2014

Myocardial Infarction
Myocardial infarction (MI; Latin: infarctus myocardii) or acute myocardial infarction (AMI),
commonly known as a heart attack, occurs when blood stops flowing properly to a part of the heart, and
the heart muscle is injured because it is not receiving enough oxygen. Usually, this is because one of
the coronary arteries that supplies blood to the heart develops a blockage due to an unstable
buildup of white blood cells, cholesterol and fat. The event is called "acute" if it is sudden and serious.
Myocardial infarction differs from cardiac arrest, although cardiac arrest can be a consequence of MI.
A person having an acute MI usually has sudden chest pain that is felt behind the sternum and sometimes
travels to the left arm or the left side of the neck. Additionally, the person may have shortness of
breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety. Women experience fewer of these
symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue.
In many cases, in some estimates as high as 64%, the person does not have chest pain or has vague
symptoms. These are called "silent" myocardial infarctions.
Important risks are previous cardiovascular disease, old age, tobacco smoking, abnormal blood levels of
certain lipids, diabetes, high blood pressure, lack of physical activity, obesity, chronic kidney
disease, excessive alcohol consumption, and the use of cocaine and amphetamines. The main ways to
determine if a person has had a myocardial infarction are electrocardiograms (ECGs) that trace the
electrical signals in the heart and testing the blood for substances associated with damage to the heart
muscle. ECG testing is used to differentiate between two types of myocardial infarction based on the
appearance of the tracing. An ST section of the tracing higher than the baseline is called an ST
elevation MI (STEMI) which usually requires more aggressive treatment. If this is not the case, the
diagnosis is confirmed with a blood test (usually troponin).
Immediate treatments for a suspected MI often include aspirin, which prevents further blood from
clotting; nitroglycerin, sometimes given to treat chest pain; and oxygen. STEMI is treated by restoring
circulation to the heart, called reperfusion therapy, and typical methods are angioplasty, where the arteries
are pushed open, and thrombolysis, where the blockage is removed using medications. Non-ST elevation
myocardial infarction (NSTEMI) may be managed with medication, although angioplasty may be required
if the person is considered to be at high risk. People, who have multiple blockages of their coronary
arteries, particularly if they also have diabetes, may also be treated with bypass surgery (CABG). Ischemic
heart disease, which includes MI, angina, and heart failure when it happens after MI, was the leading cause
of death for both men and women worldwide in 2011.

Contents

1 Signs and symptoms

2 Causes

2.1 Lifestyle

2.2 Disease

2.3 Genetic

2.4 Other

3 Pathophysiology
o

3.1 Pathological types

4 Diagnosis

4.1 Classification

4.2 Electrocardiogram

4.3 Cardiac biomarkers

4.4 Imaging

5 Prevention
o

5.1 Lifestyle

5.2 Medication

6 Management
o

6.1 STEMI

6.2 NSTEMI

6.3 Cardiac rehabilitation

6.4 Secondary prevention

7 Prognosis
o

7.1 Complications

8 Epidemiology

9 Society and culture

9.1 Economics

9.2 Legal implications

10 Research

11 References

12 External links

Signs and symptoms

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely
instantaneous. Chest pain is the most common symptom of acute MI and is often described as a sensation
of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply)
of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate
to the lower jaw, neck, right arm, back, and upper abdomen, where it may mimic heartburn. Levine's sign,
in which patients localize the chest pain by clenching their fists over their sternums, has classically been
thought to be predictive of cardiac chest pain, although a prospective observational study showed it had a
poor positive predictive value.
Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle,
causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an
excessive form of sweating),[15] weakness, light-headedness, nausea, vomiting, and palpitations. These
symptoms are likely induced by a massive surge of catecholamine from the sympathetic nervous
system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac
dysfunction. Loss (due to inadequate blood flow to the brain and cardiogenic shock) and sudden
death (frequently due to the development of ventricular fibrillation) can occur in MIs.
Female, elderly, and diabetic patients report atypical symptoms more frequently than their male and
younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average
vs. 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea, weakness,
and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring
symptoms that may manifest as long as one month before the actual clinically manifested ischemic event.
In women, chest pain may be less predictive of coronary ischemia than in men. Women may also
experience back or jaw pain during an episode.
At least one-fourth of all MIs are silent, without chest pain or other symptoms. These cases can be
discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of
related complaints. Estimates of the prevalence of silent MIs vary between 22 and 64%. A silent course is
more common in the elderly, in patients with diabetes mellitus and after heart transplantation, probably
because the donor heart is not fully innervated by the nervous system of the recipient. In people with
diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as
possible explanations for the lack of symptoms.
Any groups of symptoms compatible with a sudden interruption of the blood flow to the heart are called
an acute coronary syndrome.

The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary
embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax,
and esophageal rupture. Other noncatastrophic differentials include gastro esophageal reflux and Tietze's
syndrome.

Causes
Many of the risk factors for myocardial infarction are modifiable and thus many cases may be preventable.

Lifestyle
Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery
disease. Lack of exercise has been linked to 712% of cases. Less common causes include stress-related
causes such as job stress, which accounts for about 3% of cases, and chronic high stress levels.
Tobacco smoking, including secondhand smoke Short-term exposure to air pollution, including carbon
monoxide, nitrogen dioxide, and sulfur dioxide, but not ozone. Lack of physical activity, psychosocial
factors including, low socioeconomic status, social isolation and negative emotions increase the risk of and
are associated with worse outcomes after MI. Socioeconomic factors such as a shorter education and
lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of
MI. Alcohol prolonged exposure to high quantities of alcohol can increase the risk of heart attack.
There is little evidence that reducing dietary saturated fat or increasing polyunsaturated fat intake affects
heart attack risk. Trans fats do appear to increase risk.

Disease
Diabetes mellitus (type 1 or 2), high blood pressure, dyslipidemia/hypercholesterolemia (abnormal levels
of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and
high triglycerides Obesity (defined by a body mass index of more than 30 kg/m, or alternatively by waist
circumference or waist-hip ratio).
A number of acute and chronic infections including: Chlamydophila pneumoniae, influenza, Helicobacter
pylori, and Porphyromonas gingivalis among others have been linked to atherosclerosis and myocardial
infarction. As of 2013, there is no evidence of benefit from antibiotics or vaccination, however, calling the
association into question.

