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Free access | 10.1172/JCI106347

Experimental myocardial infarction: IV. Reduction of left ventricular compliance in the healing phase

William B. Hood Jr., Jesus A. Bianco, Raj Kumar, and Richard B. Whiting

Thorndike Memorial Laboratory, Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts 02118

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02118

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02118

Find articles by Hood, W. in: JCI | PubMed | Google Scholar

Thorndike Memorial Laboratory, Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts 02118

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02118

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02118

Find articles by Bianco, J. in: JCI | PubMed | Google Scholar

Thorndike Memorial Laboratory, Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts 02118

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02118

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02118

Find articles by Kumar, R. in: JCI | PubMed | Google Scholar

Thorndike Memorial Laboratory, Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts 02118

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02118

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02118

Find articles by Whiting, R. in: JCI | PubMed | Google Scholar

Published July 1, 1970 - More info

Published in Volume 49, Issue 7 on July 1, 1970
J Clin Invest. 1970;49(7):1316–1323. https://doi.org/10.1172/JCI106347.
© 1970 The American Society for Clinical Investigation
Published July 1, 1970 - Version history
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Abstract

Compliance of the infarcted left ventricle was studied in dogs 3-5 days after occlusion of the left anterior descending coronary artery. Compliance was assessed from postmortem pressure-volume curves and from pressure-length measurements (mercury-in-silastic segment length gauges) made both in vivo and postmortem. Postmortem pressure-volume curves showed reduced compliance compared to sham-operated animals. Postmortem pressure-length curves of infarcted and adjacent normal myocardium indicated that the diminished total compliance could be attributed to an increase in stiffness of the infarcted area. This was confirmed by in vivo end-diastolic pressure-length changes produced by transient aortic occlusion. The infarcted area was akinetic, showing neither contraction nor aneurysmal bulging. In addition, anesthetized dogs with infarcts, when compared with sham-operated animals, had similar left ventricular end-diastolic volumes (indicator dilution method), but higher left ventricular end-diastolic pressures. Taken with previous observations, which show that systolic aneurysmal bulging is uniformly present at the onset of ischemia, these results indicate that stiffening of the ischemic myocardium occurs during the first 5 days after infarction, and show that elevation of left ventricular filling pressure does not necessarily signify ventricular dilatation. The results also suggest a mechanism whereby ventricular performance may improve during recovery from acute myocardial infarction.

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