Left Ventricular Function After Cardiopulmonary Bypass Is Related to the Length-Dependent Regulation of Myocardial Function: In Response

We thank Drs. de Hert and Van der Linden for their insightful comments on our article (1) and we would like to respond on some of the issues brought forward. The aim of our study was two-fold: first, to describe our approach to quantify perioperative LV function, and second, to obtain a reference data set for future studies in patients undergoing cardiac surgery. The comments of de Hert and Van der Linden focus on the latter aspect of our study. We fully agree that the published literature indicates a substantial variability in recovery of LV function after cardiopulmonary bypass, and we acknowledge the extensive list of possible factors influencing this variable outcome. In fact, this is exactly the reason why we felt it was necessary to generate a data set that would be applicable to the anesthetic and cardioprotective approach followed in our institute. Specifically, we use low-dose target-controlled infusion of propofol, remifentanil, and sufentanil, and intermittent antegrade warm-blood cardioplegic arrest during normothermic cardiopulmonary bypass. The metabolic advantages of this approach have already been published, but few data are available on the acute hemodynamic effects. Our study was performed in patients with relatively preserved LV function undergoing elective CABG, to ensure that the possible changes in LV function could be contributed mainly to the effects of anesthesia and cardioplegic arrest, rather than to the surgical intervention. This selection may partly explain the preserved postoperative systolic function in our patient group. However, de Hert et al. studied a similar patient group and reported a more variable outcome that could not be explained by preoperative LV function (2). Therefore, differences in anesthesia and cardioplegic approaches between our study and the studies by de Hert et al. may need to be considered. One such difference is the use of normothermic arrest with blood cardioplegia in our study, whereas the studies of de Hert et al. included the use of hypothermia and crystalloid cardioplegia. This may be important because recent studies indicate less myocardial cell damage after normothermic blood cardioplegia (3). Furthermore, the use of propofol in both studies may not be comparable, because hypothermia has an important influence on propofol pharmacokinetics (4). However, we certainly agree that extrapolation of our findings to patients with poor baseline LV function and prolonged cardiac arrest should be done with caution. But despite this, we would still conclude that the new data provided by our study constitute valuable background information when interpreting the acute hemodynamic effects of complex surgical interventions such as LV reconstruction in heart failure patients in whom the same anesthesia and cardioplegia approach is used. Sven A. F. Tulner Robert J. M. Klautz Gerda L. van Rijk-Zwikker Frank H. M. Engbers Jeroen J. Bax Jan Baan Ernst E. van der Wall Robert A. Dion Paul Steendijk