Genetic
Genome-wide association studies have found 27 genetic variants that are associated with an increased risk
of myocardial infarction.[37] Strongest association of MI has been found with the 9p21 genomic locus,
which contains genes CDKN2A & 2B, although the single nucleotide polymorphisms that are implicated
are within a non-coding region. The majority of these variants are in regions that have not been previously
implicated in coronary artery disease. The following genes have an association with
MI: PCSK9, SORT1,MIA3, WDR12, MRAS, PHACTR1, LPA, TCF21, MTHFDSL, ZC3HC1, CDKN2A,
2B, ABO, PDGF0, APOA5, MNF1ASM283, COL4A1, HHIPC1, SMAD3, ADAMTS7, RAS1, SMG6,S
MG6, SNF8, LDLR, SLC5A3, MRPS6, KCNE2.

Other
At any given age, men are more at risk than women, particularly before menopause, but because in general
women live longer than men, ischemic heart disease causes slightly more total deaths in women. Family

history of ischemic heart disease or MI, particularly if one has a first-degree relative (father, brother,
mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at/or younger than
age 55 years (men) or 65 (women).
Oral contraceptive pillwomen who use combined oral contraceptive pills have a modestly increased risk
of myocardial infarction, especially in the presence of other risk factors, such as smoking.
An increased incidence of a heart attack is associated with time of day especially in the morning hours,
more specifically around 9 am.
Old age increases risk of a heart attack.

Pathophysiology
Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated
and ST-elevated MIs, which are most frequently (but not always) a manifestation of coronary artery
disease. The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial
coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the
artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall
of arteries (in this case, the coronary arteries), typically over decades.[46] Blood stream column irregularities
visible on angiography reflect artery lumen narrowing as a result of decades of advancing
atherosclerosis. Plaques can become unstable, rupture, and additionally promote the formation of a blood
clot that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the
coronary vasculature, it leads to MI (necrosis of downstream myocardium).
If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the
heart cells in the territory of the occluded coronary artery die (chiefly through necrosis) and do not grow
back. A collagen scar forms in their place. Recent studies indicate that another form of cell
death, apoptosis, also plays a role in the process of tissue damage subsequent to MI. As a result, the
patient's heart will be permanently damaged. This myocardial scarring also puts the patient at risk for
potentially life-threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can
rupture with catastrophic consequences.
Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in
conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is
believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular
fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden
cardiac death. Another life-threatening arrhythmia is ventricular tachycardia (V-tach/VT), which can cause
sudden cardiac death. However, VT usually results in rapid heart rates that prevent the heart from pumping
blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further
coronary ischemia and extension of the infarct.
The cardiac defibrillator device was specifically designed to terminate these potentially fatal arrhythmias.
The device works by delivering an electrical shock to the patient to depolarize a critical mass of the heart
muscle, in effect "rebooting" the heart. This therapy is time-dependent, and the odds of successful
defibrillation decline rapidly after the onset of cardiopulmonary arrest.
Myocardial infarction results from atherosclerosis. Inflammation is known to be an important step in the
process of atherosclerotic plaque formation. C-reactive protein (CRP) is a sensitive but
nonspecific marker for inflammation. Elevated CRP blood levels, especially measured with highsensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes. Moreover,
some drugs for MI might also reduce CRP levels. The use of high-sensitivity CRP assays as a means
of screening the general population is advised against, but it may be used optionally at the physician's
discretion in patients who already present with other risk factors or known coronary artery
disease. Whether CRP plays a direct role in atherosclerosis remains uncertain.
Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary
arteries can be detected with CT scans. Several studies have shown that coronary calcium can provide
predictive information beyond that of classical risk factors.
Hyperhomocysteinemia (high blood levels of the amino acid homocysteine) in homocysteinuria is
associated with premature atherosclerosis; whether elevated homocysteine in the normal range is causal is
controversial.

Pathological types
The two main types of acute myocardial infarction, based on pathology, are:

Transmural AMI is associated with atherosclerosis involving a major coronary artery. It can be
sub-classified into anterior, posterior, inferior, lateral, or septal. Transmural infarcts extend through the

whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood
supply. In addition, on ECG, ST elevation and Q waves are seen.

Subendocardial AMI involves a small area in the subendocardial wall of the left ventricle,
ventricular septum, or papillary muscles. The Subendocardial area is particularly susceptible to
ischemia. In addition, ST depression is seen on ECG.

Diagnosis
A diagnosis of myocardial infarction is made by integrating the history of the presenting illness and
physical examination with electrocardiogram findings and cardiac markers(blood tests for heart
muscle cell damage).A coronary angiogram allows visualization of narrowing or obstructions on the heart
vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a
myocardial infarction based on anatomy-pathological findings.
A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often
performed upon arrival to an emergency department. New regional wall motion abnormalities on

an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal
cases by the on-call cardiologist. In stable patients whose symptoms have resolved by the time of
evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used
in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or
pharmacologic stress. Thallium may also be used to determine viability of tissue, distinguishing whether
non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.

Contents

1 Diagnostic criteria

2 Physical examination

3 Electrocardiogram

4 Cardiac markers

5 Angiography

6 Histopathology

7 See also

8 References

Diagnostic criteria
According to the WHO criteria as revised in 2000, a cardiac troponin rise accompanied by either typical
symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of
MI.
Previous WHO criteria formulated in 1979 put less emphasis on cardiac biomarkers; according to these, a
patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria
are satisfied:
1. Clinical history of ischemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin

Physical examination
The general appearance of patients may vary according to the experienced symptoms; the patient may be
comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is
common and points to vasoconstriction. Some patients have low-grade fever (3839 C). Blood
pressure may be elevated or decreased, and the pulse can become irregular.
If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs
due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the
pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation,
such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound,
a pericardial friction rub and rales over the lung.

