Key result
Rheumatoid arthritis is linked to ~49% higher median hs-cTnI levels compared to controls.
Why the study?
Patients with rheumatoid arthritis have an increased incidence of heart failure, and chronic myocardial injury may be a mechanism for its development.
Are high-sensitivity cardiac troponin-I concentrations elevated in patients with rheumatoid arthritis compared to controls?
Cross-Sectional (n=254)
Are high-sensitivity cardiac troponin-I concentrations elevated in patients with rheumatoid arthritis compared to controls?
Absolute Event Rate: 1.15% vs 0.77%
p-value: p=<0.001
Patients with rheumatoid arthritis have elevated high-sensitivity cardiac troponin-I levels independent of traditional cardiovascular risk factors and inflammation, suggesting subclinical myocardial injury.
Elevated hs-cTnI in RA without HF may indicate subclinical injury; hypothesis-generating for HF mechanisms and risk stratification.
OBJECTIVES: We examined the hypothesis that cardiac-specific troponin-I (cTn-I), a biomarker of myocardial injury, is elevated in patients with rheumatoid arthritis (RA). BACKGROUND: RA patients have an increased incidence of heart failure (HF). Chronic myocardial injury in RA may be a mechanism for the development of HF. METHODS: We compared cTn-I concentrations measured by high-sensitivity immunoassay in 164 patients with RA and 90 controls, excluding prior or active heart failure. We examined the relationship between cTn-I concentrations and cardiovascular risk factors, inflammation, and coronary artery calcium score (CACS), a measure of coronary atherosclerosis. RESULTS: cTn-I concentrations were 49% higher in patients with RA (median 1.15 pg/mL [IQR 0.73-1.92] than controls (0.77 pg/mL [0.49-1.28](P<0.001). The difference remained statistically significant after adjustment for demographic characteristics (P = 0.002), further adjustment for cardiovascular (CV) risk factors (P = 0.004), inflammatory markers (P = 0.008), and in a comprehensive model of CV risk factors and inflammatory markers (P = 0.03). In patients with RA, cTn-I concentrations were positively correlated with age (rho = 0.359), Framingham risk score (FRS) (rho = 0.366), and systolic blood pressure (rho = 0.248 (all P values ≤ 0.001)), but not with measures of inflammation or RA drug therapies. cTn-I was significantly correlated with CACS in RA in univariate analysis, but not after adjustment for age, race, sex and FRS (P = 0.79). Further model adjustments for renal function and coronary artery disease confirmed the significance of the findings. CONCLUSION: High-sensitivity cTn-I concentrations are elevated in patients with RA without heart failure, independent of cardiovascular risk profile and inflammatory markers. Elevated troponin concentrations in RA may indicate subclinical, indolent myocardial injury.
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Bradham et al. (2012) conducted a cross-sectional in Rheumatoid Arthritis (n=254). Rheumatoid arthritis vs. Controls without rheumatoid arthritis was evaluated on High-sensitivity cardiac troponin-I (hs-cTn-I) concentration (pg/mL) (p=<0.001). Rheumatoid arthritis was associated with 49% higher median high-sensitivity cardiac troponin-I concentrations (1.15 pg/mL) compared to controls (0.77 pg/mL), independent of cardiovascular risk factors.
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