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Ann Thorac Surg 1992;53:464-471
© 1992 The Society of Thoracic Surgeons


Articles

Adverse effect of prearrest hypothermia in immature hearts: Rate versus duration of cooling

Teanoosh Hosseinzadeh, MD, Christo I. Tchervenkov, MD*, Mackenzie Quantz, MD, Ray C.-J. Chiu, MD, PhD

Division of Cardiovascular Surgery, The Montreal General Hospital/McGill University, Montreal, Quebec, Canada

Accepted for publication August 29, 1991.

* Address reprint requests to Dr Tchervenkov, Cardiovascular Surgery, The Montreal Children's Hospital, 2300 Tupper St, Montreal, Que, Canada, H3H 1P3.

It has been suggested that rapid cooling before the induction of arrest may be harmful to the newborn myocardium. The objective of this study was twofold: (1) to evaluate whether preancst rapid cooling is indeed detrimental to myocardial recovery and (2) if so, to evaluate whether the adverse effect of prearrest hypothermia is dependent on the rate of cooling or the total duration of cold perfusion. After an initial stabilization period isolated Langendorff hearts (n = 5 per group) from neonatal piglets (5 to 7 days old) were randomized to four groups: group 1, 5 minutes of rapid cooling to 15 °C; group 2, 20 minutes of slow cooling to 15 °C; group 3 and group 4, rapid and slow cooling, respectively, with the addition of St. Thomas cardioplegic solution. All groups were then subjected to 2 hours of ischemia at 15 °C followed by 30 minutes of reperfusion at 38.5 °C. Postischemic recovery of left ventricular developed pressure was significantly greater in group 1 versus group 2 (80% ± 3% versus 61% ± 2%; p < 0.05) and in the presence of cardioplegia, group 3 versus group 4 (72% ± 3% versus 57% ± 3%; p < 0.05). The increase in left ventricular end-diastolic pressure was significantly less in group 1 versus group 2 (8% ± 5% versus 33% ± 7%; p < 0.01). Myocardial adenosinotriphosphate content recovery correlated with ventricular recovery. To evaluate the second objective, hearts were divided into three groups: group 1, rapid cooling (5 minutes); group 2, rapid cooling (5 minutes) + cold perfusion (15 minutes) at 15 °C; and group 3, slow cooling (20 minutes). Postischemic recovery of left ventricular developed pressure was significantly greater in group 1 versus groups 2 or 3 (80% ± 3% versus 64% ± 5% or 61% ± 2%, respectively; p < 0.05). Rise in left ventricular end-diastolic pressure was significantly less in group 1 (8% ± 5%) versus group 2 (43% ±14%) or group 3 (33% ± 7%) (p < 0.05). Creatine phosphate levels correlated directly with greater recovery of ventricular function in group 1. The results demonstrate that (1) rapid cooling is not detrimental and in fact offers better protection than slow cooling, (2) the detrimental effect of cooling appears to be related to the duration and not the rate of cooling, and (3) cardioplegia does not provide any additional protection. Therefore, prolonged prearrest hypothermic perfusion is detrimental to the newborn heart and should be avoided.




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