Left ventricular function after cardiopulmonary bypass is related to the length-dependent regulation of myocardial function.

Abstract

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 in-patient 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 τ) 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 τ, 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. Stefan G. de Hert, MD, PhD Philippe J. Van der Linden, MD, PhD