Dyssynchrony and Fibrosis Persist After Resolution of Cardiomyopathy in a Swine Premature Ventricular Contraction Model

Abstract Objectives This study sought to prospectively study the development and then regression of premature ventricular contraction (PVC)-induced cardiomyopathy, with the hypothesis that structural left ventricular (LV) changes that are of potential clinical significance may endure beyond the period of exposure to PVCs. Background Recovery of LV function after eradication of PVCs in PVC-induced cardiomyopathy is incompletely defined. Methods Fifteen swine were exposed to: 1) 50% paced PVCs from the LV lateral epicardium for 12 weeks (LV PVC, n = 5); 2) no pacing for 12 weeks (Control, n = 5); or 3) 50% paced LV PVCs for 12 weeks followed by pacing cessation for 4 weeks (Recovery, n = 5). LV function was quantified biweekly in sinus rhythm with echocardiography. Dyssynchrony was measured from pressure-volume loops at baseline and terminal studies. LV fibrosis was quantified after sacrifice. Results LV ejection fraction during sinus rhythm fell between baseline and terminal studies in the LV PVC group (65.8 ± 3.0 to 39.3 ± 3.2; p  Conclusions In a swine model of PVC-induced cardiomyopathy, cessation of PVCs for 4 weeks leads to normalization of LV systolic function but significant changes in myocardial fibrosis and LV dyssynchrony during sinus rhythm persist.