Unstable angina: pathophysiology and drug therapy.

Abstract:

:Unstable angina is a clinical syndrome characterized by increased rate and severity of angina pectoris attacks and, sometimes but not always, accompanied by ECG changes similar to those seen in coronary insufficiency. According to the present conception of the pathogenesis, ruptures at points of high-grade stenosis in the epicardial coronary arteries with simultaneous apposition of thrombi and vasoconstriction cause critical narrowing of the vascular lumen, which means that with the same level of oxygen consumption, coronary blood flow might be inadequate even at rest. In this way the development of severe ischemia, sudden cardiac death or myocardial infarction is programmed. Therapy must accordingly aim at avoiding or eliminating the progression of thrombosis and at increasing the reduced coronary blood flow. The prognosis is unequivocally improved by aspirin. In addition, heparin, 400 units/kg body weight, should be given. Thrombolysis may be possible after mechanical recanalization, depending on the individual results of coronary angiography. Providing the adverse reactions are monitored, nitroglycerin given intravenously is the basic drug therapy, although comparative studies against other drugs are not available and some data show the development of tolerance during prolonged use. Therefore, an early change to sustained-release nitrates or mononitrates can be justified. beta-receptor blockers reduce the frequency of silent ischemia and of myocardial infarction. By these means, in 80% of the patients affected, unstable angina will be converted to the stable form of the disease. If symptoms persist coronary angiography is urgently indicated, to allow the selection of PTCA or aortocoronary bypass surgery according to the findings.

journal_name

Eur J Clin Pharmacol

authors

Bleifeld W

doi

10.1007/BF01417569

subject

Has Abstract

pub_date

1990-01-01 00:00:00

pages

S73-6

eissn

0031-6970

issn

1432-1041

journal_volume

38 Suppl 1

pub_type

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