, patients with an
ommendations pertaining to anticoagulant therapy atypical clinical presentation, and patients with
[13]. One of the new recommendations relates a history of cardiovascular disease [25; 41; 201].
to the use of anticoagulant therapy beyond the Compared with patients who do receive therapy,
minimum of 48 hours recommended in the earlier mortality rates are substantially higher for patients
edition of the guidelines, noting that it is prefer- who are eligible for reperfusion but do not receive
able for patients to receive anticoagulant therapy it, and rates have been higher and more discrepant
for the duration of the index hospitalization (up to for women and older patients [25; 197].
8 days). Another recommendation relates to opti- ACC/AHA guidelines for the management of a
mal dosing of anticoagulant therapy for patients patient who does not receive reperfusion therapy
undergoing PCI after fibrinolytic therapy, and the include [13]:
third recommendation notes that fondaparinux
• Loading dose (300 mg) of clopidogrel
should not be used as the only anticoagulant agent
to patients younger than 75 years of age
to support PCI after fibrinolytic therapy because of
the risk of catheter thrombosis [13]. • Treatment with clopidogrel at a dose
of 75 mg per day for 14 days
Unfractionated heparin should be used for patients
• Use of anticoagulant therapy (low-
with severe impairment of renal function, and
molecular-weight heparin or fondaparinux
unfractionated heparin or enoxaparin may be used
rather than unfractionated heparin)
for patients who are at increased risk of bleeding
given for the duration of the index
or who are likely to have early angiography [180].
hospitalization is reasonable
Researchers reviewed data on 20,479 patients to
compare outcomes for unfractionated heparin and • Aspirin
enoxaparin [179]. Significantly fewer patients in CARE AFTER REPERFUSION
the enoxaparin group had subsequent PCI within
30 days after fibrinolytic therapy [179]. There were Site of Care
no differences between the two agents with respect According to the ACC/AHA guidelines, patients
to major bleeding. with STEMI should be treated in either a coronary
care unit or a stepdown unit [12]. Care provided in
Coronary Artery a coronary care unit should be structured accord-
Bypass Graft Surgery ing to evidence-based protocols, and nursing staff
Although PCI is done more frequently, several should be certified in critical care [12]. Patients
situations call for the use of CABG. The ACC/ who are admitted to a coronary care unit may be
AHA guidelines for STEMI recommend emergent transferred to a stepdown unit after they have been
or urgent CABG when severe multivessel disease clinically stable for 12 to 24 hours [12]. Low-risk
is present or when PCI has failed [12]. Compared patients who have had successful PCI may be
with PCI, CABG requires a longer recovery time admitted directly to a stepdown unit [12].

Maintaining Coronary Blood Flow or other physicians involved in the care of the
The risk of reocclusion is a major concern in the patient) to discontinue the medication due to the
long-term management of patients following rep- patient’s need for some type of invasive procedure.
erfusion for ACS. Antiplatelet and anticoagulant To reduce the incidence of adverse consequences
therapies are used to maintain patency of the from the early discontinuation of clopidogrel/
infarct-related artery and prevent reocclusion [145; aspirin therapy, the ACC/AHA guidelines recom-
303]. As previously described, a STEMI-associated mend [79]:
thrombus consists of a fibrin-rich core and a • Before implanting a stent, the physician
platelet-rich cap. Because of this, both antiplatelet should discuss the need for dual therapy
and anticoagulant therapies play important roles in with the patient. If there is not a reasonable
maintaining patency of the infarct-related artery expectation that the patient will adhere
and preventing reocclusion [145; 303]. to dual therapy for 12 months, the use
Aspirin and Clopidogrel of drug-eluting stents should be avoided.
Combination aspirin and clopidogrel therapy has • If the patient expects to have major
become the main therapy for preventing stent surgery within the next 12 months, use
reocclusion. The 2007 focused update of the of a bare-metal stent should be considered.
ACC/AHA guidelines for STEMI include a new • A greater effort should be made by the
recommendation for clopidogrel (75 mg per day for physician to ensure that the patient and
14 days) to be added to aspirin for patients with family understand the risk of discontinuing
STEMI, regardless of whether they have reperfu- prescribed dual therapy early. Emphasize
sion with fibrinolytic therapy [13]. Stopping this that the patient must contact the prescribing
therapy early greatly increases the risk of stent cardiologist prior to stopping the therapy,
thrombosis and can result in severe adverse conse- even if requested to discontinue the
quences, including recurrent myocardial ischemia medication by another physician.
and infarction. • If the patient must have a procedure that
Patient I, a man 74 years of age, presented to the requires clopidogrel be stopped, use of
emergency department with symptoms indicative of aspirin should be continued if at all possible.
ACS. Because he had a history of a STEMI that was Therapy should be resumed as soon as
treated by the placement of two drug-eluting stents, safely possible following the procedure.
the decision was made to take the patient to the cardiac A current area of research is exploring methods
catheterization laboratory. On catheterization, the phy- similar to the use of heparin to bridge lapses in
sician found that one of Patient I’s stents was completely warfarin use that may be used to bridge oral anti-
occluded by a thrombus. The stent was re-opened, and platelet agent lapses pre-operatively in patients
the patient was transferred to the cardiac stepdown unit with intracoronary stents who are at high risk for
for monitoring. When questioned, Patient I indicated stent reocclusion.
that he quit taking the clopidogrel upon the instructions
of his urologist in preparation for a urological surgical Beta Blockers
procedure. The 2007 focused update still recommends that
oral beta blockers be used within the first 24 hours.
Multiple factors may be implicated in a patient’s
Beta blockers should not be used in patients with
decision to stop taking clopidogrel early. These
signs of heart failure, low cardiac output, increased
include the cost of the medication, incomplete
risk of cardiogenic shock, or other relative con-
understanding of the importance of continuing
traindications to beta blockade [13].
the medication as prescribed, and the instructions
of other healthcare providers (dentists, surgeons,
ACE Inhibitors them routinely and should not be administered
The use of an oral ACE inhibitor within the first during the hospitalization for any patient with
24 hours is a strong recommendation for patients STEMI [13].
with anterior infarction, pulmonary congestion, or
Non-Invasive Testing After STEMI
left ventricular ejection fraction of less than 0.40
[12]. The ACC/AHA guidelines for STEMI note Exercise testing in patients with STEMI is useful
that it is preferable to initiate treatment with an for risk stratification and assessment of functional
ACE inhibitor after fibrinolytic therapy has been capacity and should be performed to assess the
completed and the patient’s blood pressure has presence and extent of inducible ischemia in
stabilized [12]. Treatment should start at a low dose patients who have not had angiography and do not
that is gradually increased to a full dose within 24 have high-risk features [12]. The optimum time
to 48 hours. ACE inhibitors are of most benefit for to exercise test after STEMI has not been clearly
patients who are 55 to 74 years of age, have had an defined. Exercise testing before discharge can pro-
anterior infarct, or have a heart rate of at least 80 vide reassurance to patients about their functional
beats per minute [168]. Contraindications include a capacity and can also be used to establish exercise
systolic blood pressure of less than 100 mm Hg (or parameters for cardiac rehabilitation [12].
more than 30 mm Hg below baseline), the presence Echocardiography is also recommended for assess-
of clinically relevant renal failure, a history of bilat- ing left ventricular function in patients with
eral stenosis of the renal arteries, or known allergy. STEMI who have not had coronary angiography
Patients who cannot tolerate an ACE inhibitor [12]. Patients who have baseline abnormalities
should be treated with an ARB [12]. that may compromise interpretation of the ECG
findings should have stress echocardiography (or
Calcium-Channel Blockers
myocardial perfusion imaging) to assess induc-
Use of verapamil and diltiazem may be useful when ible ischemia [12]. Echocardiography and stress
beta blockers are contraindicated, if the patient echocardiography should be performed according
has well-preserved left ventricular function and to guidelines or criteria developed for their use
no clinical evidence of congestive heart failure or [18; 19].
pulmonary congestion [164; 165]. Both drugs have
been associated with significantly reduced mortal-
ity and major cardiovascular events [164; 165]. Discharge Planning
Verapamil should not be used for patients with
heart failure or bradyarrhythmias, and diltiazem Appropriate discharge planning and secondary
should not be used for patients with left ventricular prevention measures are essential, as the morbid-
dysfunction [163; 165]. ity and mortality after UA/NSTEMI or STEMI
are high (Table 11) [2]. A multidisciplinary team
NSAIDs should be involved in preparing the patient for dis-
The reported increased risk of mortality, reinfarc- charge, and detailed discharge instructions should
tion, hypertension, heart failure, and myocardial be given to both the patient and family [11; 12].
rupture associated with the use of COX-2 inhibi- Discharge instructions should be easily understood,
tors and other NSAIDs led to the inclusion of two culturally sensitive, given in the patient’s preferred
new recommendations in the 2007 focused update language, and reinforced with written instructions
of the ACC/AHA guidelines [13; 157; 158; 162]. [11]. Instructions should include detailed informa-
According to these recommendations, the use of tion on [11; 12]:
NSAIDs should be discontinued at the time of • Scheduling the first follow-up visit
presentation for patients who have been taking
• Return to normal activities
(e.g., driving, work)

