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Background: Severe COVID-19 pneumonia requiring intensive care treatment remains a clinical challenge to date. Dexamethasone was reported as a promising treatment option, leading to a reduction of mortality rates in severe COVID-19 disease. However, the effect of dexamethasone treatment on cardiac injury and pulmonary embolism remains largely elusive. Method(s): In total 178 critically ill COVID-19 patients requiring intensive care treatment and mechanical ventilation were recruited in three European medical centres and included in the present retrospective study. 113 patients (63.5%) were treated with dexamethasone for a median duration of 10 days (IQR 9-10). 65 patients (36.5%) constituted the nondexamethasone control group. Result(s): While peak inflammatory markers were reduced by dexamethasone treatment, the therapy also led to a significant reduction in peak troponin levels (231% vs. 700% indicated as relative to cut off value, p=0.001). Similar, dexamethasone resulted in significantly decreased peak D-Dimer levels (2.16 mg/l vs. 6.14mg/l, p=0.002) reflected by a significant reduction in pulmonary embolism rate (4.4% vs. 20.0%, p=0.001). The antithrombotic effect of dexamethasone treatment was also evident in the presence of therapeutic anticoagulation (pulmonary embolism rate: 6% vs. 34.4%, p<0.001). Of note, no significant changes in baseline characteristics were observed between the dexamethasone and non-dexamethasone group. Conclusion(s): In severe COVID-19, antiinflammatory effects of dexamethasone treatment seem to be associated with a significant reduction in myocardial injury. Similar, a significant decrease in pulmonary embolism, independent of anticoagulation, was evident, emphasizing the beneficial effect of dexamethasone treatment in severe COVID-19. (Figure Presented).
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Aims/Background: Severe COVID-19 pneumonia requiring intensive care treatment remains a clinical challenge to date. Dexamethasone was reported as a promising treatment option, leading to a reduction of mortality rates in severe COVID-19 disease as well as ventilator-dependent days. However, the effect of dexamethasone treatment on cardiovascular outcomes including cardiac injury monitored by cardiac enzymes remains largely elusive. Methods: For this study, we retrospectively screened 224 consecutive COVID-19 patients between 4/2020 and 1/2021 in three Europeen Hospitals. To avoid bias effects of further applied COVID-19 specific medications including tacilizumab, remdesevir and sarilumab, 46 patients treated with at least one of these substances were excluded from further analyses. In total 178 critically ill COVID-19 patients requiring intensive care treatment and mechanical ventilation were recruited. 113 patients (63.5%) were treated with dexamethasone for a median duration of 10 days (IQR 9–10). 65 patients (36.5%) constituted the non-dexamethasone group. The assessment of cardiac injury was based on cardiac enzymes. Results: Baseline charactaristics shown in Tab. 1. While peak inflammatory markers seemed to be reduced by dexamethasone treatment (CRP and a trend towards decrease of interleukin 6 levels (CRP maximum level: median: 20 ng/mL (IQR 12–28) vs. 22 ng/mL (IQR 14–37), p=0.043;IL-6 maximum level: median: 192 pg/mL (IQR 78–533) vs. 708 pg/mL (550–885), p=0.085), in the dexamethasone Group also shown a significant reduction in peak troponine levels as shown in Figure 1. CK and CK-MB do not differ significantly by Dexamethasone application. Of note, no significant changes in baseline characteristics were observed between the dexamethasone and non-dexamethasone group (Table 1). Conclusion: In severe COVID-19, antiinflammatory effects of dexamethasone treatment could be associated with a significant reduction in myocardial injury. Further studies should further evaluate whether Dexamethasone effects directly myocardial involvement in COVID 19. Funding Acknowledgement: Type of funding sources: None.Figure 1. Dynamics of hs-troponineTable 1. Baseline characteristics
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The coronavirus disease 2019 (COVID-19) affects not only the respiratory system, but also the cardiovascular system in 20-28% of cases, causing endothelial dysfunction, vasculitis, hyper-and hypocoagulation, myocarditis, endothelial dysfunction and other adverse effects. The presence of cardiovascular risk factors and diseases has been shown to worsen the disease severity and increase mortality from COVID-19. Recent studies have also found that elevations in some serum cardiovascular biomarkers can stratify the disease severity, in particular rates of hospitalizations to an internal medicine or intensive care unit, intubation, and mortality. They can be divided into markers of damage (TnT/I, creatine phosphokinase (CPK) and CPK-MB, myoglobin, NT-proBNP), coagulation (prothrombin time, fibrinogen and D-dimer), as well as prospective biomarkers for which the available evidence base is limited but there is a pathophysiological rationale (homocysteine and sST2). This review presents studies on the use of above serum biomarkers to stratify the risk of death in patients with COVID-19.