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Relationship Between Peak Troponin Values and Long-Term Ischemic Events Among Medically Managed Patients With Acute
Sarah A Goldstein1,2, L Kristin Newby3,2, Derek D Cyr1
1Duke Clinical Research Institute, Durham, NC.
Insights
Higher peak troponin levels in non-ST-segment elevation acute coronary syndromes (ACS) correlate with increased long-term mortality and ischemic events. Treatment effects of prasugrel versus clopidogrel did not vary by troponin levels.
Area of Science:
- Cardiology
- Biomarkers
- Acute Coronary Syndromes
Background:
- The prognostic value of troponin in non-ST-segment elevation acute coronary syndromes (ACS) is known.
- However, its relationship with long-term outcomes in patients managed medically with contemporary antiplatelet therapy requires further definition.
Purpose of the Study:
- To investigate the association between peak troponin levels and 30-month outcomes in medically managed non-ST-segment elevation ACS patients.
- To assess if treatment effects of prasugrel versus clopidogrel differ based on peak troponin levels.
Main Methods:
- Analysis of 6763 patients from the TRILOGY ACS trial (prasugrel vs. clopidogrel).
- Categorization of peak troponin/upper limit of normal (ULN) ratio within 48 hours of the index ACS event.
- Evaluation of 30-month composite outcomes (cardiovascular death, myocardial infarction, stroke) and all-cause death.
Main Results:
- A graded relationship was observed between increasing peak troponin levels and 30-month mortality.
- The association with composite endpoints plateaued beyond peak troponin values ≥3×ULN.
- No significant heterogeneity in treatment effect between prasugrel and clopidogrel was found across troponin categories.
Conclusions:
- In medically managed non-ST-segment elevation ACS patients, higher peak troponin levels are associated with a graded increase in long-term ischemic events.
- Peak troponin levels did not predict differential treatment efficacy between prasugrel and clopidogrel.
Background:
The relationship between troponin level and outcomes among patients with non-ST-segment elevation ACS is established, but the relationship of troponin level with long-term outcomes among medically managed non-ST-segment elevation ACS patients receiving contemporary antiplatelet therapy is inadequately defined.
Methods And Results:
In 6763 medically managed non-ST-segment elevation ACS patients randomized in TRILOGY ACS (Targeted Platelet Inhibition to Clarify the Optimal Strategy to Medically Manage Acute Coronary Syndromes) (prasugrel versus clopidogrel), we examined relationships between categories of peak troponin/upper limit of normal (ULN) ratio within 48 hours of the index ACS event (≈4.5 days before randomization) and 30-month outcomes (cardiovascular death, myocardial infarction, or stroke; cardiovascular death or myocardial infarction; and all-cause death). Patients with peak troponin levels <1×ULN were younger, were more often women, and had lower GRACE risk scores than those in other troponin groups. Those with ratios ≥5×ULN were more frequently smokers but less often had prior myocardial infarction or percutaneous coronary intervention. Diabetes mellitus prevalence, body mass index, serum creatinine, and hemoglobin were similar across groups. For all end points, statistically significant differences in 30-month event rates were observed between peak troponin categories. The relationship was linear for 30-month mortality (<1×ULN, n=1849 [6.2%]; 1 to <3×ULN, n=1203 [9.6%]; 3 to <5×ULN, n=581 [10.8%]; and ≥5×ULN, n=3405 [12.8%]) but plateaued for composite end points beyond peak troponin values ≥3×ULN. There was no statistically significant heterogeneity in treatment effect by peak troponin ratio for any end point.
Conclusions:
Among medically managed non-ST-segment elevation ACS patients selected for medical management, there was a graded relationship between increasing peak troponin and long-term ischemic events but no heterogeneity of treatment effect for prasugrel versus clopidogrel according to peak troponin.
Clinical Trial Registration:
URL: http://www.clinicaltrials.gov. Unique identifier: NCT00699998.