OUTCOMES WITHIN FIVE YEARS AFTER FIRST MI

Outcome Prevalence
40–69 Years of Age >70 Years of Age
Men Women Men Women
Recurrent MI or fatal CAD 16% 22% 24% 24%
Heart failure 7% 12% 22% 25%
Stroke 4% 6% 6% 11%
MI = myocardial infarction; CAD = coronary artery disease.
• Recommended secondary prevention after implantation of a drug-eluting stent [11; 12].

measures The 2007 update of the ACC/AHA guidelines for
• Medication dosing and frequency the management of STEMI indicate that patients
should receive clopidogrel (75 mg daily) for 14
• Plans to obtain prescribed medications
days after discharge and note that it is reasonable
immediately after discharge
to continue treatment for 1 year [13]. Questions
• Referral to cardiac rehabilitation about clopidogrel maintenance therapy remain, as
Cardiac Rehabilitation the optimal dose and duration of therapy have not
been identified [143; 243]. Another concern is the
Referral to a cardiac rehabilitation program is a
effect of stopping clopidogrel. In a 2008 study of
recommendation in ACC/AHA guidelines because
3,137 patients with ACS (treated either medically
it can help patients achieve secondary prevention
or with PCI) who took clopidogrel for a mean of 9
goals [11; 12; 20]. Rehabilitation programs are of
to 10 months, there was a significantly high risk of
particular benefit for patients who had STEMI or
adverse events in the initial 90 days after stopping
high-risk patients with UA/NSTEMI, for whom
treatment with clopidogrel [142].
supervised exercise is best [11; 12].
Warfarin is recommended as an antithrombotic
Medications for patients with UA/NSTEMI or STEMI who are
In addition to rehabilitation, four classes of medi- allergic to aspirin [11; 12; 20]. In addition, warfarin
cations are recommended after an ACS event to (with or without aspirin) is reasonable for patients
decrease the risk of reocclusion: antiplatelet/anti- with UA/NSTEMI who have a high risk for CAD,
coagulant agents (aspirin and clopidogrel or war- a low bleeding risk, and cannot tolerate clopidogrel
farin), beta blockers, ACE inhibitors (or ARBs), [11]. Warfarin is also indicated after STEMI for
and lipid-lowering agents [11; 12; 20]. patients who have persistent or paroxysmal atrial
fibrillation or had a documented left ventricu-
Antiplatelet/Anticoagulant Agents
lar thrombus [12]. Warfarin should be given to
The recommended antiplatelet therapy after dis- maintain a specific international normalized ratio
charge is a combination of aspirin and clopidogrel (INR), depending on the use of stents, underlying
[11; 12; 20]. The findings of studies have suggested cardiac disease, and the concomitant use of clopi-
that low-dose aspirin is as effective as higher doses dogrel [12]. The risk of bleeding is increased when
but has a better safety profile [152; 250; 251]. The warfarin is used in conjunction with aspirin and/
recommended daily dose of aspirin is 75–162 mg or clopidogrel, and patients treated with the three
[11; 12; 152]. Higher doses of aspirin (162–325 medications should be monitored closely [11].
mg) are recommended for 1 month after implan-
tation of bare-metal stent and for 3 to 6 months
Beta Blockers
Patients with established coronary heart
Treatment with beta blockers is recommended for disease should be identified for secondary
all patients after UA/NSTEMI or STEMI [11; 12; prevention efforts. Patients with a coronary
20]. Treatment should continue indefinitely. heart disease risk equivalent should receive
equally intensive risk factor intervention
ACE Inhibitors or ARBs as those with clinically apparent coronary
heart disease.
An ACE inhibitor is also recommended as long-
term therapy after UA/NSTEMI or STEMI [11; summary.aspx?doc_id=11333.
12; 20]. ARBs should be used in patients who are Last accessed October 21, 2010.)
unable to tolerate an ACE inhibitor and have Strength of Recommendation/Level of Evidence:
clinical or radiographic signs of heart failure or a IA (Procedure should be performed based on the
left ventricular ejection fraction of less than 0.40 evaluation of multiple population risk strata.)
[11; 12].
Lipid-Lowering Agents The class I guideline recommendations for all sec-
Even before the advent of statins, reducing lipid ondary prevention strategies can be organized into
levels through diet and previously available a simplified “ABCDE” approach to help clinicians
medications led to significant reductions in MIs implement guideline-based care [11; 108]:
[12]. Statins are now the preferred medications • A: Antianginal agents, antiplatelet
for lipid-level management, and several studies therapy, and ACE inhibitors (or ARBs)
have demonstrated their effectiveness in reducing
atherogenesis [11; 12]. A fasting lipid profile should • B: Beta blockers and blood pressure control
be determined within 24 hours of admission, and • C: Cardiac rehabilitation, cholesterol
statin therapy should begin during hospitalization, treatment, and cigarette smoking cessation
regardless of this baseline level [11; 12]. • D: Diet, depression management,
and diabetes management
secondary prevention:
risk factor modification • E: Exercise and education
Substantial evidence has demonstrated that aggres- Smoking Cessation
sive risk-reduction therapies enhance patient Mortality after an ACS event for a patient who
outcomes after ACS. ACC/AHA guidelines have smokes cigarettes is twice that for a patient who
made several recommendations for secondary does not. The rates of reinfarction and death at 1
prevention focusing on lifestyle modifications and year have been found to be reduced in persons who
medications [11; 12; 20]. Due to shortened hospital stop smoking [80; 87]. Smoking is the single most
stays, responsibility for patient education about risk important modifiable cardiovascular risk factor,
factor modification, recognition and reinforcement and use of low-tar, low-nicotine, or filtered ciga-
of positive progress involves healthcare providers rettes does not reduce cardiovascular risk. Injurious
in all practice settings. effects of tobacco and its components (nicotine and
carbon monoxide) on the cardiovascular system
include:
• Damage to the inner wall of the artery
resulting in increased stiffness and
vasoconstriction
• Increased cardiac arrhythmias
• Increased oxidation of LDL

