Introduction: Recovery of LV structure and function after eradication of PVCs in PVC-induced cardiomyopathy (PVC-CMPY) is incompletely defined.
Hypothesis: That structural and functional changes might persist after cessation of PVCs.
Methods: 15 swine were exposed to 1) 50% paced PVCs from the LV lateral epicardium for 12 weeks (LV, n=5), no pacing for 12 weeks (CTRL, n=5) or 3) 50% LV PVCs for 12 weeks followed by pacing cessation for a further 4 weeks (Recovery, n=5). LV function was quantified biweekly in sinus rhythm (SR) with echocardiography. Dyssynchrony during SR was measured from pressure-volume loops at baseline and terminal studies, as the proportion of ventricular contraction during which change in segmental volume was out of phase with change in total chamber volume. Myocardial fibrosis was quantified after sacrifice.
Results: LVEF during SR fell significantly between baseline and terminal studies in the LV PVC group (64±3% to 37±3%, P<0.05), while there was no significant change in the CTRL (72±4% to 74±3%; p=NS) and Recovery (64±4% to 62±4%, P=NS) groups (Figure). After sacrifice, % fibrosis was higher in the LV PVC group compared to CTRL (5.6±0.3% vs. 2.9±0.4%; P<0.05) and remained higher in Recovery (4.1±0.3% vs. 2.9±0.4%, p<0.05) despite return to baseline LVEF. In both the LV PVC and the Recovery groups, there were significant increases in LV dyssynchrony during SR (3±0.5% to 14±3% vs 4±0.5% to 12±2%; P<0.05 for both), with LV dyssynchrony in the Recovery group at terminal study no different from that in the LV PVC group (p=NS), despite absence of PVCs for 4 weeks and return of LVEF to baseline.
Conclusions: In a swine model of PVC-CMPY, cessation of PVCs for 4 weeks leads to normalization of LVEF but significant changes in myocardial fibrosis and dyssynchrony during SR persist. This has implications for long-term prognosis in PVC-CMPY, even after PVC elimination.