7 research outputs found
Thromboembolic and cardiovascular risk in rheumatoid arthritis: role of the haemostatic system
Circumstantial evidence suggests that the innate immune system and coagulation system share a common evolutionary origin, which explains the extensive crosstalk between inflammatory cytokines and coagulation factors, with many components being important for both systems. This crosstalk has been extensively studied in sepsis, an acute state of high-grade inflammation. However, rheumatoid arthritis (RA) as well as many other autoimmune diseases can also be considered as a prothrombotic state. More and more studies show that autoimmune diseases, including RA, are a risk factor for cardiovascular disease, and also for venous thromboembolic events, such as pulmonary embolism and deep vein thrombosis. Inflammation and its effect on the haemostatic system is probably the link between these diseases. This viewpoint gives an update of the current literature on thromboembolic risk in RA, but also documents important knowledge gaps. This viewpoint will therefore help to focus on further research topics to improve diagnostic and therapeutic options which may relieve both the proinflammatory and the prothrombotic burden of autoimmune diseases
Subclinical renal dysfunction is independently associated with cardiovascular events in rheumatoid arthritis: the CARRE Study
Background Patients with rheumatoid arthritis (RA) have double the risk of cardiovascular (CV) disease, largely independently of traditional CV risk factors. Renal dysfunction is associated with CV morbidity and mortality in the general population, but data on this association in RA are lacking. Objective To investigate the association between renal function and CV events in RA. Methods The CARRE Study is an ongoing prospective cohort study of Dutch patients with RA, which records CV events. Glomerular filtration rate (GFR) was estimated with the abbreviated Modification of Diet in Renal Disease formula. Logistic regression determined the association between estimated GFR and the occurrence of CV events. Results 353 patients were followed for 3 years, and 23 (7%) had a CV event. Patients who had an event had a significantly lower baseline GFR than those who did not (59 vs 79 ml/min, p=0.001). This association remained significant after adjustment for traditional risk factors: in this analysis, a decrease in GFR of 5 ml/min was associated with a 30% (95% CI 7% to 59%) increase in the occurrence of CV events. During follow-up, an unfavourable change in GFR was noted in patients who later had a CV event compared with those who did not. Conclusion These data confirm that, in RA, renal dysfunction is associated with a higher risk of CV disease independently of traditional CV risk factor