PATHOLOGY OF FATAL PERIOPERATIVE MYOCARDIAL-INFARCTION - IMPLICATIONSREGARDING PATHOPHYSIOLOGY AND PREVENTION

Citation
Mm. Dawood et al., PATHOLOGY OF FATAL PERIOPERATIVE MYOCARDIAL-INFARCTION - IMPLICATIONSREGARDING PATHOPHYSIOLOGY AND PREVENTION, International journal of cardiology, 57(1), 1996, pp. 37-44
Citations number
22
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
01675273
Volume
57
Issue
1
Year of publication
1996
Pages
37 - 44
Database
ISI
SICI code
0167-5273(1996)57:1<37:POFPM->2.0.ZU;2-A
Abstract
The aim of this study was to determine the pathology of fatal postoper ative myocardial infarction (MI) and compare it with that of non-opera tive myocardial infarction. Histopathological analyses of coronary art eries and myocardium were performed on autopsy heart specimens (n=67), and clinical attributes were studied. Findings of perioperative MI (n =42) were compared to those of non-perioperative MI (n=25). Significan t atherosclerotic obstruction (>50% cross-sectional narrowing) was obs erved in the majority of patients (93%). Left main (>50% cross-section al narrowing) and/or three-vessel coronary artery disease were especia lly common (44%) in this group. Evidence of unstable plaques with disr uption was noted in 55% of perioperative MI patients (n=23); plaque he morrhage was found in 45% (n=19). Predicting the site of infarction ba sed on severity of underlying stenosis would have been unsuccessful in more than half the patients in both perioperative and nonoperative MI groups. Clinical profiles of the patients in the two groups were simi lar in terms of prior cardiac history, gender and age. Fatal periopera tive MI occurs predominantly in patients with multivessel coronary dis ease, especially left main and three-vessel disease. The severity of p reexisting underlying stenosis did not predict the resulting infarct t erritory. Evidence of acute plaque disruption in the infarct-related a rtery is common. Perioperative MIs have similar coronary artery pathol ogy to non-operative MIs with regard to coronary plaque hemorrhage, ru pture, and thrombus formation and probably occur by a similar mechanis m.