Corpus overview


Overview

MeSH Disease

Human Phenotype

Transmission

Seroprevalence
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    Observations on echocardiographic findings in patients with COVID-19

    Authors: Ahsan A Khan; Sunil James; Mengshi Yuan; Latoya Woolery; Nina Huppertz; Mushidur Rahman; Chetan Varma; Stavros Apostolakis; Vinoda Sharma

    doi:10.21203/rs.3.rs-58076/v1 Date: 2020-08-12 Source: ResearchSquare

    Background The novel coronavirus (SARS-CoV-2) has created global havoc by causing Coronavirus Disease MESHD 2019 (COVID-19). Cardiovascular involvement MESHD in COVID-19 varies from troponin rise or arrhythmia HP arrhythmia MESHD/ myocarditis HP myocarditis MESHD to fulminant cardiogenic shock HP cardiogenic shock MESHD. There is limited data on echocardiographic findings in such patients. We aimed to assess abnormal echocardiographic findings and contributory factors in patients with COVID-19.Methods We performed retrospective analysis of COVID-19 positive patients who underwent a transthoracic echocardiogram (TTE) at Sandwell and West Birmingham (SWBH) NHS Trust between March 2020 and May 2020. Patients were compared based on TTE changes and divided into two groups (abnormal TTE and normal TTE).Results 66 out of 463 patients with COVID-19 had a TTE. 46 patients (69.7%) had abnormal findings on their TTE. Tricuspid regurgitation HP Tricuspid regurgitation MESHD was the most common abnormality observed (26 (56.5%) patients), followed by aortic regurgitation HP aortic regurgitation MESHD (13 (28.3%) patients) and mitral regurgitation HP mitral regurgitation MESHD (12 (26.1%) patients). Haemoglobin and LDH were predictors of abnormal TTE (Hb OR: 0.97, p = 0.049, LDH, OR: 1.00, p = 0.03). Significantly more patients in the abnormal TTE group died during their inpatient stay compared to normal TTE (p = 0.01). Having an abnormal TTE was an independent predictor of death on regression analysis (OR: 0.229, p = 0.034).Conclusions This is the first detailed observational study looking at echocardiographic changes in admitted COVID-19 patients irrespective of disease severity. The most common abnormality was valve regurgitation MESHD. Patients with abnormal TTE were more likely to die in hospital.

    Cardiac involvement in COVID-19 patients: mid-term follow up by cardiac magnetic resonance imaging

    Authors: Hui Wang; Ruili Li; Hong Jiang; Zixu Yan; Xinyan Tao; Hongjun Li; Lei Xu

    doi:10.21203/rs.3.rs-57104/v1 Date: 2020-08-11 Source: ResearchSquare

    Background: Coronavirus disease MESHD 2019 (COVID-19) induces myocardial injury MESHD, either direct myocarditis HP myocarditis MESHD or indirect injury due to systemic inflammatory response. Myocardial involvement MESHD has been proved to be one of the primary manifestations of COVID-19 infection MESHD, according to laboratory test, autopsy, and cardiac magnetic resonance imaging (CMRI). However, the middle-term outcome of cardiac involvement MESHD after the patients were discharged from the hospital is yet unknown. The present study aimed to evaluate mid-term cardiac sequelae in recovered COVID-19 patients by CMRIMethods: A total of 47 recovered COVID-19 patients were prospectively recruited and underwent CMRI examination in this study. The CMRI protocol consisted of black blood SERO fat-suppressed T2 weighted imaging (BB-T2WI), T2 star mapping, left ventricle cine imaging, pre- and post-contrast T1 mapping, and late gadolinium enhancement (LGE). Myocardium edema MESHD edema HP and LGE were assessed in recovered COVID-19 patients. The left ventricle ( LV MESHD) and right ventricle (RV) function and LV mass were assessed and compared with normal controls.Results: Finally, 44 recovered COVID-19 patients and 31 normal controls were included in this study. No edema HP edema MESHD was observed in any patient. LGE was found in 13 patients. All LGE lesions were located in the middle myocardium and/or sub-epicardium with a scattered distribution. Further analysis showed that LGE-positive patients had significantly decreased left ventricle peak global circumferential strain (LVpGCS), right ventricle peak global circumferential strain (RVpGCS), right ventricle peak global longitudinal strain (RVpGLS) as compared to non-LGE patients (p<0.05), while no difference was detected between the non-LGE patients and normal controls.Conclusion: Myocardium injury MESHD existed in about 30% of COVID-19 patients. These patients had peak right ventricle strain that decreased at the 3-month follow-up. Cardiac MRI can monitor the COVID-19-induced myocarditis HP myocarditis MESHD progression, and CMR strain analysis is a sensitive tool to evaluate the recovery of left ventricle circumferential contraction dysfunction MESHD and right ventricular dysfunction MESHD.

