Key result
Peak cTnI elevation from 1 to 10 ng/L is linked to ~60% higher composite risk.
Why the study?
The prognostic role of cardiac troponin I at presentation versus peak levels in patients with NSTEMI was unclear.
Does peak cardiac troponin I predict cardiovascular events better than cTnI at presentation in patients with NSTEMI?
Cohort (n=215)
Does peak cardiac troponin I predict cardiovascular events better than cTnI at presentation in patients with NSTEMI?
In patients with NSTEMI, peak cardiac troponin I is a significant predictor of 1-year cardiovascular events, whereas troponin at presentation is not.
May inform NSTEMI prognostication with peak troponin I; leaves open superiority to presentation values.
OBJECTIVES: Non-ST elevation myocardial infarction (NSTEMI) is one of the most common manifestations of acute coronary syndromes (ACS). We evaluated the prognostic role of cardiac troponin I (cTnI) at presentation and peak cardiac troponin I in patients with NSTEMI. METHODS: We consecutively enrolled 215 subjects presenting with NSTEMI. Subjects were followed up for 1 year. cTnI at presentation and the peak value of cTnI were measured. The primary end point was defined as cardiovascular death, readmission to hospital with heart failure and new ACS. RESULTS: The subjects who presented the primary end point (49 subjects) had significantly increased values of peak cTnI compared to subjects free of cardiovascular events [7.19 (2.97-21.32) vs. 4.09 (1.18-11.85) ng/l; p = 0.002]. Nevertheless, cTnI at presentation did not differ between subjects who presented the primary end point and those free of events (p = 0.39). Multivariate Cox regression analysis after adjustment for confounders revealed by the univariate analysis showed that for an increase in peak cTnI from 1 to 10 ng/l, there is a 60% anticipated increase in the relative risk to present the primary end point (p = 0.04). CONCLUSION: These findings documented the different prognostic significance of cTnI at presentation and peak cTnI in patients presenting with NSTEMI, and highlighted the importance of monitoring the levels of cTnI in this high-risk population.
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Siasos et al. (2016) conducted a cohort in Non-ST elevation myocardial infarction (NSTEMI) (n=215). Peak cardiac troponin I vs. Cardiac troponin I at presentation was evaluated on Cardiovascular death, readmission to hospital with heart failure and new ACS (RR 1.60, p=0.04). An increase in peak cardiac troponin I from 1 to 10 ng/l was associated with a 60% increase in the relative risk of the primary composite endpoint (p=0.04).
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