Coronary thrombosis in pathogenesis of acute myocardial infarction. Histopathological study of coronary arteries in 108 necropsied cases using serial section.

Abstract

An extensive histopathological study was carried out on the hearts of 108 patients with electrocardiographically proven acute myocardial infarction dying after admission to a coronary care unit. The occluded or the narrowest segments of the coronary arteries were examined at intervals of 100 mu using serial sections. Serial sectioning is important in such a study because the pathology of the lumen can vary considerably within a 2 to 3 mm segment. A high incidence (80.3%) of thrombus formation corresponding to the site of infarction was observed. These thrombi occluded the vessel lumen, were usually found proximally in the coronary arteries, and were associated with a ruptured atheromatous plaque in 90.8 per cent of cases. It is postulated that an increase of intraplaque pressure resulting from a honeycomb-like accumulation of foam cells, cholesterol clefts, and blood infiltration through the injured endothelial cells is the cause of rupture of the atheromatous plaque. This rupture into the vessel lumen may precede, and be responsible for, formation of thrombus and the onset of acute myocardial infarction.

Perioperative cardiac events in patients undergoing noncardiac surgery: a review of the magnitude of the problem, the pathophysiology of the events and methods to estimate and communicate risk

“…19 In 64%-100% of patients with nonoperative MIs, coronary artery plaque fissuring occurs, 20,21 and in 65%-95% there is an acute luminal thrombus. [21][22][23][24][25] The pathophysiology underlying MIs in the operative setting is less clear.…”

Coronary arterial remodeling in differing clinical presentations of unstable angina pectoris—an intravascular ultrasound study

“…[1][2][3][4] Postmortem studies show an association between large atherosclerotic plaques and acute coronary syndromes. [28][29][30][31] On the other hand, some angiographic studies report that acute coronary syndromes may arise from lesions with < 50% stenosis. [32][33][34] If the culprit lesion of the acute coronary syndrome is larger, but associated with more positive remodeling, this may in part reconcile the discrepancies between the pathologic and angiographic findings of patients with acute myocardial infarction.…”

Vulnerable Atherosclerotic Plaque

“…Our rationale begins with the fact that, in autopsy studies of victims of fatal MI, a second occlusive thrombus is found in 6% to 16% of victims, though most of these individuals have a second vulnerable plaque (rarely three). 25,26 Approximately half of these have rupture or erosion with a mural (non-infarctrelated) thrombus. In patients with stable symptoms, arterial inflammation is not diffuse, and in these patients most plaques are predominantly fibrotic.…”