New concepts for the treatment of unstable angina: role for intravenous diltiazem

Abstract

The management of unstable angina continues to undergo rapid evolution as new therapies and techniques become increasingly available to clinicians. It appears that the pathogenesis of unstable angina involves endothelial factors (plaque rupture of fissure resulting in a complex coronary stenotic lesion) together with dynamic factors (including platelet aggregation, thrombosis, and altered coronary vasomotor tone), and therefore it is clear why the approach to the patient with acute coronary syndromes has become multidimensional. This article summarizes the current views of the pathogenesis of unstable angina, and the role that the above factors may play in the clinical syndrome of acute coronary insufficiency. In addition, the newer therapeutic approaches to the pharmacologic management of unstable angina are discussed, including the use of nitrates, heparin, aspirin, and beta-blockers. Increasingly, calcium-channel blockers are being utilized in the early pharmacologic management of unstable angina, particularly because these agents have a salutary effect on reducing increased coronary vasomotor tone, reducing myocardial oxygen demand while at the same time augmenting coronary blood flow, and decreasing platelet aggregation. Numerous small clinical trials have examined the role of intravenous calcium-channel-blocker therapy for the acute management of unstable angina. In particular, intravenous diltiazem appears to be both safe and efficacious in this setting, and may offer some advantages to intravenous nitroglycerin, when used in the Coronary Care Unit setting. Because diltiazem is a heart rate-lowering vasoactive drug, it may attenuate myocardial ischemia without causing reflex tachycardia associated with other vasoactive pharmacologic therapies. Several of these studies utilizing intravenous diltiazem in unstable angina are reviewed and discussed.