• Decreased levels of HDL • Any evidence of a patient’s progress in
• Increased risk for thrombus formation smoking cessation should receive recognition
and positive reinforcement during any
• Increased platelet aggregation
encounter with a healthcare provider.
• Reduced oxygen-carrying capacity of blood
• Use of antidepressant medications to assist
• Acceleration of atherosclerotic process in the cessation process may be considered.
and formation of atherosclerotic plaque
• For some patients, use of nicotine
• Increased risk of atherosclerotic plaque replacement therapy is effective in
rupture and acute ischemic events helping achieve smoking cessation.
Current research has shown that exposure to Nicotine replacement therapy is available in patch,
environmental smoke (secondhand smoke) is also gum, inhaler, spray, or lozenge. Some forms are
a risk factor for atherosclerosis. It is recommended available over the counter; others require a pre-
that all individuals avoid all exposure to smoke, scription. It is important to note that people who
including secondhand smoke. When discussing continue to smoke should not use nicotine replace-
smoking cessation with patients and families, it ment therapies. Available pharmacological options
is important to stress the benefits. Research has include bupropion and varenicline [87].
shown that risk of MI declines within 24 hours of
complete cessation from smoking [87]. Bupropion
The current length of stay for most persons hospi- A non-nicotine oral agent approved for use in
talized with ACS is too short for effective smok- smoking cessation, bupropion may be started while
ing cessation intervention. Providing resources, the patient is still smoking. The patient should be
including referrals, that the patient can use after instructed to pick a set stop smoking date sometime
discharge is critical. Options for smoking cessation during the second week of bupropion therapy. The
help include individual counseling, structured medication may be continued for 7 to 12 weeks.
group programs, and use of strategies to prevent Persons who have not stopped smoking by the sev-
relapse [80; 87]. enth week should be instructed to discontinue the
medication. Contraindications for use of bupropion
When working with patients who smoke, it is include presence of seizure disorders, past or current
important to remember the following points [80; diagnosis of bulimia or anorexia, and concurrent
87]: use of monoamine oxidase inhibitors. Persons who
• Cigarette smoking is an addiction. The are actively in the process of stopping alcohol or
effects of nicotine impact the brain quickly; sedative use should not take this medication.
exposure to nicotine through smoking
Varenicline
must be repeated at frequent intervals to
maintain a “steady state” and avoid signs Varenicline acts by reducing the urge to smoke.
of withdrawal. In the hospital setting, The person should be instructed to set a definitive
patients who are smokers can develop signs “quit date” for stopping smoking. One week prior to
of irritability, anxiety, depression, anger, that date, varenicline is started. The dose is titrated
inability to focus, insomnia, and increased during the first week and is usually prescribed for a
appetite due to being unable to maintain minimum of 12 weeks. If the person has successfully
their smoking habit as they do at home. stopped smoking by the end of the initial 12-week
period, the medication may be prescribed for a
• Each time the patient interacts with the
second 12-week period to increase the likelihood
healthcare system, the health care provided
that the patient will remain off cigarettes.
should briefly reinforce the importance of
smoking cessation.
Online sites that offer resources for smoking ces- to the DASH diet provides an eating plan that
sation are also available for patients and families. reduces sodium intake to 1500-2300 mg per day;
They include the AHA (http://www.american- 2300 mg is considered the highest acceptable level
heart.org), the American Cancer Society (http:// by the national High Blood Pressure Education
www.cancer.org), and the American Lung Associa- Program, but the Institute of Medicine recom-
tion (http://www.lungusa.org). mends the lower intake of 1500 mg. The DASH
diet is high in fruits, vegetables, and low-fat dairy
Hypertension products. It is low in both saturated fat and total
Hypertension is a significant risk for ongoing CAD fat and rich in potassium and calcium [78; 128].
and recurrent ACS. The JNC7 defines hyperten- Research has shown that increased potassium
sion as a systolic blood pressure of 140 mm Hg or intake from foods (not supplements) has been
greater or a diastolic blood pressure of 90 mm Hg linked to better blood pressure control. Foods rich
or greater. A blood pressure of 120–139 mm Hg in potassium include potatoes, sweet potatoes,
systolic or 80–89 mm Hg diastolic is defined as bananas, apricots, cooked soybeans, cooked lentils,
pre-hypertensive. For these patients, lifestyle modi- fat-free milk, trout, and tuna fish.
fications are indicated to reduce blood pressure
Studies have supported the premise that blood pres-
into the “normal” range and prevent hypertension-
sure is reduced with an eating plan low in saturated
related complications. “Normal” blood pressure is
fat, cholesterol, and total fat that also emphasized
defined as systolic pressure less than 120 mm Hg
fruits, vegetables, and fat-free or low-fat dairy prod-
and diastolic blood pressure less than 80 mm Hg.
ucts. The DASH diet also includes whole-grain
Medication therapy is often prescribed for the products, fish, poultry, and nuts. More information
management of hypertension. A thiazide diuretic is available online at http://www.nhlbi.nih.gov/
is frequently the first drug of choice; other medi- health/public/heart/hbp/dash/new_dash.pdf.
cations used in hypertension management may
include, but are not limited to, beta blockers and Dyslipidemia
ACE-inhibitors. Two or more medications may be Another major modifiable risk factor is dyslipi-
required for adequate blood pressure control [87]. demia, or high cholesterol. The desired total cho-
lesterol target is less than 200 mg/dL; 200–239 mg/
Effective control of hypertension also includes
dL is considered “borderline,” and levels of 240 mg/
lifestyle changes; these include maintenance of
dL or greater are considered high [127]. However,
a healthy body weight (weight loss for obese per-
optimal cholesterol levels are more accurately
sons), physical activity for 30 to 45 minutes daily or
calculated by further measuring LDL, HDL, and
almost every day, reduction of sodium intake, and
triglycerides. For individuals with known CAD,
alcohol consumption in moderation for persons
the desired target for LDL is less than 100 mg/dL.
who drink [87; 128].
Levels between 100 and 129 mg/dL are considered
The DASH Diet “above optimal,” and 130–159 mg/dL is “borderline
One dietary measure that has been found effec- high.” Measurements of 160–189 mg/dL are “high,”
tive in hypertension management is the Dietary and 190 mg/dL and greater is “very high” [127].
Approaches to Stop Hypertension (DASH) diet. HDL, also known as “good cholesterol,” acts by
Following the DASH diet plan has been found to removing cholesterol from circulation and trans-
reduce sodium intake and improve blood pressure porting it to the liver. HDL levels are inversely
in hypertensive patients. It is estimated that the related to CAD risk. A level of 60 mg/dL or greater
average American diet contains about 3300 mg of is desirable; levels less than 40 mg/dL are consid-
sodium for women, and 4200 for men. Adherence ered low [127].

