Background
Premature ventricular contractions (PVCs) commonly coexist with cardiomyopathy. Recently, PVCs have been identified as possible cause of cardiomyopathy. We developed a PVC-induced cardiomyopathy animal model using a novel premature pacing algorithm to assess timeframe and reversibility of this cardiomyopathy and examine the associated histopathological abnormalities.
Methods and Results
Thirteen mongrel dogs were implanted with a specially programmed pacemaker capable of simulating ventricular extrasystoles. Animals were randomly assigned to either 12 weeks of bigeminal PVCs (n=7) or no PVCs (control, n=6). Continuous 24-hr Holter corroborated ventricular bigeminy in the PVC group (PVC 49.8% vs. control <0.01%, P < 0.0001). After 12 weeks, only the PVC group developed cardiomyopathy with a significant reduction in left ventricular (LV) ejection fraction (PVC 39.7±5.4% vs. control 60.7±3.8%, P<0.0001) and an increase in LV end-systolic dimension (LVESD, PVC 33.3±3.5mm vs. control 23.7±3.6mm, P<0.001). Ventricular effective refractory period showed a trend to prolong in the PVC group. PVC-induced cardiomyopathy was resolved within 2-4 weeks after discontinuation of PVCs. No inflammation, fibrosis, or changes in apoptosis and mitochondrial oxidative phosphorylation were observed with PVC-induced cardiomyopathy.
Conclusions
This novel PVC animal model demonstrates that frequent PVCs alone can induce a reversible form of cardiomyopathy in otherwise structurally normal hearts. PVC-induced CM lacks gross histopathological and mitochondrial abnormalities seen in other canine models of CM.