TY - JOUR
T1 - High-sensitive troponin T measurements
T2 - What do we gain and what are the challenges?
AU - Twerenbold, Raphael
AU - Jaffe, Allan
AU - Reichlin, Tobias
AU - Reiter, Miriam
AU - Mueller, Christian
N1 - Funding Information:
The authors are supported by research grants from the Swiss National Science Foundation (PP00B-102853), the Swiss Heart Foundation, Basel University, Abbott, Roche, Siemens, and the Department of Internal Medicine, University Hospital Basel.
Funding Information:
Conflict of interest: We disclose that C.M. has received research support from the Swiss National Science Foundation (PP00B- 102853), the Swiss Heart Foundation, the Novartis Foundation, the Krokus Foundation, Abbott, Astra Zeneca, Biosite, Brahms, Nano-sphere, Roche, Siemens, and the Department of Internal Medicine, University Hospital Basel, as well as speaker honoraria from Abbott, Biosite, Brahms, Roche, and Siemens. A.J. acts as a consultant for Alere, Beckman Coulter, Critical Diagnostics, and Amgen. All other authors declare that they have no conflicts of interest.
PY - 2012/3
Y1 - 2012/3
N2 - Cardiac troponin (cTn) I and T are structural proteins unique to the heart. Detection of cTn in peripheral blood indicates cardiomyocyte damage. As acute myocardial infarction (AMI) is the most important cause of cardiomyocyte damage, cTns have become an integral part in the diagnosis of AMI. For this indication, cTns are superior to all other biomarkers and therefore are the preferred marker for the diagnosis of AMI. However, cTn indicates and provides an estimate of cardiomyocyte damage irrespective of its cause. The major limitation of contemporary cTn assays is that they are often not elevated during the initial hours of AMI. Recent advances in assay technology have led to more sensitive and precise cTn assays that will have a profound impact on clinical practice. High-sensitive cTn (hs-cTn) assays have two differentiating features from contemporary cTn assays: (i) detection of cTn in a majority of healthy persons and (ii) precise definition of what is 'normal' (the 99th percentile). Recent multicentre studies have shown that hs-cTn assays improve the early diagnosis of patients with suspected AMI, particularly the early rule-out. To achieve best clinical use, cTn has to be interpreted as a quantitative variable. Rising and/or falling levels differentiate acute from chronic cardiomyocyte damage. The terms 'troponin-positive' and 'troponin negative' should therefore be avoided. 'Detectable' levels will become the norm and will have to be differentiated from 'elevated' levels. The differential diagnosis of a small amount of cardiomyocyte damage and therefore minor elevations of cTn is broad and includes acute and chronic cardiac disorders. The differential diagnosis of larger amount of injury and therefore more substantial elevations of cTn is largely restricted to AMI, myocarditis, and a rare patient with tako-tsubo cardiomyopathy.
AB - Cardiac troponin (cTn) I and T are structural proteins unique to the heart. Detection of cTn in peripheral blood indicates cardiomyocyte damage. As acute myocardial infarction (AMI) is the most important cause of cardiomyocyte damage, cTns have become an integral part in the diagnosis of AMI. For this indication, cTns are superior to all other biomarkers and therefore are the preferred marker for the diagnosis of AMI. However, cTn indicates and provides an estimate of cardiomyocyte damage irrespective of its cause. The major limitation of contemporary cTn assays is that they are often not elevated during the initial hours of AMI. Recent advances in assay technology have led to more sensitive and precise cTn assays that will have a profound impact on clinical practice. High-sensitive cTn (hs-cTn) assays have two differentiating features from contemporary cTn assays: (i) detection of cTn in a majority of healthy persons and (ii) precise definition of what is 'normal' (the 99th percentile). Recent multicentre studies have shown that hs-cTn assays improve the early diagnosis of patients with suspected AMI, particularly the early rule-out. To achieve best clinical use, cTn has to be interpreted as a quantitative variable. Rising and/or falling levels differentiate acute from chronic cardiomyocyte damage. The terms 'troponin-positive' and 'troponin negative' should therefore be avoided. 'Detectable' levels will become the norm and will have to be differentiated from 'elevated' levels. The differential diagnosis of a small amount of cardiomyocyte damage and therefore minor elevations of cTn is broad and includes acute and chronic cardiac disorders. The differential diagnosis of larger amount of injury and therefore more substantial elevations of cTn is largely restricted to AMI, myocarditis, and a rare patient with tako-tsubo cardiomyopathy.
KW - Acute myocardial infarction
KW - Diagnosis
KW - High-sensitive cardiac troponin
KW - Sensitivity
KW - Specificity
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U2 - 10.1093/eurheartj/ehr492
DO - 10.1093/eurheartj/ehr492
M3 - Review article
C2 - 22267244
AN - SCOPUS:84857937071
SN - 0195-668X
VL - 33
SP - 579
EP - 586
JO - European heart journal
JF - European heart journal
IS - 5
ER -