Rheumatoid arthritis is a chronic autoimmune disease that not only affects the joints but also increases the risk of cardiovascular events and mortality. Previous studies have shown that conventional risk factors are not sufficient to predict major adverse cardiovascular events (MACE) and mortality in rheumatoid arthritis patients. Factors such as smoking, obesity, hypertension, and even markers of systemic inflammation like C-reactive protein do not fully account for the increased risk in this population.
Researchers at Brigham and Women’s Hospital conducted a study to investigate the association between high-sensitivity cardiac troponin T (hs-cTnT) levels and cardiovascular risk in rheumatoid arthritis patients. The study followed a group of patients for an average of 5 years and found a significant correlation between positive hs-cTnT test results and subsequent MACE and all-cause mortality. Even after adjusting for standard risk factors and RA disease activity, the association remained strong with an adjusted hazard ratio of 4.29 for MACE and 4.18 for all-cause mortality.
The study included 331 rheumatoid arthritis patients with a median disease duration of 12 years. Despite the majority of patients being at relatively low risk according to standard heart risk testing, the actual 10-year MACE rate was 4.8%, and 15% of the cohort died during the follow-up period. Positive hs-cTnT results were found in 35% of patients, significantly increasing the risk of MACE even before adjusting for other risk factors.
The findings of this study suggest that hs-cTnT testing may serve as an independent risk factor for cardiovascular events and mortality in rheumatoid arthritis patients. Identifying patients with higher cardiovascular risk based on hs-cTnT levels could prompt the initiation of cardiovascular prevention medications such as statins. However, further research is needed to determine the utility of screening specific populations using hs-cTnT in clinical practice.
Future studies should focus on examining the association between hs-cTnT levels and existing atherosclerotic plaque among asymptomatic rheumatoid arthritis patients. This could help in determining the efficacy of using hs-cTnT testing as a screening tool in clinical settings. Additionally, the impact of disease-modifying treatments on MACE risk should be further investigated, as previous research has suggested a potential reduction in cardiovascular risk with such therapies.
Regular hs-cTnT testing could play a crucial role in assessing cardiovascular risk and mortality in rheumatoid arthritis patients. By identifying individuals with elevated hs-cTnT levels, healthcare providers can implement preventive strategies to mitigate the risk of MACE and improve patient outcomes. Further studies are warranted to validate the findings of this research and explore the potential benefits of incorporating hs-cTnT testing into routine care for rheumatoid arthritis patients.
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