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 myocardial 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, -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.
THE THERAPEUTIC OBJECTIVES IN THE USE OF ANTIANGINAL DRUGS:-
The major therapeutic objectives in the treatment of angina are aimed at terminating or preventing an acute attack and increasing the patient’s exercise capacity. These objectives can be achieved by reducing overall myocardial oxygen demand or by increasing oxygen supply to ischemic areas.A decrease in myocardial oxygen demand can be attained through use of the organic nitrates,calcium entry blockers,and -adrenoceptor blocking agents.
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