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LIVERPOOL -- Elevated levels of high-sensitivity troponin I (hs-TnI) were associated with excess mortality among patients with inflammatory arthritis, researchers reported here.

Among 1,022 patients enrolled in the (NOAR) from 2000 to 2009, increased risks of all cause mortality (HR 1.71, 95% CI 1.46 to 2) and cardiovascular mortality (HR 2.14, 95% CI 1.65 to 2.79) were seen for each unit increase in log transformed hs-TnI, according to Sarah Skeoch, MBBS, of the University of Manchester, U.K., and colleagues.

Inflammatory arthritis is associated with increased cardiovascular risk, and standard risk-prediction models underperform in these patients. "There's a recognition that we need to develop better ways of identifying inflammatory patients at high risk of cardiovascular disease," Skeoch said in presenting the results at the .

Cardiac troponin is released from damaged myocardium, and is detectable in the circulation within hours of myocardial injury, she explained, calling the enzyme the cornerstone of diagnosis in acute coronary syndrome.

More recently, high-sensitivity assays have been developed that can predict events in asymptomatic individuals in the general population. To see if this could be used to predict cardiovascular mortality in patients with inflammatory arthritis (including rheumatoid arthritis), the researchers analyzed data from NOAR, which is an inception cohort study of patients who have had a history of having two or more swollen joints for more than 4 weeks. Participants were recruited from 2000 to 2009 and followed from enrollment until the end of 2016 or death, with death reports obtained from the National Death Register.

Baseline medical history, cardiovascular risk factors, C-reactive protein, and creatinine were recorded, and hs-TnI was measured with a chemiluminescence assay.

At baseline the median age of patients was 56, and median symptom duration was 10.6 months. Two-thirds of the participants were women, and 61% of the total met the criteria for rheumatoid arthritis established by the American College of Rheumatology/European League Against Rheumatism.

Cardiovascular disease was present at baseline in 3.8% of the patients, and 20% were still smoking.

There were associations found between baseline characteristics and troponin, with significant associations seen for previous cardiovascular events, age, male sex, diabetes, lipids, hypertension, and creatinine level.

During 11,237 patient-years of follow-up, there were 158 deaths, with 27 from ischemic cardiovascular causes; the median time from inclusion until death was 7.4 years.

In an unadjusted model, the risk of cardiovascular death was elevated for patients with a diagnosis of rheumatoid arthritis (HR 2.10, 95% CI 1.45 to 2.95), and for individuals without previous cardiovascular disease (HR 2.11, 95% CI 1.56 to 2.86).

After adjustment for age, sex, cardiovascular risk factors, and inflammatory arthritis factors including seropositivity, disease activity scores, and symptom duration, the risks were found to be as follows:

• Whole cohort, HR 1.76 (95% CI 1.05 to 2.96)
• Patients with RA diagnosis, HR 2.32 (95% CI 1.23 to 4.36)
• Patients without previous cardiovascular disease, HR 1.62 (95% CI 0.89 to 3.04

In a subanalysis of patients meeting the criteria for rheumatoid arthritis at baseline, there were 14 deaths, and again, there was a significant association with hs-TnI (HR 2.25, 95% CI 1.10 to 4.62).

In addition, patients in the highest tertile of hs-TnI had a sixfold increased risk for cardiovascular death compared with the lowest tertile (HR 6.19, 95% CI 2.39 to 16.01).

"In this analysis we've shown that baseline troponin levels do predict cardiovascular death in inflammatory arthritis, and this association was independent of traditional risk factors," Skeoch said.

"What's not clear are the mechanisms driving the increased troponin levels in our cohort. Not only ischemic events can cause this, but other factors such as infiltrative cardiac disease, heart failure, and endothelial dysfunction can also drive troponin levels, all of which may be relevant in inflammatory arthritis."

An advantage of this approach, she added, is that assays for troponin are already clinically available, and could be rapidly introduced into practice.

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