From joints to vessels: How rheumatoid arthritis therapy alters the fate of the heart

Rheumatoid arthritis (RA) significantly increases the risk of cardiovascular diseases (CVD), including myocardial infarction (MI), stroke, and heart failure (HF). This association is linked to chronic inflammation, endothelial dysfunction, and accelerated atherosclerosis. Patients with RA have a 1.5-2 times higher risk of CVD compared to the general population, and cardiovascular mortality reaches 40%-50%. However, basic anti-inflammatory drugs such as methotrexate reduce the rate of cardiovascular events by 20%-30% due to suppression of systemic inflammation. Biological medications also demonstrate a cardioprotective effect, reducing the risk of MI by 20%-40%, although some (<i>e.g.</i>, tumor necrosis factor α inhibitors) may increase the risk of HF in predisposed patients. Janus kinase inhibitors are associated with an increased risk of thrombosis and cardiovascular events, particularly in patients with pre-existing risk factors. Therefore, optimal control of inflammation in RA can reduce cardiovascular risk; however, drug selection should consider individual safety profiles. Regular monitoring of cardiovascular risk factors and a multidisciplinary approach are key to managing patients with RA and minimizing complications.