Ischemic heart disease (IHD) is defined as lack of oxygen and decreased or no

blood
flow to the myocardium resulting from coronary artery narrowing or obstruction.
It may present as acute coronary syndrome (ACS), which includes unstable angina
and nonST-segment elevation (NSTE) or ST-segment elevation (STE) myocardial
infarction (MI), chronic stable exertional angina, ischemia without symptoms, or
ischemia due to coronary artery vasospasm (variant or Prinzmetal angina).
PATHOPHYSIOLOGY
Major determinants of myocardial oxygen demand (MVo2) are heart rate (HR),
contractility,
and intramyocardial wall tension during systole. Because the consequences
of IHD usually result from increased demand with a fixed oxygen supply,
alterations
in MVo2 are important in producing ischemia and for interventions intended to
alleviate it.
The double product (DP) is the heart rate multiplied by the systolic blood
pressure
(DP = HR SBP) and serves as an indirect estimate of MVo2.
The caliber of resistance vessels delivering blood to the myocardium and MVo2
are
the primary determinants in the occurrence of ischemia.
Large epicardial or surface coronary vessels (R1) offer little resistance to
myocardial
flow and intramyocardial arteries and arterioles (R2), which branch into a dense
capillary network to supply basal blood flow. Under normal circumstances,
resistance
in R2 is much greater than that in R1. Myocardial blood flow is inversely related to

arteriolar resistance and directly related to coronary driving pressure.

Atherosclerotic lesions occluding R1 increase arteriolar resistance, and R2 can
vasodilate
to maintain coronary blood flow. With greater degrees of obstruction, this
response is inadequate, and the coronary flow reserve afforded by R2 vasodilation
is
insufficient to meet oxygen demand.
The diameter and length of obstructing lesions and the influence of pressure drop
across an area of stenosis also affect coronary blood flow. Dynamic coronary
obstruction
can occur in normal vessels and vessels with stenosis in which vasomotion or a
spasm may be superimposed on a fixed stenosis. Persisting ischemia may promote
growth of collateral blood flow.
Relatively severe stenosis (>70%) may provoke ischemia and symptoms at rest.
Lesions creating obstruction of 50% to 70% may reduce blood flow, but these
obstructions are not consistent, and vasospasm and thrombosis superimposed on a
noncritical lesion may lead to clinical events such as MI.
Regional loss of ventricular contractility may impose a burden on remaining
myocardial
tissue, resulting in heart failure (HF), increased MVo2, and rapid depletion
of blood flow reserve. Zones of tissue with marginal blood flow may develop that
are at risk for more severe damage if the ischemic episode persists or becomes
more
severe. Nonischemic areas of myocardium may compensate for severely ischemic
and border zones of ischemia by developing more tension than usual in attempt to
maintain cardiac output. The left or right ventricular dysfunction that ensues may
be

associated with an S3 gallop, dyspnea, orthopnea, tachycardia, fluctuating blood

pressure,
transient murmurs, and mitral or tricuspid regurgitation. Impaired diastolic and
systolic function leads to elevated left ventricular filling pressure.
CLINICAL PRESENTATION
Many ischemic episodes are asymptomatic (silent ischemia). Patients often have
a
reproducible pattern of pain or other symptoms that appear after a specific amount
of
exertion. Increased symptom frequency, severity, or duration, and symptoms at rest
suggest an unstable pattern that requires immediate medical evaluation.
Ischemic Heart Disease 11
CHAPT ER
103
Ischemic Heart Disease | CHAPTER 11
Symptoms may include a sensation of pressure or burning over the sternum or
near it, which often radiates to the left jaw, shoulder, and arm. Chest tightness and
shortness of breath may also occur. The sensation usually lasts from 30 seconds to
30 minutes.
Precipitating factors include exercise, cold environment, walking after a meal,
emotional
upset, fright, anger, and coitus. Relief occurs with rest and within 45 seconds
to 5 minutes of taking nitroglycerin.
Patients with variant (Prinzmetal) angina secondary to coronary spasm are more
likely to experience pain at rest and in the early morning hours. Pain is not usually
brought on by exertion or emotional stress or relieved by rest; the
electrocardiogram

(ECG) pattern demonstrates current injury with ST-segment elevation rather than
depression.
Unstable angina is stratified into categories of low, intermediate, or high risk for
short-term death or nonfatal MI. Features of high-risk unstable angina include:
(1) accelerating tempo of ischemic symptoms in the preceding 48 hours; (2) pain
at rest lasting more than 20 minutes; (3) age older than 75 years; (4) ST-segment
changes; and (5) clinical findings of pulmonary edema, mitral regurgitation, S3,
rales,
hypotension, bradycardia, or tachycardia.
Episodes of ischemia may also be painless, or silent, perhaps due to a higher
threshold
and tolerance for pain than in patients who have pain more frequently.
DIAGNOSIS
Obtain medical history to identify the nature or quality of chest pain, precipitating
factors, duration, pain radiation, and response to nitroglycerin or rest. Ischemic
chest
pain may resemble pain from noncardiac sources, and diagnosis of anginal pain
may
be difficult based on history alone.
Ask the patient about personal risk factors for coronary heart disease (CHD),
including
smoking, hypertension, and diabetes mellitus.
Obtain family history that includes information about premature CHD,
hypertension,
lipid disorders, and diabetes mellitus.
Findings on cardiac examination may include abnormal precordial systolic bulge,

