++
PATHOPHYSIOLOGY OF ISCHEMIC HEART DISEASE
++
Angina pectoris, the primary symptom of ischemic heart disease, is caused by transient episodes of myocardial ischemia that are due to an imbalance in the myocardial oxygen supply–demand relationship. This imbalance may be caused by an increase in myocardial oxygen demand (which is determined by heart rate, ventricular contractility, and ventricular wall tension) or by a decrease in myocardial oxygen supply (primarily determined by coronary blood flow, but occasionally modified by the oxygen-carrying capacity of the blood) or sometimes by both (Figure 27–1). Because blood flow is inversely proportional to the fourth power of the artery's luminal radius, the progressive decrease in vessel radius that characterizes coronary atherosclerosis can impair coronary blood flow and lead to symptoms of angina when myocardial O2 demand increases, as with exertion (so-called typical angina pectoris). In some patients, anginal symptoms may occur without any increase in myocardial O2 demand, but rather as a consequence of an abrupt reduction in blood flow, as might result from coronary thrombosis (unstable angina) or localized vasospasm (variant or Prinzmetal angina). Regardless of the precipitating factors, the sensation of angina is similar in most patients. Typical angina is experienced as a heavy, pressing substernal discomfort (rarely described as a "pain"), often radiating to the left shoulder, flexor aspect of the left arm, jaw, or epigastrium. However, a significant minority of patients note discomfort in a different location or of a different character. Women, the elderly, and diabetics are more likely to experience myocardial ischemia with atypical symptoms. In most patients with typical angina, whose symptoms are provoked by exertion, the symptoms are relieved by rest or by administration of sublingual nitroglycerin.
++
++
Angina pectoris is a common symptom, affecting more than 9 million Americans (Rosamond et al., 2008). Angina pectoris may occur in a stable pattern over many years or may become unstable, increasing in frequency or severity and even occurring at rest. In typical stable angina, the pathological substrate is usually fixed atherosclerotic narrowing of an epicardial coronary artery, on which exertion or emotional stress superimposes an increase in myocardial O2 demand. In variant angina, focal or diffuse coronary vasospasm episodically reduces coronary flow. Patients also may display a mixed pattern of angina with the addition ...