Characterization of the electrophysiological substrate in patients with Barlow's disease.
mitral valve prolapse
papillary muscles
premature ventricular complexes
risk stratification
sudden death
ventricular fibrillation
ventricular tachycardia
Journal
Journal of cardiovascular electrophysiology
ISSN: 1540-8167
Titre abrégé: J Cardiovasc Electrophysiol
Pays: United States
ID NLM: 9010756
Informations de publication
Date de publication:
12 2021
12 2021
Historique:
revised:
27
09
2021
received:
30
06
2021
accepted:
11
10
2021
pubmed:
20
10
2021
medline:
22
2
2022
entrez:
19
10
2021
Statut:
ppublish
Résumé
Myxomatous mitral valve prolapse (MVP) and mitral-annular disjunction (Barlow disease) are at-risk for ventricular arrhythmias (VA). Fibrosis involving the papillary muscles and/or the infero-basal left ventricular (LV) wall was reported at autopsy in sudden cardiac death (SCD) patients with MVP. We investigated the electrophysiological substrate subtending VA in MVP patients with Barlow disease phenotype. Twenty-three patients with VA were enrolled, including five with syncope and four with a history of SCD. Unipolar (Uni < 8.3 mV) and bipolar (Bi < 1.5 mV) low-voltage areas were analyzed with electro-anatomical mapping (EAM), and VA inducibility was evaluated with programmed ventricular stimulation (PES). Electrophysiological parameters were correlated with VA patterns, electrocardiogram (ECG) inferior negative T wave (nTW), and late gadolinium enhancement (LGE) assessed by cardiac magnetic resonance. Premature ventricular complex (PVC) burden was 12 061.9 ± 12 994.6/24 h with a papillary-muscle type (PM-PVC) in 18 patients (68%). Twelve-lead ECG showed nTW in 12 patients (43.5%). A large Uni less than 8.3 mV area (62.4 ± 45.5 cm Low unipolar low voltage areas can be identified with EAM in the basal inferolateral LV region and in the papillary muscles as a potential electrophysiological substrate for VA and SCD in patients with MVP and Barlow disease phenotype.
Sections du résumé
BACKGROUND
Myxomatous mitral valve prolapse (MVP) and mitral-annular disjunction (Barlow disease) are at-risk for ventricular arrhythmias (VA). Fibrosis involving the papillary muscles and/or the infero-basal left ventricular (LV) wall was reported at autopsy in sudden cardiac death (SCD) patients with MVP.
OBJECTIVES
We investigated the electrophysiological substrate subtending VA in MVP patients with Barlow disease phenotype.
METHODS
Twenty-three patients with VA were enrolled, including five with syncope and four with a history of SCD. Unipolar (Uni < 8.3 mV) and bipolar (Bi < 1.5 mV) low-voltage areas were analyzed with electro-anatomical mapping (EAM), and VA inducibility was evaluated with programmed ventricular stimulation (PES). Electrophysiological parameters were correlated with VA patterns, electrocardiogram (ECG) inferior negative T wave (nTW), and late gadolinium enhancement (LGE) assessed by cardiac magnetic resonance.
RESULTS
Premature ventricular complex (PVC) burden was 12 061.9 ± 12 994.6/24 h with a papillary-muscle type (PM-PVC) in 18 patients (68%). Twelve-lead ECG showed nTW in 12 patients (43.5%). A large Uni less than 8.3 mV area (62.4 ± 45.5 cm
CONCLUSIONS
Low unipolar low voltage areas can be identified with EAM in the basal inferolateral LV region and in the papillary muscles as a potential electrophysiological substrate for VA and SCD in patients with MVP and Barlow disease phenotype.
Substances chimiques
Contrast Media
0
Gadolinium
AU0V1LM3JT
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
3179-3186Informations de copyright
© 2021 Wiley Periodicals LLC.
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