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Quantitative troponin and death, cardiogenic shock, cardiac arrest and new heart failure in patients with non-ST-segement elevation acute coronary syndromes (NSTE ACS): insights from the Global Registry of Acute Coronary Events
  1. Sanjit S Jolly1,
  2. Heather Shenkman2,
  3. David Brieger3,
  4. Keith A Fox4,
  5. Andrew T Yan5,6,
  6. Kim A Eagle7,
  7. P Gabriel Steg8,
  8. Ki-Dong Lim5,6,
  9. Ann Quill9,
  10. Shaun G Goodman5,6,
  11. for the GRACE Investigators
  1. 1Population Health Research Institute, Department of Medicine, Hamilton Health Sciences, McMaster University, Hamilton, Ontario, Canada
  2. 2California Cardiac Institute, Glendale, California, USA
  3. 3Coronary Care Unit, Concord Hospital, Sydney, Australia
  4. 4Cardiovascular Research, Division of Medical & Radiological Sciences, The University of Edinburgh, Edinburgh, UK
  5. 5Canadian Heart Research Centre, Division of Cardiology, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada
  6. 6Terrence Donnelly Heart Centre, Division of Cardiology, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada
  7. 7University of Michigan Medical Center, Ann Arbor, Michigan, USA
  8. 8Département de Cardiologie, INSERM U-698, Université Paris 7, Paris, France
  9. 9University of Massachusetts Medical School, Worcester, Massachusetts, USA
  1. Correspondence to Sanjit S. Jolly, Rm. C3 118 CVSRI Building, Hamilton General Hospital, 237 Barton St. East, Hamilton, ON, Canada, L8L 2X2; jollyss{at}mcmaster.ca

Abstract

Background The objective of this study was to determine if the extent of quantitative troponin elevation predicted mortality as well as in-hospital complications of cardiac arrest, new heart failure and cardiogenic shock.

Design 16 318 patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS) from the Global Registry of Acute Coronary Events (GRACE) were included. The maximum 24 h troponin value as a multiple of the local laboratory upper limit of normal was used. The population was divided into five groups based on the degree of troponin elevation, and outcomes were compared. An adjusted analysis was performed using quantitative troponin as a continuous variable with adjustment for known prognostic variables.

Results For each approximate 10-fold increase in the troponin ratio, there was an associated increase in cardiac arrest, sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) (1.0, 2.4, 3.4, 5.9 and 13.4%; p<0.001 for linear trend), cardiogenic shock (0.5, 1.4, 2.0, 4.4 and 12.7%; p<0.001), new heart failure (2.5, 5.1, 7.4, 11.6 and 15.8%; p<0.001) and mortality (0.8, 2.2, 3.0, 5.3 and 14.0%; p<0.001). These findings were replicated using the troponin ratio as a continuous variable and adjusting for covariates (cardiac arrest, sustained VT or VF, OR 1.56, 95% CI 1.39 to 1.74; cardiogenic shock, OR 1.87, 95% CI 1.61 to 2.18; and new heart failure, OR 1.57, 95% CI 1.45 to 1.71). The degree of troponin elevation was predictive of early mortality (HR 1.61, 95% CI 1.44 to 1.81; p<0.001 for days 0–14) and longer term mortality (HR 1.18, 95% CI 1.07 to 1.30, p=0.001 for days 15–180).

Conclusion The extent of troponin elevation is an independent predictor of morbidity and mortality.

  • Myocardial infarction
  • mortality
  • shock
  • heart failure
  • prognosis
  • angina - unstable
  • NSTEMI
  • STEMI

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Footnotes

  • Funding GRACE is supported by an unrestricted educational grant from Sanofi-Aventis to the Center for Outcomes Research, University of Massachusetts Medical School. Sanofi-Aventis had no involvement in the collection, analysis and interpretation of data, in the writing of the report and in the decision to submit the paper for publication.

  • Competing interests SSJ, DB, KAF, KAE, PGS, SGG were speakers for, and received reconsulting honoraria and a research grant from Sanofi-Aventis.

  • Ethics approval This study was conducted with the approval of the review boards of all participating hospitals.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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