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J Thorac Cardiovasc Surg 1997;113:1091-1099
© 1997 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Received for publication August 30, 1996 revisions requested Oct. 11, 1996; revisions received Nov. 5, 1996 accepted for publication Nov. 11, 1996. Address for reprints: Daniel Burkhoff, MD, Department of Medicine, 630 West 168th St., New York, NY 10032.
Abstract
Objective: The purpose of this study was to quantify the magnitude of interaction between the right and left ventricles in conditions of heart failure. Methods: Human hearts were taken from transplant recipients diagnosed with dilated cardiomyopathy at the time of transplantation and were restored to beating condition with use of an isolated perfusion circuit. Left ventricularright ventricular interaction was determined by ramping volume in the left ventricle while holding right ventricular volume constant. Right ventricular pressure gain was plotted against left ventricular pressure and the slope of the linear regression determined the left ventricularright ventricular interaction. A similar procedure was used to determine right ventricularleft ventricular interaction. Two normal hearts were obtained from transplant donors not suitable for cardiac donation to serve as control hearts. Results: Mean left ventricularright ventricular interaction was 0.22 in the hearts with dilated cardiomyopathy compared with 0.06 in the control hearts. Mean right ventricularleft ventricular interaction was 0.14 in the hearts with dilated cardiomyopathy compared with 0.09 in the control hearts. A marked increase in left ventricularright ventricular interaction was noted in the hearts with dilated cardiomyopathy compared with control hearts. Although observed values of right ventricularleft ventricular interaction also correspond to previously published results, no significant increase was observed in the dilated cardiomyopathy condition. Conclusions: These studies confirm previously published values for systolic ventricular interaction obtained with animal models and demonstrate a marked increase in the dependence of the right ventricle on left ventricular function to maintain systolic pressure generation during conditions of dilated cardiomyopathy.
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