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.
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
Sudden ischaemic death results either from an episode of acute myocardial ischaemia consequent upon coronary thrombosis or from an arrhythmia arising within a scarred left ventricle. Very different proportions of these two groups have been reported in both clinical studies in resuscitated subjects with out-of-hospital ventricular fibrillation, and in necropsy series. In 168 cases of sudden death due to ischaemic heart disease coming to necropsy 73 (43.5%) had mural intraluminal coronary thrombi, 50 (29.8%) had occlusive intraluminal thrombi, and 45 (26.7%) had no intraluminal thrombi, giving a ratio of 2.7:1 for those with and without coronary thrombosis. Single vessel disease, the presence of acute infarction at autopsy and prodromal symptoms were positively associated with the presence of coronary thrombosis. Conversely, the presence of old myocardial infarction at necropsy, a known clinical history of ischaemic heart disease and triple vessel disease were associated with the absence of acute thrombosis. The reported variation in the incidence of coronary thrombi in sudden ischaemic death can be largely explained by selection of subjects with those clinical characteristics which are positively or negatively associated with coronary thrombosis.
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