The majority of dietary fat intake is in the form Lipid-lowering medication therapy should be
of triglycerides. Like LDL, excess levels of triglyc- combined with lifestyle modification and initiated
erides are associated with adverse cardiovascular before patient is discharged. If LDL is not less than
effects. A normal level is defined as any measure- 100 mg/dL despite medication therapy, dosage
ment less than 150 mg/dL. Levels of 500 mg/dL are should be increased or combination therapy should
considered “very high” [127]. be prescribed. Recommended lifestyle modifica-
tions include increased consumption of omega-3
Dietary changes can help to reduce or maintain
fatty acids and aerobic exercise.
cholesterol and triglyceride levels within the target
or desired ranges. In general, following a healthy Lipid-Lowering Medications
eating plan is recommended, balancing calorie Available categories of medications found to lower
intake against calorie expenditure. This includes LDL include statins, bile acid-binding resins, and
[87]: niacin. Of these, statins are considered the most
• Reducing consumption of saturated fats. powerful [87].
Patients should consume no more than Statins available for the treatment of dyslipidemia
7% of daily calories from fat and no more include lovastatin, simvastatin, pravastatin, and
than 200 mg/day of cholesterol. atorvastatin [87; 88]. Because cholesterol biosyn-
• Use canola oil or olive oil; avoid tropical thesis is the most active in early morning hours,
oils and hydrogenated vegetable oils. statins should be taken at bedtime. It is important
• Increase intake of soluble fiber to 10–25 to counsel patients taking statins to limit their
g per day. Sources of soluble dietary fiber consumption of grapefruit juice. When taken at
include oats, legumes, grains, vegetables, about the same time as the statin, components in
and fruits. the grapefruit juice interfere with the breakdown of
• Severely limit consumption of any foods the medication, resulting in a potentially hazardous
containing trans fats. high level of medication in the body.
Bile acid-binding resins are also useful in the treat-
Encouraging consumption of omega-3 ment of dyslipidemia [87; 88]. Examples of avail-
fatty acids in the form of fish or in capsule able agents in this class include cholestyhramine/
form (1 g per day) for risk reduction in questran and colestipol. The agents are available
UA/NSTEMI patients may be reasonable. in a variety of forms, each requiring specific patient
For treatment of elevated triglycerides,
education. Powder forms should be mixed with
higher doses (2 to 4 g per day) may be
used for risk reduction. liquid to form a gritty solution; however, tablets
should not be cut, crushed, or chewed. Bile acid-
summary.aspx?doc_id=11333. binding resins should be taken with the largest
Last accessed October 21, 2010.) meal of the day and other medications should be
Strength of Recommendation/Level of Evidence: IIbB taken either 1 hour before or 4 hours after admin-
(Treatment may be considered based on the evaluation istration.
of limited population risk strata.)
Niacin is also known as vitamin B3 or nicotinic
acid and acts to both lower LDL and raise HDL
For persons with known CAD, it is important that levels in the blood [87; 88]. It is generally admin-
dyslipidemia is managed medically [11; 87]. A lipid istered at doses of 1000–2000 mg twice a day, but
profile should be obtained within 24 hours of any side effects have been reported with higher doses.
admission for ACS. For patients whose initial LDL Aspirin may be given 30 minutes before a dose to
is greater than 70 mg/dL, therapy to decrease the reduce the side effect of severe flushing. Niacin
level further (to less than 70 mg/dL) is indicated. should also be taken with food to minimize gas-
trointestinal side effects.
Depression a recent ACS event), compliance with guideline-
An ACS event can be distressing for many recommended medications has ranged from 18% to
patients, leading to a heightened fear of dying 55%. Approximately 54% of individuals have been
and anxiety about adjusting to life with cardiac compliant with all of their initial medications,
disease [141]. These emotions can substantially and compliance decreases over time [105; 122;
affect a patient’s psychosocial status and lead to 131]. Several other factors have been found to be
depression [12; 139; 140]. Some degree of clinically associated with noncompliance with medications,
significant depression has been reported to occur including [105; 122; 131]:
in up to one-half of patients with ACS, with major • Choice of medication
depression occurring in 15% to 20% of patients
• Tolerability
[12; 140]. Depression has been found more often
in women with ACS compared with men [138]. • Duration of treatment
In addition to the negative effect on the patient’s • Dosing frequency
quality of life, depression has also been shown to • Higher number of prescribed medications
be associated with lack of adherence to secondary • Lack of symptoms as indication for the
prevention measures and with increased mortal- medication
ity [12; 132; 136; 139]. Evaluation of a patient’s
• Uncertainty about how to take the
psychosocial status, with particular attention paid
medication
to signs of depression, is a recommendation in the
ACC/AHA guidelines for STEMI, and screening • Lack of transportation to the pharmacy
for depression and referral and/or treatment is a Anecdotal information from patients, families, and
recommendation in the ACC/AHA guidelines medical personnel involved in patient care indicate
for UA/NSTEMI [11; 12]. At each visit, clinicians that another major barrier to adherence is the cost
should ask patients about anxiety, sleep disor- of the medications.
ders, social support, and symptoms of depression.
Cognitive-behavior therapy, sertraline, or selec- Patient Education
tive serotonin-reuptake inhibitors may be useful Patient education is an integral component of
for enhancing the quality of life for patients with treatment for patients with ACS and should begin
symptoms of depression [12; 140]. during hospitalization and continue throughout
follow-up care [11; 12]. Adequate time for appro-
Diabetes priate education during the index hospitalization
For patients with diabetes, adverse events after has been challenged by shorter hospital stays and
UA/NSTEMI or STEMI may be reduced by tight reduced staffing [12; 104]. The responsibility of
glucose control. This is defined as a hemoglobin patient education has thus shifted to the healthcare
A1C level of less than 7% [11; 12; 20]. Diet modi- team. Surveys have shown that nearly half of indi-
fication and use of medications and/or insulin are viduals are not knowledgeable about ACS-related
often necessary to maintain a health blood glucose symptoms or their level of risk, even after having
level and to avoid cardiovascular complications. an ACS event [104]. Men, older individuals, and
individuals with less formal education were less
COMPLIANCE ISSUES
likely to be knowledgeable about their risk and
Lack of patient compliance with medications is symptoms [104]. This lack of knowledge can con-
also a serious problem and has been referred to as tribute to lack of compliance with recommended
an “unrecognized risk factor for CAD” due to its secondary prevention strategies.
association with significant increases in adverse
events and health costs [117; 122]. Among indi- Research has shown that patient education should
viduals with CAD (many of whom had experienced focus on the importance of [11; 12; 103]:

