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 1 h (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.
Bibliographical noteFunding Information:
This work was supported in part by a grant from Medtronic, Inc. The authors would like to thank Monica Mahre, William Gallagher, and Charles Soule for their technical assistance. Additionally, we would like to thank Dr. Hartmuth Bittner for his expert assistance and insight. Finally, we would like to thank B. Braun Medical Inc. for their generous supply of hetastarch.