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J Thorac Cardiovasc Surg 1996;112:1378-1386
© 1996 Mosby, Inc.

CARDIOPULMONARY BYPASS,
MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

ISCHEMIC PRECONDITIONING IN CARDIAC SURGERY: A WORD OF CAUTION

Louis P. Perrault, MD FRCSCa, Philippe Menasché, MD PhDa, Alain Bel, MDa, Thierry de Chaumaray, MDa, Jacqueline Peynet, MDa, Adrian Mondry, MDb, Patricia Oliverob, Rodica Emanoil-Ravier, PhDc, Jean-Marie Moalic, PhDb

Dr. Perrault is supported by the Clinician-Scientist program (phase I) of the Medical Research Council of Canada.

Received for publication May 1, 1996 Revisions requested May 13, 1996; revisions received June 17, 1996 Accepted for publication June 17, 1996 Address for reprints: Philippe Menasché, MD, PhD, Hôpital Lariboisière, 2 rue Ambroise Paré, Paris Cedex, France.

Abstract

Objective: Ischemic preconditioning is now established as an effective means of reducing infarct size. However, it remains uncertain whether preconditioning can improve the myocardial protection afforded by cardioplegia. The present study was designed to address this issue. Methods: After the institution of cardiopulmonary bypass, 10 patients were preconditioned with 3 minutes of aortic crossclamping followed by 2 minutes of reperfusion before the onset of retrograde continuous warm cardioplegic arrest. Ten case-matched patients served as controls. Three blood samples were drawn simultaneously from the radial artery and the coronary sinus before bypass, at the end of the 5-minute preconditioning protocol or after 5 minutes of bypass in control patients, and at the end of cardioplegic arrest. These samples were assayed for creatine kinase MB isoenzyme and lactate. Right atrial biopsy specimens taken at the same time points were processed by Northern blotting for the expression of messenger ribonucleic acid of both c-fos and heat shock protein 70. Results: At the end of arrest, the release of creatine kinase MB from the myocardium was markedly greater in preconditioned patients than in the controls. The transmyocardial lactate gradient was shifted toward production in the preconditioned group (+0.22 ± 0.13 mmol/L) and toward extraction in the control group (-0.06 ± 0.21 mmol/L). Molecular biology data did not suggest a protective effect of preconditioning. There were no clinical adverse events related to preconditioning. Conclusions: Preconditioning does not enhance cardioplegic protection and might even be deleterious. These results do not dismiss its use in cardiac operations. They rather emphasize the need for identifying pharmacologic mediators that could safely and effectively duplicate the cardioprotective effects of ischemic preconditioning. (J THORAC CARDIOVASC SURG 1996;112:1378-86)




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