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 alteration of electrophysiologic properties, including refractoriness, strength–interval relations and conduction, with the development of heart failure 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 compared with those in six control dogs before and after rapid infusion of 800 ml of intravenous saline. Results. The right ventricular (RV) and left ventricular (LV) effective refractory period (ERP) and absolute refractory period (ARP) were significantly longer in dogs with pacing-induced 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 loading in cardiomyopathic animals, posterior and anterior LV ERPs became prolonged to 178 ± 5 ms (p = 0.004) and 189 ± 14 ms (p = 0.065), respectively, shifting the strength–interval relation in the direction of longer S1S2coupling intervals. Anterior LV monophasic action potential durations at 90% repolarization also became prolonged from 192 ± 10 ms to 222 ± 23 ms (p < 0.012) with volume loading. These findings were not altered by subsequent sodium nitroprusside. Local conduction times parallel and perpendicular to fiber orientation were not altered by development of cardiomyopathy or volume alterations. Conclusions. The development of dilated cardiomyopathy results in significant prolongation of refractoriness and repolarization that is increased further by volume augmentation but is not reversed by pharmacologic load reduction. Although these abnormalities may contribute to the environment needed for a non-reentrant, triggered or stretch-mediated arrhythmogenic process in cardiomyopathic states, additional studies will be required to demonstrate such a focal mechanism conclusively.