EXTENSIVE MYOCYTOLYSIS AS A MARKER OF SUDDEN CARDIAC DEATH

Citation
Pa. Adegboyega et al., EXTENSIVE MYOCYTOLYSIS AS A MARKER OF SUDDEN CARDIAC DEATH, Cardiovascular pathology, 5(6), 1996, pp. 315-321
Citations number
26
Categorie Soggetti
Pathology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
10548807
Volume
5
Issue
6
Year of publication
1996
Pages
315 - 321
Database
ISI
SICI code
1054-8807(1996)5:6<315:EMAAMO>2.0.ZU;2-7
Abstract
Colliquative myocytolysis, an intracellular vacuolization of myocardia l cells, is considered an indicator of acute myocardial ischemia. Alth ough often present in ischemic cardiac death, this lesion is often eit her overlooked, or not utilized as a criterion for diagnosing ischemia . This study reports light microscopic and ultrastructural studies of six autopsied patients who died suddenly and showed extensive myocytol ysis as the only pathologic finding. In two of these patients, the cli nical history and electrocardiogram findings documented an acute ische mic episode 1 to 3 hours antemortem. Six control patients with matched age and postmortem intervals did not show the intracellular vacuoliza tion characteristic of myocytolysis. The postmortem intervals ranged f rom 2 to 12 hours. Ultrastructurally, myocytolysis was seen as a well- defined large intracellular vacuole without any lining membrane and as sociated with disrupted myofibrils, prominent Z band degeneration, and a few fat droplets. The mitochondria showed swelling and disruption, as well as electron dense amorphous inclusions. The swelling and disru ption of mitochondria are well-known postmortem artefacts, and the mit ochondrial amorphous inclusions, large intracellular vacuoles, promine nt Z band degeneration, and fat droplets are not seen with autolysis. We conclude that myocytolysis, especially if extensive and restricted to an area supplied by a major coronary artery, can be a helpful patho logic marker of myocardial ischemia, particularly in sudden deaths wit hout any other histologic findings. (C) 1996 by Elsevier Science Inc.