Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death.

Abstract

A specific search for intramyocardial platelet aggregates was made in 90 patients who died suddenly of ischemic heart disease. Platelet aggregates in small intramyocardial vessels were found in 27 (30%). There was a significant difference (p < .05) in the incidence of platelet aggregates in patients with chest pain of recent onset (unstable angina) before death (16/36, 44.4%) and that in those without it (1 1/54, 20.4%). Multifocal microscopic necrosis with involvement of the full thickness of the ventricular wall, including the subpericardial zone, was significantly more common (p = < .005) in the patients with platelet emboli (55.6% vs 12.7%). With one exception, aggregates were confined to the segment of myocardium immediately downstream of a major epicardial coronary artery containing an atheromatous plaque that had undergone fissuring and on which mural thrombus had developed. The results support the view that platelet aggregates in the myocardium represent an embolic phenomenon and are a potential cause of unstable angina. The association of myocardial necrosis with such emboli could precipitate sudden death from ventricular fibrillation. Circulation 73, No. 3, 418-427, 1986. WHEN PATIENTS with stable and unstable angina are compared the degree and distribution of stenosis is similar, but unstable angina is associated with stenotic lesions that have a characteristic angiographic morphology.' These type II lesions have morphologic features, including an irregular outline and the presence of intraluminal filling defects outlined by contrast medium,2 that are observed on postmortem angiograms.3'4 Under these circumstances histologic examination reveals atheromatous plaques that have undergone fissuring, rupture, or ulceration and over which nonocclusive (mural) thrombus has formed.When thrombus projects into, but does not totally occlude, the lumen of an artery, there is the potential for emboli to pass distally into the segment of myocardium supplied by that artery. Such embolization has been postulated to be responsible for the crescendo

Recognition of the Importance of Embolization in Atherosclerotic Vascular Disease

“…[1][2][3][4][5] This event leads to exposure of subendothelial matrix, with attendant platelet aggregation, thrombus, and occlusion of a major epicardial vessel. In a continuum, unstable angina and non-ST-segment-elevation MI also are indexed to a breech of the arterial wall, but the resultant thrombus is usually mural, not occlusive.…”

“…Embolization of plaque contents of plateletthrombus into the microvasculature has been reported in some patients with these acute coronary syndromes, but it has been generally believed to be uncommon. 1,2,6,7 In some cases of sudden death, the process of embolization has been speculated to play an important role. It is nevertheless surprising that systematic pathological studies of the microvasculature of the postmortem heart infarct territory have not been performed.…”

Relation of Nonperfused Myocardial Volume and Surface Area to Left Ventricular Performance in Coronary Microembolization

“…5 The total volume of myocardium that is rendered ischemic after such ME is too small to solely explain the magnitude of LV contractile dysfunction and other adverse consequences of ME. 6,7 Coronary ME, because of its frequent incidence after coronary interventions and the subsequent adverse outcomes in patients with ME, has recently been the focus of investigations. 8 -10 Inflammatory cytokines have been shown to depress myocardial function 11 ; hence, it is likely that MEinduced generation of proinflammatory cytokines plays a role in myocardial contractile dysfunction after ME.…”

Intracoronary Thrombus and Platelet Glycoprotein IIb/IIIa Receptor Blockade With Tirofiban in Unstable Angina or Non–Q-Wave Myocardial Infarction

“…1 Histologically, plaque hemorrhage, fissure, and intraluminal thrombus are common in patients dying of acute ischemic syndrome. [2][3][4][5][6] Culprit lesions often have a complex appearance on angiography and angioscopy 4,5 with an intraluminal thrombus. 5,6 Blood markers of platelet activity and fibrin generation are usually increased.…”