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J Thorac Cardiovasc Surg 1994;108:467-476
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Effects of perfusion-induced edema on diastolic stress-strain relations in intact swine papillary muscle

New York, N.Y.

Supported in part by U.S. Public Health Service grants 1RO1HL41163 and 1F32HL07706.

Presented in part at the Thirty-ninth Annual Scientific Session of the American College of Cardiology.

Received for publication Aug. 25, 1993. Accepted for publication Jan. 9, 1994. Address for reprints: Henry M. Spotnitz, MD, Department of Surgery, Columbia University College of Physicians & Surgeons, 630 West 168th St., New York, NY 10032.

Abstract

The mechanism through which edema reduces left ventricular compliance has not been defined. Accordingly, diastolic properties of in situ left ventricular swine papillary muscles were studied in three groups: control (n= 6, 4°to 6°C), edematous (150 mOsm/L coronary perfusion, n= 6, 4°to 6°C), and ischemic contracture (n= 8, 28°C). Lagrangian stress () and strain () were calculated from slow stretch data and approximated by=(e^ß- 1). The natural logarithm of stress versus strain was linear over the physiologic range of 0.05 < strain < 0.40. Hypotonic perfusions (1 Lx3) progressively shifted the stress-strain relationship upward and to the left. Compared to baseline,increased significantly (p< 0.05) after perfusion 3 (6.7±2.1 baseline, 12.2±6.6 perfusion 1, 12.7±3.5 perfusion 2, and 42.9±16.3 gm/cm²perfusion 3). The constantßdid not change significantly (13.0±1.5 baseline, 13.1±1.6 perfusion 1, 13.2±1.6 perfusion 2, and 14.1±1.4 perfusion 3). Right ventricular water content increased after each perfusion (77.1%±1.4% baseline, 81.6%±1.3%, 84.7%±1.5%, and 86.9%±1.7%, p< 0.05). With ischemic contracture,increased from 61.9±17.8 to 173.1±61.5 gm/cm²(p> 0.05) andßincreased insignificantly from 6.5±0.6 to 10.6±1.8 (p= NS). In the control group all variables were unchanged after 210 minutes. We conclude that myocardial stiffness increases with myocardial edema. This may explain decreased compliance in the edematous left ventricle. (J THORACCARDIOVASCSURG1994;108:467-76)

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