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.

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.

• 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.