Introduction

The Big Heart Disease Lie

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During the past two decades the pathophysiologic mechanisms considered responsible for the acute coronary syndromes (ST-segment elevation myocardial infarction [MI], ST-segment depression MI, and unstable angina) have been evolving dramatically. In the mid-to-late 1970s, episodic coronary vasospasm was thought to be responsible for the development of unstable angina and acute MI (AMI) (1,2). In the mid-to-late 1980s and mid-1990s, plaque rupture and subsequent thrombus formation were considered paramount (3,4), and coronary vasoconstriction was considered quite inconsequential. The different acute coronary syndromes were perceived simply to represent different points on a single continuum of plaque rupture and thrombus formation: the continuum ranged from a ruptured plaque with little or no thrombus (often asymptomatic), to a ruptured plaque with moderate thrombus leading to only partial coronary occlusion (unstable angina and MI associated with ST-segment depression), to a ruptured plaque with extensive thrombus and complete occlusion of the artery (MI associated with ST-segment elevation). In the mid-to-late 1990s, however, it has been appreciated that this two-component pathophysiologic model of the acute coronary syndromes may be simplistic and inadequate for some patients. Recent evidence from atherectomy samples, for example, indicate that a substantial number of patients with unstable angina, and perhaps a subset of patients with ST-segment deviation MI as well, may be manifesting disease due to a rapid cellular proliferation of the atherosclerotic plaque itself, with little contri-

From: Contemporary Cardiology: Management of Acute Coronary Syndromes, Second Edition Edited by: C. P. Cannon © Humana Press Inc., Totowa, NJ

bution from either major thrombus formation or vasoconstriction (5,6). These three mechanisms (ruptured plaque, thrombus formation, and rapid cellular proliferation) may also be closely interrelated in a given patient, with a substantial contribution from each.

As the understanding of culprit mechanisms has evolved, the targets of therapeutic intervention have likewise evolved. Because the predominant pathophysiology of the acute coronary syndromes relates to an abrupt cessation of coronary blood flow and myocardial oxygen supply, therapeutic strategies have focused on restoration of coronary blood flow: therapies to limit thrombus formation and enhance thrombus dissolution (thrombolytic therapy, thrombin inhibitors, and platelet inhibitors) and therapies to "debulk" the luminal obstruction mechanically (percutaneous transluminal coronary angioplasty, stent, atherectomy, laser, and so on). A critical foundation in the therapeutic approach to patients with the acute coronary syndromes remains, however, the reduction in myocardial oxygen demand since this approach may limit the amount of infarction for a given amount of ischemia, and it may also widen the window of time within which other therapeutic interventions may be effective. The purpose of this chapter is to focus on the role of the conventional antiischemic therapies, i.e., b-adrenergic blockers, calcium channel blockers, and nitrates, in the management of the acute coronary syndromes. Although an effort is made to review the experience with these agents separately for patients who present with ST-segment elevation compared with those who present with ST-segment depression or unstable angina, this distinction often cannot be made from many of the clinical trials conducted before the thrombolytic era. Entry criteria for most of the older studies included persistent ST-segment elevation or depression ±1.0 mm, whereas many of the newer studies include only those with persistent ST-segment elevation if thrombolytic therapy was administered.

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