TY - JOUR
T1 - Cardiac Troponin for Assessment of Myocardial Injury in COVID-19
T2 - JACC Review Topic of the Week
AU - Sandoval, Yader
AU - Januzzi, James L.
AU - Jaffe, Allan S.
N1 - Funding Information:
Dr. Sandoval has served on the Advisory Boards for Roche Diagnostics (past) and Abbott Diagnostics without personal compensation; and has served as a speaker without personal financial compensation for Abbott Diagnostics. Dr. Januzzi is a Trustee of the American College of Cardiology; has received grant support from Novartis Pharmaceuticals and Abbott Diagnostics; has received consulting income from Abbott Diagnostics, Janssen, MyoKardia, Novartis, and Roche Diagnostics; and has participated in clinical endpoint committees/data safety monitoring boards for Abbott, AbbVie, Amgen, Bayer, CVRx, Janssen, and Takeda. Dr. Jaffe has consulted for or presently consults for most of the major diagnostics companies, including Beckman, Abbott, Siemens, ET Healthcare, Roche, Quidel, Sphingotec, Brava, Blade, and Novartis. Kuang-Yuh Chyu, MD, served as Guest Editor for this paper. P.K. Shah, MD, served as Guest Editor-in-Chief for this paper.
Publisher Copyright:
© 2020 American College of Cardiology Foundation
PY - 2020/9/8
Y1 - 2020/9/8
N2 - Increases in cardiac troponin indicative of myocardial injury are common in patients with coronavirus disease-2019 (COVID-19) and are associated with adverse outcomes such as arrhythmias and death. These increases are more likely to occur in those with chronic cardiovascular conditions and in those with severe COVID-19 presentations. The increased inflammatory, prothrombotic, and procoagulant responses following severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection increase the risk for acute nonischemic myocardial injury and acute myocardial infarction, particularly type 2 myocardial infarction, because of respiratory failure with hypoxia and hemodynamic instability in critically ill patients. Myocarditis, stress cardiomyopathy, acute heart failure, and direct injury from SARS-CoV-2 are important etiologies, but primary noncardiac conditions, such as pulmonary embolism, critical illness, and sepsis, probably cause more of the myocardial injury. The structured use of serial cardiac troponin has the potential to facilitate risk stratification, help make decisions about when to use imaging, and inform stage categorization and disease phenotyping among hospitalized COVID-19 patients.
AB - Increases in cardiac troponin indicative of myocardial injury are common in patients with coronavirus disease-2019 (COVID-19) and are associated with adverse outcomes such as arrhythmias and death. These increases are more likely to occur in those with chronic cardiovascular conditions and in those with severe COVID-19 presentations. The increased inflammatory, prothrombotic, and procoagulant responses following severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection increase the risk for acute nonischemic myocardial injury and acute myocardial infarction, particularly type 2 myocardial infarction, because of respiratory failure with hypoxia and hemodynamic instability in critically ill patients. Myocarditis, stress cardiomyopathy, acute heart failure, and direct injury from SARS-CoV-2 are important etiologies, but primary noncardiac conditions, such as pulmonary embolism, critical illness, and sepsis, probably cause more of the myocardial injury. The structured use of serial cardiac troponin has the potential to facilitate risk stratification, help make decisions about when to use imaging, and inform stage categorization and disease phenotyping among hospitalized COVID-19 patients.
KW - cardiac troponin
KW - coronavirus disease 2019
KW - myocardial injury
KW - type 2 myocardial infarction
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U2 - 10.1016/j.jacc.2020.06.068
DO - 10.1016/j.jacc.2020.06.068
M3 - Review article
C2 - 32652195
AN - SCOPUS:85089804137
SN - 0735-1097
VL - 76
SP - 1244
EP - 1258
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 10
ER -