TY - JOUR
T1 - Papillary muscle ventricular arrhythmias in patients with arrhythmic mitral valve prolapse
T2 - Electrophysiologic substrate and catheter ablation outcomes
AU - Enriquez, Andres
AU - Shirai, Yasuhiro
AU - Huang, Jason
AU - Liang, Jackson
AU - Briceño, David
AU - Hayashi, Tatsuya
AU - Muser, Daniele
AU - Fulton, Brian
AU - Han, Yuchi
AU - Perez, Armando
AU - Frankel, David S.
AU - Schaller, Robert
AU - Supple, Gregory
AU - Callans, David
AU - Marchlinski, Francis
AU - Garcia, Fermin
AU - Santangeli, Pasquale
PY - 2019/6
Y1 - 2019/6
N2 - 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.
AB - 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.
KW - catheter ablation
KW - mitral valve prolapse
KW - papillary muscles
KW - sudden cardiac death.
KW - ventricular arrhythmias
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U2 - 10.1111/jce.13900
DO - 10.1111/jce.13900
M3 - Article
C2 - 30879029
AN - SCOPUS:85063048598
VL - 30
SP - 827
EP - 835
JO - Journal of Cardiovascular Electrophysiology
JF - Journal of Cardiovascular Electrophysiology
SN - 1045-3873
IS - 6
ER -