Cardiovascular (CV) disease (CVD) co-morbidity and mortality is one of the largest drivers of the excess morbidity and pre-term mortality in patients with rheumatoid arthritis (RA) [1–3]. The mechanisms behind the increased CV morbidity and mortality in RA likely include a complex interplay between RA-related inflammation, beneficial as well as detrimental effects of anti-rheumatic drugs, and an increased prevalence of traditional risk factors for cardiovascular disease. Some of these CV risk factors may occur in excess already at RA diagnosis, others will occur and act as mediators of effects primarily due to RA-related inflammation and its treatment(s) [3].