Electrocardiogram

The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad,
symptomatic emergency department populations. A serial ECG may be used to follow rapid changes in
time. The standard 12 lead ECG does not directly examine the right ventricle, and is relatively poor at
examining the posterior basal and lateral walls of the left ventricle. In particular, acute myocardial
infarction in the distribution of the circumflex artery is likely to produce a non-diagnostic ECG. The use of
additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may
improve sensitivity for right ventricular and posterior myocardial infarction.
The 12 lead ECG is used to classify patients into one of three groups:
1. those with ST segment elevation or new bundle branch block (suspicious for acute injury and a
possible candidate for acute reperfusion therapy with thrombolytics or primary PCI),
2. those with ST segment depression or T wave inversion (suspicious for ischemia), and
3. Those with a so-called non-diagnostic or normal ECG.
A normal ECG does not rule out acute myocardial infarction. Mistakes in interpretation are relatively
common, and the failure to identify high risk features has a negative effect on the quality of patient care.
It should be determined if a person is at high risk for myocardial infarction before conducting imaging tests
to make a diagnosis. People who have a normal ECG and who are able to exercise, for example, do not
merit routine imaging. Imaging tests such as stress radionuclide myocardial perfusion imaging or
stress echocardiography can confirm a diagnosis when a person's history, physical exam, ECG and cardiac
biomarkers suggest the likelihood of a problem.

Cardiac markers
Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their
damaged cell membranes into the bloodstream. Until the 1980s, the enzymes SGOT and LDH were used to
assess cardiac injury. Now, the markers most widely used in detection of MI are MB subtype of the
enzyme creatine kinase and cardiac troponins T and I as they are more specific for myocardial injury. The
cardiac troponins T and I which are released within 46 hours of an attack of MI and remain elevated for
up to 2 weeks and have nearly complete tissue specificity and are now the preferred markers for assessing
myocardial damage. Heart-type fatty acid binding protein is another marker, used in some home test kits.
Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial
infarction in the near future. New markers such as glycogen phosphorylase isoenzyme BB are under
investigation.
The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes).
When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for
them are taken over a 24-hour period. Because these enzyme levels are not elevated immediately following
a heart attack, patients presenting with chest pain are generally treated with the assumption that a
myocardial infarction has occurred and then evaluated for a more precise diagnosis.

Angiography
In difficult cases or in situations where intervention to restore blood flow is appropriate,
coronary angiography can be performed. A catheter is inserted into an artery (usually the femoral artery)
and pushed to the vessels supplying the heart. A radio-opaque dye is administered through the catheter and
a sequence of x-rays (fluoroscopy) is performed. Obstructed or narrowed arteries can be identified,
and angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill,
especially in emergency settings. It is performed by a physician trained in interventional cardiology.

Histopathology

Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a
normal microscope are so-called wavy fibers. Subsequently, the myocyte cytoplasm becomes
more eosinophilic (pink) and the cells lose their transversal striations, with typical changes and eventually
loss of the cell nucleus. The interstitium at the margin of the infarcted area is initially infiltrated
with neutrophils, then with lymphocytes and macrophages, who phagocytose ("eat") the myocyte debris.
The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the
infarct with a fibrous (collagenous) scar (which are typical steps in wound healing). The interstitial space
(the space between cells outside of blood vessels) may be infiltrated with red blood cells.
These features can be recognized in cases where the perfusion was not restored; re-perfused infarcts can
have other hallmarks, such as contraction band necrosis.
A cardiac troponin rise accompanied by typical symptoms, pathological Q waves, ST elevation or
depression, or coronary intervention is diagnostic of MI.
WHO criteria formulated in 1979 has classically been used to diagnose MI; a patient is diagnosed with MI
if two (probable) or three (definite) of the following criteria are satisfied:
1. Clinical history of ischemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers
At autopsy, a pathologist can diagnose an MI based on anatomy-pathological findings.

Classification
Myocardial infarctions are generally classified into ST elevation MI (STEMI) and non-ST elevation MI
(NSTEMI). A STEMI is the combination of symptoms related to poor oxygenation of the heart with
elevation of the ST segments on the electrocardiogram followed by an increase in proteins in the blood
related to heart muscles death. They make up about 25 to 40 percent of cases.
The phrase "heart attack" is often used non-specifically to refer to a myocardial infarction and to sudden
cardiac death. An MI is different from, but can cause cardiac arrest, which is the stopping of the heartbeat.
It is also distinct from heart failure, in which the pumping action of the heart is impaired. However, an MI
may lead to heart failure.
A 2007 consensus document classifies MI into five main types:

Type 1 spontaneous MI related to ischemia due to a primary coronary event such as plaque
erosion and/or rupture, fissuring, or dissection

Type 2 MI secondary to ischemia due to either increased oxygen demand or decreased supply,
e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension

Type 3 sudden unexpected cardiac death, including cardiac arrest, often with symptoms
suggestive of myocardial ischemia, accompanied by new ST elevation, or new left bundle branch
block (LBBB), or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy,
but death occurring before blood samples could be obtained, or at a time before the appearance of
cardiac biomarkers in the blood

Type 4 associated with coronary angioplasty or stents:

Type 4a MI associated with percutaneous coronary intervention (PCI)

Type 4b MI associated with stent thrombosis as documented by angiography or at

autopsy

Type 5 MI associated with CABG

Electrocardiogram
For a person to qualify as having a STEMI, in addition to reported angina, the ECG must show new ST
elevation in two or more adjacent ECG leads. This must be greater than 2 mm (0.2 mV) for males and
greater than 1.5 mm (0.15mV) in females if in leads V2 and V3 or greater than 1 mm (0.1 mV) if it is in
other ECG leads. A left bundle branch block that is believed to be new used to be considered the same as
ST elevation; however, this is no longer the case. In early STEMIs there may just be peaked T waves with
ST elevation developing later.

Cardiac biomarkers
While there are a number of different biomarkers, troponins are considered to be the best and reliance on
older tests (such as CK-MB) or myoglobin is discouraged. Copeptin may be useful to rule out MI rapidly
when used along with troponin.

