Erschienen in:
28.10.2020 | COVID-19 | IM - COMMENTARY
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Cardiac injury as prognostic value in COVID-19: more remains to be clarified
verfasst von:
Nicola Mumoli, Marco Cei, Antonino Mazzone, Giulia Conte
Erschienen in:
Internal and Emergency Medicine
|
Ausgabe 2/2021
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Excerpt
Coronavirus disease 2019 (COVID-19) is a newly recognized infectious disease, caused by the severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2), with a high rate of morbidity and mortality [
1,
2]. In particular, with COVID-19 infection, mortality rates are highest in older patients (14.8% in those > 80 years) and in patients with cardiovascular disease. Currently, there is no evidence-based treatment for COVID-19, consequently, the mainstay of treatment is supportive care [
3]. Acute respiratory distress syndrome (ARDS) is considered to be an acute process confined to the lungs, with an overall case-fatality rate for COVID 19 which varies between 1.4% and 2.3%. However, there is more and more evidence which identifies myocardial injury as COVID-19 related-complication, manifesting as left ventricular dysfunction and troponin elevation, with an incidence ranging from 7.2% to 12% [
4]. Nevertheless, while an American College of Cardiology clinical bulletin pointed out the cardiac implications of COVID-19, the link between COVID-19–associated cardiac injury and risk of mortality remains unclear. Recent studies have highlighted the association between myocardial injury and fatal outcomes of COVID-19 disease. Particularly, inflammation caused by SARS-COV 2 appears to result in myocardial injury, leading to impairment of cardiac function, and increased incidence of ventricular tachyarrhythmias. Conversely, the prognosis of patients without myocardial injury appears relatively favorable, even for those with underlying cardiovascular disease. Patients with myocardial injury have elevated levels of myocardial markers, such as circulating cardiac troponin, a marker related but not limited to myocardial injury. In particular, troponin elevation, during COVID-19 infection, is likely to be multifactorial and it is not only attributable to atherothrombotic coronary occlusion. For example, in critically unwell patients, the oxygen supply–demand occurs at a cellular level in the majority of organ systems, but the sensitivity of cardiac troponin testing substantially is one of the earliest and most precise indicators of end-organ dysfunction, thus allowing an early start of the oxygen supplement to improve tissue oxygenation and perfusion. Moreover, the elevation of troponin in this kind of patients seems to play a negative prognostic role. In a cohort study of 191 patients with confirmed COVID-19 infection, the elevation of troponin was closely related to mortality increase [
5]. In another study, the number of patients with an elevation of troponin concentration was more likely to require invasive or noninvasive ventilation and to develop acute respiratory distress syndrome or acute kidney injury [
1]. Nevertheless, data about the clinical significance of cardiac injury in non-critically ill COVID-19 patients and about the correlation between cardiac injury and mortality are still lacking and unclear. In particular, the interaction between heart damage, comorbidity, and mortality is not well defined. …