Turning the Corner on CV Risk in Rheumatoid Arthritis Save
Cardiovascular (CV) disease remains the leading cause of mortality in rheumatoid arthritis (RA). A number of studies progressed our knowledge in the session Rheumatoid arthritis - comorbidity and clinical aspects – I on Thursday at EULAR 2021.
Kazuki Yoshida presented abstract #OP0101 examining the influence of disease activity in RA over time on the subsequent risk of major adverse CV events (MACE). They followed 40,721 patients using the Clinical Disease Activity Index from first visit through the end of follow up or to first MACE. During the first 6 months of follow-up hazard ratios [HRs] for first MACE were 1.61 [0.93, 2.77] for low CDAI, 1.97 [1.13, 3.43] for moderate CDAI, and 2.11 [1.13, 3.96] for high CDAI. This excess diminished over time, normalising by the third year at the latest. The authors constructed hypothetical models demonstrating that earlier transition to low CDAI (ie early aggressive therapy) would improve MACE-free survival.
Elena Myasoedova presented data from the Mayo Clinic, abstract #OP0102, assessing trends in heart failure in RA over time and comparing the incidence of heart failure in RA patients compared to population-based non-RA comparators over time. They included 905 RA patients. They found no statistically significant difference in heart failure rates in RA patients in the 2000’s (HR 0.73; 95%CI 0.46-1.18) or 1990’s (HR 0.91, 95% CI 0.62-1.35) compared to 1980’s. In the 903 general population comparators there was also no difference in the incidence of heart failure over time. However, when they compared the risk of heart failure in RA and non-RA, patients with RA in 2000s had no excess heart failure risk compared to the general population (HR 1.14, 95%CI 0.73-1.78). This contrasted with a 2-fold excess risk of heart failure in RA patients in the 1980s (HR 2.20, 95%CI 1.44-3.34) and 1.5-fold increase in the 1990s (HR 1.54, 95%CI 1.04-2.29).
Dr Lam and colleagues presented abstract #OP0103 evaluating the 5-year cardiovascular event rate among early RA patients managed by a treat-to-target strategy compared with a cardiovascular risk factor-matched non-RA population. They included 261 patients with early RA and 783 matched controls. Cardiovascular events occurred in 2.3% early RA patients and in 3.3% controls over 5 years, demonstrating no excess risk in RA patients treated with the treat-to-target strategy. Among the early RA group, longer remission duration appeared protective, HR 0.46 (95% CI 0.23-0.93), while high baseline HAQ was predictive of cardiovascular events, HR 5.2 (95% CI 1.2-23).
Overall, these data are promising and suggest that we are improving cardiovascular outcomes in RA patients while also illustrating the tools we have available to maximise this effect. It certainly appears that achieving remission, especially in the early stages of the disease, is crucial in reducing cardiovascular risk in RA.