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

International journal of cardiology. Heart & vasculature (2018-09-28)
Luis Dos Santos, Ednei L Antonio, Andrey J Serra, Amanda Yoshizaki, Larissa Seibt, Flavio A Silva, Gisele K Couto, Luciana V Rossoni, Paulo Tucci, Angelo A de Paola, Guilherme Fenelon
RESUMEN

Atrial 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. Wistar 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. Mild 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. Rats with RF-induced CHF exhibit pronounced atrial structural remodeling and enhanced AF vulnerability. This model may be useful for studying AF substrate in CHF.

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Anti-Collagen Type I/III, Cyanogen Bromide Fragments Rabbit pAb, liquid, Calbiochem®