Autopsy findings in sudden coronary death reveal that both ischemic injury to the conduction system and survival of anoxia-resistant fibers, along with neuropathologic changes, contribute to fatal arrhythmias.
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Suggests dual arrhythmia substrates in sudden coronary death; hypothesis-generating and should not yet change practice.
The arrhythmogenic substrates for sudden coronary death were studied in 13 autopsied hearts and in 2 left stellate ganglia (surgically excised). Diffuse or segmentary obstruction of nutritional arteries accounted for acute ischemic injury of the conduction system, which was the underlying cause of high-risk bradycardic arrhythmias in one-third of the cases. However, in one-quarter of the cases the survival of anoxia-resistant subendocardial specialized fibers was probably responsible for reentrant lethal tachycardic arrhythmias. In other cases, early infarct damage could have fatal arrhythmias of either type. Intrinsic and/or extrinsic neuropathologic changes, unbalancing the autonomic action on the heart, were often seen to participate in the arrhythmogenic features of sudden coronary death.
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Lino Rossi (1982) studied this question.
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