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Introduction of High-sensitivity Troponin Assays: Impact on Myocardial Infarction Incidence and Prognosis - 17/11/12

Doi : 10.1016/j.amjmed.2012.07.015 
Tobias Reichlin, MD a, b, c, Raphael Twerenbold, MD b, Miriam Reiter, MD b, Stephan Steuer, MD d, Stefano Bassetti, MD e, Cathrin Balmelli, MD b, Katrin Winkler, MD f, g, Sabine Kurz, MD b, Claudia Stelzig, MS b, Michael Freese, RN b, Beatrice Drexler, MD b, Philip Haaf, MD b, Christa Zellweger, MD b, Stefan Osswald, MD a, Christian Mueller, MD a, b,
a Department of Cardiology, University Hospital, Basel, Switzerland 
b Department of Internal Medicine, University Hospital, Basel, Switzerland 
c Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass 
d Limmattalspital Zürich, Switzerland 
e Kantonsspital Olten, Switzerland 
f Servicio de Pneumologia, Hospital del Mar - IMIM, UPF, CIBERES, ISC III, Barcelona, Spain 
g Servicio de Urgencias, Hospital del Mar - IMIM, Barcelona, Spain 

Requests for reprints should be addressed to Christian Mueller, MD, Department of Cardiology, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland

Abstract

Objective

The study objective was to compare the incidence and prognosis of acute myocardial infarction when using high-sensitivity cardiac troponin assays instead of a standard cardiac troponin assay for the diagnosis of acute myocardial infarction.

Methods

In a prospective international multicenter study, we enrolled 1124 consecutive patients presenting with suspected acute myocardial infarction. Final diagnoses were adjudicated by 2 independent cardiologists 2 times using all available clinical information: first using standard cardiac troponin levels and second using high-sensitivity cardiac troponin T levels for adjudication. Patients were followed up for a mean of 19±9 months.

Results

The use of high-sensitivity cardiac troponin T instead of standard cardiac troponin resulted in an increase in the incidence of acute myocardial infarction from 18% to 22% (242 vs 198 patients), a relative increase of 22%. Of the 44 additional acute myocardial infarctions, 35 were type 1 acute myocardial infarctions and 9 were type 2 acute myocardial infarctions. This was accompanied by a reciprocal decrease in the incidence of unstable angina (unstable angina, 11% vs 13%). The most pronounced increase was observed in patients adjudicated with cardiac symptoms of origin other than coronary artery disease with cardiomyocyte damage (83 vs 31 patients, relative increase of 268%). Cumulative 30-month mortality rates were 4.8% in patients without acute myocardial infarction, 16.4% in patients with a small acute myocardial infarction detected only by high-sensitivity cardiac troponin T but not standard cardiac troponin, and 23.9% in patients with a moderate/large acute myocardial infarction according to standard cardiac troponin assays and high-sensitivity cardiac troponin T (P<.001).

Conclusions

The introduction of high-sensitivity cardiac troponin assays leads to only a modest increase in the incidence of acute myocardial infarction. The novel sensitive assays identify an additional high-risk group of patients with increased mortality, therefore appropriately classified with acute myocardial infarction (Advantageous Predictors of Acute Coronary Syndromes Evaluation; NCT00470587).

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Keywords : Acute myocardial infarction, Biomarker, High-sensitivity troponin, Incidence, Prognosis, Troponin


Plan


 Funding: The study was supported by research grants from the Swiss National Science Foundation (PP00B-102853), the Swiss Heart Foundation, Abbott, Brahms, Roche, Siemens, and the Department of Internal Medicine, University Hospital Basel.
 Conflict of Interest: Dr Reichlin has received research grants from the Swiss National Science Foundation (PASMP3-136995), the Swiss Heart Foundation, the Prof Cloetta Foundation, the University of Basel, and the Department of Internal Medicine, University Hospital Basel, as well as speaker honoraria from BRAHMS and Roche. Dr Mueller has received research support from the Swiss National Science Foundation (PP00B-102853), the Swiss Heart Foundation, Abbott, ALERE, Beckman Coulter, BRAHMS, Bühlmann Nanosphere, Roche, Siemens, and the Department of Internal Medicine, University Hospital Basel, as well as speaker honoraria from Abbott, ALERE, BRAHMS, Roche, and Siemens. All other authors declare that they have no conflict of interest. The high-sensitivity cardiac troponin T assay was donated by Roche, which had no role in the design of the study, the analysis of the data, the preparation of the manuscript, or the decision to submit the manuscript for publication.
 Authorship: All authors had access to the data and played a role in writing this manuscript.


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Vol 125 - N° 12

P. 1205 - décembre 2012 Retour au numéro
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