Cardiac troponin after percutaneous coronary intervention and 1-year mortality in non-ST-segment elevation acute

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.
Abstract

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