Imaging
A chest radiograph and routine blood tests may indicate complications or precipitating causes, and are
often performed upon arrival to an emergency department. New regional wall motion abnormalities on
an echocardiogram are also suggestive of an MI. Echo may be performed in equivocal cases by the on-call
cardiologist.[63] In stable patients whose symptoms have resolved by the time of evaluation, technetium
(99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to
visualize areas of reduced blood flow in conjunction with physiological or pharmacological
stress. Thallium may also be used to determine viability of tissue, distinguishing whether nonfunctional
myocardium is actually dead or merely in a state of hibernation or of being stunned. Medical societies
recommend that the physician confirm a person is at high risk for myocardial infarction before conducting
imaging tests to make a diagnosis. Patients who have a normal ECG and who are able to exercise, for
example, do not merit routine imaging. Imaging tests such as stress radionuclide myocardial perfusion
imaging or stress echocardiography can confirm a diagnosis when a patient's history, physical exam, ECG,
and cardiac biomarkers suggest the likelihood of a problem.

Prevention
Myocardial infarction and other related cardiovascular diseases can be prevented to a large extent by a
number of interventions in terms of lifestyle and medical treatments.
On a population level, public health measures may be used to reduce unhealthy diets (excessive salt,
saturated fat and trans fat) including food labeling and marketing requirements as well as requirements for
catering and restaurants, and stimulating physical activity. This may be part of regional cardiovascular
disease prevention programmes, or through the health impact assessment of regional and local plans and
policies.

Lifestyle
People considered at high risk of cardiovascular disease or with previous cardiovascular problems are
advised to keep a diet where less than 30% of the energy intake derives from fat, a diet that contains less
than 7% of the energy intake in the form saturated fat, and a diet that contains less than 300 mg/day of
cholesterol. Replacing saturated with mono- polyunsaturated fat is also recommended, as the consumption

of polyunsaturated fat instead of saturated fat can decrease coronary heart disease. Olive oil, rape-seed
oil and related products are to be used instead of saturated fat. Other recommendations include: increased
intake of wholegrain starch, reduced sugar intake (particularly of refined sugar), consumption of 5 portions
of fruit and vegetables daily, consumption of 2 or more portions of fish per week, and 45 portions of
unsalted nuts, seeds or legumes per week. Vitamins and mineral supplements are of no proven benefit, and
neither are plant stanols or sterols.
Physical activity can reduce the risk of cardiovascular disease, and people at risk are advised to engage in
150 minutes of moderate or 75 minutes of vigorous intensity aerobic exercise a week. Keeping a healthy
weight, drinking alcohol within the recommended limits, and smoking cessation are measures that may
reduce the risk of cardiovascular disease.

Medication
Aspirin has been studied extensively in people considered at increased risk of myocardial infarction. Based
on numerous studies in different groups (e.g. people with or without diabetes), there does not appear to be
a benefit strong enough to outweigh the risk of excessive bleeding. Nevertheless, many clinical practice
guidelines continue to recommend aspirin for primary prevention, and some researchers feel that those
with very high cardiovascular risk but low risk of bleeding should continue to receive aspirin.
Cholesterol-lowering drugs from the statin class may be used in those at an elevated risk of cardiovascular
disease; this can be calculated with validated risk prediction tools such as QRISK2.

Management
Management of acute coronary syndrome is targeted against the effects of reduced blood flow to the
afflicted area of the heart muscle, usually because of a blood clot in one of the coronary arteries, the
vessels that supply oxygenated blood to the myocardium. This is achieved with urgent hospitalization and
medical therapy, including drugs that relieve chest pain and reduce the size of the infarct, and drugs that
inhibit clot formation; for a subset of patients invasive measures are also employed (coronary angiography
and percutaneous coronary intervention). Basic principles of management are the same for all types
of acute coronary syndrome. However, some important aspects of treatment depend on the presence or
absence of elevation of the ST segment on the electrocardiogram, which classifies cases upon presentation
to either ST segment elevation myocardial infarction (STEMI) or non-ST elevation acute coronary
syndrome (NST-ACS); the latter includes unstable angina and non-ST elevation myocardial infarction
(NSTEMI). Treatment is generally more aggressive for STEMI patients, and reperfusion therapy is
reserved for them. Long term therapy is necessary for prevention of recurrent events and complications.

Contents

1 General principles

2 Patient-dependent initial measures

3 Emergency services

4 Initial diagnostic approach

5 Relief of angina
o

5.1 Nitrates

5.2 Beta blockers

5.3 Oxygen therapy

5.4 Analgesics

6 Antiplatelet drugs
o

6.1 Aspirin

6.2 P2Y12 inhibitors

6.3 Glycoprotein IIb/IIIa inhibitors

7 Anticoagulants

8 Reperfusion

9 Rehabilitation

10 Special cases
o

10.1 Cocaine

10.2 Wilderness setting

10.3 Air travel

General principles
Acute coronary syndromes are caused by sudden and critical reduction of blood flow in one of the
coronary arteries, the vessels that supply oxygenated blood to the myocardium (heart muscle), typically by
a blood clot. The principal symptom is typically chest pain, known as angina pectoris; people who present
with angina must prompt evaluation for possible acute coronary syndrome.
Acute coronary syndromes are classified to two major categories, according to the patient's
electrocardiogram, and specifically the presence or absence of persistent (>20 min) ST segment
elevation (or left bundle branch block). Patients with acute coronary syndrome and ST elevation are said to
suffer from ST-elevation myocardial infarction (STEMI) and they tend to have one of their coronary
arteries totally blocked. Damage is reversible for approximately 20-30 minutes after complete obstruction
of blood flow; thereafter myocardial cell death ensues and progresses as time passes. Therefore, complete
and sustained restoration of blood flow must be as prompt as possible to ensure maximum salvage of
functional myocardium, a principle expressed in the maxim "time is muscle". This is achieved with
reperfusion therapy, which is based on invasive reopening of the afflicted coronary artery with primary

