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.

HMG-CoA reductase inhibitors (statins) reduce cardiovascular morbidity and mortality by around 25–50% and are widely used in primary and secondary prevention of vascular disease syndromes.^2–4 Although operating in part through lipid modulation, recent studies demonstrate broader properties for statins, particularly in altering inflammatory pathways.⁵ There is considerable current interest, therefore, in the broader clinical uses of statins, in particular in disease states more clearly associated with high grade inflammation.

Many in vitro and animal studies now describe the potential anti-inflammatory effects of statins. After exposure to statins, endothelial cells exhibit increased endothelial nitric oxide synthase and tissue plasminogen activator antigen with reduced plasminogen activator inhibitor 1, tissue factor, and endothelin expression (reviewed by …