Antirheumatic drugs and cardiovascular disease in rheumatoid arthritis

Abstract

There is increased cardiovascular (CV) morbidity and mortality in rheumatoid arthritis (RA) and other rheumatic and musculoskeletal diseases (RMDs). Systemic inflammation is highly involved in atherogenesis. Non-steroidal anti-inflammatory drugs (NSAIDs), primarily COX-2 inhibitors might increase CV risk. Corticosteroids might act as a double-edged sword as they exert both beneficial and negative effectson the CV system. NSAIDs and corticosteroids are anti-inflammatory, but, on the other hand, they might be potentially atherogenic. Conventional synthetic DMARDs (csDMARDs), such as antimalarials, methotrexate, sulfasalazine, leflunomide and cyclosporine A have good CV safety, however, leflunomide and cyclosporine A might cause hypertension. Biologic DMARDs, by suppressing inflammation and disease activity, might either reduce CV risk or at least not cause any harm in that respect. Recently, tofacitinib and most likely other Janus kinase inhibitors have been associated with increased CV risk, at least in RMD patients with high CV risk at baseline. In clinical practice, EULAR and other recommendations guide the rheumatologist when screening for and managing CV comorbidities.