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Published on: August 25, 2015
The potential benefits of 1.5% hetastarch as a cardioplegia additive
James A Coles1, Daniel C Sigg, Paul A Iaizzo
1Department of Surgery, University of Minnesota, 420 Delaware St. SE, MMC 107, Minneapolis, MN 55455, USA.
Introduction:
Myocardial edema is a clinically relevant problem found in post-ischemic reperfused hearts. The objective of this study was to understand the effects of hetastarch-supplemented cardioplegia on post-ischemic edema and cardiac function.
Materials And Methods:
Swine hearts were arrested with either St. Thomas Hospital cardioplegia with (n=6) or without (n=7) 1.5% hetastarch. Following hypothermic global ischemia, hearts were crystalloid reperfused in a four-chamber isolated working mode.
Results:
Hetastarch decreased myocardial water content gains after three hours of reperfusion (control versus hetastarch, hour 0: 67+/-5% versus 67+/-3%, NS; hour 3: 82+/-2% versus 78+/-1%, p=0.1). Post-ischemic control group left ventricular end-diastolic pressures were elevated after 1h (in mm Hg, hour 0: 13+/-2, hour 1: 19+/-3, hour 2: 19+/-3, hour 3: 20+/-2) but remained stable (<16 mm Hg) in the hetastarch group. Post-reperfusion creatine phosphokinase perfusate levels in the hetastarch treated hearts were decreased (control: 1.6 IU/l/g versus hetastarch: 0.6 IU/l/g, p=0.15).
Discussion/Conclusions:
Hetastarch treatment delayed myocardial edema development and attenuated myocardial creatine kinase efflux, thereby preserving diastolic function.
