Cardiovascular risk and rheumatoid arthritis: from mechanisms of atherosclerosis to therapeutic approach.
Large epidemiological studies showed that one of the most important causes of death in patients with rheumatoid arthritis (RA) is represented by cardiovascular disease. Thus, the presence of RA is associated with an increased risk of the occurrence of stable angina, myocardial infarction, heart failure and stroke. However, studies performed during the last years failed to bring us clear evidence regarding the role of traditional cardiovascular risk factors (hyperlipidemia, diabetes mellitus, hypertension, smoking and obesity) in the pathogenesis of cardiovascular disease in these patients. Recently, the role of inflammation and its mediators not only in the atherosclerosis plaque development but also in the mechanisms of vulnerable plaque was clearly demonstrated. From this point of view, recent studies showed that inflammatory cells and mediators of inflammation are both markers of an increased cardiovascular risk and unfavorable cardiovascular outcome, and also cardiovascular risk factors that act in an active manner in the processes that promote atherosclerosis. Taking into account the fact that RA is a systemic inflammatory status, recent reports demonstrated the involvement of inflammation mediators in connection with prothrombotic factors and endothelial dysfunction in the development of cardiovascular disease in RA patients. There are only scarce data in the literature regarding the benefice of cardiovascular risk reduction therapies in this group. Further studies are required for the refinement of the cardiovascular risk stratification algorithms and for the improvement of the cardiovascular risk management in rheumatoid arthritis.
Jurcuţ
Ciprian
C
Internal Medicine I Department, Central Military Hospital, Bucharest, Romania.
Jurcuţ
Ruxandra
R
Tănăsescu
Coman
C
D001172:Arthritis, Rheumatoid / Q000150:complications* / Q000276:immunology* / Q000628:therapy; D050197:Atherosclerosis / Q000209:etiology / Q000276:immunology / Q000628:therapy; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000276:immunology* / Q000628:therapy; D016207:Cytokines / Q000276:immunology; D004730:Endothelium, Vascular / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000276:immunology*; D012307:Risk Factors
D016207:Cytokines