RELATIONSHIP BETWEEN INFLAMMATORY CYTOKINES AND ELECTRICAL REMODELLING IN CARDIAC RESYNCHRONIZATION THERAPY

D. Zizek, M. Cvijic, B. Antolic, I. Zupan

Department of Cardiology, University Medical Centre Ljubljana, Slovenia

Abstract

Introduction: Cardiac remodelling in advanced heart failure (HF) is associated with increased inflammation, leading to ventricular fibrosis and subsequent impairment of intraventricular conduction. In addition, scar-related anisotropy provides conditions for re-entry ventricular tachyarrhythmias (VTs). The aim of our study was to evaluate the relation between inflammatory cytokines, intrinsic QRS duration (iQRS) and VT occurrence after cardiac resynchronization therapy (CRT).
Methods: We prospectively included 55 patients with advanced HF (age 66 ± 10; 37 male (67%); New York Heart Association class II-IV; EF 26.4 ± 6.2%; QRS 162 ± 21ms; 26 ischaemic aetiology (47.3%)) who underwent implantation of a CRT device. Clinical, electrocardiographic and plasma levels of inflammatory parameters (interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor ? (TNF-?)) were evaluated before and after 6 months of CRT. Biventricular pacing at 6 months was temporarily inhibited to record iQRS. Reverse electrical remodelling was defined as a decrease in iQRS duration by ?10 ms.
Results: After 6 months of CRT reverse electrical remodelling was accompanied by significant reduction of IL-6, IL-10 and TNF-?. Electrical remodelling was identified in 31 patients (56%). This group of patients demonstrated significant decrease of cytokine levels (IL-6: 2.6 ng/L (1.7-4.4) to 2.1 ng/L (1.1-3.3), p=0.028; IL-10: 8.1 ng/L (0.9-17.8) to 4.2 ng/L (1.7-11.3), p=0.020; TNF-?: 7.4 ng/L (5.0-9.9) to 5.6 ng/L (3.2-7.1), p=0.001); whereas no changes were observed in patients without electrical remodelling. In median follow-up 30 (24-34) months, VTs were registered in 18 patients (32.7%). Patients with electrical remodelling experienced significantly less VTs compared to patients without electrical remodelling.
Conclusions: Reduction of inflammatory cytokines after CRT could have a pathophysiological role in improvement of intraventricular conduction and consequent amelioration of arrhythmogenic substrate.