    The Spectrum of Cardiovascular Complications MESHD in COVID-19- A Comprehensive Literature Review

    Authors: Raja Shakeel Mushtaque; Rabia Mushtaque; Shahbano Baloch; Aadil Raza; Haseeb Bhatti; Zohaib Khan

    id:10.20944/preprints202008.0257.v1 Date: 2020-08-11 Source: Preprints.org

    A newly identified novel coronavirus named as severe acute respiratory syndrome MESHD-related coronavirus2 (SARS‐CoV 2) has given rise to the global pandemic. SARS-CoV2 which causes coronavirus disease MESHD 2019 (COVID-19), is a positive-stranded RNA virus with nucleocapsid. It binds to host angiotensin-converting enzyme2 (ACE2) receptor through surface glycoprotein (S protein). These ACE 2 receptors are attached to the cell membranes of many organs. Thus, COVID-19 does not only result in acute respiratory distress syndrome MESHD respiratory distress HP syndrome but also affects multiple organ systems, requiring a multidisciplinary approach to manage this disease. COVID-19 can damage the myocardial cells and result in fulminant myocarditis HP myocarditis MESHD, acute cardiac injury MESHD, cardiomyopathy HP cardiomyopathy MESHD, heart failure MESHD, cardiogenic shock HP cardiogenic shock MESHD, or arrhythmia HP arrhythmia MESHD. COVID-19 seeds harmful immune response through cytokine storm leading to indirect organ damage. In this literature review, the available data is comprehended regarding cardiovascular complications in COVID-19, and the correlation of biomarkers with the disease activity is discussed. This literature review also highlights the important treatment options and outcomes of the individual study.

    Life-threatening cardiogenic shock HP cardiogenic shock MESHD in a pediatric patient with SARS-CoV-2-associated myocarditis HP myocarditis MESHD treated with remdesivir: a case description and report of similar cases from the Literature

    Authors: Silvia Molinari; Lucia M.D. Colasanto; Maria L. Melzi; Alessandro Cattoni; Roberto Panceri; Michela Bombino; Giuseppe Lapadula; Andrea Biondi

    doi:10.21203/rs.3.rs-34802/v1 Date: 2020-06-12 Source: ResearchSquare

    BackgroundChildren are relatively spared from Coronavirus disease MESHD 2019 (COVID-19), but some severe cases have been reported. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection MESHD in children TRANS may affect the cardiovascular system. We hereby report about a case of myocarditis HP myocarditis MESHD evolving to cardiogenic shock HP cardiogenic shock MESHD in a SARS-CoV-2 positive child TRANS.Case presentationAn otherwise healthy 12-year-old patient was admitted with fever HP fever MESHD, vomiting HP vomiting MESHD, diarrhoea and drowsiness MESHD drowsiness HP, without any respiratory symptoms. He was diagnosed with COVID-19 on nasopharyngeal swab. He developed hypotension HP hypotension MESHD and cardiogenic shock HP cardiogenic shock MESHD. Bedside echocardiography revealed left ventricular impairment MESHD with an ejection fraction (LVEF) below 25%. Plasmatic markers of myocardial injury MESHD were remarkably raised, as well as inflammatory biomarkers, including procalcitonin (highest recorded value: 66 ng/mL) and interleukin-6 (8209 pg/mL). The child TRANS was transferred to Intensive Care Unit and he was treated with catecholamine support, mechanical ventilation and empiric anti-infectious therapy, including broad spectrum antibiotics and the antiviral agent remdesivir. All additional microbiological investigations yielded negative results. We observed a gradual improvement of LVEF within 5 days. A cardiac magnetic resonance confirmed the suspicion of myocarditis HP myocarditis MESHD. After 21 days of hospitalisation, the child TRANS was discharged without sequelae.ConclusionsOur hypothesis is that the child TRANS suffered from SARS-CoV-2-induced fulminant myocarditis HP myocarditis MESHD, probably in the setting of cytokine release syndrome (CRS). The peculiarity of this SARS-CoV-2 infection MESHD is the presence of cardiac failure MESHD in a previously healthy child TRANS without a respiratory illness MESHD. The positive outcome is in line with published Literature about the overall better prognosis of COVID-19 children TRANS compared to adults TRANS. Remdesivir, an investigational antiviral therapy, may have played a role on the clinical improvement of the child TRANS.

