Epidemiology and predictors of cardiovascular diseases in rheumatoid arthritis
Authors:   , Raadsen Reinder 
Published: May 2024

In chapter 2 we explored changes in lipid-profile and NT-proBNP throughout the development of RA. Thirty-eight patients were followed from the preclinical phase until up to 6 months treatment with bDMARDs. Most changes in lipid-profile and NT-proBNP seemed to be related to changes in CRP. These changes were already present at the moment of diagnosis, indicating the need for timely intervention to prevent atherosclerosis development and thus future CVD. However, these results should be interpreted with caution, as larger studies are needed to confirm our findings.

In chapter 3 we investigated the longitudinal effects of four years of anti-rheumatic therapy on several markers for subclinical atherosclerosis in RA patients and compared baseline values with OA patients. Although IMT remained stable throughout the entire follow up, AIx and PWV decreased in the first six months of anti-inflammatory therapy. Additionally, we found a positive correlation between disease activity and IMT, AIx, and PWV. These results suggest modest beneficial changes in surrogate markers for subclinical CVD. This should be investigated further in larger, prospective studies with a comparative, matched control group during the entire follow up period.

In chapter 4 we described CV risk management procedures of 125 consecutive, newly diagnosed RA patients. We found that the majority of patients already had either dyslipidemia, hypertension, or both, with a higher prevalence in male patients. Of the female patients, only 4% had a high CV mortality risk, while 50% of male patients had a high or very high risk. Of these high-risk patients, only 26% were started on preventive medication by their general practitioner within a year of screening. We concluded that CV risk screening needs to be part of standard care, to reduce the CV burden of RA patients.

In chapter 5 we investigated the presence of CVD in patients with IA compared to healthy controls in a large cross-sectional study. We found that the prevalence of CV risk factors was increased for all IA patient groups. Additionally, the prevalence of CVD was increased in IA patients. Adjusting results for CV risk factors highly attenuated the odds ratios, suggesting that the current CVD risk in IA patients is heavily influenced by these risk factors. More attention needs to be paid to screening for and treatment of traditional CV risk factors, not only in RA patients, but in individuals with PsA and SpA as well.

In chapter 6 we extended the CARRÉ cohort study to a follow up of 20 years. We found increased HRs for both RA patients and DM patients without prevalent CVD compared to healthy controls. When the analyses were adjusted for ‘traditional’ CV factors, no significant ‘RA-specific’ risk remained, while a ‘DM-specific’ risk was retained. This suggests that the increased CVD risk in RA patient without previous CVD is mainly attributable to increased prevalences of CV risk factors as hypertension and dyslipidemia. With better control of inflammation in RA due to modern, early treatment, structural CV risk screening and management needs to be implemented to further decrease the CVD risk.

Finally, in chapter 7 we studied the activation of the coagulation system of RA patients during treatment with either TNF-blockers or JAK-inhibitors. The coagulation markers were measured at baseline, and after one, three and six months of follow up. In TNF-blocker users, both D-dimer and fibrinogen levels significantly declined, while TAT levels significantly increased after 6 months follow up. In JAK-inhibitor users, only vWF levels significantly declined. Our data suggests that an increased VTE risk due to treatment with either medication type is unlikely, however, this needs to be verified in larger studies with a longer follow up duration.