Patient education on cardiovascular aspects of rheumatoid disease: an unmet need

Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis affecting nearly one in 100 adults [1]. Cardiovascular disease (CVD) occurs at rates higher than expected in the general population, is the most prevalent comorbidity and most common cause of death in RA patients [2–5]. The exact reasons remain unclear, but both classical CVD risk factors (such as hypertension and dyslipidaemia) and novel mechanisms (such as systemic inflammation), and their interplay, appear to be important [6, 7]. Classical risk factors may be fixed (e.g. age, sex, family history) or modifiable (e.g. smoking, hypertension, dyslipidaemia, obesity, sedentarity). The latter are an obvious target for identification and intervention [7, 8], neither of which appears to be happening systematically in the current rheumatology health care environment [3, 9]. This is partly due to lack of sufficient awareness of health professionals and information/education of patients on this aspect of their disease. Interestingly, many of the medications used for the management of RA may have a significant impact upon these factors, with the clearest example being the potential cardiovascular effects of the commonly used non-steroidal anti-inflammatory drugs (NSAIDs) and coxibs [10], the hypertensive effects of some disease-modifying anti-rheumatic drugs (DMARDs) such as cyclosporine and leflunomide, or potential beneficial lipid effects of others, such as hydroxychloroquine [7]. Non-pharmacological interventions are of equal, if not more, importance: for example, there is excellent quality evidence to suggest that exercise provides significant functional benefits in RA patients, together, of course, with important cardiovascular benefits, such as improvements in lipid profile and insulin sensitivity, reduction of prothrombotic states and body fat content, and diminished risk of death from CVD in the general population and high risk groups therein [11]. The importance of systemic inflammation is more controversial: there is clear evidence that atherosclerosis is an inflammatory disease [12] and that RA appears to associate with premature peripheral atherosclerotic changes [13]; there is also evidence that better control of systemic inflammation leads to survival benefits in RA [14–17]. However, it remains unclear whether this is a direct effect or whether it operates through amelioration of the multiple metabolic and vascular effects of inflammation [18, 19]. Uncertainties also remain as to the best way to achieve sufficient control of high-grade inflammation without adverse effects to the vasculature.