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Overview

MeSH Disease

Human Phenotype

Transmission

Seroprevalence
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    Causal associations between COVID-19 and Atrial Fibrillation HP Atrial Fibrillation MESHD: A bidirectional Mendelian randomization study

    Authors: Xiaoyu Zhang; Biyan Wang; Di Liu; Jinxia Zhang; Qiuyue Tian; Xiaoni Meng; Jie Zhang; Haifeng Hou; Manshu Song; Wei Wang; Youxin Wang; Steven Y Chang; Tisha Wang; Nida Qadir; Rachel Vreeman; Joseph Masci; Nick A Maskell; Shaney Barratt

    doi:10.1101/2020.08.13.20174417 Date: 2020-08-14 Source: medRxiv

    Abstract Background Observational studies showed that coronavirus disease MESHD 2019 (COVID-19) attacks universally and its most menacing progression uniquely endangers the elderly TRANS with cardiovascular disease MESHD ( CVD MESHD). Whether COVID-19 is causally related to increasing susceptibility and severity of atrial fibrillation HP atrial fibrillation MESHD ( AF MESHD), the main form of CVD MESHD, remains still unknown. Methods The study aims to investigate the bidirectional causal relations of COVID-19 with AF MESHD using two-sample Mendelian randomization (MR) analysis. Results MR evidence suggested genetically predicted severe COVID-19 was significantly associated with higher risk of AF MESHD (odds ratio [OR], 1.041; 95% confidence interval (CI), 1.007-1.076; P = 0.017), while genetically predicted AF MESHD was not causally associated with severe COVID-19 (OR, 0.831; 95% CI, 1.619-1.115; P=0.217). There was limited evidence to support association of genetically proxied COVID-19 with risk of AF MESHD (OR, 1.051; 95% CI, 0.991-1.114; P=0.097), and vice versa (OR, 0.163; 95% CI, 0.004-6.790; P=0.341). MR-Egger indicated no evidence of pleiotropic bias MESHD. Conclusion Overall, severe COVID-19 may causally affect AF MESHD through independent biological pathway. Survivors from severe COVID-19 might be of high risk of AF MESHD in the future. Key words Coronavirus disease MESHD 2019; Atrial Fibrillation HP Atrial Fibrillation MESHD; Bidirectional mendelian randomization

    Characteristics of Ischemic Stroke HP Stroke MESHD in COVID-19: A Need for Early Detection and Management

    Authors: Dinesh V. Jillella; Nicholas J. Janocko; Fadi Nahab; Karima Benameur; James G. Greene; Wendy L. Wright; Mahmoud Obideen; Srikant Rangaraju

    doi:10.1101/2020.05.25.20111047 Date: 2020-05-26 Source: medRxiv

    Objective: In the setting of the Coronavirus Disease MESHD 2019 (COVID-19) global pandemic caused by SARS-CoV-2, a potential association of this disease with stroke HP stroke MESHD has been suggested. We aimed to describe the characteristics of patients who were admitted with COVID-19 and had an acute ischemic stroke HP ischemic stroke MESHD ( AIS MESHD). Methods: This is a case series of PCR-confirmed COVID-19 patients with ischemic stroke HP ischemic stroke MESHD admitted to an academic health system in metropolitan Atlanta (USA) between March 24th,2020, and May 5th, 2020. Demographic, clinical, and radiographic characteristics were described. Results: Of 124 ischemic stroke HP ischemic stroke MESHD stroke MESHD patients admitted during this study period, 8 (6.5%) were also diagnosed with COVID-19. The mean age TRANS of patients was 64.3 +/- 6.5 years, 5 (62.5%) male TRANS, mean time from last-normal was 4.8 days [SD 4.8], and none received acute reperfusion therapy. All 8 patients had at least one stroke HP stroke MESHD-associated co-morbidity. The predominant pattern of ischemic stroke HP ischemic stroke MESHD was embolic MESHD; 3 were explained by atrial fibrillation HP atrial fibrillation MESHD while 5 (62.5%) were cryptogenic. In contrast, cryptogenic strokes HP strokes MESHD were seen in 20 (16.1%) of 124 total stroke HP stroke MESHD admissions during this time. Conclusions: In our case series, ischemic stroke HP ischemic stroke MESHD affected COVID-19 patients with traditional stroke HP stroke MESHD risk factors with an age TRANS of stroke HP stroke MESHD presentation typically seen in non-COVID populations. We observed a predominantly embolic pattern of stroke MESHD stroke HP with a higher than expected rate of cryptogenic strokes HP strokes MESHD and with a prolonged median time to presentation and symptom recognition limiting the use of acute reperfusion treatments. These results highlight the need for increased community awareness, early identification, and management of AIS in COVID-19 patients.

