Ischemic preconditioning protects against arrhythmogenesis through maintenance of both active as well as passive electrical properties in ischemic canine hearts.

Background: The mechanisms for the antiarrhythmogenic effects of preconditioning in ischemic hearts, although well demonstrated, are not clear. We measured indices of activation and repolarization using data from a high-resolution epicardial sock electrode array in preconditioned (PC) and non-PC hearts in an attempt to gain further insight into protective mechanisms.

Methods And Results: Five canine hearts were subjected to a coronary artery occlusion lasting at least 1 hour, and 5 were subjected to a similar occlusion preceded by a preconditioning protocol. Epicardial electrograms were recorded using a 490-electrode sock. Representative beats were selected at intervals of 1 minute for analysis. The mean ST elevation for the PC group both rose slowly after occlusion and also resolved more slowly than the non-PC group. Electrocardiographic markers for propagation such as Total Activation Time, the QRSRMS width, and magnitude of steepest downstroke of the QRS complex all showed that the PC group maintained conduction velocity initially and also varied less dramatically than the control group. The regression line slope computed on a scatter plot of QT width vs cycle length was 0.23 for the PC group and 0.58 for non-PC. During occlusion, the incidence of premature ventricular contractions (PVCs) peaked at approximately 17 minutes followed by a second peak at approximately 27 minutes in the non-PC group, the PC group showed similar peaks at approximately 24 and approximately 53 minutes respectively.

Conclusion: The slower rate of resolution of ST elevation in PC hearts suggests a delay in gap junction closure, thus maintaining intracellular resistivity and reducing the likelihood of arrhythmia. The speed of conduction is adequately maintained during the early stages of ischemia in PC hearts. The mQTi-mRR regression line, a surrogate measure of rate dependency of repolarization (restitution), has a lower slope in the PC case, thus suggesting a mechanism of reduced arrhythmogenesis. The conclusions are supported by a delay of peak PVCs in PC hearts.