Thrombosis and Acute Coronary-Artery Lesions in Sudden Cardiac Ischemic Death

Abstract

The nature of the pathologic lesion in sudden cardiac ischemic death is in dispute. Among 100 subjects who died of ischemic heart disease in less than six hours, coronary thrombi were found in 74. There was no difference in incidence between those who died in less than 15 minutes, those who died in 15 to 60 minutes, and those who died after one hour. Among 26 cases without an intraluminal thrombus, plaque fissuring was found in 21; thus, in only 5 cases was no acute arterial lesion demonstrated. No intraluminal thrombi were found in age-matched controls. Forty-eight of the 74 thrombi were found at sites of preexisting high-grade stenosis; 14 were found at points of previous stenosis of less than 50 per cent of the diameter of the lumen. Forty-seven per cent of the thrombi were found in the right coronary artery. Only 30 per cent were found in the left anterior descending coronary artery. The pathologic process in sudden ischemic death involves a rapidly evolving coronary-artery lesion in which plaque fissuring and resultant thrombus formation are present. These findings have implications for the prevention of sudden cardiac death by antithrombotic therapy.

Residual flow to the infarct zone against lethal ventricular tachyarrhythmias during the acute phase of myocardial infarction

“…1 Several studies have attempted to identify determinants that will predict lethal ventricular tachyarrhythmias. Infarct size, [8][9][10] infarct location, 11 and preinfarct angina 12 have been reported as determinants of these arrhythmias, but residual flow has not yet been studied. It has been shown that residual flow to the myocardium at risk, either through collateral vessels or by anterograde flow, is a powerful determinant of enhanced myocardial salvage and good prognosis.…”

“…It was interesting to note that patients with the right coronary as the culprit artery were prone to develop ventricular tachyarrhythmias, but these associations seem to be rather inconsistent. [8][9][10] Further studies may be needed to test the earlier hypothesis that acute occlusion of the right coronary artery, which usually supplies the conduction system, may be more related to life-threatening arrhythmias. 8 Preinfarct angina tended to protect against lethal ventricular tachyarrhythmias, but this did not achieve statistical significance (p = 0.09), suggesting a minor contribution of preinfarct angina to the prevention of these arrhythmias.…”

γ‐Glutamyltransferase and Risk of Sudden Cardiac Death in Middle‐Aged Finnish Men: A New Prospective Cohort Study

“…Given the length of time between baseline measurements of GGT and subsequent occurrence of SCD in our study (>20 years), there is a likelihood that the effects of inflammation on SCD are mediated through a chronic process, which is most likely to be the development and progression of coronary atherosclerosis 7. Indeed, pathological signs of inflammation are evident in the coronary atherosclerotic lesions and vulnerable plaques that are found in the majority of cases of SCD 31, 32. The GGT–SCD association observed in our study remained robust after adjusting for CRP.…”

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.…”