Popkova Tatyana V, Novikova Diana S, Gasparyan Armen Yuri, Nasonov Evgeny L
Department of Vascular Pathology of Rheumatic Diseases, V.A. Nasonova Research Institute of Rheumatology, Russian Academy Sciences, Kashirskoe Shosse, 34A, Moscow, 115522, Russian Federation.
Curr Med Chem. 2015;22(16):1903-10. doi: 10.2174/0929867322666150415122039.
Cardiovascular events such as myocardial infarction (MI) and stroke due to enhanced inflammatory atherosclerosis account for increased premature mortality in rheumatoid arthritis (RA). Accumulated evidence suggests that accelerated atherosclerosis and related cardiovascular comorbidities in RA are confounded not only by traditional risk factors (TRF) but also by a number of immune and inflammatory pathways. Since chronic inflammation and autoimmune disorders play a key role in atherosclerosis and related cardiovascular complications in RA, effective suppression of systemic inflammation can be viewed as a strategy for cardiovascular therapy and prevention in this disease. This article overviews some mechanisms of action of methotrexate on TRF, clinical and subclinical manifestations of RA-induced atherosclerosis, and related cardiovascular morbidity and mortality.
由于炎症性动脉粥样硬化加剧导致的心血管事件,如心肌梗死(MI)和中风,是类风湿关节炎(RA)患者过早死亡增加的原因。越来越多的证据表明,RA中加速的动脉粥样硬化和相关心血管合并症不仅受到传统危险因素(TRF)的影响,还受到多种免疫和炎症途径的影响。由于慢性炎症和自身免疫性疾病在RA的动脉粥样硬化和相关心血管并发症中起关键作用,有效抑制全身炎症可被视为该疾病心血管治疗和预防的一种策略。本文概述了甲氨蝶呤对TRF的一些作用机制、RA诱导的动脉粥样硬化的临床和亚临床表型,以及相关的心血管发病率和死亡率。