Cardiovascular manifestations of rheumatic diseases have been thoroughly examined over the past decades. It has been established that all structures of the heart can be affected due to the long-term systemic inflammation and specific autoimmune and autoinflammatory factors [1]. Classic clinical models of cardiovascular phenomenon in rheumatic diseases are rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), which are associated with enhanced course of atherosclerosis and various atherothrombotic events. Numerous large cohort studies of RA and SLE have provided evidence of atypical and severe course of myocardial infarction and heart failure in these autoimmune diseases, necessitating specific early diagnostic and preventive approaches.

The intensity of systemic inflammation confounds cardiovascular manifestations across rheumatic diseases. Accordingly, inflammation-induced atherosclerosis is believed to be a more pressing issue in RA and SLE than in autoinflammatory disorders [2]. Methotrexate therapy improves lipid profiles and reduces atherothrombotic risk in RA by diminishing production of C-reactive protein (CRP) and suppressing systemic inflammation [3]. Biologic agents may also protect from enhanced atherogenesis in RA by potently suppressing pro-inflammatory cytokines, such as interleukin-6 and tumor necrosis factor alpha [4]. Although there are no specifically designed trials of colchicine therapy in atherogenesis due autoinflammatory disorders, this anti-neutrophilic agent is viewed as cardioprotective and essential for cohorts of patients with inflammatory amyloidosis and pericarditis [5].