Abstract

Introduction: Left ventricular (LV) post-extrasystolic potentiation (PESP) and dyssynchrony (LVD) are proposed mechanisms that may trigger premature ventricular contraction-induced cardiomyopathy (PVC-CM). While long-coupled (LC) PVCs are characterized by higher LVD and lower PESP, short-coupled (SC) PVCs have higher PESP and lower LVD. Methods: Twenty-four mongrel dogs implanted with right ventricular epicardial pacemakers were randomized to short-coupled (PVC-SC; 200 to 220-ms, n = 10), long-coupled (PVC-LC; 320 to 340-ms, n = 7) bigeminal PVCs, or no PVCs (sham; n = 7). Holter monitors were obtained to confirm PVC burdens. Echocardiograms were performed at baseline and regular intervals up to 12 weeks after assignment to assess for LV remodeling by investigators blinded to group assignments. Intra- and inter-group comparisons were performed at each time point. PVC-CM was defined as LV ejection fraction < 50%. Results: Holter monitors confirmed similar PVC burdens in PVC-LC and PVC-SC groups. After 12 weeks (Table 1), PVC-CM developed in 9 (90%) PVC-SC and 5 (71%) PVC-LC animals (p = 0.5368) with similar LVEF reduction in both groups (PVC-SC: 44.4 ± 1.5%; PVC-LC: 44.7 ± 4.0%; p = 0.9953) compared to sham (62.6 ± 1.5%). LV end-diastolic volume was greater in the PVC-LC (67.5 ± 4.6 mL) compared to PVC-SC (57.5 ± 2.7 mL; p = 0.0171) and sham (52.1 ± 1.5 mL; p = 0.0004) groups. LV end-systolic volume and indices of LV mass were similarly elevated in PVC-SC and PVC-LC groups compared to sham. Conclusions: Short- and long-coupled PVCs did not differentially impact the incidence or severity of LV remodeling in this translational animal model of PVC-CM. This finding is compatible with preliminary clinical observations that PVC coupling interval does not predict the development of PVC-CM in humans. Our data suggest that PESP and LV dyssynchrony play equally important roles in the development of PVC-CM.

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