percutaneous coronary intervention, or non-invasive breaking up of the responsible blood clot with
a thrombolytic drug.
Patients without ST segment elevation are said to suffer from non-ST-elevation acute coronary syndrome
and tend not to have full occlusion of a coronary artery. If there is evidence of myocardial cell death
(especially elevated cardiac biomarkers) they are considered to have a non-ST-elevation myocardial
infarction (NSTEMI); otherwise they are classified as suffering from unstable angina. Their management is
based on the estimation of their risk for adverse events. Patients at low risk can be adequately treated with
medical therapy, in many ways similar to the one used for STEMI (but excluding thrombolytics). Those at
moderate to high risk benefit from an early invasive strategy, which includes coronary angiography and, if
necessary, revascularization with percutaneous coronary intervention or coronary artery bypass surgery.
Medical therapy for acute coronary syndromes is based on drugs that act against ischemia and resultant
angina and limit the infarct size (i.e., the area of myocardium that is affected); as well as drugs that inhibit
clot formation. The latter include antiplatelet agents, which block the activation and aggregation
of platelets (cellular blood components that contribute to clot formation), and anticoagulant agents (which
attenuate the coagulation cascade). Long-term therapy in acute coronary syndrome survivors is targeted
against recurrence and long term complications (secondary prevention).

Patient-dependent initial measures

Because of the relationship between the duration of myocardial ischemia and the extent of damage to heart
muscle, patients experiencing possible acute coronary syndrome symptoms or people around them are
encouraged to immediately call emergency medical services. Patients with known coronary artery
disease who have been prescribed nitroglycerin should promptly take one dose, and call emergency
medical services if their symptoms do not improve within 5 minutes. Patients should not be transported to
hospital by private vehicles instead of an ambulance. Chewing nonenteric-coated aspirin (162325 mg) is
encouraged (unless there are contraindications).
Health care professionals are responsible for teaching their patients at risk of acute coronary syndrome
what the symptoms of this condition are, and that it is imperative to seek urgent medical attention in case
they present.

Emergency services
Emergency Medical Services (EMS) Systems vary considerably in their ability to evaluate and treat
patients with suspected acute myocardial infarction. Some provide as little as first aid and early
defibrillation. Others employ highly trained paramedics with sophisticated technology and advanced
protocols. Paramedic
services
are
capable
of
providing
oxygen,
IV
access,
sublingual nitroglycerine, morphine, and aspirin. Some advanced paramedic systems can also perform 12lead ECGs.[15] If a STEMI is recognized the paramedic may be able to contact the local PCI hospital and
alert the emergency room physician, and staff of the suspected AMI. Some Paramedic services are capable
of providing thrombolytic therapy in the pre-hospital setting, allowing reperfusion of the myocardium.
With primary PCI emerging as the preferred therapy for ST-segment elevation myocardial
infarction, EMS can play a key role in reducing door-to-balloon intervals (the time from presentation to a
hospital ER to the restoration of coronary artery blood flow) by performing a 12-lead ECG in the field and
using this information to triage the patient to the most appropriate medical facility. In addition, the 12-lead
ECG can be transmitted to the receiving hospital, which enables time saving decisions to be made prior to
the arrival of the patient. This may include a "cardiac alert" or "STEMI alert" that calls in off duty
personnel in areas where the cardiac cath lab is not staffed 24 hours a day. Even in the absence of a formal
alerting program, pre-hospital 12-lead ECGs are independently associated with reduced door to treatment
intervals in the emergency department.

Initial diagnostic approach

In patients with symptoms typical of myocardial ischemia an electrocardiogram must be immediately
obtained - e.g., within 10 minutes from first contact with medical or paramedical personnel, including prehospital setting; the electrocardiographic findings will guide the subsequent management. Patients

with elevation of the ST segment (or presumed new left bundle branch block) are treated based on
guidelines for ST elevation myocardial infarction (STEMI) and must undergo reperfusion therapy as soon
as possible. Serum cardiac biomarkers are routinely obtained and their elevation is necessary for
confirming diagnosis of myocardial infarction; however, reperfusion must not be delayed by waiting for
the results. Patients without the above findings are initially classified as suffering from non ST elevation
acute coronary syndrome, and subsequent cardiac biomarker results will differentiate between true non ST
elevation myocardial infarction(NSTEMI) and unstable angina.

Relief of angina
Relief of the pain of angina is of paramount importance, not only for humane reasons but because the pain
is associated with sympathetic activation that causes vasoconstriction and increases the workload of the
heart.[24] The pain of myocardial ischemia is likely to respond to any intervention that improves the
relationship between oxygen demand and supply, like nitrates, beta blockers and oxygen.

Nitrates
Nitrates, like nitroglycerin, dilate blood vessels, which is beneficial against myocardial ischemia in two
ways: By increasing blood flow in the coronary arteries and the amount of oxygen that arrives to heart
muscle; and by relaxing all blood vessels in the body, thereby reducing the workload that heart needs to
produce against them and the oxygen it consumes. The preferred mode of administration is sublingually.
By relaxing blood vessels nitrates also reduce blood pressure, which must be carefully monitored; they
must not be used if hypotension is present. They must also be avoided in patients who have
taken sildenafil or other phosphodiesterase type 5 inhibitors (used for erectile dysfunction) within the
previous 2448 hours, as the combination of the two could cause a serious drop in blood
pressure. Intravenous nitrates are useful in patients with hypertension or pulmonary edema.

Beta blockers
By reducing sympathetic stimulation of the heart, beta blockers decrease heart rate, blood pressure
and cardiac output, and hence heart oxygen consumption. Beta-blockers alleviate ischemic pain, and have
also been proved to reduce the size of infarcted heart muscle, the risk of arrhytmias, and the proportion of
patients with acute coronary syndrome who actually evolve STEMI. However, they have also been shown
to increase the risk of acute heart failure. Their early use is contraindicated if there are signs of
congestive (e.g., Killip class II or above) or hypotension, along with other contraindications to beta
blockers (slow heart rate, atrioventricular block); in the absence of contraindications beta blocker therapy
should begin in the first 24 hours. It may be prudent to prefer oral rather than intravenous forms.

