Ospedale Guglielmo da Saliceto, Piacenza, Italy.
Hospital Puerta del Mar, Cadiz, Spain.
Heart Rhythm. 2017 Dec;14(12):1864-1870. doi: 10.1016/j.hrthm.2017.07.025. Epub 2017 Jul 27.
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.
频发室性早搏(PVC)可诱发或加重左心室(LV)收缩功能障碍。
本研究旨在确定初诊为“单纯 PVC 诱发”心肌病患者的临床特征。
本前瞻性多中心研究纳入 155 例连续就诊的 LV 功能障碍伴频发 PVC 患者(年龄 55 ± 12 岁,男性 96 例[62%],平均 PVC 负荷 23% ± 12%),这些患者接受消融治疗并随访至少 12 个月。研究排除了先前诊断为结构性心脏病的患者(50 例[32%])和随访过程中未完全消除 PVC 且 LV 射血分数(LVEF)未恢复正常的患者(24 例[15%])。
在剩余的 81 例患者中,41 例(51%)消融成功且 LVEF 未恢复正常,被归类为 PVC 加重的非缺血性心肌病;40 例(49%)LVEF 恢复正常,被归类为单纯 PVC 诱发的心肌病。后者组患者的基础 PVC 负荷更高(27% ± 12% vs 12% ± 8%;P <.001),LV 舒张末期直径更小(58 ± 5 mm vs 60 ± 6 mm;P =.05),固有 QRS 更短(105 ± 12 ms vs 129 ± 24 ms;P <.001)。任何以下基线特征都能准确识别消融后 LVEF 无法恢复正常的患者(85%的敏感性,98%的特异性):固有 QRS >130 ms、基础 PVC 负荷 <17%以及 LV 舒张末期直径 >63 mm。
频发 PVC 且 LVEF 降低的原因不明患者中,近一半在持续消除 PVC 后 LVEF 恢复正常,这些患者可以在消融前识别。