Citation, DOI & article data
Myocardial injury is defined by an elevation of cardiac troponin values above the 99th percentile upper reference limit. It is considered a prerequisite for the diagnosis of myocardial infarction but also an entity in itself and can arise from non-ischemic or non-cardiac conditions 1,2.
The term 'myocardial injury' might be used in the setting of direct cardiac damage such as cardiac contusion but it might also occur in diverse other clinical scenarios such as myocardial infarction, myocardial inflammation, sepsis, and iatrogenic injury 1-3.
A myocardial injury might present with cardiac symptoms like chest pain and/or dyspnea. Depending on the etiology and extent there will be characteristic changes on the electrocardiogram. It can be reliably detected biochemically with serologic markers and is defined by an elevation of cardiac troponin values above the 99th percentile upper reference limit 1. The creatine kinase MB isoform is another serologic marker 4,5.
Presumed mechanisms of myocardial injury include the following 4:
- direct cardiac damage with cardiomyocyte injury
- myocardial strain as a result of excessive wall stress
- myocardial ischemia due to myocardial oxygen supply and demand mismatch
Myocardial injury might be irreversible and is often associated with myocardial necrosis or apoptosis 4. However, the concept of troponin release in the setting of reversible injury such as extreme exercise has been suggested 4.
Myocardial injury can have the following causes 1-4, 6,7:
- primary myocardial ischemia / myocardial infarction
- atherosclerotic plaque rupture with thrombosis
- mismatch in myocardial oxygen supply and demand
- non-ischemic myocardial injury
- multifactorial and systemic causes
Due to the excellent sensitivity and fast availability of serologic biomarkers, imaging methods have no real role in the detection of myocardial necrosis but the localization and the search for the etiology for non-ischemic or indeterminate cases.
Myocardial injury is associated with myocardial necrosis and myocardial edema. Therefore it can be depicted on MRI with cardiac tissue characterization techniques including T2-weighted imaging/STIR, late gadolinium enhancement and myocardial mapping techniques 2.
- T2/STIR: hyperintensity
- T2-mapping: increased T2 [ms]
- T1-mapping: increased T1 [ms]
- ECV: increased
- typically subendocardial to transmural late gadolinium enhancement in case of an acute myocardial infarction
- no enhancement in the no-reflow zone in case of microvascular obstruction
- focal subepicardial or patchy mid-wall enhancement in the setting of myocardial inflammation or direct cardiac damage such as cardiac contusion
The radiological report should include a description and localization of the following:
- 1. Thygesen K, Alpert J, Jaffe A et al. Fourth Universal Definition of Myocardial Infarction (2018). Eur Heart J. 2018;40(3):237-69. doi:10.1093/eurheartj/ehy462
- 2. Chapman A, Adamson P, Mills N. Assessment and Classification of Patients with Myocardial Injury and Infarction in Clinical Practice. Heart. 2016;103(1):10-8. doi:10.1136/heartjnl-2016-309530 - Pubmed
- 3. Friedrich M. Tissue Characterization of Acute Myocardial Infarction and Myocarditis by Cardiac Magnetic Resonance. JACC Cardiovasc Imaging. 2008;1(5):652-62. doi:10.1016/j.jcmg.2008.07.011 - Pubmed
- 4. Park K, Gaze D, Collinson P, Marber M. Cardiac Troponins: From Myocardial Infarction to Chronic Disease. Cardiovasc Res. 2017;113(14):1708-18. doi:10.1093/cvr/cvx183 - Pubmed
- 5. Kemp M, Donovan J, Higham H, Hooper J. Biochemical Markers of Myocardial Injury. Br J Anaesth. 2004;93(1):63-73. doi:10.1093/bja/aeh148 - Pubmed
- 6. Scalone G, Niccoli G, Crea F. Editor’s Choice- Pathophysiology, Diagnosis and Management of MINOCA: An Update. European Heart Journal: Acute Cardiovascular Care. 2018;8(1):54-62. doi:10.1177/2048872618782414 - Pubmed
- 7. Guensch D, Yu J, Nadeshalingam G, Fischer K, Shearer J, Friedrich M. Evidence for Acute Myocardial and Skeletal Muscle Injury After Serial Transthoracic Shocks in Healthy Swine. PLoS One. 2016;11(9):e0162245. doi:10.1371/journal.pone.0162245 - Pubmed