Oxygen therapy
Initial administration of oxygen to all patients with acute coronary syndrome is common practice; however,
there is evidence that supplemental oxygen might be harmful for cardiac patients who do not need it. It is
currently recommended to give oxygen only to breathless patients or when blood oxygen saturation is low,
e.g. <90%.

Analgesics
Analgesic agents that are most commonly used are opioids, and especially morphine, which is considered
the analgesic of choice in patients with ST elevation. Along with its pain-controlling properties, morphine
also reduces the work of breathing, alleviates breathlessness, reduces anxiety and has favorable action
on hemodynamic parameters and cardiac oxygen consumption. However, in patients presenting without ST
elevation, morphine has been shown to have adverse events potential, and its use is considered acceptable
only after inadequate pain relief by medication specific against angina. Non-steroidal anti-inflammatory
drugs are contraindicated for both categories of patients.

Antiplatelet drugs
All patients with acute coronary syndrome must immediately receive antiplatelet therapy, including aspirin
and generally a second oral antiplatelet agent. Bleeding is the most important side-effect of antiplatelets.

Aspirin

Aspirin inhibits platelet aggregation and formation of blood clots. It is effective across the entire spectrum
of acute coronary syndromes, and it actually has been shown to reduce the rate of death in patients with
STEMI and in patients presenting without ST elevation. Aspirin is contraindicated in patients with
documented allergy or known platelet disorder. Patients who have had long gastrointestinal symptoms
while on long-term aspirin therapy are usually able to tolerate aspirin in the short term. For patients with
true intolerance to aspirin clopidogrel is recommended. Lower doses need days to achieve full antiplatelet
effect; therefore a loading dose is necessary for patients who are not already on aspirin.

P2Y12 inhibitors
Aside of aspirin, three antiplatelet agents taken by mouth have been approved for use in acute coronary
syndromes, clopidogrel, ticagrelor and prasugrel; all reduce platelet aggregation by inhibiting
the P2Y12 receptor, a type of adenosine phosphate receptor, on platelet surface. Not all three of them are
equally indicated in all types of acute coronary syndromes. In patients with ST elevation the choice of
P2Y12 inhibitor depends on reperfusion strategy; for patients undergoing primary percutaneous coronary
intervention ticagrelor and prasugrel are considered superior to clopidogrel, as they are more potent and
have more rapid onset of action, at the cost of some increase in bleeding risk; for STEMI patients who are
treated with fibrinolysis and those who do not undergo reperfusion treatment only clopidogrel is indicated.
Prasugrel must not be given to patients with a history of ischemic stroke or aged 75 years or older. In
patients with non-ST elevation acute coronary syndrome current guidelines also recommend dual
antiplatelet therapy; clopidogrel and ticagrelor are indicated in this setting, with ticagrelor considered
superior for patients undergoing early invasive strategy (see later). However, emerging evidence questions
this strategy. As with aspirin, it is necessary to administer a loading dose.

Glycoprotein IIb/IIIa inhibitors

Glycoprotein IIb/IIIa inhibitors is a class of intravenous antiplatelet agents used in patients undergoing
percutaneous coronary intervention, consisting of abciximab, eptifibatideand tirofiban. Patients presenting
with ST elevation that will be re-perfused with percutaneous coronary intervention may receive one of the
above agents at the time of catheterization, or perhaps before. Administering eptifibatide or tirofibane may
also be reasonable in patients presenting with NST-ACS who are considered of intermediate or high risk
and are treated with early invasive strategy.

Anticoagulants
Anticoagulants in acute coronary syndrome are targeted against the coronary blood clot, as well as towards
prevention of thrombotic complications, like formation of blood clots in the ventricles, stroke, pulmonary
embolism or deep vein thrombosis. Patients undergoing PCI also need an anticoagulant to
prevent catheter thrombosis. Options include unfractionated heparin, enoxaparin (a low molecular weight
heparin), fondaparinux (a pentasaccharide antagonist of factor Xa) and bivalirudin (a direct thrombin
inhibitor); all the above agents are given parenterally (subcutaneously or intravenously). Unfractionated
heparin has the disadvantage of requiring dose adjustment based on a laboratory exam, activated (APTT).
In STEMI patients choice depends on the reperfusion strategy used (see below); bivalirudin is used when
PCI is employed only, while in the same case fodaparinux is not preferred. Similarly, in Non-STE ACS
bivalirudin too is only used when an early invsive strategy is chosen.

Reperfusion
The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction,
that we are said to be in the reperfusion era. Patients who present with suspected acute myocardial
infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are
presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates
for immediate reperfusion, either with thrombolytic therapy, percutaneous coronary intervention (PCI) or
when these therapies are unsuccessful, bypass surgery.

Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or
non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial
therapies and are often stabilized with antiplatelet drugs and anticoagulated. If their condition remains
(hemodynamically) stable, they can be offered either latecoronary angiography with subsequent restoration
of blood flow (revascularization), or non-invasive stress testing to determine if there is significant ischemia
that would benefit from revascularization. If hemodynamic instability develops in individuals with
NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of
thrombolytic agents is contraindicated in this patient subset, however.
The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically
due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden
narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium.
Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding.
At least 10% of patients with STEMI do not develop myocardial necrosis (as evidenced by a rise in cardiac
markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow
to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial
infarction. If treated within the hour, about 25% of STEMIs can be aborted.

Rehabilitation
Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances. This requires
monitoring in acoronary care unit and protocolised administration of antiarrhythmic agents.
Antiarrhythmic agents are typically only given to individuals with life-threatening arrhythmias after a
myocardial infarction and not to suppress the ventricular ectopy that is often seen after a myocardial
infarction.
Cardiac rehabilitation aims to optimize function and quality of life in those afflicted with a heart disease.
This can be with the help of a physician, or in the form of a cardiac rehabilitation program.
Physical exercise is an important part of rehabilitation after a myocardial infarction, with beneficial effects
on cholesterol levels, blood pressure, weight, stress and mood. Some patients become afraid of exercising
because it might trigger another infarct. Patients are stimulated to exercise, and should only avoid certain
exerting activities. Local authorities may place limitations on driving motorized vehicles. In most cases,
the advice is a gradual increase in physical exercise during about 68 weeks following an MI. If it doesn't
feel too hard for the patient, the advice about exercise is then the same as applies to anyone else to gain
health benefits, that is, at least 2030 minutes of moderate exercise on most days (at least five days per
week) to the extent of getting slightly short of breath.
Some people are afraid to have sex after a heart attack. Most people can resume sexual activities after 3 to
4 weeks. The amount of activity needs to be dosed to the patient's possibilities.

