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Letter by Bengueddache and Bendjelid Regarding Article, "Mild Hypothermia in Cardiogenic Shock Complicating Myocardial Infarction: Randomized SHOCK-COOL Trial".

Circulation. 2019;140:e154–e155. DOI: 10.1161/CIRCULATIONAHA.119.040185 e154 Samir Bengueddache, MD Karim Bendjelid, MD, PhD To the Editor: We read with great interest the article “Mild Hypothermia in Cardiogenic Shock Complicating Myocardial Infarction: Randomized SHOCK-COOL Trial” by Fuernau et al,1 and we highlight some questions regarding the methodology and the rationalizations made by the authors regarding their results in the present SHOCKCOOL Trial 1. Several pathophysiological concepts concerning the impact of hypothermia on the DO2–Vo2 relationship have been totally overlooked by the authors. Our team has already published data about the same physiological question.2 First, little information was given regarding baseline hemodynamic parameters of the 2 groups of patients, especially concerning what truly matters when looking for the impact of hypothermia on the heart. With those parameters in hand, one would have a better insight into the studied population and the impact of hypothermia on cardiac output, heart rate, acid–base status, and SvO2. 2 Moreover, it would have been interesting to statistically compare the baseline temperature of the 2 groups at inclusion, which based on Figure 2 seems truly different. Indeed, because cardiogenic shock is well known as a cold shock, one could argue that a lower baseline temperature in the intervention group at the moment of catheterization during laboratory admission (which seems conceivable in Figure 2) could suggest more severe low-flow shock in the present group. Therefore, more information about baseline characteristics would have been helpful to conduct a deeper conceptual reflection. Furthermore, it seems to us very inconsistent to not display changes in cardiac output during the entire protocol, because it is well known that hypothermia decreases the heart rate. Indeed, it has been shown multiples times that hypothermia has a negative chronotropic effect on heart rate.3 This probably explains why we found a higher rate of use of norepinephrine in this group during the first 12 h of hypothermia. For instance, Figure 3D shows a higher mean arterial pressure in the intervention group during the first 8 h, which seems statistically significant. One can presume that by lowering the temperature and consequently the heart rate and the coupled cardiac output, the authors have decreased tissue perfusion in the hypothermic group, and that condition has led to an increased need for a vasopressor to maintain sufficient mean arterial pressure. Indeed, during heart failure the important decrease in stroke volume is physiologically compensated by an increase in heart rate. The same observation seems to also explain the lactate elevation during the 24 h of hypothermia. Indeed, hypothermic subjects have been exposed to more stressors than the control group. In addition, it is well known that catecholamine increases lactate level by positive action on the turnover of glycolytic metabolism.4 © 2019 American Heart Association, Inc. LETTER TO THE EDITOR