Atrial fibrillation promotion in a rat model of heart failure induced by left ventricle radiofrequency ablation

Abstract

BackgroundAtrial fibrillation (AF) frequently coexists with congestive heart failure (CHF). The increased susceptibility to AF in CHF has been attributed to a variety of structural and electrophysiological changes in the atria, particularly dilation and interstitial fibrosis. We evaluated atrial remodeling and AF vulnerability in a rat model of CHF induced by left ventricle (LV) radiofrequency (RF) ablation.MethodsWistar rats were divided into 3 groups: RF-induced CHF (Ab, n = 36), CHF animals treated with spironolactone (AbSpi, n = 20) and sham controls (Sham, n = 29). After 12 weeks, animals underwent echocardiographic and electrophysiological evaluation and were sacrificed for histological (atrial fibrosis) and Western blotting (TGF-β1, collagen I/III, connexin 43 and CaV1.2) analysis.ResultsMild LV dysfunction and marked atrial enlargement were noted in both ablated groups. AF inducibility (episodes ≥2 s) increased in the Ab group compared to sham animals (31/36, 86%; vs. 15/29, 52%; p = 0.005), but did not differ from the AbSpi group (16/20, 80%; p = NS). Sustained AF (>30 s) was also more frequent in the Ab group compared to shams (56% vs. 28%; p = 0.04). Spironolactone reduced atrial fibrosis (p < 0.01) as well as TGF-β1 (p < 0.01) and collagen I/III (p < 0.01) expression but did not affect connexin 43 and CaV1.2 expression.ConclusionsRats with RF-induced CHF exhibit pronounced atrial structural remodeling and enhanced AF vulnerability. This model may be useful for studying AF substrate in CHF.

Highlights from the International Journal of Cardiology Heart & Vasculature: Heart failure, atrial fibrillation, coronary artery disease and myocardial infarction

“…Symptoms in AF patients include palpitations and reduced exercise tolerance, partly due to reduced oxygen uptake and impaired heart rate responses [21], [22]. Concomitant risk factors such as hypertension, HF, obesity, metabolic syndrome, sleep apnea and ageing lead to structural remodeling processes in the atria, which contribute to the progressive nature of AF and the reduced efficacy of pharmacological and catheter-based rhythm-control strategies [19], [23], [24]. Fibrosis is a prominent feature of atrial remodeling, with epicardial fat tissue importantly contributing to the arrhythmogenic fibrotic substrate, thereby promoting the recurrence of AF in patients undergoing ablation procedures [25].…”