Special cases
Cocaine
Cocaine associated myocardial infarction should be managed in a manner similar to other patients with
acute coronary syndrome except beta blockers should not be used and benzodiazepines should be
administered early. The treatment itself may have complications. If attempts to restore the blood flow are
initiated after a critical period of only a few hours, the result may be a reperfusion injury instead of
amelioration.

Wilderness setting
In wilderness first aid, a possible heart attack justifies evacuation by the fastest available means, often
meaning the initiation of a MEDEVAC. The suspicion or provisional diagnosis of an MI means that it is
inappropriate for the patient to walk out of the wilderness setting and will require them to be carried or
conveyed in a vehicle. Aspirin, nitroglycerin, and oxygen can all be given with relative ease in a wilderness
setting and should be administered as soon as possible in suspected cases of MI. Wilderness management
of cardiac arrest differs slightly from that carried out in an urban setting in that it is generally considered

acceptable to terminate a resuscitation attempt after 30 minutes if there has been no change in the patient's
condition.

Air travel
Certified personnel traveling by commercial aircraft may be able to assist an MI patient by using the onboard first aid kit, which may contain some cardiac drugs (such as glyceryl trinitrate spray, aspirin,
or opioid painkillers), an AED, and oxygen. Pilots may divert the flight to land at a nearby airport. Cardiac
monitors are being introduced by some airlines, and they can be used by both on-board and ground-based
physicians.
An MI requires immediate medical attention. Treatment attempts to save as much viable heart muscle as
possible and to prevent further complications, hence the phrase "time is [heart] muscle". Aspirin and
nitroglycerin may be administered. Nitroglycerin (administered under the tongue or intravenously) may be
administered to improve the blood supply to the heart. Morphine may be used if nitroglycerin is not
effective. Other analgesics such as nitrous oxide are of unknown benefit.
In the past, high flow oxygen was recommended for everyone with possible myocardial infarction. More
recently, routine use was found to lead to increased mortality and infarct size. Therefore, oxygen is
currently only used if oxygen levels are found to be low or someone is in respiratory distress.

STEMI
The current definitive treatment modalities for MI with ECG evidence of ST elevation (STEMI)
include thrombolysis and percutaneous coronary intervention.
Thrombolysis involves the administration of medication that activates the enzymes that normally destroy
blood clots. The first thrombolysis agent was streptokinase, but most thrombolysis agents used currently
are
artificial
forms
of
the
human
enzyme tissue
plasminogen
activator (tPA): reteplase, alteplase and tenecteplase. They are administered intravenously. Once a STEMI
has been diagnosed, and no contraindications are present (such as a high risk of bleeding), thrombolysis
can be administered in the pre-hospital or in-hospital setting. There is inconclusive evidence whether prehospital thrombolysis reduces death in people with STEMI compared to in-hospital thrombolysis. Prehospital thrombolysis reduces time to receipt of thrombolytic treatment, based on studies conducted in
higher income countries. If despite thrombolysis there is significant cardiogenic shock, continued severe
chest pain, or less than a 50% improvement in ST elevation on the ECG recording after 90 minutes, then
rescue PCI is indicated emergently.
Primary percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be
performed in a hospital in a timely manner.
If PCI cannot be performed within 90 to 120 minutes then thrombolysis, preferably within 30 minutes of
arrival to hospital, is recommended. After PCI, people are generally placed on dual antiplatelet therapy for
at least a year (which is generally aspirin and clopidogrel).

NSTEMI
In the absence of ST elevation, formal diagnosis of MI is delayed until a blood test for biomarkers (usually
troponin) can be performed; this is 36 hours after the onset of symptoms. The scenario is referred to as
"non-ST elevation acute coronary syndrome" (NSTEACS). In the meantime, the calculated risk of further
cardiovascular events (e.g. using the GRACE score) and the presence of other ECG changes and clinical
features determine ongoing management.
People with an acute coronary syndrome where no ST elevation is demonstrated (non-ST elevation ACS or
NSTEACS) are treated with aspirin. Clopidogrel is added in many cases, particularly if the risk of
cardiovascular events is felt to be high and early PCI is being considered. Depending on whether early PCI
is planned, an inhibitor of antithrombin (fondaparinux or low molecular weight heparin) may be added. In
very
high-risk
scenarios, inhibitors
of
the
platelet
glycoprotein
IIb3a receptor such
aseptifibatide or tirofiban may be used.
Heparins in those who have had an NSTEMI or unstable angina do not change the risk of death. They do
decrease the risk of having a further myocardial infarction.

P2Y12 inhibitors such as clopidogrel or ticagrelor do not change the risk of death when given to people
with a suspected NSTEMI prior to PCI. They do however increase the risk of bleeding and decrease the
risk of further cardiovascular problems. Thus their routine use prior to PCI is of questionable value.

Cardiac rehabilitation
Cardiac rehabilitation benefits many who have experienced myocardial infarction, even if there has been
substantial heart damage and resultant left ventricular failure; ideally other medical conditions that could
interfere with participation should be managed optimally. It should start soon after discharge from hospital.
The programme may include lifestyle advice, exercise, social support, as well as recommendations
about driving, flying, sport participation, stress management, and sexual intercourse.

Secondary prevention
A number of lifestyle recommendations are available to those who have experienced myocardial infarction.
This includes the adoption of a Mediterranean-type diet, maintaining alcohol intake within recommended
limits, exercising to the point of mild breathlessness for 2030 minutes every day, stopping smoking, and
trying to achieve a healthy weight.
People are usually started on several long-term medications after an MI, with the aim of preventing further
cardiovascular events such as MIs, congestive heart failure, or strokes.

