Cardiovascular mortality and cardiovascular event rates in patients with inflammatory rheumatic diseases in the CARdiovascular in rheuMAtology (CARMA) prospective study—results at 5 years of follow-up

Abstract

Objectives To determine cardiovascular (CV) mortality and incidence of the first CV event (CVE) in patients with chronic inflammatory rheumatic diseases (CIRD) after 5 years of follow-up. Methods This is an analysis of the CARdiovascular in rheMAatology (CARMA) study after 5 years of follow-up. It includes patients with RA (n = 775), AS (n = 738) and PsA (n = 721), and individuals without CIRD (n = 677) attending outpatient rheumatology clinics from 67 public hospitals in Spain. Descriptive analyses were performed for the CV mortality at 5 years. The Systematic COronary Risk Evaluation (SCORE) function at 5 years was calculated to determine the expected risk of CV mortality. Poisson models were used to estimate the incidence rates of the first CVE. Hazard ratios of the risk factors involved in the development of the first CVE were evaluated using the Weibull proportional hazard model. Results Overall, 2382 subjects completed the follow-up visit at 5 years. Fifteen patients died due to CVE. CV deaths observed in the CIRD cohort were lower than that predicted by SCORE risk charts. The highest incidence rate of CVE [7.39 cases per 1000 person-years (95% CI 4.63, 11.18)] was found in PsA patients. However, after adjusting for age, sex and CV risk factors, AS was the inflammatory disease more commonly associated with CVE at 5 years [hazard ratio 4.60 (P =0.02)], compared with those without CIRD. Conclusions Cardiovascular mortality in patients with CIRD at 5 years of follow-up is lower than estimated. Patients with AS have a higher risk of developing a first CVE after 5 years of follow-up.

Rheumatoid Arthritis and Cardiovascular Risk: Retrospective Matched-Cohort Analysis Based on the RECORD Study of the Italian Society for Rheumatology

“…At that time, the CARMA project member speculated on the protective effect of the biologic therapy administered to a high number of patients, due to the favorable effect of biologics on the insulin resistance, lipid composition, and other beneficial metabolic effects mediated by these agents, as well as the effect on reducing inflammation. Likewise, the greater knowledge of the EULAR recommendation for the management of traditional CV risk factors among the members of the CARMA project may also have explained these favorable results ( 31 ). The discrepancy supports the gap in proper stratification and treatment of the patients with RA in our cohort.…”

The Risk of Cardiovascular Diseases in Axial Spondyloarthritis. Current Insights

“…A low level of education and general comorbidities (including CV diseases) were identified as predictors of death ( 16 ). In a Spanish study analyzing CV mortality and CV events at 5 years in different IRD, AS was found to have the highest risk of a first CV event [HR: 4.6 (1.32–15.99)], but without increased CV deaths ( 17 ). Finally, a recent meta-analysis concluded that CV mortality in AS was increased, with a relative risk (RR) of 1.46 [1.15–1.86] ( 18 ).…”

Factors associated with risk of major adverse cardiovascular events in patients with rheumatoid arthritis: a nationwide, population-based, case-control study

“…However, the CARdiovascular in rheuMAtology (CARMA) project in Spanish patients revealed a lower rate of cardiovascular events and cardiovascular deaths in patients with chronic inflammatory rheumatic diseases, including RA. 29 Different genetic components and biologics usage percentage in the two groups might be parts of the possible explanations. López-Mejías et al 30 summarized the genetic factors associated with the risk of cardiovascular disease in RA patients, including the HLA class II histocompatibility antigen, DRB1 beta chain ( HLA-DRB1 ) gene, especially the HLA-DRB1*04 shared epitope (SE) alleles, and some polymorphisms inside and outside the HLA region such as the TNFA rs1800629 polymorphism (located at TNFA promoter), the C -C chemokine receptor type 5 ( CCR5)Δ32 rs333 polymorphism (a 32-basepairs deletion), and the methylenetetrahydrofolate reductase (MTHFR) rs1801131 polymorphism.…”