• Recognition of symptoms Recognition of Symptoms
• Timeliness of care Many individuals still believe that the onset of
• Acknowledgment of risk factors for ACS an MI will be “dramatic,” with chest pain that
is severe and crushing [11; 12; 237]. However,
• Compliance with secondary prevention
among individuals who have had an acute MI,
strategies
only 40% interpreted their symptoms as cardiac
Education in these areas should be tailored to in nature [95]. In addition, chest pain and other
individuals, as perceptions of cardiac disease and ACS-related symptoms are interpreted differently
risk differ across subgroups of patients according to by men and women. Men were more likely to think
age, gender, and race/ethnicity [95; 103]. Table 12 the symptoms were cardiac in nature if the chest
provides a summary of strategies that nurses, physi- pain was severe and if they had a history of CAD.
cians, and other healthcare team members can use In contrast, women did not relate severity of chest
to facilitate effective education with patients and pain with a cardiac origin [95]. Healthcare profes-
families [89; 90; 91; 92; 94]. sionals should talk to patients about the “real” signs
and symptoms of ACS, emphasizing the diversity
in symptoms [104].
STRATEGIES FOR EFFECTIVE
EDUCATION FOR ACS PATIENTS Timeliness of Care
Ask the patient what language he or she prefers for On average, individuals wait 2 hours before seek-
educational resources and use that language for ing medical care for ACS-related symptoms, and
oral education and written resources (as much this delay has not changed over time despite
as possible).
many national public campaigns emphasizing the
Assess the patient’s baseline understanding of the
importance of timely care [11]. Furthermore, up to
disease and treatment.
50% of individuals with ACS-related symptoms
Ask the patient what and how much he or she
wants to know. are transported to the hospital by means other
Discuss epidemiologic and clinical evidence.
than EMS, which can increase delays [12; 93].
Individuals have given several reasons for delays in
Involve other healthcare specialists in the
educational process. seeking medical care (Table 13) [237]. Individuals
Use a variety of educational resources in a variety and their families or caregivers should be told that
of media. immediate action is needed for ACS-related symp-
Try innovative approaches, such as interactive toms, including calling EMS, taking nitroglycerin
modules. for ischemic pain, and taking aspirin.
Offer online resources to patients (e.g., the AHA
website, http://www.americanheart.org, or the
NHLBI website, http://www.nhlbi.nih.gov). REASONS FOR DELAY IN SEEKING
MEDICAL ATTENTION FOR CHEST PAIN
Ascertain potential barriers to compliance.
Develop an action plan. Expected more severe chest pain
Have the patient focus on one behavior change Believed chest pain would resolve
at a time, if necessary. Did not think symptoms were serious
Involve family members in educational efforts. Decided on “wait and see” approach
Reinforce recommendations at all office visits. Thought symptoms were related to another condition
Provide positive reinforcement for each step toward (muscle strain, heartburn)
goals. Was not aware of benefit of rapid action
Provide telephone follow-up. Feared embarrassment if symptoms were not related
to cardiac event
Source: [89; 90; 91; 92; 94] Table 12
Underestimated risk of cardiac event
Acknowledgement of Risk Factors ing their patients to prevent CAD and manage risk
The need for better understanding of risk among factors [50]. Of particular note is the percentage of
individuals who have had ACS is evidenced by respondents who were not aware that CAD leads
studies that have shown that perceptions of per- to more deaths among women than among men;
sonal risk are lower than actual risk [104; 237]. only 8% of primary care physicians, 13% of obste-
Healthcare professionals should reinforce infor- tricians/gynecologists, and 17% of cardiologists
mation about modifiable risk factors and provide recognized this fact [50]. Clinicians have noted
patients with educational resources that describe several barriers to adhering to CAD prevention
risk factors and their effect on the potential for guidelines, including [49; 50]:
future events. One useful resource is the Risk • Cost of medications
Assessment Tool on the AHA website, which
• Lack of reimbursement, especially
allows individuals to assess their risk of an MI
for lifestyle interventions
or cardiac death within 10 years. This tool may
be accessed at http://www.americanheart.org/ • Lack of adequate time for counseling
presenter.jhtml?identifier=3003499. Patients’ • Lack of patient education tools
individual risk factors should be discussed in an • Existence of multiple guidelines
ongoing manner, with a focus on positive changes
• Lack of knowledge and skills to recommend
through lifestyle modifications and medications.
dietary changes and facilitate patient
Compliance with Secondary adherence
Prevention Strategies Efforts should be directed at alleviating these bar-
Compliance with prevention strategies can be riers to enable healthcare professionals to evaluate
enhanced by identifying the barriers for each patients’ risk factors adequately and to develop
individual patient and working together to address ways to help patients understand their risk and
the problem [12; 20]. Primary care clinicians and the importance of prevention strategies. A mul-
other healthcare professionals should ask patients tidisciplinary team approach is needed to provide
about medication compliance at each office visit expertise in all areas. In addition, initiatives should
and should emphasize the importance of maintain- emphasize the risk of CAD among women.
ing drug therapy. Ongoing education about the
benefit gained from medications as well as lifestyle
modifications is vital to ensuring high compliance Simulated case studies
and low risk of adverse events.
Case Study 1
Patient E is a man, 54 years of age, who presented to
Adherence to Evidence- his primary care physician’s office with complaints
Based Guidelines of chest pain. Upon arrival at the primary care
physician’s office, he was chest pain free. A 12-lead
Sub-optimal adherence to guidelines for man- ECG was performed and showed no changes from
agement and prevention of CAD contributes to previous ECGs. The patient’s vital signs were found
increased ACS risk. Adherence has been less than to be stable and within his normal range: blood
effective, especially among patients at low risk for pressure 135/78 mm Hg, heart rate 68 beats per
disease [49; 50]. In one survey, primary care physi- minute and regular, and respirations 16 breaths per
cians, obstetricians/gynecologists, and cardiologists minute and unlabored. He was afebrile.
did not rate themselves as being effective in help-

