The increased cardiovascular risk in rheumatoid arthritis: when does it start?Nowadays it is well known that patients with established rheumatoid arthritis (RA) suffer from an increased cardiovascular risk in comparison with the general population, and both traditional cardiovascular risk factors as well as the underlying chronic inflammatory process contribute to this excess cardiovascular risk. Little is known, however, about the cardiovascular risk in early RA patients - hence the recent article by Södergren and colleagues could be an important contribution to the field [1] .
The increased cardiovascular risk in RA is mainly due to atherosclerotic events. Until recently atherosclerosis was considered an accumulation of lipoproteins within the arterial wall. During the past decade, however, atherosclerosis has been recognized as a chronic inflammatory process in the artery. The first step in the process is endothelial dysfunction caused by traditional cardiovascular risk factors such as smoking. The endothelium becomes more permeable - to lipids, for example - and becomes procoagulant instead of anti-coagulant. The inflammatory response further results in an entry of inflammatory cells and muscle cells. Foam cells are formed and result in fatty streaks. This lesion progresses and a fibrous cap is formed, consisting of smooth muscle cells and a collagen matrix that separates this atherosclerotic plaque from the arterial lumen. Ultimately, the plaque may rupture and the subsequent thrombosis causes a myocardial infarction.
Wow,