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Ann Thorac Surg 1986;42:675-680
© 1986 The Society of Thoracic Surgeons


Articles

Temperature-Specific Effects of Adjuvant Diltiazem Therapy on Myocardial Energetics Following Potassium Cardioplegic Arrest

Irvin B. Krukenkamp, M.D., Norman A. Silverman, M.D.*, Dag Sorlie, M.D., Ara Pridjian, M.D., Sidney Levitsky, M.D.

From the Department of Surgery, University of Illinois College of Medicine, Chicago, IL

Accepted for publication February 6, 1986.

* Address reprint requests to Dr. Silverman, Department of Surgery, University of Illinois Medical Center, PO Box 6998, Chicago, IL

Adjuvant slow calcium channel blockade theoretically minimizes the calcium influx attendant to potassium-induced cardioplegic arrest, particularly if clinically acceptable levels of cardiac hypothermia are not maintained. The present study assessed the efficacy of diltiazem therapy in ameliorating perturbations of myocardial oxygen consumption that could be attributable to postischemic intracellular calcium accumulation. In 30 canine hearts, myocardial oxygen consumption was determined during incremental isovolumic pressure-volume loading before and 30 minutes after 2 hours of either 20 or 28°C potassium cardioplegic arrest. The intracoronary perfusate in randomized hearts was modified by the addition of diltiazem, 150 µg/kg. Although systolic performance (as defined by peak developed pressure as compared with balloon volume curves) was unchanged after 20°C ischemia, adjuvant diltiazem therapy prevented the 44 ± 2% (p < .01) decrease in peak developed pressure after 28°C arrest. Moreover, the 39% augmentation of postischemic myocardial oxygen consumption at specific peak developed pressure following both 20 and 28°C ischemia was attenuated with diltiazem only after the warmer ischemic interval. This difference was characterized by a larger (35 ± 2 vs. 26 ± 2%; p < .025) decrease in postischemic oxygen extraction despite a comparable hyperemia. These data suggest that adjuvant diltiazem therapy during potassium-induced cardioplegic arrest preserves energy-efficient pump function only after warmer ischemia, thereby limiting the clinical application of this myoprotective regimen.




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T. Hamasaki, H. Kuroda, and T. Mori
Temperature Dependency of Calcium-Induced Reperfusion Injury in the Isolated Rat Heart
Ann. Thorac. Surg., March 1, 1988; 45(3): 306 - 310.
[Abstract] [PDF]




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