Thoracic Epidural Anesthesia Reduces the Severity of Myocardial Ischemia in Conscious Dogs

To the Editor: In their recent study, Rolf et al. [1] concluded in their title that thoracic epidural anesthesia (TEA) "improves functional recovery from myocardial stunning in conscious dogs." We do not fully agree with Rolf et al.'s conclusion that TEA improves functional recovery of the postischemic-reperfused ("stunned") myocardium. In contrast, the improved functional recovery observed in this experimental setting may reflect the well known antiischemic action of a sympathectomy by TEA during the coronary occlusion, for the following reasons: 1. There is experimental evidence that the contractile function of ischemic-reperfused myocardium is increased by sympathetic nervous [2] or beta-adrenergic stimulation [3,4], and beta-adrenergic blockade of stunned myocardium with esmolol has no inotropic effect on regional contractile function [5]. Therefore, it is unlikely that the reduction of the sympathetic drive of the stunned myocardium by TEA is the direct reason for the better contractile function observed in the study. 2. The severity of postischemic dysfunction (stunning) is determined primarily by the severity and duration of the antecedent ischemia [for review see [6]]. By studying ischemic collateral blood flow, the authors were able to exclude differences in the severity of blood flow reduction during coronary occlusion, which is one important determinant of the rate of recovery of the postischemic-reperfused myocardium [7]. However, by reducing sympathetic output toward the myocardium, TEA reduces myocardial contractility and oxygen demand and may thereby reduce the severity of ischemia in dogs with coronary occlusion [8,9] and patients with unstable angina [10]. In the study of Rolf et al. [1], global hemodynamic variables were relatively stable after TEA: only dP/dt as a variable of global contractility was reduced by 10% (not reaching statistical significance). However, systolic outward bulging of the ischemic myocardium was markedly reduced in the presence of TEA: wall-thickening fraction during coronary occlusion was -28.0% +/- 5.1% without and -15.5% +/- 5.3% with TEA, P = 0.0007 if data are compared by using a t-test. This is in contrast to the authors' conclusion that "ischemic dysfunction was not different be-tween study groups" because using a (in principle correct) two-way analysis of variance that also takes into account the WTF data before (WTF 100% +/- 0%) and after ischemia; this difference could not be detected as "statistically significant." A reduced outward bulging during TEA indicates a better preservation of the function of the ischemic myocardium, a finding that is consistent with the concept proposed by Gallagher [11] that a reduction of myocardial oxygen demand by a negative inotropic intervention during ischemia will result in a better regional myocardial function at a given ischemic collateral perfusion because of an improvement of the oxygen supply/demand relationship. In conclusion, we are not convinced that TEA has a direct influence on the function of postischemic-reperfused (stunned) myocardium, as suggested in the title of the study of Rolf et al. [1]. Instead, their findings may be explained by the antiischemic effect of a thoracic TEA during the antecedent ischemic period. Wolfgang Schlack, MD, DEAA* Volker Thamer, MD, PhD Institut fur *Klinische Anaesthesiologie and Herz- und Kreislaufphysiologie; Heinrich-Heine-Universitat; D-40225 Dusseldorf, Germany