Abstract
BackgroundSevere 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.MethodsIn 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. One hundred thirteen patients (63.5%) were treated with dexamethasone for a median duration of 10 days (IQR 9–10). Sixty five patients (36.5%) constituted the non-dexamethasone control group.ResultsWhile 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. 6.14 mg/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.ConclusionIn severe COVID-19, anti-inflammatory 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.
Highlights
Acute Respiratory Distress Syndrome (ARDS) caused by coronavirus disease 2019 (COVID-19) remains one of the major challenges in current intensive care treatment worldwide [1]
While peak inflammatory markers were reduced by dexamethasone treatment, the therapy led to a significant reduction in peak troponin levels (231 vs. 700% indicated as relative to cut off value, p = 0.001)
The antithrombotic effect of dexamethasone treatment was evident in the presence of therapeutic anticoagulation
Summary
Acute Respiratory Distress Syndrome (ARDS) caused by coronavirus disease 2019 (COVID-19) remains one of the major challenges in current intensive care treatment worldwide [1]. First studies have proposed high rates of myocardial injury in COVID-19 infection [4, 5]. According to recent studies, cardiac involvement may not represent a specific feature of COVID-19 but is more likely the result of a high inflammatory burden in the context of a severe disease process [7]. In addition to cardiac injury, an increased thrombogenicity resulting in high rates of pulmonary embolism and other thromboembolic events has been observed in COVID19 [10, 11]. 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. The effect of dexamethasone treatment on cardiac injury and pulmonary embolism remains largely elusive
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