Angina pectoris is a clinical manifestation that results from coronary atherosclerotic heart disease. An acute anginal attack (secondary angina) is thought to occur because of an imbalance between myocardial oxygen supply and demand owing to the inability of coronary blood flow to increase in proportion to increases in myocardial oxygen requirements. This is generally the result of severe coronary artery atherosclerosis. Angina pectoris (variant, primary angina) may also occur as a result of vasospasm of large epicardial coronary vessels or one of their major branches. In addition, angina in certain patients may result from a combination of coronary vasoconstriction, platelet aggregation, plaque rupture, and an increase in myocardial oxygen demand (crescendo or unstable angina).

Antianginal drugs may relieve attacks of acute myo-cardial ischemia by increasing myocardial oxygen supply or by decreasing myocardial oxygen demand or both. Three groups of pharmacological agents have been shown to be effective in reducing the frequency, severity, or both of primary or secondary angina. These agents include the nitrates, p-adrenoceptor antagonists, and calcium entry blockers. To understand the beneficial actions of these agents, it is important to be familiar with the major factors regulating the balance between myocardial oxygen supply and demand. These factors are summarized in Table 17.1.

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