Exercise-Induced Cardiac Troponin Elevations: From Underlying Mechanisms to Clinical Relevance
Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is...
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| Published in | Circulation (New York, N.Y.) Vol. 144; no. 24; pp. 1955 - 1972 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Lippincott Williams & Wilkins
14.12.2021
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field. |
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| AbstractList | Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field. Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field.Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field. Supplemental Digital Content is available in the text. Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field. |
| Author | Baggish, Aaron L. Mingels, Alma M.A. Ørn, Stein Thompson, Paul D. Chung, Eugene H. George, Keith Eijsvogels, Thijs M.H. Shave, Rob E. Aengevaeren, Vincent L. Kleiven, Øyunn |
| AuthorAffiliation | Cardiology Department, Stavanger University Hospital, Norway (Ø.K., S.Ø.) Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Vancouver, Canada (R.E.S.) Division of Cardiology, Hartford Hospital, CT (P.D.T.) Radboud Institute for Health Sciences, Departments of Physiology (V.L.A., T.M.H.E.), Radboud University Medical Center, Nijmegen, The Netherlands Cardiovascular Performance Program, Massachusetts General Hospital, Boston (A.L.B.) Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, United Kingdom (K.G.) Department of Clinical Chemistry, Central Diagnostic Laboratory, Maastricht University Medical Center Maastricht, The Netherlands (A.M.A.M.) Michigan Medicine, University of Michigan, Ann Arbor (E.H.C.) |
| AuthorAffiliation_xml | – name: Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, United Kingdom (K.G.) – name: Department of Clinical Chemistry, Central Diagnostic Laboratory, Maastricht University Medical Center Maastricht, The Netherlands (A.M.A.M.) – name: Cardiology Department, Stavanger University Hospital, Norway (Ø.K., S.Ø.) – name: Radboud Institute for Health Sciences, Departments of Physiology (V.L.A., T.M.H.E.), Radboud University Medical Center, Nijmegen, The Netherlands – name: Cardiovascular Performance Program, Massachusetts General Hospital, Boston (A.L.B.) – name: Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Vancouver, Canada (R.E.S.) – name: Division of Cardiology, Hartford Hospital, CT (P.D.T.) – name: Michigan Medicine, University of Michigan, Ann Arbor (E.H.C.) |
| Author_xml | – sequence: 1 givenname: Vincent L. surname: Aengevaeren fullname: Aengevaeren, Vincent L. organization: Radboud Institute for Health Sciences, Departments of Physiology (V.L.A., T.M.H.E.), Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 2 givenname: Aaron L. surname: Baggish fullname: Baggish, Aaron L. organization: Cardiovascular Performance Program, Massachusetts General Hospital, Boston (A.L.B.) – sequence: 3 givenname: Eugene H. surname: Chung fullname: Chung, Eugene H. organization: Michigan Medicine, University of Michigan, Ann Arbor (E.H.C.) – sequence: 4 givenname: Keith surname: George fullname: George, Keith organization: Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, United Kingdom (K.G.) – sequence: 5 givenname: Øyunn surname: Kleiven fullname: Kleiven, Øyunn organization: Cardiology Department, Stavanger University Hospital, Norway (Ø.K., S.Ø.) – sequence: 6 givenname: Alma M.A. surname: Mingels fullname: Mingels, Alma M.A. organization: Department of Clinical Chemistry, Central Diagnostic Laboratory, Maastricht University Medical Center Maastricht, The Netherlands (A.M.A.M.) – sequence: 7 givenname: Stein surname: Ørn fullname: Ørn, Stein organization: Cardiology Department, Stavanger University Hospital, Norway (Ø.K., S.Ø.) – sequence: 8 givenname: Rob E. surname: Shave fullname: Shave, Rob E. organization: Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Vancouver, Canada (R.E.S.) – sequence: 9 givenname: Paul D. surname: Thompson fullname: Thompson, Paul D. organization: Division of Cardiology, Hartford Hospital, CT (P.D.T.) – sequence: 10 givenname: Thijs M.H. surname: Eijsvogels fullname: Eijsvogels, Thijs M.H. organization: Radboud Institute for Health Sciences, Departments of Physiology (V.L.A., T.M.H.E.), Radboud University Medical Center, Nijmegen, The Netherlands |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34898243$$D View this record in MEDLINE/PubMed |
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| Keywords | apoptosis cardiomegaly, exercise-induced athletes necrosis heart heart injuries |
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| Snippet | Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or... Supplemental Digital Content is available in the text. Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in... |
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| SubjectTerms | Cardiovascular Diseases - metabolism Exercise Humans Kinetics State of the Art Troponin - metabolism |
| Title | Exercise-Induced Cardiac Troponin Elevations: From Underlying Mechanisms to Clinical Relevance |
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