Clinical recognition of pure premature ventricular complex-induced cardiomyopathy at presentation

Abstract

Frequent premature ventricular complexes (PVCs) can induce or worsen left ventricular (LV) systolic dysfunction. The purpose of this study was to identify the clinical pattern of patients having a "pure PVC-induced" cardiomyopathy at presentation. This prospective multicenter study included 155 consecutive patients (age 55 ± 12 years, 96 men [62%], 23% ±12% mean PVC burden) with LV dysfunction and frequent PVCs submitted for ablation and followed up for at least 12 months. Patients with a previously diagnosed structural heart disease (50 [32%]) and those without complete PVC abolition during follow-up who did not normalize LV ejection fraction (LVEF) (24 [15%]) were excluded from the analysis. Of the remaining 81 patients, 41 (51%) had a successful sustained ablation, did not have normalized LVEF, and were classified as having PVC-worsened nonischemic cardiomyopathy, and 40 (49%) who had normalized LVEF were considered as having pure PVC-induced cardiomyopathy. The latter group had higher baseline PVC burden (27% ± 12% vs 12% ± 8%; P <.001), smaller LV end-diastolic diameter (58 ± 5 mm vs 60 ± 6 mm; P = .05), and shorter intrinsic QRS (105 ± 12 vs 129 ± 24 ms; P <.001). Any of the following baseline characteristics accurately identified patients who will not normalize LVEF after PVC ablation (85% sensitivity, 98% specificity): intrinsic QRS >130 ms, baseline PVC burden <17%, and LV end-diastolic diameter >63 mm. Almost half of patients with frequent PVCs and low LVEF of unknown origin normalize LVEF after sustained PVC abolition, and these patients can be identified before ablation.