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Free access | 10.1172/JCI106477

Experimental myocardial infarction: VIII. Chronotropic augmentation of cardiac function in left ventricular failure of acute and healing stages in intact conscious dogs

Raj Kumar, Julio Joison, David P. Gilmour, Farouk A. Molokhia, C. A. S. Pegg, and William B. Hood Jr.

Thorndike Memorial Laboratory, Harvard Medical Unit, Boston, Massachusetts 02130

Sears Surgical Laboratory, Harvard Surgical Service, Boston City Hospital, Boston, Massachusetts 02130

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02130

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02130

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

Thorndike Memorial Laboratory, Harvard Medical Unit, Boston, Massachusetts 02130

Sears Surgical Laboratory, Harvard Surgical Service, Boston City Hospital, Boston, Massachusetts 02130

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02130

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02130

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

Thorndike Memorial Laboratory, Harvard Medical Unit, Boston, Massachusetts 02130

Sears Surgical Laboratory, Harvard Surgical Service, Boston City Hospital, Boston, Massachusetts 02130

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02130

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02130

Find articles by Gilmour, D. in: PubMed | Google Scholar

Thorndike Memorial Laboratory, Harvard Medical Unit, Boston, Massachusetts 02130

Sears Surgical Laboratory, Harvard Surgical Service, Boston City Hospital, Boston, Massachusetts 02130

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02130

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02130

Find articles by Molokhia, F. in: PubMed | Google Scholar

Thorndike Memorial Laboratory, Harvard Medical Unit, Boston, Massachusetts 02130

Sears Surgical Laboratory, Harvard Surgical Service, Boston City Hospital, Boston, Massachusetts 02130

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02130

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02130

Find articles by Pegg, C. in: PubMed | Google Scholar

Thorndike Memorial Laboratory, Harvard Medical Unit, Boston, Massachusetts 02130

Sears Surgical Laboratory, Harvard Surgical Service, Boston City Hospital, Boston, Massachusetts 02130

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02130

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02130

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

Published January 1, 1971 - More info

Published in Volume 50, Issue 1 on January 1, 1971
J Clin Invest. 1971;50(1):217–225. https://doi.org/10.1172/JCI106477.
© 1971 The American Society for Clinical Investigation
Published January 1, 1971 - Version history
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Abstract

The hemodynamic effects of tachycardia induced by atrial pacing were investigated in left ventricular failure of acute and healing experimental myocardial infarction in 20 intact, conscious dogs. Myocardial infarction was produced by gradual inflation of a balloon cuff device implanted around the left anterior descending coronary artery 10-15 days prior to the study. 1 hr after acute myocardial infarction, atrial pacing at a rate of 180 beats/min decreased left ventricular end-diastolic pressure from 19 to 8 mm Hg and left atrial pressure from 17 to 12 mm Hg, without change in cardiac output. In the healing phase of myocardial infarction 1 wk later, atrial pacing decreased left ventricular end-diastolic pressure from 17 to 9 mm Hg and increased the cardiac output by 37%. This was accompanied by evidence of peripheral vasodilation. In two dogs with healing anterior wall myocardial infarction, left ventricular failure was enhanced by partial occlusion of the circumflex coronary artery. Both the dogs developed pulmonary edema. Pacing improved left ventricular performance and relieved pulmonary edema in both animals. In six animals propranolol was given after acute infarction, and left ventricular function deteriorated further. However the pacing-induced augmentation of cardiac function was unaltered and, hence, is not mediated by sympathetics.

The results show that the spontaneous heart rate in left ventricular failure of experimental canine myocardial infarction may be less than optimal and that maximal cardiac function may be achieved at higher heart rates.

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