PMC:7102662 / 10999-13470 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7102662","sourcedb":"PMC","sourceid":"7102662","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7102662","text":"2.2.1 Acute myocardial injury\nAcute myocardial injury is the most commonly described CV complication in COVID-19 (Table 1). Different reports have used different definitions for acute myocardial injury, including rise in cardiac enzymes (different biomarkers and cut-offs) and/or electrocardiographic abnormalities. However, an elevation of high-sensitivity cardiac troponin I (cTnI) above 99th percentile upper reference limit is the most commonly used definition.Table 1\nThe overall incidence of acute cardiac injury has been variable but roughly 8–12% of the positive cases are known to develop significant elevation of cTnI [10]. The aforementioned meta-analysis of the Chinese studies [4] reported 8% incidence of acute cardiac injury whereas another study including only those patients who had had a definite outcome (death or discharge from hospital) reported 17% incidence of cTnI elevation [5]. Regardless of the actual incidence, acute cardiac injury has been consistently shown to be a strong negative prognostic marker in patients with COVID-19 [5,6,8]. The patients admitted to ICU or having severe/fatal illness have several-fold higher likelihood of troponin elevation. In contrast, the incidence of elevated troponin has been very low (only 1–2%) in patients having mild illness not requiring ICU admission.\nAny of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus.\nNo study has described the incidence of ST-segment elevation myocardial infarction in COVID-19, but it appears to be low. Similarly, the incidence of left ventricular systolic dysfunction, acute left ventricular failure and cardiogenic shock have also not been described. Only one Chinese study reported incidence of heart failure in COVID-19 patients [5]. Heart failure had occurred in 52% of the patients who subsequently died and in 12% of the patients who were discharged from the 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