The Rationale for Comparative Studies of Accelerated Atherosclerosis in Rheumatic Diseases

Abstract

The inflammatory pathogenesis of atherosclerosis is now well-established, owing to in vitro and in vivo studies and the application of high sensitivity assays for C-reactive protein (CRP) in the general population and specific groups at risk for cardiovascular disease (CVD). In view of the complexity of inflammation-induced atherosclerosis, the rationale for comparative studies of atherogenesis in rheumatic diseases with diverse inflammatory pathogenesis seems obvious; they are human in vivo models to study inflammatory mechanisms involved in atherosclerosis and the impact of treatment. Factors implicated in atherogenesis in systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), familial Mediterranean fever (FMF) and Behçet's disease (BD) are discussed in this review. Evidence suggests that enhanced atherosclerosis causes premature cardiovascular events in the autoimmune disease, SLE, and the "high-grade" inflammatory rheumatic disease, RA. Preliminary data suggest that enhanced atherogenesis may accompany FMF in the absence of sufficient suppression of inflammation by colchicine. In the setting of BD, the role of atherosclerosis in the premature manifestation of coronary pathology has not been confirmed; coronary vasculitis and aneurysms appear to constitute the basis of myocardial infarction (MI) in BD. A variety of established and novel risk factors are believed to influence enhanced atherogenesis in rheumatic diseases. Antiphospholipid antibodies are thought to be intimately involved in atherogenesis in SLE and to a lesser extend in RA. CRP may play a more universal role in all rheumatic diseases. The application of high resolution ultrasound of peripheral arteries and other non-invasive techniques may allow targeted use of statins, ACE inhibitors, antiplatelet agents and other cardioprotective drugs in patients with rheumatic diseases, but this needs to be evaluated specifically in prospective studies.

Investigation of the arterial stiffness and associated factors in patients with familial Mediterranean fever

“…The drug of choice for the prevention of attacks and the development of amilodosis in patients with FMF is colchicine, which has anti-neutrophilic, anti-inflammatory, anti-fibrotic, and anti-proliferative effects (20). Preliminary data propose that enhanced atherogenesis may accompany FMF in the absence of a sufficient suppression of inflammation by colchicine (21). In our study, we found that stiffness measurements get higher in the attack period.…”

Alexithymia and Tissue Inflammation

“…In addition, since the lifestyle-related factors BMI [20], smoking [20] and alcohol use [21] have been suggested to affect levels of inflammatory markers, a two-step cluster analysis was performed to create a single variable from these lifestyle risk factors [22]. In model 2, we evaluated the effect of the chronic inflammation-relevant disorders rheumatoid arthritis [23] and coronary heart disease [24] together with the factors from model 1. These chronic disorders were also pooled into one variable in order to control the number of degrees of freedom in the analyses.…”

Does mean platelet volume influence the attack or attack-free period in the patients with Familial Mediterranean fever?

“…In this context, it was reported that the prothrombotic pathways and atherosclerosis can be suppressed by using colchicine [5,6]. Platelet size is correlated with platelet function and activation.…”