Enriquez Andres, Shirai Yasuhiro, Huang Jason, Liang Jackson, Briceño David, Hayashi Tatsuya, Muser Daniele, Fulton Brian, Han Yuchi, Perez Armando, Frankel David S, Schaller Robert, Supple Gregory, Callans David, Marchlinski Francis, Garcia Fermin, Santangeli Pasquale
Division of Cardiology, Queen's University, Kingston, Ontario, Canada.
Section of Cardiac Electrophysiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
J Cardiovasc Electrophysiol. 2019 Jun;30(6):827-835. doi: 10.1111/jce.13900. Epub 2019 Mar 18.
Mitral valve prolapse (MVP) is a common valve condition and has been associated with sudden cardiac death. Premature ventricular contractions (PVCs) from the papillary muscles (PMs) may play a role as triggers for ventricular fibrillation (VF) in these patients.
To characterize the electrophysiological substrate and outcomes of catheter ablation in patients with MVP and PM PVCs.
Of 597 patients undergoing ablation of ventricular arrhythmias during the period 2012-2015, we identified 25 patients with MVP and PVCs mapped to the PMs (64% female). PVC-triggered VF was the presentation in 4 patients and a fifth patient died suddenly during follow-up. The left ventricle ejection fraction (LVEF) was 50.5% ± 11.8% and PVC burden was 24.4% ± 13.1%. A cardiac magnetic resonance imaging was performed in nine cases and areas of late gadolinium enhancement were found in four of them. A detailed LV voltage map was performed in 11 patients, three of which exhibited bipolar voltage abnormalities. Complete PVC elimination was achieved in 19 (76%) patients and a significant reduction in PVC burden was observed in two (8%). In patients in which the ablation was successful, the PVC burden decreased from 20.4% ± 10.8% to 6.3% ± 9.5% (P = 0.001). In 5/6 patients with depressed LVEF and successful ablation, the LV function improved postablation. No significant differences were identified between patients with and without VF.
PM PVCs are a source of VF in patients with MVP and can induce PVC-mediated cardiomyopathy that reverses after PVC suppression. Catheter ablation is highly successful with more than 80% PVC elimination or burden reduction.
二尖瓣脱垂（MVP）是一种常见的瓣膜疾病，与心源性猝死有关。来自乳头肌（PMs）的室性早搏（PVCs）可能在这些患者中作为室颤（VF）的触发因素起作用。
描述二尖瓣脱垂和乳头肌室性早搏患者的电生理基质及导管消融结果。
在2012年至2015年期间接受室性心律失常消融的597例患者中，我们确定了25例二尖瓣脱垂且室性早搏定位到乳头肌的患者（64%为女性）。4例患者表现为室性早搏触发的室颤，另有1例患者在随访期间突然死亡。左心室射血分数（LVEF）为50.5%±11.8%，室性早搏负荷为24.4%±13.1%。9例患者进行了心脏磁共振成像，其中4例发现钆延迟增强区域。11例患者进行了详细的左心室电压图检查，其中3例表现为双极电压异常。19例（76%）患者实现了室性早搏的完全消除，2例（8%）患者的室性早搏负荷显著降低。在消融成功的患者中，室性早搏负荷从20.4%±10.8%降至6.3%±9.5%（P = 0.001）。在6例左心室射血分数降低且消融成功的患者中，5例患者消融后左心室功能改善。有室颤和无室颤的患者之间未发现显著差异。
乳头肌室性早搏是二尖瓣脱垂患者室颤的一个来源，可诱发室性早搏介导的心肌病，在室性早搏抑制后可逆转。导管消融非常成功，超过80%的患者室性早搏消除或负荷降低。
