Nicorandil in Atherosclerosis Risk in Patients With Rheumatoid Arthritis

Overview

The goal of this clinical trial is to learn about the effects of adding nicorandil to conventional Disease-Modifying Antirheumatic Drugs(DMARDs) in treatment of patients with rheumatoid arthritis. The main questions it aims to answer are: Does adding nicorandil to conventional DMARDs in treatment of patients with rheumatoid arthritis reduce the risk of plaque buildup in arteries (atherosclerosis) ? and What medical problems may participants have when taking nicorandil ? Participants will: Take nicorandil added to DMARDs or DMARDs only for 3 months patient will be assessed at baseline and 3 months after for disease activity and risk of plaque formation over vascular wall Keep a diary of their symptoms and possible side effects

RA is associated with significant risk of cardiovascular (CV) disease. Atherosclerosis is notably accelerated in RA patients, driven by a combination of chronic systemic inflammation, endothelial dysfunction, and traditional CV risk factors including hypertension, dyslipidemia, and insulin resistance. the conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), effectively control joint inflammation and disease activity, but doesnot affect the risk of atherosclerosis. Nicorandil is a hybrid drug that combines nitrate-like vasodilatory properties with the activation of ATP-sensitive potassium (K\_ATP) channels. It has been extensively studied in cardiovascular medicine for its vasodilatory, anti-ischemic, and endothelial-stabilizing effects. Recent preclinical and clinical evidence suggests that nicorandil also possesses anti-inflammatory properties, making it a promising candidate for vascular protection in inflammatory conditions such as RA. Carotid intima-media thickness (CIMT) is a validated, non-invasive imaging biomarker for subclinical atherosclerosis. It reflects structural arterial changes and is predictive of future cardiovascular events. In RA, CIMT is frequently elevated even in the absence of overt CV disease, correlating with disease duration, activity, and systemic inflammation. Changes in CIMT serve as a surrogate endpoint for evaluating the progression or regression of atherosclerosis in interventional trials. Lipoprotein(a) \[Lp(a)\] has emerged as a promising biomarker for predicting atherosclerotic risk. Elevated Lp(a) levels contribute to accelerated atherogenesis by promoting endothelial dysfunction, oxidative stress, and recruitment of pro-inflammatory immune cells within the vascular wall. Patients with RA often exhibit elevated Lp(a) levels compared to healthy individuals, which has been associated with a higher risk of atherosclerosis. Among autoimmune disorders, RA exhibits the strongest association with elevated Lp(a) in the context of atherosclerosis. both will be used to assess risk reduction.