The risk of cardiovascular disease (CVD) is up to twofold increased in patients with inflammatory joint disorders (IJD). This increased CVD risk is due to both traditional risk CVD risk factors such as hypertension, smoking and dyslipidemia as well as the underlying chronic systemic inflammation in IJD. Traditional CV risk factors are more often present in IJD and partially a consequence of changes in physical function related to the underlying IJD. Approximately 50% of the increased CV risk is due to traditional CV risk factors and 50% due to the inflammatory process. Inflammation may have a negative impact on CV risk factors, but this effect only marginally explains the increased prevalences of CV risk factors.
CV risk management should thus not only target the inflammation but also CV risk factors. It has three main principles: non-pharmacological interventions, pharmacological management of CV risk factors, and control of disease activity.
Non-pharmacological strategies Life style management should include counselling for smoking cessation (albeit that the favorable cardiovascular effects of smoking cessation might be less than in the general population) as well as increasing physical activity, and healthy (Mediterranean) diet.
Treatment of CV-risk factors Thus far, adequate CV endpoint trials with statins and or antihypertensive agents have not been published. However, population and databases investigations indicate that antihypertensive agents and statins do not work less than in the general population. Indeed, statins have additional anti-inflammatory effects, that might be important from a CV point of view.
Disease activity There is mounting evidence that cumulative disease activity as well as the number and duration of flares over time do contribute to the cardiovascular risk.
Hence, inflammation reduction is important for CVD risk reduction, but it appears that the type of treatment is less important. Nowadays, tapering of biologicals is becoming more and more standard of care and has several benefits, but one of the drawbacks might be the possible negative effect on thrombotic markers. As thrombotic markers normalize with biologicals therapy, this favorable effect might be reversed and thus exposing our patients to an increased CV-risk.
Furthermore, it is important to realize that it cannot be excluded some biologic agents as well as targeted synthetic DMARDs might have adverse cardiovascular effects. Finally, NSAIDs/COXIBs and steroids might have a negative impact on the cardiovascular risk profile.
Conclusions The increased CV risk in IJD is widely acknowledged for about a decade. Nonetheless, CV mortality has hardly improved, despite major improvements in antirheumatic therapy. Hence, targeting disease activity only is just NOT enough to reduce the CV risk of our patients. In line of this, most (recent) studies indicate poor CV risk management in daily clinical practice and thus the CV challenge for the future is optimizing CV risk management and its implementation.
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Disclosure of Interest None declared
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