Use of troponin to diagnose periprocedural myocardial infarction: effect on composite endpoints in the British Bifurcation Coronary Study (BBC ONE)
James Cockburn1, Miles Behan, Adam de Belder
1Sussex Cardiac Centre, Brighton and Sussex University Hospitals NHS Trust, Brighton, UK.
Insights
Using troponin for diagnosing periprocedural myocardial infarction (PMI) significantly increases detection rates. This heightened sensitivity challenges the justification of PMI within composite endpoints in interventional trials.
Area of Science:
- Cardiology
- Interventional Cardiology
- Biomarker Analysis
Background:
- Periprocedural myocardial infarction (PMI) diagnosis relies on cardiac enzyme elevation.
- Current guidelines suggest troponin over creatine kinase (CK) for PMI diagnosis.
- The clinical relevance of minor troponin increases remains unclear.
Purpose of the Study:
- To evaluate the impact of troponin-based PMI definition on composite endpoint incidence.
- To analyze changes in PMI and composite endpoint rates in the BBC ONE trial.
Main Methods:
- The British Bifurcation Coronary Study (BBC ONE) randomized 500 patients with coronary bifurcation lesions.
- Patients were assigned to simple or complex stenting strategies.
- The composite primary endpoint included death, myocardial infarction (MI), and target vessel failure at 9 months.
Main Results:
- Troponin use would increase PMI diagnosis fivefold, from 7.4% to 37.0%.
- The incidence of PMI would rise from 3.6% to 28.4% in the simple group and 11.2% to 45.6% in the complex group.
- Composite endpoint rates would increase from 8% to 32% (simple) and 15.2% to 48% (complex) with troponin use.
Conclusions:
- Troponin-based diagnosis leads to a substantial increase in PMI detection.
- The clinical significance of these elevated troponin levels needs further investigation.
- Incorporating PMI into composite endpoints may require re-evaluation in interventional trials.
Background:
Periprocedural myocardial infarction (PMI; ESC/ACC type 4a) is diagnosed on the basis of elevation of cardiac enzymes more than three times the 99th centile upper reference limit. Recent guidelines recommend the use of troponin instead of creatine kinase (CK) to diagnose PMI, but this assay increases diagnostic sensitivity, while the clinical significance of small increases in troponin remains undetermined. We examined the effects of using the new definition on the incidence of a composite endpoint (previously defined by CK) in a contemporary clinical randomised trial-the British Bifurcation Coronary Study (BBC ONE).
Methods:
The BBC ONE trial randomly allocated 500 patients with coronary bifurcation lesions to either a simple or complex stenting strategy. The composite primary endpoint (CPEP) included death, myocardial infarction (MI) (PMI plus subsequent MI) and target vessel failure, at 9 months.
Results:
In BBC ONE the CPEP occurred in 8% versus 15.2% in the simple and complex groups, respectively (HR 2.02, 95% CI 1.17 to 3.47, p=0.009). This difference was largely driven by PMI, which occurred in nine (3.6%) versus 28 (11.2%) patients (HR 3.24, 95% CI 1.53 to 6.86, p=0.001). Using troponin, PMI would have occurred in 71 (28.4%) versus 114 (45.6%) patients, respectively (HR 1.61, 95% CI 1.27 to 2.05, p=0.001), and the CPEP in 32% versus 48% of patients (HR 1.50, 95% CI 1.2 to 1.87, p=0.001). Use of troponin increased MI detection fivefold, from 7.4% to 37.0% overall.
Conclusions:
Use of troponin would have led to a fivefold increase in diagnosis of PMI in the BBC ONE trial. Incorporation of PMI into a composite endpoint may no longer be justified in many interventional trials.
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