Risk stratification in patients with unstable angina using absolute serial changes of 3 high-sensitive troponin assays

  • Claudia Maushart
  • Raphael Twerenbold
  • Tobias Reichlin
  • Miriam Reiter
  • Berit Moehring
  • Nora Schaub
  • Cathrin Balmelli
  • Maria Rubini Gimenez
  • Rebeca Hoeller
  • Konstantin Sakarikos
  • Beatrice Drexler
  • Philip Haaf
  • Stefan Osswald
  • Christian Mueller

Abstract

Background: It is unknown whether unstable angina (UA) results in previously nondetectable low-level myocardial necrosis. We compared the pattern of myocardial necrosis between patients with UA, acute myocardial infarction (AMI), and noncardiac chest pain (NCCP) using 3 high-sensitive cardiac troponin (hs-cTn) assays. Methods: In a multicenter study, we enrolled 842 unselected patients with acute chest pain in the emergency department. Roche hs-cTnT, Beckman Coulter hs-cTnI, and Siemens hs-cTnI were determined in a blinded fashion at presentation and after 1, 2, 3, and 6 hours. The final diagnosis was adjudicated by 2 independent cardiologists. Results: A change in hs-cTn of ≥2 ng/L within the first hour after presentation as assessed with Roche hs-cTnT, Beckman Coulter hs-cTnI, and Siemens hs-cTnI was observed in 26%, 31%, and 32% of patients with UA (n = 115) compared with 91%, 92%, and 96% in patients with AMI (n = 120) and 12%, 23%, and 16% in patients with NCCP (n = 415; P <.001 for all comparisons between UA and AMI, P >.05 for all comparisons between UA and NCCP). In patients with UA, such a 1-hour change in hs-cTn of ≥2 ng/L was associated with an increased risk of death or AMI during the 30-day follow-up (P =.003,.03,.03) and 2-year follow-up (P <.001,.002, and.006). Conclusions: In marked contrast to patients with AMI, most patients with UA do not exhibit relevant hs-cTn changes. The minority of UA with hs-cTn changes, however, has a significantly worse short- and long-term outcome.

Bibliografische Daten

OriginalspracheEnglisch
ISSN0002-8703
DOIs
StatusVeröffentlicht - 03.2013
Extern publiziertJa

Anmerkungen des Dekanats

Funding Information:
Dr Reichlin has received research grants from the Swiss Natinoal Science Foundation (PASMP3-136995), the Swiss Heart Foundation, the University of Basel, the Professor Max Cloetta Foundation, and the Department of Internal Medicine, University Hospital Basel, as well as speaker honoraria from Brahms and Roche. Dr Mueller has received research grants from the Swiss National Science Foundation ( PP00B-102853 ) and the Swiss Heart Foundation; research support from Abbott, Biosite, Brahms, Nanosphere, Roche, Siemens, and the Department of Internal Medicine, University Hospital Basel; and speaker honoraria from Abbott, Biosite, Brahms, Roche, and Siemens. All other authors declare that they have no conflict of interest with this study.