Acute elevation of coronary venous pressure does not affect left ventricular contractility in the normal and stressed swine heart: Implications for the Fontan operation

Byline: Robert J.M. Klautz, Gerda L. van Rijk-Zwikker, Paul Steendijk, Jim Wilde, David F. Teitel, Jan Baan Abstract: Objective: After the Fontan operation the right atrium and, thus, the coronary sinus are connected to the pulmonary arterial system, which causes the coronary venous pressure to increase. We investigated the acute effects of elevation of coronary venous pressure on baseline hemodynamics, coronary venous flow, and left ventricular contractility. Methods: In acutely instrumented pigs, during complete right heart bypass and during constant cardiac output, pressure in the right atrium, right ventricle, and coronary sinus was altered by a height-adjustable reservoir. At various levels of coronary venous pressure (up to 4 kPa or up to 30 mm Hg), flow from the reservoir was measured and left ventricular hemodynamics and contractility were measured from catheter-derived left ventricular pressure and (conductance) volume data. Contractility of the left ventricle was assessed by the end-systolic pressure-volume relationship derived during an unloading intervention by adjusting the bypass pump speed. Results: Left ventricular end-diastolic pressure increased slightly (about 5%) with each kilopascal increase in coronary venous pressure, most likely related to diastolic ventricular interaction. No other changes in hemodynamic parameters occurred. Neither coronary venous flow nor left ventricular contractility was influenced by changes in coronary venous pressure. Imposing myocardial stress with dobutamine, 10 [mu]g/kg per minute, did not change these findings. Conclusion: Increasing coronary venous pressure to 4 kPa in the intact circulation with intact autoregulation does not affect coronary flow or left ventricular contractility. We found no experimental evidence for the usefulness of diversion of the coronary sinus to the left atrium during Fontan-type operations. (J Thorac Cardiovasc Surg 1997;114:560-7) Article History: Received 4 December 1996; Revised 15 January 1997; Revised 23 April 1997; Accepted 28 April 1997 Article Note: (footnote) [star] From the Cardiac Physiology Laboratory, Departments of Cardiologya and Cardiothoracic Surgery,b University Hospital Leiden, The Netherlands, and Cardiovascular Research Institute,c University of California, San Francisco, Calif., [star][star] This study was made possible by a grant from The Netherlands Heart Foundation (grant 90.293)., a Address for reprints: Jan Baan, PhD, Cardiac Physiology Laboratory, Department of Cardiology, C5-P University Hospital Leiden, P.O. Box 9600, 2300 RC Leiden, The Netherlands., aa *Current address: Department of Cardiothoracic Surgery, University Hospital Rotterdam/Dijkzigt, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands., acents 0022-5223/97 $5.00 + 0 12/1/82919