Cardiac troponin after percutaneous coronary intervention and 1-year mortality in non-ST-segment elevation acute coronary syndrome using systematic evaluation of biomarker trends
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Published on: January 28, 2020
Pierluigi Tricoci1, Sergio Leonardi2, Jennifer White1
1Duke Clinical Research Institute, Durham, North Carolina.
Insights
Elevated cardiac troponin (cTn) after percutaneous coronary intervention (PCI) in non-ST-segment elevation acute coronary syndrome (NSTE ACS) significantly predicts 1-year mortality. This finding aids in defining post-PCI myocardial infarction and preventing related myonecrosis.
Area of Science:
- Cardiology
- Biomarkers
- Interventional Cardiology
Background:
- The prognostic significance of cardiac troponin (cTn) following percutaneous coronary intervention (PCI) remains debated.
- Distinguishing cTn elevations due to PCI versus index myocardial infarction (MI) in non-ST-segment elevation acute coronary syndrome (NSTE ACS) is challenging.
Purpose of the Study:
- To analyze cTn trends in NSTE ACS patients undergoing PCI within the EARLY ACS and SYNERGY trials.
- To investigate the association between post-PCI cTn levels and 1-year mortality.
Main Methods:
- Cardiac troponin (cTn) and time data were analyzed for 10,199 patients.
- A methodology was employed to differentiate post-PCI cTn elevations from index MI.
- Cox modeling evaluated the relationship between peak post-PCI cTn and 1-year mortality, adjusting for clinical variables.
Main Results:
- A reliable method identified post-PCI cTn elevation distinct from index MI in 57% of patients.
- Peak post-PCI cTn elevation was significantly associated with a 7% increase in 1-year mortality (HR 1.07 per 10× ULN increase).
- Peak post-PCI creatine kinase-myocardial band also showed a significant association with 1-year mortality (HR 1.13 per 1× ULN increase).
Conclusions:
- A novel methodology successfully differentiated post-PCI cTn elevations in over half of NSTE ACS patients.
- A significant correlation exists between post-PCI cTn levels and 1-year mortality.
- Findings support refining MI definitions and strategies to mitigate PCI-related myonecrosis.
Objectives:
This study sought to review cardiac troponin (cTn) trends during non-ST-segment elevation acute coronary syndrome (NSTE ACS) in patients undergoing percutaneous coronary intervention (PCI) in the EARLY ACS (Early Glycoprotein IIb/IIIa Inhibition in Non-ST-Segment Elevation Acute Coronary Syndromes) and SYNERGY (Superior Yield of the New Strategy of Enoxaparin, Revascularization and Glycoprotein IIb/IIIa Inhibitors) studies and to study the relationship between post-PCI cTn and mortality.
Background:
The prognostic value of cTn post-PCI is controversial. In patients with NSTE ACS, it is especially difficult to distinguish between cTn elevations due to PCI or index myocardial infarction (MI).
Methods:
Time and cTn (indexed by upper limit of normal [ULN]) data pairs were plotted for 10,199 patients and independently reviewed by 2 physicians to identify patients in whom post-PCI cTn elevation could be distinguished from that of index MI. Post-PCI cTn peak was identified for each plot, and its relationship with 1-year mortality was evaluated using Cox modeling, correcting for 15 clinical variables from the EARLY ACS 1-year mortality model (including baseline cTn). We used an identical methodology to assess the association between creatine kinase-myocardial band and 1-year mortality.
Results:
Patients with cTn (re-)elevation post-PCI not evaluable were identified and excluded from further analysis (4,198 [41%] with cTn rising prior to PCI; 229 [2%] with missing cTn). Among the remainder (n = 5,772 [57%]), in the multivariable model, peak cTn post-PCI was associated with a 7% increase in mortality (hazard ratio [HR] for 10 × ULN increase: 1.07, 95% confidence interval [CI]: 1.02 to 1.11; p = 0.0038). Peak post-PCI creatine kinase-myocardial band was significantly associated with 1-year mortality (HR for 1 × ULN increase: 1.13, 95% CI: 1.05 to 1.21; p = 0.0013).
Conclusions:
We used a methodology that differentiated post-PCI cTn (re-)elevation from that of presenting MI in more than one-half of patients with NSTE ACS undergoing PCI. This identified a highly significant relationship between post-PCI cTn and 1-year mortality, with implications for both incorporating a cTn post-PCI MI definition and preventing PCI-related myonecrosis.
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