decreased intensity of S1, paradoxical splitting of S2, presence of S3 or S4, apical

systolic
murmur, and diastolic murmur.
Laboratory tests: hemoglobin, fasting glucose (to exclude diabetes), and fasting
lipid
panel. High-sensitivity C-reactive protein (hsCRP); homocysteine level; evidence
of
Chlamydia infection; and elevations in lipoprotein (a), fibrinogen, and
plasminogen
activator inhibitor may be helpful. Cardiac enzymes are normal in stable angina.
Troponin T or I, myoglobin, and creatinine kinase myocardial band (CK-MB) may
be elevated in unstable angina.
Resting ECG is normal in about half of patients with angina who are not
experiencing
acute ischemia. Typical STT-wave changes include depression, T-wave inversion,
and ST-segment elevation. Variant angina is associated with ST-segment elevation,
whereas silent ischemia may produce elevation or depression. Significant ischemia
is
associated with ST-segment depression greater than 2 mm, exertional hypotension,
and reduced exercise tolerance.
Exercise tolerance (stress) testing (ETT), thallium myocardial perfusion
scintigraphy,
radionuclide angiocardiography, ultrarapid computed tomography, and coronary
angiography may be performed in certain circumstances. Obtain a chest radiograph
if the patient has HF symptoms.
TREATMENT

 Goals of Treatment: Short-term goals are to reduce or prevent anginal symptoms

that
limit exercise capability and impair quality of life. Long-term goals are to prevent
CHD events such as MI, arrhythmias, and HF and to extend the patients life.
104
SECTION 2 | Cardiovascular Disorders
NONPHARMACOLOGIC THERAPY
Primary prevention through modification of risk factors should reduce prevalence
of
IHD. Secondary intervention is effective in reducing subsequent morbidity and
mortality.
Risk factors for IHD are additive and can be classified as alterable or unalterable.
Unalterable risk factors include gender, age, family history or genetic composition,
environmental influences, and, to some extent, diabetes mellitus. Alterable risk
factors include smoking, hypertension, hyperlipidemia, obesity, sedentary lifestyle,
hyperuricemia, psychosocial factors such as stress, and use of drugs that may be
detrimental (eg, progestins, corticosteroids, calcineurin inhibitors).
PHARMACOLOGIC THERAPY
-Adrenergic Blockers
Decreased HR, contractility, and blood pressure reduce MVo2 and oxygen
demand
in patients with effort-induced angina. -Blockers do not improve oxygen supply,
and, in certain instances, unopposed -adrenergic stimulation may lead to coronary
vasoconstriction.
-Blockers improve symptoms in approximately 80% of patients with chronic
exertional

stable angina, and objective measures of efficacy demonstrate improved exercise

duration
and delay in the time at which ST-segment changes and initial or limiting
symptoms
occur. -Blockade may allow angina patients previously limited by symptoms to
perform
more exercise and improve cardiovascular performance through a training effect.
Ideal candidates for -blockers include patients in whom physical activity is a
prominent
cause of attacks; those with coexisting hypertension, supraventricular arrhythmias,
or post-MI angina; and those with anxiety associated with anginal episodes.
-Blockers may be used safely in angina and HF.
-Blockade is effective in chronic exertional angina as monotherapy and in
combination
with nitrates and/or calcium channel blockers (CCBs). -Blockers are first line in
chronic angina requiring daily maintenance therapy because they are more
effective
in reducing episodes of silent ischemia and early-morning peak of ischemic
activity
and improving mortality after Q-wave MI than nitrates or CCBs.
If -blockers are ineffective or not tolerated, monotherapy with a CCB or
combination
therapy may be instituted. Reflex tachycardia from nitrates can be blunted with
-blocker therapy, making this a useful combination.
Initial doses of -blockers should be at the lower end of the usual dosing range
and

titrated to response. Treatment objectives include lowering the resting HR to 50 to

60
beats/min and limiting maximal exercise HR to approximately 100 beats/min or
less.
HR with modest exercise should be no more than approximately 20 beats/min
above
resting HR (or a 10% increment over resting HR).
There is little evidence to suggest superiority of any particular -blocker. Those
with
longer half-lives may be administered less frequently, but even propranolol may
be given
twice daily in most patients. Membrane-stabilizing activity is irrelevant in angina
treatment.
Intrinsic sympathomimetic activity appears to be detrimental in patients with rest
or severe angina because the reduction in HR would be minimized, limiting
reduction
in MVo2. Cardioselective -blockers may minimize adverse effects such as
bronchospasm,
intermittent claudication, and sexual dysfunction. Combined nonselective - and
-blockade with labetalol may be useful in patients with marginal left ventricular
(LV)
reserve.
Adverse effects of -blockade include hypotension, decompensated HF,
bradycardia,
heart block, bronchospasm, altered glucose metabolism, fatigue, malaise, and
depression.
Abrupt withdrawal has been associated with increased severity and number of

anginal episodes and MI. Tapering of therapy over several days should minimize
risk
of withdrawal reactions if therapy is to be discontinued.
Nitrates
Nitrates reduce MVo2 secondary to venodilation and arterial-arteriolar dilation,
leading to a reduction in wall stress from reduced ventricular volume and pressure