In a majority of cases, the “culprit lesion” in patients who suffer an MI was not critically stenotic or even symptomatic before its rupture. As noted previously, anginal symptoms typically occur with fixed lesions exhibiting greater than 70% chronic occlusion. Pathologic and clinical studies show that two thirds of ruptured plaques are less than or equal to 50% stenotic before plaque rupture, and 85% exhibit initial stenotic occlusion of less than or equal to 70%. Thus, the worrisome conclusion is that a large number of asymptomatic adults are at significant risk for a catastrophic coronary event. At present, it is impossible to predict plaque rupture in any given patient.
Plaque disruption and ensuing non-occlusive thrombosis also are common, repetitive, and often clinically silent complications of atheromas. The healing of such subclinical plaque disruption and overlying thrombosis is an important mechanism by which atherosclerotic lesions progressively enlarge (
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Angina pectoris is an intermittent chest pain caused by transient, reversible myocardial ischemia. The pain is a consequence of the ischemia-induced release of adenosine, bradykinin, and other molecules that stimulate autonomic nerves. The following three variants are recognized:
Typical or stable angina is predictable episodic chest pain associated with particular levels of exertion or some other increased demand (e.g., tachycardia). The pain is described as a crushing or squeezing substernal sensation that often radiates down the left arm or to the left jaw (referred pain). The pain usually is relieved by rest (reducing demand) or by drugs such as nitroglycerin, a vasodilator that increases coronary perfusion.
Prinzmetal or variant angina occurs at rest and is caused by coronary artery spasm. Although such spasms typically occur on or near existing atherosclerotic plaques, a completely normal vessel can be affected. Prinzmetal angina typically responds promptly to vasodilators such as nitroglycerin and calcium channel blockers.
Unstable angina (also called crescendo angina) is characterized by increasingly frequent pain, precipitated by progressively less exertion or even occurring at rest. Unstable angina is associated with plaque disruption and superimposed thrombosis, distal embolization of the thrombus, and/or vasospasm; it can be a harbinger of MI, portending complete vascular occlusion.
Myocardial infarction (MI), also commonly referred to as “heart attack,” is necrosis of the heart muscle resulting from ischemia. The major underlying cause of IHD is atherosclerosis; while MIs can occur at virtually any age, the frequency rises progressively with aging and with increasing risk factors for atherosclerosis (Chapter 10). Nevertheless, approximately 10% of MIs occur before 40 years of age, and 45% occur before 65 years of age. Blacks and whites are equally affected. Men are at greater risk than women, although the gap progressively narrows with age. In general, women tend to be protected against MI during their reproductive years. However, menopause—with declining estrogen production—is associated with exacerbation of coronary artery disease, and IHD is the most common cause of death in older adult women.
The vast majority of MIs are caused by acute thrombosis within coronary arteries (