Do statins offer therapeutic potential in inflammatory arthritis?

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Abstract
Rheumatoid arthritis (RA) is associated with accelerated vascular risk with attendant early mortality (pooled standardised mortality rate 1.7) and excess morbidity.1 Optimal treatment of RA disease activity should therefore reasonably deal with vascular risk modification in addition to the well recognised objectives of treatment—namely, to suppress inflammation, improve function, prevent articular damage, and modify psychosocial implications of disease. Intriguingly, vascular specialists are now exercised with the realisation that inflammation is central to the pathogenesis of atherogenesis. Striking similarities in the atherogenic lesion in the vessel have been drawn with the chronic synovitis characteristic of RA, particularly to plaque structure and the role of extracellular matrix degradation in subsequent rupture. That said, vascular inflammation is not reflected in the same degree of local tissue destruction, nor the sustained substantial increase in the acute phase response as in RA, but rather with a lower grade chronic inflammatory response relying on high sensitivity assays for detection of the persistent inflammatory load. Thus, although not necessarily exemplary of shared aetiology, these parallels suggest that shared interventions may be possible.