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J Thorac Cardiovasc Surg 2006;132:884-890
© 2006 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Myocardial protection in the failing heart: II. Effect of pulsatile cardioplegic perfusion under simulated left ventricular restoration

^a Department of Biomedical Engineering, University of California, Irvine
^b Department of Medicine, University of California, San Diego
^c Department of Surgery, David Geffen School of Medicine at University of California, Los Angeles
^d Option on Bioengineering, California Institute of Technology, Pasadena
^e Department of Pediatrics and Cardiovascular Research Institute, University of California, San Francisco.

Received for publication September 29, 2005; accepted for publication April 11, 2006.

^_* Address for reprints: Gerald D. Buckberg, MD, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, 62-258 CHS, Los Angeles, CA 90095. (Email: gbuckberg{at}mednet.ucla.edu).

Objective: The open ventricle was studied in pacing-induced experimental heart failure to determine the extent of coronary perfusion and distribution during either continuous or pulsatile cardioplegic perfusion compared with whole blood in the beating heart.

Methods: In 5 animals that underwent pacing-induced heart failure and in 6 control swine, regional coronary blood flows were measured on bypass in the open left ventricle (simulating exposure for left ventricle restoration) during (1) beating, (2) nonpulsatile cardioplegia, and (3) pulsatile cardioplegia modalities. Mean perfusion pressure was maintained at 80 mm Hg.

Results: Flow magnitude and distribution differed in control and failing hearts in the open left ventricle. In control hearts, transmural and endocardial cardioplegic flow of nonpulsatile and pulsatile flow (which were similar to each other) exceeded beating flow by 63% and 70%, respectively, in the open left ventricle condition. Transmural and subendocardial vascular resistance increased in failing hearts during cardioplegic delivery, resulting in lower subendocardial flow under nonpulsatile conditions for the same perfusion pressure. In failing hearts, subendocardial perfusion conditions did not change in the beating state (0.89 vs 0.78 mL/min/g in control and failing open beating states, respectively), but nonpulsatile cardioplegic flow was significantly reduced by 154%, and became lower than beating flow by 32.2% (0.78 vs 0.59 mL/min/g). Conversely, pulsatile cardioplegic delivery improved endocardial flow in the open failing hearts, as cardioplegic perfusion with pulsatility exceeded beating flow by 41%. In heart failure, pulsatility from either the beating heart, which causes extrinsic compression of coronary vessels, or intrinsic vessel distension during pulsatile cardioplegic perfusion preserved endocardial perfusion better than nonpulsatile cardioplegia at the same perfusion pressure.

Conclusion: In the failing open ventricle (simulated geometry during ventricular restoration), subendocardial blood flow was maintained in the beating state, but decreased significantly from control values during nonpulsatile cardioplegic perfusion. Conversely, pulsatile cardioplegic delivery improved subendocardial perfusion of the open failing ventricle. These findings of improved subendocardial perfusion during pulsatile delivery (either during beating or cardioplegic perfusion) compared with nonpulsatile cardioplegic delivery may have important implications for myocardial protection in failing hearts.

Related Article

Myocardial protection in the failing heart: I. Effect of cardioplegia and the beating state under simulated left ventricular restoration

Monica Kostelec, James Covell, Gerald D. Buckberg, Ahmad Sadeghi, Julien I.E. Hoffman, and Ghassan S. Kassab
J. Thorac. Cardiovasc. Surg. 2006 132: 875-883. [Abstract] [Full Text] [PDF]

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