Comments and Rationale: Persons who present was approximately 30 pounds overweight. When
in any healthcare setting with a complaint of chest the physician mentioned his need for weight loss,
pain should be evaluated for the presence of signs and the patient’s usual reply was, “It’s either the weight
symptoms of ACS. Appropriate assessment measures or the smoking. I can’t manage both.”
include vital signs and a 12-lead ECG to assess for
Comments and Rationale: A careful history and
changes suspicious for ischemia or infarct. Patient E
physical can provide information necessary to triage
was chest pain free on arrival, his ECG did not show
patients who present with chest pain and stratify their
any acute ischemic changes, and his vital signs were
risk for serious consequences such as acute MI. Major
stable. Further assessment by the healthcare provider
risk factors for ACS include a known history of CAD,
is indicated.
history of occlusions that have required intervention to
The physician questioned Patient E about his chest restore blood flow and oxygen supply, and the presence
pain episodes. The patient reported that, until of modifiable risk factors such as obesity, dyslipidemia,
about a week ago, he just had been having his smoking, and hypertension.
“usual” occasional chest pain when he “worked too
Given the patient’s known CAD, previous history
long, too hard in the yard.” However, over the last
of CABG and PCI with stents, and his continuing
week, his chest pain attacks had been lasting longer
risk factors, the physician instructed Patient E to go
and requiring more sublingual nitroglycerin tablets
to the emergency department of the local hospital.
for relief. The previous night he had experienced a
The patient declined transport by EMS and insisted
prolonged episode of chest pain at rest and decided
on driving himself to the hospital.
to seek medical attention.
Comments and Rationale: ACC/AHA guidelines
Comments and Rationale: Chest pain that occurs
strongly recommend that persons with possible ACS be
in a predictable pattern, is generally triggered by the
transported to the hospital by EMS [11]. Transport by
same level of exertion, and is readily relieved by rest
EMS provides the opportunity for skilled healthcare pro-
and sublingual nitroglycerin can be classified as “stable
viders to assess the patient, obtain an immediate ECG,
angina.” Stable angina is a hallmark symptom of CAD
and administer aspirin and other therapies as indicated.
but is rarely indicative of acute myocardial ischemia.
In addition, EMS can notify the receiving emergency
However, chest pain attacks that increase in frequency,
department to expect the patient so immediate triage
severity, and/or require additional nitroglycerin tablets
and evaluation are facilitated. ACC/AHA guidelines
to achieve relief and severe chest pain that occurs at
strongly discourage persons with possible ACS from
rest are indications that the patient’s angina has become
driving themselves or asking friends or family members
“unstable.” Immediate medication evaluation and
for transport to the emergency department.
intervention is indicated [87].
In the emergency department, Patient E developed
The physician reviewed Patient E’s medical record
an episode of chest pain. He rated the pain as 10
and noted that he had a history of CABG surgery 5
out of 10 and located the pain on the left side of
years previously. Two years ago, Patient E required
his chest, substernal region. He was slightly dia-
placement of a drug-eluting stent to open a block-
phoretic with a blood pressure of 170/90 mm Hg
age in one of the saphenous vein grafts from his
and a heart rate of 110 beats per minute.
prior CABG surgery. Patient E was also prescribed
medication for dyslipidemia; his most recent labo- Comments and Rationale: Severe, intense chest pain
ratory tests showed his LDL was borderline high located in the left substernal area of the chest coupled
at 135 mg/dL. He stopped smoking following the with diaphoresis and vital sign changes is a strong
stent placement two years previously. The patient indicator of ACS.
The emergency physician activated the chest pain After receiving morphine, Patient E reported that
protocol. Patient E received 325 mg of aspirin he was chest pain free. His blood pressure and heart
with instructions to chew it before swallowing. rate returned to the “usual” level. His initial car-
He was also given sublingual nitroglycerin, and diac biomarkers were returned negative for cardiac
supplemental oxygen at 2 liters per nasal cannula damage. The physician made the decision to admit
was started. A 12-lead ECG was performed, and the patient to the telemetry/stepdown floor for
blood work, including a CK-MB and troponin T further observation and monitoring. His admitting
level, were drawn. diagnosis was UA/possible ACS, and his admitting
orders included orders for serial biomarker monitor-
Comments and Rationale: In ACS, aspirin is given
ing, continuous ECG monitoring, and immediate
immediately for its antiplatelet action to decrease the
12-lead ECG with chest pain.
risk of thrombus formation. Sublingual nitroglycerin
acts a vasodilator, reducing myocardial workload while Comments and Rationale: The combination of
increasing myocardial oxygen supply. It also helps to Patient E’s increasingly severe and frequent chest
lower elevated blood pressure. pain episodes coupled with the presence of non-specific
changes on 12-lead ECG and his previous history of
The 12-lead ECG showed non-specific ST-segment
CAD, CABG, and stent placements are indicators that
and T-wave changes. Five minutes after one sublin-
the patient is at increased risk for MI. Serial biomarkers
gual nitroglycerin tablet, the patient reported that
can provide important diagnostic information and may
his chest pain was 10/10; his blood pressure was
be used to confirm or rule out a diagnosis of NSTEMI.
140/88 mm Hg. A second sublingual nitroglycerin
Continuous ECG monitoring provides information
tablet was given; 5 minutes later, Patient E reported
about ST-segment changes indicative of ischemia and
his pain was 8/10, and his blood pressure remained
infarct. A 12-lead ECG recorded during chest pain
at about 140/88 mm Hg. A third sublingual nitro-
can also provide information about possible ischemia/
glycerin tablet was administered, and minutes later,
infarction and what part of the heart is at risk.
the patient reported that his pain was 5/10. His
blood pressure was measured as 132/80 mm Hg. Patient E’s second set of cardiac biomarkers
The physician ordered 2 mg of morphine IV. returned showing an elevated CK-MB level. A
repeat ECG indicated no evidence of ischemia or
Comments and Rationale: In patients with clini-
infarct. A third set of cardiac biomarkers approxi-
cal symptoms of ACS, non-specific ST-segment and
mately 8 hours later showed that the CK-MB eleva-
T-wave changes are worrisome. Serial ECGs may be
tion increased and the troponin T was positive
indicated to identify the presence of an evolving MI.
for myocardial damage. A diagnosis of NSTEMI
Sublingual nitroglycerin may be given every 5 minutes
was confirmed. Another ECG taken immediately
up to 3 doses if the patient does not become hypoten-
after the return of the laboratory work did not
sive. The goal of analgesic therapy in ACS is to get the
show any evidence of ischemia; however, minutes
patient “chest pain free.” Morphine may be used to
later, Patient E developed chest pain. ST-segment
treat chest pain that does not resolve after 3 sublingual
depression in the inferior leads was noted on con-
nitroglycerin tablets. Morphine acts as a vasodilator,
tinuous ECG monitoring.
decreasing myocardial oxygen demands and increasing
myocardial oxygen supply [11; 14; 73; 87].