    Human iPSC-Derived Cardiomyocytes are Susceptible to SARS-CoV-2 Infection MESHD

    Authors: Arun Sharma; Gustavo Garcia Jr.; Vaithilingaraja Arumugaswami; Clive N Svendsen

    doi:10.1101/2020.04.21.051912 Date: 2020-04-21 Source: bioRxiv

    Coronavirus disease 2019 (COVID-19) is a viral pandemic caused by the severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2). COVID-19 is predominantly defined by respiratory symptoms, but cardiac complications including arrhythmias HP arrhythmias MESHD, heart failure MESHD, and viral myocarditis HP myocarditis MESHD are also prevalent. Although the systemic ischemic MESHD and inflammatory responses caused by COVID-19 can detrimentally affect cardiac function, the direct impact of SARS-CoV-2 infection MESHD on human cardiomyocytes is not well-understood. We used human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) as a model system to examine the mechanisms of cardiomyocyte-specific infection by SARS-CoV-2. Microscopy and immunofluorescence demonstrated that SARS-CoV-2 can enter and replicate within hiPSC-CMs, localizing at perinuclear locations within the cytoplasm. Viral cytopathic effect induced hiPSC-CM apoptosis MESHD and cessation of beating after 72 hours of infection MESHD. These studies show that SARS-CoV-2 can infect hiPSC-CMs MESHD in vitro, establishing a model for elucidating the mechanisms of infection MESHD and potentially a cardiac-specific antiviral drug screening platform.

    Myocyte Specific Upregulation of ACE2 in Cardiovascular Disease MESHD: Implications for SARS-CoV-2 mediated myocarditis HP myocarditis MESHD

    Authors: Nathan R Tucker; Mark Chaffin; Kenneth C Bedi Jr.; Irinna Papangeli; Amer-Denis Akkad; Alessandro Arduini; Sikander Hayat; Gökcen Eraslan; Christoph Muus; Roby Bhattacharyya; Christian M Stegmann; - Human Cell Atlas Lung Biological Network; Kenneth B Margulies; Patrick T Ellinor

    doi:10.1101/2020.04.09.20059204 Date: 2020-04-14 Source: medRxiv

    Coronavirus disease 2019 (COVID-19) is a global pandemic caused by a novel severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2). SARS-CoV-2 infection MESHD of host cells occurs predominantly via binding of the viral surface spike protein to the human angiotensin-converting enzyme 2 (ACE2) receptor. Hypertension HP Hypertension MESHD and pre-existing cardiovascular disease MESHD are risk factors for morbidity from COVID-19, and it remains uncertain whether the use of angiotensin converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB) impacts infection MESHD and disease. Here, we aim to shed light on this question by assessing ACE2 expression in normal and diseased human myocardial samples profiled by bulk and single nucleus RNA-seq.

