Key result
High-sensitivity troponin I >26 ng/L was associated with an increased 3-year risk of cardiovascular death, MI, or stroke compared to <1.9 ng/L (18.6% vs 5.0%; HR 2.70; 95% CI 1.96-3.71; P<0.001).
Why the study?
Does elevated high-sensitivity troponin I predict increased risk of cardiovascular events in stable patients with established atherosclerosis?
RCT (n=15,833)
Does elevated high-sensitivity troponin I predict increased risk of cardiovascular events in stable patients with established atherosclerosis?
Hazard Ratio: 2.7 (95% CI 1.96–3.71)
Absolute Event Rate: 18.6% vs 5%
p-value: p=<0.001
In stable patients with established atherosclerosis, higher hs-TnI concentrations independently predict a higher 3-year risk of cardiovascular events and may identify patients who derive greater absolute benefit from secondary prevention therapies like vorapaxar.
hs-TnI stratifies CV risk independently in stable atherosclerosis; extends ACS prognostic data to chronic secondary prevention.
BACKGROUND: Cardiac troponin I, measured with a high-sensitivity assay (hs-TnI), is well-established for risk prediction in acute coronary syndromes. However, its prognostic role in stable atherosclerotic disease, particularly for future myocardial infarction (MI), is less well defined. METHODS: We measured hs-TnI (Abbott ARCHITECT) in 15833 patients with prior MI, ischemic stroke, or peripheral arterial disease from the placebo-controlled Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2°P)-Thrombolysis in Myocardial Infarction (TIMI) 50 trial of the platelet inhibitor vorapaxar, excluding patients with recent MI (<30 days). hs-TnI was categorized into 5 groups based on the detection limit (1.9 ng/L), 99th percentile reference limit (26 ng/L), and tertiles in between (1.9-26 ng/L), as well as sex-specific reference limits. RESULTS: Higher hs-TnI concentration was associated with older age, male sex, and increased atherosclerosis burden. hs-TnI identified a graded 3-year risk of cardiovascular death, MI, or stroke from 5.0% to 18.6% (P < 0.001), driven by cardiovascular death and MI (P < 0.001). This risk was independent of established clinical risk indicators, B-type natriuretic peptide and C-reactive protein [adjusted hazard ratio 2.70 (95% CI, 1.96-3.71), P < 0.001 for hs-TnI >26 ng/L vs <1.9 ng/L]. In patients with prior MI, there was a pattern of greater absolute benefit with vorapaxar in patients with an increased hs-TnI (absolute risk difference 1.9% with hs-TnI >26 ng/L vs 0.3% with hs-TnI <1.9 ng/L; P interaction = 0.82). CONCLUSIONS: In stable patients with established atherosclerosis, hs-TnI concentrations effectively stratified the risk of new or recurrent cardiovascular (CV) events, in particular CV death and MI. High-risk patients with prior MI identified by increased hs-TnI had a substantial absolute improvement in net clinical outcome with vorapaxar.
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Eisen et al. (2016) conducted an RCT in Stable atherosclerotic disease (n=15,833). High-sensitivity troponin I (hs-TnI) >26 ng/L vs. hs-TnI <1.9 ng/L was evaluated on cardiovascular death, MI, or stroke (adjusted HR 2.70, 95% CI 1.96-3.71, p=<0.001). High-sensitivity troponin I >26 ng/L was associated with an increased 3-year risk of cardiovascular death, MI, or stroke compared to <1.9 ng/L (18.6% vs 5.0%; HR 2.70; 95% CI 1.96-3.71; P<0.001).
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