Cardiac troponin I (cTnI) is a key biomarker of myocardial damage that is central to the diagnosis of acute myocardial infarction (MI), as well as risk prediction of coronary heart disease, heart failure hospitalization, and overall mortality in the general population. A previous study reported that highly sensitive cTnI (>1.5 pg/mL) was an independent predictor of occult coronary plaque burden and composition on coronary computed tomography angiography (CTA) in patients with established rheumatoid arthritis (RA). The current study examines whether high cTnI also predicts for incident long-term cardiovascular (CV) events and optimizes CV risk stratification in the Prospective Evaluation of Lateral Coronary Atherosclerosis in RA (PROTECT-RA) trial after 5 years of follow-up.
Eligible patients with RA (n = 159) without symptoms or prior diagnosis of CV disease (CVD) underwent a baseline 64-slice CTA for plaque evaluation; blood was also collected for laboratory evaluations, including for biomarker assessments. Patients were followed for a mean of 60 ± 26 months for incident CV events. The study end points were composite rates of ischemic (cardiac death, nonfatal MI, ischemic stroke, peripheral arterial ischemia) and nonischemic (new-onset heart failure hospitalization) CV events. Using Cox regression analysis, the association between high cTnI (>1.5 pg/mL) and CV events was evaluated.
In the total population, the majority of patients were female, with median age of 54 years; RA disease duration was 9 (range, 5-15) years, with swollen joint count of 0.5 (range, 0-3). Disease Activity Score 28–C-reactive protein was 2.30 (range, 1.8-3.3). During the 5-year follow-up period, 11 patients suffered incident events (1.54/100 patient-years). Of these, 8 were ischemic CV events, including 1 cardiac death, 3 MIs, 2 strokes, and 2 peripheral arterial ischemic events requiring emergent revascularizations; and 3 were nonischemic events, including new onset, hospitalization, and systolic heart failure.
The CV cohort showed an increased number of traditional CV risk factors, including diabetes (4/11 patients), hypertension (8/11 patients), and D’Agostino Framingham score (15.6). The CV cohort also showed unfavorable coronary plaque burden and associated biomarkers, including coronary artery calcium, segment involvement score, segment stenosis score, plaque burden score, and mixed plaque score.
Patients who experienced CV events had higher levels of highly sensitive cTnl compared with those who did not (2.6 [2.1-4.4] vs 1.5 [1.0-2.6] pg/mL; P <.01). Measurement of highly sensitive cTnl was higher in patients with plaque versus those without. Coronary plaque presence, burden, and complexity were enriched in patients with higher levels of highly sensitive cTnl. Importantly, higher levels of highly sensitive cTnI predicted the risk for incident CV events independently of demographic and traditional cardiac risk factors, including age, sex, hypertension, diabetes, dyslipidemia, smoking, body mass index, and prednisone use (hazard ratio, 5.4; confidence interval, 1.1-25.9; P = .037). Moreover, patients with low cTnI (<1.5 pg/mL) were found to be 82% less likely to suffer a CV event.
The authors concluded, albeit from a small patient cohort, that highly sensitive cTnI is associated with presence, burden, and composition of occult coronary plaque in RA beyond traditional risk factors or CV scores, and may provide prognostic information on long-term CV event risk in patients with RA without symptoms or known history of CVD.
Karpouzas G, et al. ACR 2017. Abstract 867.