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Readers should learn how to interpret cardiac troponins (cTn) in patients with suspected acute coronary syndrome (ACS).
Should become familiar with the Universal myocardial infarction (MI) definition and subtypes of MI.
Should know how to select between the different diagnostic algorithms for diagnosis of MI.
Should learn about the most common limitations and caveats of testing with high-sensitivity (hs) cTn assays.
Should be aware of non-ACS-related reasons for cTn and particularly hsTn elevations.
Should know how to use cTn for risk stratification in pulmonary embolism and other acute settings such as acute heart failure.
Should consider serial cTn measurements for monitoring of chemotoxicity in cancer treatment and monitoring of response to pharmacological therapy in heart failure treatment.
Cardiac troponins (cTn) are components of the thin filament of the sarcomere of striated muscle regulating excitation–contraction coupling in the heart.1 2 Owing to their superior sensitivity and cardiac tissue specificity compared with cardiac enzymes or creatine kinase-MB mass, cardiac troponin T or I (cTn) are now considered the preferred biomarkers for the diagnosis of myocardial injury.3 4 Reasons for elevated cTn with or without kinetic changes are numerous and sometimes multifactorial while in some cases a reason cannot be identified despite intensive diagnostic work-up.4
Use of high-sensitivity (hs) troponin assays allow more accurate and earlier detection of myocardial infarction (MI).5–7 Higher analytical sensitivity increases the number of patients with analytically true positive cTn result due to non-ST-elevation MI but also due to numerous acute or chronic diseases in the absence of overt ischaemic heart disease. Use of hsTn has also enabled to determine a 99th percentile value of a healthy reference population and to demonstrate lower reference values for women than for men.5 8 For diagnosis, prognosis and management of acute coronary syndrome (ACS), cTn should—with few exceptions—be measured serially …
Contributors EG and HAK contributed equally for concept and draft.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests HAK received honoraria from Bayer Vital, Roche Diagnostics, Daiichi Sankyo. EG received honoraria from Bayer Vital, AstraZeneca, Roche Diagnostics, BRAHMS Germany, MSD Deutschland, Daiichi Sankyo.
Patient consent Not required.
Provenance and peer review Commissioned; externally peer reviewed.
Author note References that include a * have been selected as key references for this paper.