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J Thorac Cardiovasc Surg 1994;107:850-859
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

The effects of dynamic cardiac compression on ventricular mechanics and energetics: Role of ventricular size and contractility

Osaka and Okayama, Japan

Suppported in part by grants-in-aid for scientific research (04237219, 04454267, 04557041) from the Ministry of Education, Science and Culture; research grants for cardiovascular diseases (3A-2, 4C-4) from the Ministry of Health and Welfare; and a grant from Japan Cardiovascular Research Foundation and Nakatani Electric Measuring Technology Association of Japan.

Received for publication Feb. 18, 1993. Accepted for publication Aug. 19, 1993. Address for reprints: Osamu Kawaguchi, MD, Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka 565, Japan.

Abstract

The purpose of this study was to determine the role of ventricular size or contractility in the effectiveness of dynamic cardiac compression in terms of the pressure-volume relationship and myocardial oxygen consumption. In 10 isolated cross-circulated dog hearts, the ventricle was directly compressed during systole. For the volume run, measurements for slope of the end-systolic pressure-volume relation, pressure-volume area, external work, coronary blood flow, and myocardial oxygen consumption were achieved before and during a fixed amount of dynamic cardiac compression. Left ventricular volume was then increased while stroke volume was kept constant, and measurements were repeated. For the contractility run, after the control measurements were taken, left ventricular contractility was significantly increased or decreased by infusion of either dobutamine or propranolol into the coronary circulation. Measurements were repeated before and during dynamic cardiac compression at the control level of end-diastolic and stroke volumes. Dynamic cardiac compression significantly increased slope of the end-systolic pressure-volume relation, pressure-volume area, and external work (p < 0.01), whereas coronary blood flow and myocardial oxygen consumption were not affected. The increase in pressure-volume area caused by dynamic cardiac compression was greater with the larger volume. Despite the significant differences in the native left ventricular contractility, the increases in slope of the end-systolic pressure-volume relation, pressure-volume area, and external work did not differ among the three groups. We conclude that dynamic cardiac compression enhances left ventricular systolic function independent of ventricular contractility and without affecting coronary blood flow or myocardial oxygen consumption. Mechanical enhancement is more effective in the dilated heart. (J THORACCARDIOVASCSURG1994;107:850-9)

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