Premature ventricular contractions on healthy and diseased hearts: Differential acute effect of coupling interval and location

Background The precise pathophysiological mechanisms underlying premature ventricular contraction (PVC)-induced cardiomyopathy remain unclear. Objective This study aimed to compare the acute physiological effects of PVCs delivered at different coupling intervals (CIs) and anatomic sites in healthy hearts and in hearts with an established dilated cardiomyopathy. Methods 10 swine were studied: 5 served as controls, and 5 underwent pacemaker implantation with 180 beats/min pacing for 4 weeks to induce nonischemic dilated cardiomyopathy (NIDCM). PVCs were delivered from 14 left ventricular (LV) and 6 right ventricular sites at 4 CIs in both groups. QRS duration and hemodynamic parameters (aortic flow, maximal rate of pressure rise, and maximal rate of pressure fall) were assessed. Results PVC QRS duration increased as CI shortened in both groups (control 85 ± 7 ms at 500 ms vs 93 ± 7 ms at 350 ms, P <.01; NIDCM 103 ± 6 ms vs 119 ± 6 ms, P <.01). Hemodynamic deterioration paralleled QRS prolongation and was more pronounced in the NIDCM group. PVCs from the LV had a greater hemodynamic impact. Conclusion Shorter PVC CIs prolong QRS duration and worsen hemodynamics, with these effects more pronounced in the dilated cardiomyopathic hearts. This could correlate with a greater long-term decline in the LV ejection fraction, thereby increasing the risk of developing PVC-induced cardiomyopathy.