Catheter ablation of ventricular arrhythmias in left ventricular noncompaction cardiomyopathy

Juan José Sánchez Muñoz1, Carmen Muñoz-Esparza1, Pablo Peñafiel Verdú1

  • 1Arrhythmia Unit and Electrophysiology, Department of Cardiology, Virgen de la Arrixaca University Hospital, Murcia, Spain; Inherited Cardiac Disease Unit, Department of Cardiology, Virgen de la Arrixaca University Hospital, European Reference Networks (Guard-Heart), European Commission, Brusels, Belgium; Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, Spain; Red de Investigación Cardiovascular (CIBERCV) Instituto de Salud Carlos III, Spain.

Heart Rhythm
|December 21, 2020
PubMed

Insights

Ventricular arrhythmias (VAs) in left ventricular noncompaction (LVNC) cardiomyopathy have a varied origin, including outflow tracts and Purkinje fibers. Ablation strategies are tailored to these diverse substrates, offering new insights into managing VAs in LVNC.

Area of Science:

  • Cardiology
  • Genetics
  • Electrophysiology

Background:

  • Limited data exist on ventricular arrhythmias (VAs) in left ventricular noncompaction (LVNC) cardiomyopathy.
  • LVNC is a rare congenital heart defect characterized by abnormal myocardial development.

Purpose of the Study:

  • To analyze the clinical and electrocardiographic characteristics of VAs in patients with LVNC.
  • To understand the arrhythmogenic substrate in LVNC.

Main Methods:

  • Retrospective analysis of 42 patients with LVNC and VAs.
  • Evaluation of clinical presentation, electrocardiography, and electrophysiological study findings.
  • Endocardial and epicardial mapping and ablation were performed in selected patients.

Main Results:

  • VAs in LVNC were associated with isolated LVNC, dilated cardiomyopathy, or hypertrophic cardiomyopathy.
  • Premature ventricular complexes (PVCs), non-sustained and sustained ventricular tachycardias (VTs), and ventricular fibrillation were observed.
  • Arrhythmia origins included ventricular outflow tracts, Purkinje system, and endocardial scar patterns.

Conclusions:

  • The substrate for VAs in LVNC cardiomyopathy is heterogeneous.
  • Origins include ventricular outflow tracts, Purkinje system, and scar-like areas.
  • These findings aid in guiding ablation strategies for VAs in LVNC.
Abstract

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