Comments and Rationale: ECG changes and cardiac Patient E was taken to the cardiac catheterization
biomarker elevation indicative of myocardial ischemia laboratory for diagnostic coronary angiography and
and infarction can develop over a period of minutes to possible PCI. Cardiac catheterization revealed that
hours. In persons who have persistent chest pain with he had an area of blockage in his right coronary
initial negative ECG findings and cardiac biomarker artery. The patient’s previous stent remained open,
levels, serial measurements are indicated. As was the and the other vein grafts from previous surgery were
case with Patient E, biomarker changes indicative also patent. A PCI with placement of a bare-metal
of infarct may develop several hours after the initial stent was performed.
episode of chest pain. Presence of elevated cardiac
Comments and Rationale: Intracoronary stents
troponin levels, in the absence of ST-segment elevation,
are deployed during PCI to help to keep the lumen of
is diagnostic for NSTEMI.
the affected vessel open. The choice of type of stent
The physician ordered a continuous heparin (bare-metal or drug-eluting) is left to the interventional
infusion along with a bolus dose of eptifibatide cardiologist performing the procedure.
followed by a continuous infusion. Patient E
Following recovery in the cardiac catheterization
had been administered aspirin in the emergency
area, Patient E was returned to his room. The post-
department; on the floor, he received 600 mg of
catheterization orders included instructions for
clopidogrel along with a low dose of a beta blocker.
bedrest for 4 hours, continuation of the eptifibatide
Patient E developed another episode of chest pain
drip for a total of 18 hours following the conclu-
that was not relieved by sublingual nitroglycerin
sion of the PCI procedure, and serial monitoring
or IV morphine. As a result, the physician ordered
of cardiac biomarkers and complete blood count.
a continuous nitroglycerin drip.
Nursing care included continuous ECG monitor-
Comments and Rationale: The immediate goal of ing, frequent vital sign checks, frequent monitoring
treatment in NSTEMI is to relieve ischemia and pre- of the arterial puncture site for evidence of bleeding
vent on-going infarction. Key elements of management or hematoma, and assessment for signs of recurrent
include aspirin (chewed) and clopidogrel to reduce chest pain (indicative of reocclusion of the infarct-
platelet formation and aggregation, and nitroglycerin related vessel) or severe left flank pain (indicative
and morphine for relief of ischemic pain through reduc- of retroperitoneal bleed). Patient E was encouraged
tion of myocardial workload and decrease in myocardial to drink fluids, and his urine output was monitored
oxygen demand. Chest pain unrelieved by sublingual and recorded.
nitroglycerin may be treated with a continuous nitro-
Comments and Rationale: Key elements of care dur-
glycerin infusion titrated to relieve chest pain and main-
ing the immediate post-PCI period include monitoring
tain a blood pressure within a prescribed range. A third
for bleeding, maintaining the eptifibatide drip as ordered
major element in the management of acute NSTEMI
to decrease the risk of stent occlusion, and monitoring
is anticoagulation. A continuous heparin infusion is
the patient for changes in vital signs, heart rhythm, or
one option for anticoagulation; use of heparin may be
the development of chest pain. Potential complications
combined with the use of a glycoprotein IIb/IIIa inhibi-
during this period include bleeding from the puncture
tor. In acute stages of NSTEMI, a glycoprotein IIb/IIIa
site and reocclusion in the coronary artery.
inhibitor such as eptifibatide may be used. Eptifibatide
may be initiated prior to cardiac catheterization, and
the infusion can be maintained for a specified period of
time following catheterization and stent placement.
Patient E’s initial blood work following the PCI Comments and Rationale: At the time of admission
showed a drop in his platelet count from the high to the emergency department, Patient Z shows no signs
normal to borderline low range. A second set of of acute ischemia or infarct; she is chest pain free, her
blood work sent 6 hours later showed a dramatic ECG shows no ST-segment elevation or ST-segment
and significant drop in his platelet count. The phy- depression, and her initial cardiac troponin level is
sician was notified and ordered the discontinuation equivocal. However, she has at least one major risk
of the eptifibatide infusion. Appropriate nursing factor for CAD and subsequent ACS: hypertension
interventions included close monitoring of the that appears poorly controlled. Her ECG also shows
patient for any signs of bleeding. evidence (i.e., a pathologic Q wave with no evidence
of ST-segment elevation or T-wave inversion) that she
Comments and Rationale: Use of glycoprotein IIb/
had experienced an MI sometime in the past.
IIIa inhibitors can cause an unsafe drop in platelet
counts in some individuals. Careful monitoring of The emergency department physician admitted
platelet levels at specified intervals during the infusion Patient Z to the telemetry unit with hypertension
is indicated to identify this complication promptly and and possible ACS/UA. Serial cardiac biomarkers
intervene in timely fashion. remained essentially unchanged from the initial
levels. Repeat 12-lead ECG 8 hours after admis-
Case Study 2 sion showed no indications of acute ischemia or
Patient Z, a woman 63 years of age, presented to infarct. Patient Z had several episodes of epigastric
the emergency department with a complaint of discomfort/chest discomfort following her transfer
intermittent epigastric and chest discomfort. She to the telemetry unit. She developed nausea and
reported that the discomfort had occurred inter- emesis with one episode. Sublingual nitroglycerin
mittently over the previous 2 to 3 weeks. When was effective in relieving her discomfort. Oral
questioned, she admitted that she had felt more medications to lower her blood pressure were
fatigued and had periods of shortness of breath and effective and subsequent measurements indicated
light-headedness over the same time period. a blood pressure of 150/88 mm Hg. When asked,
Comments and Rationale: While women may pres- the patient denied any history of a previous MI.
ent with ACS symptoms similar to men, they may also When asked if a physician had ever instructed her
present with symptoms labeled as “atypical.” Epigastric to take a lipid-lowering medication, she replied
pain, fatigue, and light-headedness have been identified that she “couldn’t afford it.”
as “atypical” symptoms associated with ACS. Comments and Rationale: Risk stratification indi-
At the time of presentation to the emergency cates that Patient Z has risk factors for CAD and ACS
department, Patient Z reported that she was expe- but is not currently experiencing an acute episode. An
riencing no discomfort. Her blood pressure was early conservative approach, including a stress test, is
elevated at 210/120 mm Hg, her heart rate was 84 indicated.
beats per minute, her respirations were even and The physician ordered a fasting lipid panel, to
easy, and she did not appear to be in acute distress. evaluate for dyslipidemia, and an exercise stress
An initial ECG showed no signs of acute ischemia test.
or infarct but did reveal a pathologic Q wave. The
Comments and Rationale: The focus of medical
initial cardiac troponin I returned indicating the
therapy for Patient Z will be on continued risk stratifi-
level to be “borderline” but not yet elevated. When
cation and risk factor reduction. Exercise stress testing
asked, Patient Z admitted that she has had high
will provide information about presence of ischemic
blood pressure “for a while” and that she does not
disease and risk for adverse cardiac events.
always take her medications as prescribed.

