Elevated Cardiac Troponin Levels Do Not Predict Adverse Outcomes in Hospitalized Patients without Clinical Manifestations of Acute Coronary Syndromes

Cardiology ◽  
2000 ◽  
Vol 93 (1-2) ◽  
pp. 1-6 ◽  
Author(s):  
Eddy Barasch ◽  
Vinod Kaushik ◽  
Richa Gupta ◽  
Pinky Ronen ◽  
Beth Hartwell
2008 ◽  
Vol 101 (10) ◽  
pp. 1384-1388 ◽  
Author(s):  
Miry Blich ◽  
Anat Sebbag ◽  
Judith Attias ◽  
Doron Aronson ◽  
Walter Markiewicz

2010 ◽  
Vol 21 (6) ◽  
pp. 363-368 ◽  
Author(s):  
Peter S.C. Wong ◽  
Gopala K. Rao ◽  
Antony L. Innasimuthu ◽  
Yawer Saeed ◽  
Charles van Heyningen ◽  
...  

2003 ◽  
Vol 22 (4) ◽  
pp. 303-309 ◽  
Author(s):  
Svetlana Ignjatovic

Although the use of troponin to diagnose acute myocardial infarction (AMI) has been previously proposed, the Committee on Standardization of Markers of Cardiac Damage (C-SMCD) of the International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) made a recommendation in 1999 to expand on the enzyme diagnostic criteria for AMI to include cardiac-specific proteins. In September 2000, a joint committee of the European Society of Cardiology and the American College of Cardiology (ESC/ACC) published a new definition of AMI that for first time officially included troponin. According to these criteria, as the best biochemical indicator for detecting myocardial necrosis is "a concentration of cardiac troponin exceeding the decision limit (defined as the 99th percentile of a reference control group) on at least one occasion during the first 24 hours after the onset of clinical event". The use of creatine kinase MB (CK-MB), measured by mass assays, is still considered as an acceptable alternative only if cardiac troponin assays are not available. It is very important to standardize the clinical use of troponin in diagnosis and management of acute coronary syndromes and to clearly define decision thresholds. Two strategies have competed as the most appropriate for the use of new markers. The first relies on the use of a combination of two markers - a rapid rising marker such as myoglobin, and a marker that takes longer to rise but is more specific, such as cardiac troponin - to enable detection of AMI in patients who present early and late after symptom onset. In the second strategy, only measurement of cardiac troponin is suggested. One of the most important problems in the practical use of the cardiac-specific troponin is the right definition of decision limits. As diagnostic cut-off for clinical use, the IFCC C-SMCD recommends for troponin assays a total imprecision, expressed as coefficient of variation (CV), of <10% at the 99th percentile of a reference control group. For troponin assays that cannot presently meet the 10% CV at the 99th percentile value, a predetermined higher concentration that meets this imprecision goal should be used as cut-off for AMI until the goal of a 10% CV can be achieved at the 99th percentile. It is very important that clinically relevant biomarker, such as cardiac troponin, on which critical decisions will rest, can be measured with highly reliable and standardized methods. There are problems in assay standardization, imprecision interference, and of pre-analytical variability. Cardiac troponin is currently the most sensitive and specific biochemical marker of myocardial damage and is the best marker for diagnosis, risk stratification, and guidance of therapy in acute coronary syndromes.


2002 ◽  
Vol 39 ◽  
pp. 305
Author(s):  
Ronnier J. Aviles ◽  
Arman T. Askari ◽  
E.Magnus Ohman ◽  
Kenneth W. Mahaffy ◽  
L.Kristin Newby ◽  
...  

Author(s):  
Evangelos Giannitsis ◽  
Hugo A Katus

Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.


2019 ◽  
Vol 132 (7) ◽  
pp. 869-874 ◽  
Author(s):  
Yader Sandoval ◽  
Ian L. Gunsolus ◽  
Stephen W. Smith ◽  
Anne Sexter ◽  
Sarah E. Thordsen ◽  
...  

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