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Catheter Cardiovasc Interv. 2012 Nov 1;80(5):768-76. doi: 10.1002/ccd.23446. Epub 2012 Mar 14.

Angiographic investigation of the pathophysiology of perioperative myocardial infarction.

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Department of Medicine, Mount Sinai Medical Center, New York, New York 10029, USA.



The study of the pathophysiologic mechanism of perioperative myocardial infarctions is limited to two small autopsy studies suggesting a major role for plaque rupture and thrombosis. However, the perioperative period is characterized by increased cardiac metabolic demand that may lead to infarction in patients with otherwise stable obstructive coronary artery disease. The purpose of this study is to investigate the pathophysiology of perioperative myocardial infarctions.


Hospital records and coronary angiograms from patients from 1998 to 2006 who underwent noncardiac surgery complicated by a perioperative myocardial infarction (MI) were reviewed. The culprit lesion was identified based on ECG, left ventriculography, and coronary angiography. Degree of stenosis, TIMI flow, ACC thrombus grade, calcification score, and lesion morphology were evaluated. Based on these criteria, MIs were categorized as thrombotic, demand, or nonobstructive.


Sixty-six patients (average age, 71 years and 44% male), 77% of whom underwent an intermediate risk surgery with a 2% perioperative mortality, were identified. The distribution of demand, thrombotic, and nonobstructive MI was 55%, 26%, and 19%, respectively. There was neither statistical difference in the occurrence of prolonged hypotension or tachycardia between groups nor was there any difference in the use of antiplatelets, β-blockers, or statins.


This study identified demand ischemia as the predominant etiology of perioperative MIs in this cohort. An improved understanding of the pathophysiologic mechanism of perioperative MIs may facilitate the evaluation and management of preoperative patients.

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