IMPACT OF VOLUME LOADING AND LOAD REDUCTION ON VENTRICULAR REFRACTORINESS AND CONDUCTION PROPERTIES IN CANINE CONGESTIVE-HEART-FAILURE

Objectives. This investigation was undertaken to examine the alteratio n of electrophysiologic properties, including refractoriness, strength -interval relations and conduction, with the development of heart fail ure and to characterize the impact of volume loading on these indexes in the cardiomyopathic setting. Methods. Electrophysiologic properties in eight dogs with pacing-induced dilated cardiomyopathy were compare d with those in six control dogs before and after rapid infusion of 80 0 ml of intravenous saline. Results. The right ventricular (RV) and le ft ventricular (LV) effective refractory period (ERP) and absolute ref ractory period (ARP) were significantly longer in dogs with pacing ind uced cardiomyopathy than in control dogs: RV ERP 181 +/- 11 ms versus 138 +/- 7 ms (mean +/- SD) (p < 0.0001) and anterior LV ERP 177 +/- 13 ms versus 128 +/- 11 ms (p < 0.0001), respectively; ARP 159 +/- 14 ms versus 114 +/- 7 ms (p < 0.0001) at the RV site and 153 +/- 12 versus 117 +/- 5 ms (p < 0.0001) at the anterior LV site. After volume loadi ng in cardiomyopathic animals, posterior and anterior LV ERPs became p rolonged to 178 +/- 5 ms (p = 0.004) and 189 +/- 14 ms (p = 0.065), re spectively, shifting the strength-interval relation in the direction o f longer S1S2 coupling intervals. Anterior LV monophasic action potent ial durations at 90% repolarization also became prolonged from 192 +/- 10 ms to 222 +/- 23 ms (p < 0.012) with volume loading, These finding s were not altered by subsequent sodium nitroprusside, Local conductio n times parallel and perpendicular to fiber orientation were not alter ed by development of cardiomyopathy or volume alterations. Conclusions . The development of dilated cardiomyopathy results in significant pro longation of refractoriness and repolarization that is increased furth er by volume augmentation but is not reversed by pharmacologic load re duction. Although these abnormalities may contribute to the environmen t needed for a nonreentrant, triggered or stretch-mediated arrhythmoge nic process in cardiomyopathic states, additional studies will be requ ired to demonstrate such a focal mechanism conclusively. (C) 1997 by t he American College of Cardiology.