The association of galectin-3 level with ventricular arrhythmias and left ventricular strain in heart failure patients with implantable cardioverter defibrillator

Abstract

Background

Ventricular arrhythmias are life-threatening complications of heart failure (HF). Galectin-3, an indicator of fibrosis, is associated with incident HF and was found to be related to poor prognosis in these patients. We aimed to investigate the association of galectin-3 level with left ventricular (LV) arrhythmias in HF.

Methods

A total of 92 non-ischaemic HF patients who had implantable cardioverter-defibrillator were included in this study. Patients were divided into two groups based on the galectin-3 level. Ventricular arrhythmic events and LV strain indices were compared between the two groups. Negative binomial regression was used to detect the independent predictors of total arrhythmic events in HF patients.

Results

The median age was 65 (54–71) in the high galectin-3 group (HGAL) and 62 (52–68) in the low galectin-3 group (LGAL). Ventricular arrhythmic events were more frequent in HGAL than in LGAL, including non-sustained ventricular tachycardia (VTnon), sustained-VT (VTs), and ventricular fibrillation (VF) (p < 0.0001, p = 0.002, and p = 0.026, respectively). There were no statistically significant differences between HGAL and LGAL in terms of LV strain measurements. Galectin-3 level was positively significantly correlated with total arrhythmic events (r = 0.58, p < 0.001), but no correlation was found between galectin-3 and LV global longitudinal strain (r = 0.15, p = 0.16). Galectin-3 was an independent predictor of total ventricular arrhythmic events in HF patients (p < 0.0001).

Conclusion

VTnon, VTs, and VF events were higher in HGAL compared to LGAL. Galectin-3 was an independent predictor of total ventricular arrhythmic events in HF patients and might be used to detect high-risk HF patients for arrhythmic events.

Keywords:

• Heart failure
• galectin-3
• arrhythmia
• left ventricular strain
• biomarker
• myocardial fibrosis

Disclosure statement

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Author contributions

All authors contributed to: (1) substantial contributions to conception and design, or acquisition of data, or analysis and interpretation of data, (2) drafting the article or revising it critically for important intellectual content, and (3) final approval of the version to be published.