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Department of Anesthesiology, University Hospital Antwerp, Antwerp, Belgium
To the Editor:
We read with interest the paper of Tulner et al. (1), in which they reported, in eight coronary surgery patients, the use of the conductance catheter method for the perioperative assessment of left ventricular (LV) function. After cardiopulmonary bypass (CPB), the authors observed a preserved systolic function, an acceleration of LV pressure fall, and an increase in end-diastolic pressure (EDP). They suggested that these data may constitute useful reference values for further studies in patients undergoing cardiac surgery. We think that some caution is indicated with respect to this statement.
Recovery of LV function after CPB is a complex phenomenon and various patterns have been described over the years, most of them reporting a transient decrease in cardiac function. Different factors may be responsible for this variability. Apart from differences inpatient population and cardioprotective strategies, specific weaning procedures and the choice of the anesthetic regimen may also influence post-CPB myocardial recovery. For instance, early restoration of preload conditions can prevent the transient depression of both systolic and diastolic dysfunction after weaning from CPB (2) (ref. 30 in the article by Tulner et al.). Similarly, the use of a volatile anesthetic regimen was associated with a better early recovery of myocardial function than a total IV regimen (3,4).
More important however is the individual variability in cardiac functional reserve. It has been shown in coronary surgery patients that an increase in cardiac load resulted in a variable hemodynamic response that could not be explained by differences in preoperative variables. Some patients showed an improvement, whereas other patients showed either no change or even an impairment of LV function. These patients developed a decrease in maximal rate of pressure development (dP/dtmax), a delayed myocardial relaxation (increase in 
) with enhanced load dependence of LV pressure fall and a major increase in EDP. These patients showed systolic and diastolic dysfunction post-CPB and necessitated inotropic support to be weaned from CPB (5). This latter response has been attributed to a deficient length-dependent regulation of myocardial function (6). On the other hand, patients who developed improvement of myocardial function with an increase in cardiac load (manifested by an increase in dP/dtmax, an acceleration of LV pressure fall with a decrease in , less load dependence of LV pressure fall, and a minor change in EDP) typically showed no (or only minor) decrease in myocardial function post-CPB (5).
In view of these data, it seems that the results reported by Tulner et al. concern a subgroup of patients with good cardiac functional reserve and an adequate length-dependent regulation of myocardial function, resulting in a preserved myocardial function post-CPB. Therefore, this particular response, although present in some patients, cannot be withheld as the sole reference for the patient population undergoing coronary surgery with CPB.
References
Leiden University Medical Center, Leiden, The Netherlands
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.
References
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