Patients with rheumatoid arthritis (RA) are likely to benefit from regular high-sensitivity cardiac troponin T (hs-cTnT) testing, researchers said.
In a group of RA patients followed for a mean of 5 years, positive hs-cTnT test results were significantly associated with subsequent risk for major adverse cardiovascular events (MACE) even after adjusting for all standard risk factors and C-reactive protein (CRP) levels, with an adjusted hazard ratio (aHR) of 4.29 (95% CI 1.31-14.10), according to Katherine P. Liao, MD, MPH, and colleagues at Brigham and Women’s Hospital in Boston.
All-cause mortality was also associated with detectable hs-cTnT to nearly the same degree (aHR 4.18, 2.60-6.72), the researchers reported in the Journal of Rheumatology.
While RA patients have long been known to experience increased risks of cardiovascular events and mortality, it’s also been recognized that it’s not because their conventional risk factors are increased commensurately — there’s more going on in RA than is accounted for by smoking, obesity, hypertension, and other factors generally used to assess MACE risk. Even adding in additional factors such as CRP, an indicator of systemic inflammation, and measures of RA disease activity doesn’t fully predict MACE risk. Event rates are clearly elevated among patients not identified as being at high risk with conventional predictive models such as “hard” Framingham score.
“From a clinical standpoint, the identification of patients with RA who have a higher CV [cardiovascular] risk, prompting initiation of CV prevention medications (i.e., statins), remains a challenge,” Liao and colleagues explained.
The researchers had the idea of checking whether hs-cTnT might fill in the gap. Some years ago, another group had found that high-sensitivity testing for a related substance, troponin I, improved prediction of cardiovascular events and atherosclerotic plaque burden. As it happens, Brigham and Women’s Hospital has been running a longitudinal study of RA patients called BRASS that began in 2003 in which blood samples are collected and stored annually. Thus, Liao’s group had the ability to run hs-cTnT tests on those samples; for the current analysis, up to 10 years of samples were tested. The researchers were also able to calculate conventional cardiovascular risk scores for participants at baseline from their medical records.
Out of a total of more than 1,500 BRASS participants, Liao and colleagues identified 331 with sufficient data to examine 10-year MACE and mortality risk. About 83% were women and the mean age at baseline was 58. Median RA disease duration was 12 years. Treatments were typical: just over half were using methotrexate at baseline and 42% were on tumor necrosis factor inhibitors; one-quarter were taking oral corticosteroids.
Some 23% of patients had hypertension, 5% had type 2 diabetes, 9% had hyperlipidemia, and 8% were current smokers — in general, all substantially lower than most people of similar age. Under standard heart risk testing, the median predicted MACE risk over 10 years was 3.87% (interquartile range 1.18%-9.87%), indicating that most patients were at relatively low risk. Yet the actual 10-year MACE rate was 4.8%, and 15% of the cohort died during the decade-long follow-up.
Positive hs-cTnT results were seen in 35%, and this alone was associated with a massively increased MACE risk prior to adjustment for other risk factors (HR 7.13, 95% CI 2.29-22.10) relative to those negative for the marker. As noted above, such adjustments brought down the extra risk somewhat; however, further adjustment for disease activity via the DAS28 score did not make a notable difference.
All this suggests that hs-cTnT is an independent risk factor for cardiovascular risk and mortality that may be worth tracking in people with established RA, Liao and colleagues indicated, pending further studies. These should “examine the association of hs-cTnT and existing atherosclerotic plaque among asymptomatic patients with RA to determine the utility of screening specific populations using hs-cTnT in the clinic,” the group wrote.
What effect disease-modifying treatments might have had on MACE risk wasn’t examined in the study; past research has suggested that such therapies do reduce it somewhat.
![author['full_name']](https://clf1.medpagetoday.com/media/images/author/johnGever_188.jpg)
John Gever was Managing Editor from 2014 to 2021; he is now a regular contributor.
Disclosures
Support for the study came from the National Institutes of Health, the American Heart Association, and several charitable foundations. Co-authors reported relationships with numerous pharmaceutical companies and other commercial entities.
Primary Source
Journal of Rheumatology
Source Reference: Weber B, et al “The association between high-sensitivity cardiac troponin T and major adverse cardiovascular events in rheumatoid arthritis” J Rheumatol 2024; DOI: 10.3899/jrheum.2024-0168.
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