Low-grade chronic inflammation has been proposed to play a central role in atherosclerosis1,2, as well as in other types of vascular damage, and measuring the level of inflammatory markers in the blood can provide prognostic information regarding cardiovascular disease (CVD) risk1,2. A serum level of C-reactive protein (CRP), determined with a high-sensitivity assay, is at the moment the best studied inflammatory marker, and CRP has been used to enhance risk prediction based on Framingham risk score and Reynolds risk score in apparently healthy women and men1,2,3.
In this issue of The Journal, Provan and colleagues4 report interesting data regarding the putative role of low-grade chronic inflammation in CVD with special reference to the well established increased CVD risk seen in patients with rheumatoid arthritis (RA)5. Provan and colleagues4 studied a cohort of a little more than 100 patients with RA, and they found that serum levels of CRP above the median (> 3.80 mg/l) at baseline were associated with increased central artery stiffness at followup 15 years later. As increased central or large artery stiffness is a well established marker of increased CVD risk6, Provan and colleagues4 speculate that poor control of RA, as reflected by higher levels of CRP, and thereby accompanying inflammatory damage to the elastic arteries, may explain the increased CVD risk seen in patients with RA. As a consequence, they discuss that early active disease management by use of disease modifying antirheumatic drugs to control inflammation may help to reduce the risk of later CVD in patients with RA. However, although it certainly would be desirable if tight control of the inflammatory processes caused by RA would eventually lead to a decreased risk of …
Address correspondence to Dr. Jeppesen. E-mail: jj{at}heart.dk Supported by a grant from the Novo Nordisk Foundation.