Left ventricular dysfunction is associated with prolonged average ventricular fibrillation cycle length in patients

Guilherme Fenelon1, Bruce S Stambler, Etienne Huvelle

  • 1Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. guilhermefenelon@uol.com.br

Insights

Left ventricular dysfunction prolongs ventricular fibrillation cycle length (VFCL) in patients with implantable cardioverter defibrillators. This finding suggests altered ventricular refractoriness in heart failure, increasing arrhythmia risk.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Heart Failure Research

Background:

  • Cellular studies indicate prolonged ventricular refractoriness in heart failure (CHF), but clinical data are limited.
  • Ventricular fibrillation cycle length (VFCL) correlates with local refractoriness, offering a potential clinical marker.
  • Left ventricular (LV) dysfunction is a known risk factor for malignant ventricular arrhythmias.

Purpose of the Study:

  • To investigate the relationship between LV dysfunction and intracardiac VFCL in patients with implantable cardioverter-defibrillators (ICDs).
  • To determine if VFCL is prolonged in patients with reduced LV ejection fraction (LVEF).

Main Methods:

  • Analysis of intracardiac VFCL data from 49 patients (mean LVEF 41%) using Ventak MINI ICDs.
  • Patients were stratified based on LVEF (>/= 50% vs. < 50%).
  • Exclusion of patients on antiarrhythmic drugs, including beta-blockers.

Main Results:

  • Mean median VFCL was 186 ms.
  • Patients with LVEF < 50% exhibited significantly longer median VFCL (191 ms) compared to those with LVEF >/= 50% (171 ms; p=0.002).
  • Median VFCL showed a significant negative correlation with LVEF (r=-0.41; p=0.003) and a positive correlation with age (r=0.28; p=0.04). LVEF was the sole significant predictor of VFCL.

Conclusions:

  • Left ventricular dysfunction is associated with prolonged averaged VFCL in patients at risk for ventricular arrhythmias.
  • The observed prolongation of VFCL may be linked to underlying alterations in ventricular refractory periods.
  • These findings highlight a potential electrophysiological mechanism contributing to arrhythmias in heart failure.
Abstract

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