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Papillary muscle ventricular arrhythmias in patients with arrhythmic mitral valve prolapse: Electrophysiologic substrate and catheter ablation outcomes
Author(s) -
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
Publication year - 2019
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/jce.13900
Subject(s) - medicine , cardiology , ejection fraction , catheter ablation , ventricle , ablation , mitral valve prolapse , ventricular fibrillation , cardiomyopathy , heart failure , mitral valve
Background 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. Objectives To characterize the electrophysiological substrate and outcomes of catheter ablation in patients with MVP and PM PVCs. Methods 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. Conclusions 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.