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J Thorac Cardiovasc Surg 1997;114:1070-1080
© 1997 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

ISCHEMIC INTERVALS DURING WARM BLOOD CARDIOPLEGIA IN THE CANINE HEART EVALUATED BY PHOSPHORUS 31-MAGNETIC RESONANCE SPECTROSCOPY

This study was supported in part by grant HL12777 from the National Institutes of Health and by generous gifts from Mr. Anthony A. Borgatti, Jr., Mr. and Mrs. Milton J. Silverman, and the Leon S. Newton Foundation.

Received for publication Feb. 5, 1997 Revisions requested May 15, 1997 Revisions received June 23, 1997 Accepted for publication June 25, 1997 Address for reprints: W. M. Daggett, MD, Department of Surgery, Massachusetts General Hospital, BUL-119, Fruit St., Boston, MA 02114.

Abstract

Objective: Warm blood cardioplegia requires interruption by ischemic intervals to aid visualization. We evaluated the safety of repeated interruption of warm blood cardioplegia by normothermic ischemic periods of varying durations. Methods: In three groups of isolated cross-perfused canine hearts, left ventricular function was measured before and for 2 hours of recovery after arrest, which comprised four 15-minute periods of cardioplegia alternating with three ischemic intervals of 15, 20, or 30 minutes (I₁₅, I₂₀, and I₃₀). Metabolism was continuously measured by phosphorus 31–magnetic resonance spectroscopy. Results: Adenosine triphosphate levels fell progressively as ischemia was prolonged; after recovery, adenosine triphosphate was 99% ± 6%, 90% ± 1% ( p = 0.0004 vs control), and 68% ± 3% ( p = 0.0002) of control levels in I₁₅, I₂₀, and I₃₀, respectively. Intracellular acidosis with ischemia was most marked in I₃₀. After recovery, left ventricular maximal systolic elastance at constant heart rate and coronary perfusion pressure was maintained in I₁₅ but fell to 85% ± 3% in I₂₀, ( p = 0.003) and to 65% ± 6% ( p = 0.003) of control values in I₃₀, while relaxation (tau) was prolonged only in I₃₀ ( p = 0.007). Conclusions: Hearts recover fully after three 15-minute periods of ischemia during warm blood cardioplegia, but deterioration, significant with 20-minute periods, is profound when the ischemic periods are lengthened to 30 minutes. This suggests that in the clinical setting warm cardioplegia can be safely interrupted for short intervals, but longer interruptions require caution.

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