Cardiac injury as prognostic value in COVID-19: more remains to be clarified
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Cardiac injury as prognostic value in COVID‑19: more remains to be clarified Nicola Mumoli1 · Marco Cei2 · Antonino Mazzone1 · Giulia Conte1 Received: 4 October 2020 / Accepted: 12 October 2020 © Società Italiana di Medicina Interna (SIMI) 2020
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 evidencebased 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 * Nicola Mumoli [email protected] 1
Department of Internal Medicine, ASST Ovest Milanese, Ospedali di Magenta e Legnano, Ospedale Fornaroli, via al Donatore di Sangue 50, 20013 Magenta, MI, Italy
Department of Internal Medicine, Cecina Hospital, Cecina, LI, Italy
2
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 s
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