Hemodynamic consequences of premature ventricular contractions: Association of mechanical bradycardia and postextrasystolic potentiation with premature ventricular contraction-induced cardiomyopathy

Abstract

The relationships between hemodynamic consequences of premature ventricular contractions (PVCs) and development of premature ventricular contraction-induced cardiomyopathy (PVC-CM) have not been investigated. The purpose of this study was to correlate concealed mechanical bradycardia and/or postextrasystolic potentiation (PEP) to PVC-CM. Invasive arterial pressure measurements from 17 patients with PVC-CM and 16 controls with frequent PVCs were retrospectively analyzed. PVCs were considered efficient (ejecting PVCs) when generating a measurable systolic arterial pressure. PEP was defined by a systolic arterial pressure of the post-PVC beat ≥5 mm Hg higher than the preceding sinus beat. Every PVC was analyzed for 10 minutes before ablation, and the electromechanical index (EMi = number of ejecting PVCs/total PVC) and postextrasystolic potentiation index (PEPi = number of PVCs with PEP/total PVC) were calculated. EMi was 29% ± 31% in PVC-CM and 78% ± 20% in controls (P <.0001). PEPi was 41% ± 28% in PVC-CM and 14% ± 10% in controls (P = .001). There was no control in groups of low EMi or high PEPi. EMi and PEPi were not significantly correlated to left ventricular dimensions or function in PVC-CM patients. PVC coupling interval was related to both ejecting PVCs and PEP. Patients with PVC-CM more often display nonejecting PVCs and PEP compared to controls.