ABSTRACT
Background: Multiple studies have described acute effects of the Covid-19 infection on the heart, but little is known about the long-term cardiac and pulmonary effects and complications after recovery. The aim of this analysis was to deliver a comprehensive report of symptoms and possible long-term impairments after hospitalization because of Covid-19 infection as well as to try to identify predictors for Long-Covid. Method(s): This was a prospective, multicenter registry study. Patients with verified Covid-19 infection, who were treated as in-patients at our dedicated Covid hospital (Clinic Favoriten), have been included in this study. In all patients, testing was performed approximately 6 months post discharge. During the study visit the following tests and investigations were performed: Detailed patient history and clinical examination, transthoracic echocardiography, electrocardiography, cardiac magnetic resonance imaging (MRI), chest computed tomography (CT) scan, lung function test and a comprehensive list of laboratory parameters including cardiac bio markers. Result(s): Between July 2020 and October 2021, 150 patients were recruited. Sixty patients (40%) were female and the average age was 53.5+/-14.5 years. Of all patients, 92% had been admitted to our general ward and 8% had a severe course of disease, requiring admission to our intensive care unit. Six months after discharge the majority of patients still experienced symptoms and 75% fulfilled the criteria for Long-Covid. Only 24% were completely asymptomatic (figure 1). Echocardiography detected reduced global longitudinal strain (GLS) in 11%. Cardiac MRI revealed pericardial effusion in 18%. Furthermore, cardiac MRI showed signs of former peri-or myocarditis in 4%. Pulmonary CT scans identified post-infectious residues, such as bilateral ground glass opacities and fibrosis in 22%. Exertional dyspnea was associated with either reduced forced vital capacity measured during pulmonary function tests in 11%, with reduced GLS and/or diastolic dysfunction, thus providing evidence for a cardiac and/or pulmonary cause. Independent predictors for Long-Covid were markers of a more severe disease course like length of in-hospital stay, admission to an intensive care unit, type of ventilation as well as higher NT-proBNP and/or troponin levels. Conclusion(s): Even 6 months after recovery from Covid-19 infection, the majority of previously hospitalized patients still suffer from at least one symptom, such as chronic fatigue and/or exertional dyspnea. While there was no association between fatigue and cardiopulmonary abnormalities, impaired lung function, reduced GLS and/or diastolic dysfunction were significantly more prevalent in patients presenting with exertional dyspnea. On chest CT approximately one fifth of all patients showed post infectious changes in chest CT including evidence for myo-and pericarditis as well as accumulation of pericardial effusions.
ABSTRACT
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).
ABSTRACT
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
ABSTRACT
Introduction: The severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) pandemic of 2020 has an influence on people's lives worldwide, impacting global health and putting pressure on health care systems. Multiple studies have described acute effects of the Covid-19 infection on the heart, but little is known about the long-term cardiac effects and complications after recovery. The aim of this analysis was to deliver a comprehensive report of symptoms and long-term impairment after Covid-19 infection. Methods: This study was a prospective, multicenter registry study. Patients with verified COVID-19 infection, who were treated at our dedicated COVID hospital (Klinik Favoriten), have been included in this study. In all patients, testing was performed approximately 6 months post discharge. During each study visit the following tests and investigations were performed: detailed patient history and clinical examination, transthoracic echocardiography, electrocardiography, cardiac magnetic resonance imaging (MRI), pulmonary computed tomography (CT) scan, lung function test, spiroergometry and six-minute walk test (6MWT), and a comprehensive list of laboratory parameters including cardiac bio markers such as brain natriuretic peptide (NTpro BNP) and troponin T. Results: In this interim analysis of an ongoing trial, the first 65 patients are presented. Baseline values are shown in table 1: 34 (59%) were male and the median age was 48.5 years (36.4-59.3). 86% of all patients included so far had an only mild to moderate course of disease and 14% of them had a severe course and were admitted to our intensive care unit. At the time of the study visit, the majority of patients still complained about symptoms: 40% presented with fatigue and weakness, 36% with exertional dyspnea, 21% with vertigo, 17% had an impaired taste or smell. Only 28% were completely asymptomatic (figure 1). From a cardiac perspective, the only abnormal findings noted in echocardiography studies were reduced left ventricular global longitudinal strain. Cardiac MRI revealed pericardial effusion in 19%, however, these were only minimal (≤9mm) and not visible in echocardiography. Furthermore, cardiac MRI showed positive late gadolinium enhancement in 11%. Pulmonary function tests were abnormal in 16%. Pulmonary CT scans showed post infectious residues like bilateral ground glass opacities and fibrosis in 45%. Exercise capacity as measured by the 6-minute walk test with BORG Dyspnea Score and by spiroergometry was reduced in almost 40% of our study participants. Conclusions: This interim analysis showed that most previously hospitalized patients still suffer from chronic fatigue, exertional dyspnea and impaired cardiopulmonary function after Covid-19 infection. Furthermore, even though cardiac and pulmonary imaging revealed numerous pathologic findings, and exercise capacity was reduced, no correlations could be found with persisting symptoms.