Impact of Resveratrol on Arrhythmias in Chronic Ischemic Heart Failure: Insights from Biochemical, Molecular, and Histopathological Studies in a Rat Model

Background Ventricular arrhythmias (VAs) frequently arise as complications in chronic ischemic heart failure (CIHF). Purpose We evaluated the effectiveness of resveratrol (RES) in a CIHF-induced rat model of VAs and explored the underlying mechanisms. Methods Animals received the left anterior descending coronary artery ligation to simulate CIHF and were subsequently treated daily with RES for 2 months. The subjects were categorized into five groups: normal control, VAs model, VAs model receiving simvastatin, and VAs models treated with RES at doses of 10 and 50 mg/kg. Key lipid factors, including high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), were evaluated using a biochemical analyzer. Serum concentrations of inflammatory markers like interleukin-1β (IL-1β), interleukin-8 (IL-8), 6-keto-PGF1α, TXB2, endothelin (ET), and nitric oxide (NO) were quantified through radioimmunoassay (RIA). Real-time polymerase chain reaction (PCR) analyzed the VCAM-1, ICAM-1, and caspase-3 expression in the left anterior descending coronary artery, and Kv4.2, Cav1.2, and nerve growth factor (NGF) in the left ventricle. Results RES treatment led to significant improvements ( p < .05) in lipid profiles, characterized by decreased concentrations of LDL-C, TG, and TC, alongside an elevation in HDL-C. Additionally, RES significantly ( p < .05) lowered inflammatory cytokines and the ICAM-1 and VCAM-1 expression, while enhancing the Cav1.2, Kv4.2, and NGF expression ( p < .05). Furthermore, RES significantly ( p < .05) elevated 6-keto-PGF1α concentrations and increased ET and TXB2 levels. Conclusion RES emerges as an appropriate candidate for treating VAs.