Page 177 - THE EVOLUTION OF EARLY ARTHRITIS AND CARDIOVASCULAR RISK Samina A. Turk

CONCLUSION, DISCUSSION AND FUTURE PERSPECTIVES
From part I of this thesis we conclude that there are many risk factors of varying strength for the development of RA, most of which confer only a low risk on their own. It is im- portant to note that there is not yet a proven intervention, medicinal or otherwise, to prevent RA during the at-risk phase. However, primary prevention of RA is an important and widely studied topic, and we look forward to the results of several drug trials, such as the STAtins To Prevent Rheumatoid Arthritis (STAPRA) study, Arthritis Prevention in the Pre-Clinical Phase of RA with Abatacept (APIPPRA) study, TREAT EARLIER study (us- ing methotrexate and intramuscular corticoids) and the Strategy to Prevent the Onset of Clinically-Apparent Rheumatoid Arthritis (StopRA) study in which RA prevention is attempted with hydroxychloroquine. Until primary prevention has been developed, it is of great importance that patients are diagnosed with their disease as early as possible, for a prompt initiation of anti-rheumatic treatment.
Part II showed that the body composition of arthritis patients was already unfavorable at the moment of diagnosis in comparison with the general population. For future per- spectives, it would be of interest to determine body composition before the onset of arthritis, i.e. in persons with an increased risk of arthritis, to determine when this un- favorable composition develops and whether this could possibly be prevented. Also, it should be determined whether the unfavorable body composition, which is present at the onset of arthritis, can be normalized. Furthermore, the prevalence of conduction disorders was not increased at baseline, but it would be interesting to follow these pa- tients over time to determine if they develop more conduction disorders when they are exposed to inflammation for a longer period of time. Remarkably, we found a decreased heart rate of 7 beats/ min when comparing the lowest with the largest improvement of disease activity. On a population level this would mean a ten-year CV mortality risk difference of 24% between no or minimal versus substantial improvement in Disease Activity Score (DAS).
The last chapter showed that different CV risk results are obtained, depending on which CV risk prediction tool was used. Therefore, follow-up research is necessary to deter- mine which CV risk screening model is optimal in RA patients. Of interest would be to see in ten years which CV risk model best predicted the CV outcome of the pres- ent cohort and if additional corrections for RA-associated factors can improve this risk prediction model. Obviously, this model should be validated in other cohorts. Another important conclusion is that the advice for preventive CV risk medication, according to the Dutch SCORE and risk management guidelines, varied widely before and after four weeks of anti-rheumatic treatment. Overall, RA patients should be in remission or have minimal disease activity in the long-term course of their disease. Therefore, it appears rational to perform CV risk management at a time of low disease activity. Our findings indicate that CV risk management should not be implemented at disease onset but at least four weeks after initiation of anti-rheumatic treatment. To further optimize
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GENERAL DISCUSSION
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