Recovery of transmural and subepicardial wall thickening after subendocardial infarction

David C. Homans, Todd Pavek, David D. Laxson, Robert J Bache

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Objectives. This study tested the hypothesis that there is preferential recovery of subepicardial wall thickening after nontransmural myocardial infarction. Background. Previous studies have demonstrated gradual recovery of mechanical function after reperfusion in acute myocardial infarction, Because myocardial necrosis is primarily subendocardial, it was hypothesized that recovery of mechanical function would occur primarily in the subepicardial layers. Methods. Eleven mongrel dogs were instrumented with ultrasonic crystals to measure transniural and outer wall thickening. Animals performed treadmill exercise before and 8 days after nontransmural infarction produced by coronary occlusion for 90 min. Results. Coronary artery occlusion reduced myocardial blood flow to inner layers more than that to outer wall layers (mean [±SD] 0.19 ± 0.35 vs. 0.38 ± 0.38 ml/g per min, p < 0.05). Infarct size (% of risk region) was also greater in subendocardial layers (33.3 ± 24.3% inner vs. 8.3 ± 9.7% outer). Rest transmural wall thickening was 22.4 ± 7.5% versus 14.4 ± 6.3% for outer wall layers. During coronary artery occlusion, transmural and outer wall thickening decreased similarly (3.2 ± 7.7% vs. 0.2 ± 5.9%). Eight days after reperfusion, thickening of the entire wall recovered to 7.5 ± 4.7%; however, outer wall thickening had only recovered to 0.0 ± 5.8%. Myocardial blood flow was abnormal during exercise 8 days after reperfusion, with markedly reduced subendocardial perfusion. However, thickening of the inner and outer layers was similar, with transmural thickening of 8.5 ± 9.3% and outer wall thickening of 1.6 ± 6.2%. Conclusions. Despite preferential blood flow and less necrosis, thickening of the outer layer is not preserved 8 days after subendocardial infarction. The severity of subendocardial injury appears to be the major determinant of regional function after nontransmural infarction.

Original languageEnglish (US)
Pages (from-to)1109-1116
Number of pages8
JournalJournal of the American College of Cardiology
Issue number4
StatePublished - Oct 1994

Bibliographical note

Funding Information:
From the Department of Medicine, Cardiovascular Division, University of Minnesota Medical School. Minneapolis, Minnesofa. This study was supported in part by Grants HLO1162 and HL32427 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland and a Grant-in-Aid from the American Heart Association, Minnesota AIiXate. Manuscript received September 28, lYY2: revised manuscript received March Ih, 1994, accepted May 10,1YY4. Gddressfor: Dr. David C. Homans, University of Minnesota, Cardiovascular Division, Box 37.5 UMHC, Minneapolis, Minnesota 55455.


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