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Updated: May 24, 2026
Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Angiographic investigation of the pathophysiology of perioperative myocardial infarction
W Lane Duvall1, Brett Sealove, Chetan Pungoti
1Department of Medicine, Mount Sinai Medical Center, New York, New York 10029, USA. william.duvall@msnyuhealth.org
Insights
Demand ischemia, not plaque rupture, is the primary cause of perioperative myocardial infarction (MI). Understanding this mechanism aids in evaluating and managing patients before surgery.
Area of Science:
- Cardiology
- Cardiovascular Surgery
- Anesthesiology
Background:
- Limited autopsy studies suggest plaque rupture and thrombosis cause perioperative myocardial infarctions (MIs).
- Perioperative period increases cardiac metabolic demand, potentially causing MIs in patients with stable coronary artery disease.
Purpose of the Study:
- Investigate the pathophysiology of perioperative myocardial infarctions (MIs).
Main Methods:
- Reviewed hospital records and coronary angiograms of 66 patients (1998-2006) with noncardiac surgery-associated MIs.
- Identified culprit lesions using ECG, ventriculography, and angiography.
- Categorized MIs as thrombotic, demand, or nonobstructive based on stenosis, flow, thrombus, calcification, and morphology.
Main Results:
- Demand MIs (55%) predominated over thrombotic (26%) and nonobstructive (19%) MIs.
- No significant differences in hypotension, tachycardia, or medication use (antiplatelets, beta-blockers, statins) between groups.
- Identified 66 patients (average age 71, 44% male) with 2% perioperative mortality.
Conclusions:
- Demand ischemia is the primary cause of perioperative MIs in this cohort.
- Understanding perioperative MI pathophysiology can improve preoperative patient evaluation and management.
Background:
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.
Methods:
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.
Results:
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.
Conclusion:
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.
