Coronary Arterial Spasm and Vasomotion (Part 2): Current Concepts Regarding their Role in Ischemic Heart Disease

Abstract

Acxrst MYOCARDIAL INFARCTION Formany years, coronary th ombosis wacon sidered the sole and immediate cause of myo cardial infarction. This conclusion was understand ably reached because of the high prevalence of coronary thrombi in fatal acute infarction when death occurred more than six hours after the onset of symptoms. It was assumed that the thrombus was present at the moment of infarction and mi tiated the event. In fact, however, the pathologist is hindered in his attempts to understand the initia lion of infarction because myocardial necrosis can not be detected by conventional hematoxylin-eosin stain and light microscopy until six or more hours have elapsed. Electron microscopy and dehydro genase stains allow earlier detection of infarction, but nevertheless, it is not possible to confidently diagnose acute infarction during the critical early hours. Consequenfly, the presence and prevalence of coronary thrombosis at the time infarction begins is unknown. When the onset of chest pain, rather than the presence of necrosis, is used to signal the time of infarction, a thrombus is rarely found when death occurs within an hour or two.36'37 In two patients who died suddenly after the occurrence of chest pain and in one instance ST-segment elevation as well, a ruptured plaque with platelet aggregates adhering to subintimal collagen was present, but no occlusive thrombus had formed by the time of death.37 This suggests that some factor other than thrombosis caused the acute plaque changes and, pan passu, myocardial infarction. Recent clinical observations have established that a coronary thrombus is often present as early as two to six hours after the onset of an infarction and that the thrombus can be lysed by intracoronary streptokinase.@'39 However, this does not preclude the possibility that spasm and or plaque rupture did not occur earlier and lead to occlusion of the vessel and, subsequently, thrombosis. Failure to detect spasm in many of these patients may be due to a number of reasons : 1 ) spasm has not been systematically sought by the intracoronary injection of nitroglycerin before streptokinase administra tion; 2 ) spasm may be refractory even to intra coronary nitroglycerin; 3 ) intracoronary nitroglyc erin is given as a bolus injection over 30 seconds while intracoronary streptokinase is given as a con tinuous infusion over 30 to 90 minutes; 4) intra coronary nitroglycerin is injected into the coronary ostium while intracoronary streptokinase is often injected through a small catheter in close prox imity to the thrombus or the thrombus is pene trated with a guidewire to allow more exposure of the thrombus to the drug. These studies help to fill the void created by the dearth of pathologic information regarding the presence of coronary thrombi during the first few hours of infarction, but they do not help elucidate the initiation of the in farction process.