Aspirin as well as another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet
therapy" or DAPT) is continued for up to twelve months, followed by asprin indefinitely. If someone
has another medical condition that requires anticoagulation (e.g. with warfarin) this may need to be
adjusted based on risk of further cardiac events as well as bleeding risk. In those who have had a stent
more than 12 months of clopidogrel plus aspirin does not affect the risk of death.

Beta blocker therapies such as metoprolol or carvedilol are recommended to be started within 24
hours, provided there is no acute heart failure or heart block. The dose should be increased to the
highest tolerated. Contrary to what was long believed, the use of beta blockers does not appear to
affect the risk of death, possibly because other treatments for MI have become better. They should not
be used in those who have recently taken cocaine.

ACE inhibitor therapy should be commenced when stable and continued indefinitely at the highest
tolerated dose. Those who cannot tolerate ACE inhibitors may be treated with angiotensin II receptor
antagonist.

Statin therapy has been shown to reduce mortality and morbidity. The protective effects of statins
may be due to more than their LDL lowering effects. The general consensus is that statins have the
ability to stabilize plaques and multiple other ("pleiotropic") effects that may prevent myocardial
infarction in addition to their effects on blood lipids.

Aldosterone antagonists (spironolactone or eplerenone) may be used if there is evidence of left

ventricular dysfunction after an MI, ideally after commencing an ACE inhibitor.

Previous studies suggesting a benefit from omega-3 fatty acid supplementation has not been
confirmed.

Prognosis

The prognosis after MI varies greatly depending on a person's health, the extent of the heart damage, and
the treatment given.
In those who have an STEMI in the United States, between 5 to 6 percent die before leaving hospital and 7
to 18 percent die within a year.
Using variables available in the emergency room, people with a higher risk of adverse outcome can be
identified. One study found 0.4% of patients with a low-risk profile died after 90 days, whereas in highrisk people it was 21.1%.
Some risk factors for death include: age, hemodynamic parameters (such as heart failure, cardiac arrest on
admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes,
serum creatinine, peripheral vascular disease, and elevation of cardiac markers. Assessment of left
ventricular ejection fraction may increase the predictive power. Prognosis is worse if a mechanical
complication such as papillary muscle or myocardial free wall rupture occurs. Morbidity and mortality
from myocardial infarction has improved over the years due to better treatment.

Complications

Myocardial infarction complications may occur immediately following a heart attack (in
the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious
complication is a second infarction, which may occur in the domain of another atherosclerotic coronary
artery, or in the same zone if there are any live cells left in the infarct.

Contents

1 Congestive heart failure

2 Myocardial rupture

3 Arrhythmia

4 Pericarditis

5 Cardiogenic shock

6 References

Congestive heart failure

A myocardial infarction may compromise the function of the heart as a pump for the circulation, a state
called heart failure. There are different types of heart failure; left- or right-sided (or bilateral) heart failure
may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the
heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided
coronary occlusion that disrupts the blood supply of the papillary muscles. The incidence of heart failure is
particularly high in patients with diabetes and requires special management strategies. [1]

Myocardial rupture
Myocardial rupture is most common three to five days after myocardial infarction, commonly of small
degree, but may occur one day to three weeks later. In the modern era of early revascularization and
intensive pharmacotherapy as treatment for MI, the incidence of myocardial rupture is about 1% of all
MIs. This may occur in the free walls of the ventricles, the septum between them, the papillary muscles, or
less commonly the atria. Rupture occurs because of increased pressure against the weakened walls of the
heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to
ventricular aneurysm, a localized dilation or ballooning of the heart chamber.
Risk factors for myocardial rupture include completion of infarction (no revascularization performed),
female sex, advanced age, and a lack of a previous history of myocardial infarction. In addition, the risk of
rupture is higher in individuals who are revascularized with a thrombolytic agent than with PCI. The shear
stress between the infarcted segment and the surrounding normal myocardium (which may be
hypercontractile in the post-infarction period) makes it a nidus for rupture.
Rupture is usually a catastrophic event that may result a life-threatening process known as cardiac
tamponade, in which blood accumulates within the pericardium or heart sac, and compresses the heart to
the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating
the left and right ventricles) causes a ventricular septal defect with shunting of blood through the defect
from the left side of the heart to the right side of the heart, which can lead to right ventricular failure as
well as pulmonary over circulation. Rupture of the papillary muscle may also lead to acute mitral
regurgitation and subsequent pulmonary edema and possibly even cardiogenic shock.

Arrhythmia

Since the electrical characteristics of the infarcted tissue change (see pathophysiology
section), arrhythmias are a frequent complication.[6]The re-entry phenomenon may cause rapid heart rates
(ventricular tachycardia and even ventricular fibrillation), and ischemia in the electrical may cause
a complete heart block (when the impulse from the sinoatrial node, the normal cardiac pacemaker, does not
reach the heart chambers).

Pericarditis
As a reaction to the damage of the heart muscle, inflammatory cells are attracted. The inflammation may
reach out and affect the heart sac. This is called pericarditis. In Dressler's syndrome, this occurs several
weeks after the initial event.

Cardiogenic shock
A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks
following is cardiogenic shock. Cardiogenic shock is defined as a hemodynamic state in which the heart
cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the
tissues of the body.
While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data
suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75
years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of
cardiogenic shock is less than 18 hours. If the patient with cardiogenic shock is not going to be
revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon
pump if not contraindicated.[9] If diagnostic coronary angiography does not reveal a culprit blockage that is
the cause of the cardiogenic shock, the prognosis is poor.[9]
Complications may occur immediately following the heart attack (in the acute phase), or may need time to
develop (a chronic problem). Acute complications may include heart failure if the damaged heart is no
longer able to pump blood adequately around the body; aneurysm or rupture of the myocardium; mitral
regurgitation, in particular if the infarction causes dysfunction of the papillary muscle; Dressler's
syndrome; and arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation, and
heart block. Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a
second MI.