    First Case of COVID-19 Complicated with Fulminant Myocarditis MESHD Myocarditis HP: A case Report and Insights

    Authors: Jia Hui Zeng; Ying-Xia Liu; Jing Yuan; Fu-Xiang Wang; Wei-Bo Wu; Jin-Xiu Li; Li-Fei Wang; Hong Gao; Yao Wang; Chang-Feng Dong; Yi-Jun Li; Xiao-Juan Xie; Cheng Feng; Lei Liu

    id:202003.0180/v2 Date: 2020-04-06 Source: Preprints.org

    Background: Coronavirus Disease MESHD 2019 (COVID-19) has been demonstrated to be the cause of pneumonia HP pneumonia MESHD. Nevertheless, it has not been reported as the cause of acute myocarditis HP myocarditis MESHD or fulminant myocarditis HP myocarditis MESHD. Case presentation: A 63-year-old male TRANS was admitted with pneumonia HP pneumonia MESHD and cardiac symptoms MESHD. He was genetically confirmed as having COVID-19 according to sputum testing on the day of admission. He also had elevated troponin I (Trop I) level (up to 11.37 g/L) and diffuse myocardial dyskinesia MESHD dyskinesia HP along with a decreased left ventricular ejection fraction (LVEF) on echocardiography. The highest level of interleukin-6 was 272.40 pg/ml. Bedside chest radiographs showed typical ground-glass changes indicative of viral pneumonia MESHD pneumonia HP. Laboratory test results for viruses that cause myocarditis HP myocarditis MESHD were all negative. The patient conformed to the diagnostic criteria of the Chinese expert consensus statement for fulminant myocarditis HP myocarditis MESHD. After receiving antiviral therapy and mechanical life support, Trop I was reduced to 0.10 g/L, and interleukin-6 was reduced to 7.63 pg/ml. Moreover, the LVEF of the patient gradually recovered to 68%. The patient died of aggravation of secondary infection on the 33rd day of hospitalization. Conclusion: COVID-19 patients may develop severe cardiac complications MESHD such as myocarditis HP myocarditis MESHD and heart failure MESHD. This is the first report of COVID-19 complicated with fulminant myocarditis HP myocarditis MESHD. The mechanism of cardiac pathology caused by COVID-19 needs further study.

    Discovery of potential drugs for COVID-19 based on the connectivity map

    Authors: Zhonglin Li; Tao Bai; Ling Yang; Xiaohua Hou

    doi:10.21203/rs.2.24684/v1 Date: 2020-02-25 Source: ResearchSquare

    Background: Corona virus infective disease MESHD 19 (COVID-19) is the disease caused by severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) and spreads very rapidly, which become a worldwide public healthy crisis. Until now, there is no effective antivirus drugs or vaccines specifically used for its treatment. So it is urgent to discover efficient therapeutic methods. The same as SARS-CoV, SARS-CoV-2 MESHD also invades organism by combining with Angiotensin-converting enzyme 2 (ACE2). Recently, there are reports about SARS-CoV-2 infected MESHD host not only through the respiratory tract, but also gastrointestinal tract. However, it is proved that ACE2 plays a key role in protecting subjects from lung injury MESHD and resisting the inflammation MESHD caused by intestinal epithelial damage. Interestingly, the expression of ACE2 protein is reduced after SARS-CoV infection MESHD. Methods: According to the dataset of genes co-expressed with ACE2 in the colonic epithelial cells, we established a protein-protein interaction (PPI) Network and selected hub genes from them. The cluster analysis was performed to find out the dense region of the PPI Network. Then, gene ontology (GO) and pathway enrichment analysis were performed to explore the main function of genes co-expressed with ACE2. Finally, we predicted the potential drugs for the treatment of COVID-19 based on the connectivity map (Cmap) . Results: We constructed a PPI network containing 125 hub genes of genes co-expressed with ACE2 in the colonic epithelial cells and obtained two modules through cluster analysis. The GO analysis and the KEGG pathway revealed these genes were aggregated in ribosome, exosomes, extracellular cellular components; structure constituent of ribosome, G-protein coupled receptor activity, MHC class I and II receptor activity biological processes; immune response, protein metabolism, signal transduction biological processes; and ribosome, graft-versus-host disease MESHD, viral myocarditis MESHD myocarditis HP pathways. The result from Cmap indicated ikarugamycin, molsidomine had highly correlated scores with the query files. Conclusion: We found out that ikarugamycin and molsidomine were the potential drugs for the treatment of COVID-19.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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