Elsevier

Cardiovascular Pathology

Volume 8, Issue 3, May–June 1999, Pages 133-139
Cardiovascular Pathology

Articles
Histological Analysis of Coronary Artery Lesions in Fatal Postoperative Myocardial Infarction

https://doi.org/10.1016/S1054-8807(98)00032-5Get rights and content

Abstract

We sought to evaluate the underlying coronary pathology of fatal postoperative myocardial infarction (MI). It has been hypothesized that most MIs following noncardiac surgery occur in the setting of increased oxygen demand that exceeds coronary blood supply. However, most MIs not associated with surgery are caused by plaque rupture and intracoronary thrombosis. In a retrospective cohort study, we reviewed 1841 consecutive autopsy records from 1981 to 1995 at two institutions and identified 26 cases of postoperative MI with coronary arteries available. Plaque rupture was present in 12 cases (46%, 95% confidence interval [CI] 27%–67%). Of the 9 (35%) patients with intracoronary thrombus, 5 (56%; 19% of entire group) had total occlusion. Thrombus occurred on a >50% stenosis (by cross-sectional area) in a total of 33% (95% CI 16%–55%) of patients. The only statistically significant difference in clinical variables between patients with and without plaque rupture was longer interval from surgery to death in patients with plaque rupture (7.8 ± 4.4 days versus 4.4 ± 4.8 days; p = 0.047). In this autopsy series, coronary plaque rupture was associated with almost half of fatal postoperative MI cases. Strategies aimed at reducing triggers of plaque rupture with coronary occlusion might reduce postoperative MI fatality.

Section snippets

Patients

To identify cases of postoperative MI, we reviewed a total of 1841 consecutive autopsy records at two institutions (Deaconess Hospital, January 1, 1988 to December 31, 1995, n = 894; and Lahey-Hitchcock Medical Center, January 1, 1981 to December 31, 1995, (n = 947). The study was approved by the Institutional Review Boards of both hospitals. We excluded patients who had not received general anesthesia and patients with a history of coronary artery bypass surgery or with postoperative MI

Results

We identified 26 patients (age 68 ± 13 years; 9 females) who had suffered a fatal postoperative MI whose coronary histology was available for review. All MIs appeared to be ⩽72 hours in age. Fatal MI complicated the following types of surgical procedures: general surgery (10), vascular surgery (9), thoracic surgery (4), orthopedic surgery (2), and neurosurgery (1). Surgery was elective in all but one case. Death occurred a mean of 6.0 ± 4.9 (range, 0 to 17) days after surgery. Within the entire

Discussion

In this study of patients with fatal postoperative MI, we identified signs of plaque rupture in nearly half of cases. The morphology of coronary lesions and incidence of plaque disruption that we observed is similar to previous studies of sudden cardiac ischemic death 1, 2, 3, 4, 6, 7 in which close serial sections of coronary arteries were examined. Thus, fatal postoperative MI may have similar pathophysiologic mechanisms of onset as MI not associated with surgery.

Our findings confirm those of

Conclusions

In this autopsy study, plaque rupture in coronary arteries was associated with almost half of fatal postoperative MI cases. Despite a relatively insensitive methodology, our results are consistent with the findings of other investigations of sudden ischemic cardiac deaths not associated with surgery. Further prospective investigations, including randomized controlled clinical trials, are necessary to define the mechanisms and optimal, cost-effective, preventive strategies for adverse

Acknowledgements

The authors thank Mark Silverman, Department of Pathology, Lahey-Hitchcock Medical, Burlington, Massachusetts, for his assistance, and Murray Mittleman and Richard Nesto, Cardiovascular Division, Beth Israel Deaconess Medical Center, for their careful, constructive criticism of the manuscript. M. C. Cohen was partially supported by Public Health Service Fellowship No. 1-F32-HL08912-01-PSF.

Presented at the 46th Annual Scientific Session of the American College of Cardiology, Anaheim, California,

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