Coronary Artery Disease and Congestive Heart Failure

Myocardial ischemia is a result of myocardial oxygen demand exceeding available supply. In nonatherosclerotic canine coronary vessels, resting distal coronary blood flow can be maintained until the arterial diameter is constricted by 85%. Myocardial contractile function is lost by 75% following reduction of blood flow. However, maximal coronary artery blood flow declines when arterial diameter is constricted by 30–45% (1), a circumstance clinically analogous to conditions of increased oxygen demand such as anemia, fever, hypertension, or exercise in the setting of mild atherosclerosis. The human condition differs from experimental nonatherosclerotic animals as to the presence of paradoxical vasoconstriction, resulting from endothelial dysfunction and diffuse atherosclerosis that leads to long-narrowed segments of coronary arteries. Although autoregulatory range in humans with single vessel coronary artery disease and normal left-ventricular function is similar to experimental animals, in the setting elevated venous pressure (i.e., congestive heart failure [CHF]), left-ventricular hypertrophy (i.e., diastolic dysfunction), diabetes or chronic hypertension, microvascular autoregulation is impaired, and subendocardial ischemia results (2,3). Therefore, a lesser severity of stenosis may cause ischemia at minimal exertion.