During the exercise stress test, Patient Z developed that she preferred written information in English,
chest pain, diaphoresis, and nausea before reaching so written material on reducing cholesterol and
the targeted heart rate. She underwent a follow-up triglyceride consumption were provided as well as
cardiac catheterization with placement of a stent a list of local resources. The nurse also reviewed all
in her right coronary artery. Following a conversa- of Patient Z’s current medications with her when
tion with the patient regarding adherence to dual she administered them, stressing the importance
antiplatelet therapy, the interventional cardiologist of taking them as prescribed and making sure that
chose to implant a bare-metal stent. the patient understood the purpose and prescribed
dosage of all her new medications. Provided educa-
Comments and Rationale: Inability to reach a heart
tion and the patient’s responses were recorded in
rate target due to development of chest pain or other
the patient’s medical record.
ischemia-associated symptoms during a stress test
is an indication of ischemic disease and high risk for Comments and Rationale: Patient education should
future ischemia an infarct. Cardiac catheterization is be provided in the language and format that the patient
indicated; it provides direct visualization of coronary prefers. Teaching about new medications and facili-
circulation and permits percutaneous intervention if tating the patient’s ability to obtain medications after
indicated. Implantation of drug-eluting stents should discharge through referral to social work or appropriate
generally be avoided in persons for whom adherence to resources is very important. Short hospital stays do not
dual antiplatelet therapy is unlikely. permit time for exhaustive, extensive education. Writ-
ten materials and referrals that the patient can use to
Patient Z recovered uneventfully from the PCI.
follow up on recommended lifestyle changes are there-
Her prescribed medications included simvastatin,
fore helpful. Risk reduction for Patient Z will involve
metoprolol, hydrochlorothiazide, additional oral
major lifestyle changes. Healthcare practitioners in all
antihypertensive medications, her “usual” oral
settings who encounter this patient will have a role to
hypoglycemic medications, aspirin, and clopi-
play in promoting increased adherence to recommended
dogrel. Patient Z’s fasting lipid panel showed a LDL
measures.
of 190 mg/dL and a total cholesterol of 250 mg/dL.
The discharge nurse began planning for Patient Z’s
return home. Conclusion
Comments and Rationale: Unless complications
develop, patients only remain in the hospital 24 to 48 The identification of the pathophysiologic process
hours after PCI. Therefore, assessment of discharge leading to ACS has redefined the treatment of
needs and initial teaching must begin immediately. this spectrum of cardiac disorders, and researchers
continue to refine therapeutic options to produce
The nurses caring for Patient Z noted that she was optimal patient outcomes. Despite a shared ini-
taking several medications that are new to her: tiating event (plaque rupture or erosion), UA/
simvastatin, metoprolol, aspirin, and clopidogrel. NSTEMI and STEMI are distinct clinical enti-
From the admission assessment, the nurse saw ties, with differences in pathophysiology, clinical
that the patient stopped taking her previously presentation, treatment, and prognosis. The diag-
prescribed statin because of its cost. She also noted nosis of UA/NSTEMI relies primarily on elevated
that Patient Z’s fasting lipid levels were high; levels of cardiac biomarkers (troponins) and the
some diet teaching might be helpful in assisting lack of ST-segment elevation on ECG [11; 12]. By
the patient to modify her diet and reduce this contrast, the diagnosis of STEMI is made solely
risk factor. The nurse referred Patient Z to social on ECG findings [11; 12]. After the type of MI
work for possible financial assistance with medica- has been determined, complex decision making
tions and to the dietician for assistance with diet is required to determine the appropriate course of
changes. When questioned, the patient stated treatment.
The goal of immediate treatment of UA/NSTEMI have tried to capitalize on the advantages of both
is relief of ischemia and prevention of recurrent approaches by combining them, but studies have
ischemic events. Risk stratification is essential for shown that this approach (facilitated PCI) has led
determining optimal treatment for patients, as an to significantly higher rates of adverse outcomes
early invasive approach is recommended for most [195]. Ancillary therapy with antiplatelet agents
patients except those at low risk for adverse events. (aspirin, clopidogrel, and glycoprotein IIb/IIIa
The topic of early invasive versus early conserva- inhibitors) and heparin or fondaparinux is used to
tive treatment has been addressed extensively in maintain patency of the infarct-related artery and
the literature, and findings led to a 2007 update of prevent reocclusion.
the ACC/AHA guidelines for the management of Review of data from several large-scale studies,
UA/NSTEMI. The updated guidelines recommend cardiac registries, and quality improvement ini-
more aggressive antiplatelet/anticoagulant therapy, tiatives has shown that adherence to guideline
regardless of whether an early invasive or early con- recommendations for the diagnosis, treatment, and
servative approach is chosen [11; 12]. Such therapy secondary prevention of UA/NSTEMI and STEMI
reduces platelet formation and aggregation, integral are suboptimal, particularly for older individuals,
components in the formation of a thrombus after women, and minority populations [21; 22; 23; 24;
plaque disruption. Antiplatelet agents used to treat 25; 26; 27; 28; 29; 30; 31; 32; 33; 34; 35; 36; 37;
UA/NSTEMI include aspirin and clopidogrel, and 38; 39]. In addition, an inverse relationship has
glycoprotein IIb/IIIa inhibitors have been found to been found between risk and treatment, with more
enhance outcomes [11; 12]. Anticoagulant therapy low-risk patients than high-risk patients receiving
with heparin, fondaparinux, or direct thrombin aggressive treatment [25; 27; 37]. The data have
inhibitors is also recommended [11; 12]. also demonstrated a clear benefit in survival and
With STEMI, the goal of immediate treatment is outcomes when guideline recommendations are
re-establishment of blood flow to the heart, as the followed. Thus, nurses practicing in any health-
precipitating factor in STEMI is a thrombus that care setting must become familiar with these
completely occludes an artery. The crucial factor guidelines in order to help facilitate adherence in
for determining the treatment approach is timing their individual practice settings. The develop-
from the onset of symptoms to treatment and from ment and use of protocols, clinical pathways, and
arrival in the emergency department to treatment. standardized order forms can help to ensure that
The preferred option for reperfusion is PCI, but the all patients receive appropriate care in a timely
recommended 90-minute door-to-balloon time is manner. After discharge, effective communication
difficult to achieve in most cases. The other option among members of the healthcare team and the
for reperfusion, fibrinolytic therapy, has the advan- patient and family is essential for ensuring long-
tage of immediately re-establishing blood flow, term compliance with lifestyle modifications and
but it is associated with lower rates of reperfusion medications, which will help reduce the risk of
and higher risks compared with PCI. Researchers future cardiac events.

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Acute Coronary Syndrome: An Overview For Nurses: How To Receive Credit

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Course #3091 — 15 CONTACT HOURS

Acute Coronary Syndrome:

Copyright © 2010 CME Resource

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OVERVIEW OF CORONARY CIRCULATION

Source: [73; 87] Table 1

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ECG CHANGES AND DIAGNOSIS OF STEMI

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COMPARISON OF PRIMARY CARDIAC BIOMARKERS

MI = myocardial infarction; CK-MB = cardiac-specific isoenzyme of creatine kinase.

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RISK FACTORS FOR CORONARY ARTERY DISEASE (CAD) ACCORDING TO

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Dobutamine Stress Echocardiogram (DSE) • Advanced age (65 years or older)

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ADJUNCTIVE TREATMENT FOR PATIENTS WITH UNSTABLE ANGINA/

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ADJUNCTIVE TREATMENT FOR PATIENTS WITH UNSTABLE ANGINA/

ADJUNCTIVE TREATMENT FOR PATIENTS WITH UNSTABLE ANGINA/

SIZE OF TREATMENT EFFECT FOR RECOMMENDED INTERVENTIONS

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COMPARISON OF FIBRINOLYTIC THERAPY AND PCI

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COMPARISON OF FIBRINOLYTIC AGENTS FOR TREATMENT

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OUTCOMES WITHIN FIVE YEARS AFTER FIRST MI

• Recommended secondary prevention after implantation of a drug-eluting stent [11; 12].

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Source: [237] Table 13

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Evidence-Based Practice Recommendations Citations

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