    Investigation of the genetic variation in ACE2 on the structural recognition by the novel coronavirus (SARS-CoV-2)

    Authors: Xingyi Guo; Zhishan Chen; Yumin Xia; Weiqiang Lin; Hongzhi Li

    doi:10.21203/rs.3.rs-29037/v1 Date: 2020-05-14 Source: ResearchSquare

    Background: The outbreak of coronavirus disease MESHD (COVID-19) was caused by severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), through its surface spike glycoprotein (S protein) recognition on the receptor Angiotensin-converting enzyme 2 (ACE2) in humans. However, it remains unclear how genetic variations in ACE2 may affect its function and structure, and consequently alter the recognition by SARS-CoV-2. Methods: We have systemically characterized missense variants in the gene ACE2 using data from the Genome Aggregation Database (gnomAD; N = 141,456). To investigate the putative deleterious role of missense variants, six existing functional prediction tools were applied to evaluate their impact. We further analyzed structural flexibility of ACE2 and the protein-protein interface with the S protein of SARS-CoV-2 using our developed Legion Interfaces Analysis (LiAn) program. Results: Here, we characterized a total of 12 ACE2 putative deleterious missense variants. Of those 12 variants, we further showed that p.His378Arg could directly weaken the binding of catalytic metal atom to decrease ACE2 activity and p.Ser19Pro could distort the most important helix to the S-protein. Another seven missense variants may affect secondary structures (i.e. p.Gly211Arg; p.Asp206Gly; p.Arg219Cys; p.Arg219His, p.Lys341Arg, p.Ile468Val, and p.Ser547Cys), whereas p.Ile468Val with AF MESHD = 0.01 is only present in Asian. Conclusions: We provide strong evidence of putative deleterious missense variants in ACE2 that are present in specific populations, which could disrupt the function and structure of ACE2. These findings provide novel insight into the genetic variation in ACE2 which may affect the SARS-CoV-2 recognition and infection MESHD, and COVID-19 susceptibility and treatment.

    Investigation of the genetic variation in ACE2 on the structural recognition by the novel coronavirus (SARS-CoV-2)

    Authors: Xingyi Guo; Zhishan Chen; Yumin Xia; Weiqiang Lin; Hongzhi Li

    doi:10.21203/rs.3.rs-29037/v2 Date: 2020-05-14 Source: ResearchSquare

    Background: The outbreak of coronavirus disease MESHD (COVID-19) was caused by severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), through its surface spike glycoprotein (S-protein) recognition on the receptor Angiotensin-converting enzyme 2 (ACE2) in humans. However, it remains unclear how genetic variations in ACE2 may affect its function and structure, and consequently alter the recognition by SARS-CoV-2. Methods: We have systemically characterized missense variants in the gene ACE2 using data from the Genome Aggregation Database (gnomAD; N = 141,456). To investigate the putative deleterious role of missense variants, six existing functional prediction tools were applied to evaluate their impact. We further analyzed the structural flexibility of ACE2 and its protein-protein interface with the S-protein of SARS-CoV-2 using our developed Legion Interfaces Analysis (LiAn) program.Results: Here, we characterized a total of 12 ACE2 putative deleterious missense variants. Of those 12 variants, we further showed that p.His378Arg could directly weaken the binding of catalytic metal atom to decrease ACE2 activity and p.Ser19Pro could distort the most important helix to the S-protein. Another seven missense variants may affect secondary structures (i.e. p.Gly211Arg; p.Asp206Gly; p.Arg219Cys; p.Arg219His, p.Lys341Arg, p.Ile468Val, and p.Ser547Cys), whereas p.Ile468Val with AF MESHD = 0.01 is only present in Asian.Conclusions: We provide strong evidence of putative deleterious missense variants in ACE2 that are present in specific populations, which could disrupt the function and structure of ACE2. These findings provide novel insight into the genetic variation in ACE2 which may affect the SARS-CoV-2 recognition and infection MESHD, and COVID-19 susceptibility and treatment.

    Prevalence SERO and Impact of Myocardial Injury MESHD in Patients Hospitalized with COVID-19 Infection

    Authors: Anuradha Lala; Kipp W Johnson; Adam J Russak; Ishan Paranjpe; Shan Zhao; Sulaiman Solani; Akhil Vaid; Fayzan Chaudhry; Jessica K De Freitas; Zahi A Fayad; Sean P Pinney; Matthew Levin; Alexander Charney; Emilia Bagiella; Jagat Narula; Benjamin S Glicksberg; Girish Nadkarni; James Januzzi; Donna M Mancini; Valentin Fuster

    doi:10.1101/2020.04.20.20072702 Date: 2020-04-24 Source: medRxiv

    Background: The degree of myocardial injury MESHD, reflected by troponin elevation, and associated outcomes among hospitalized patients with Coronavirus Disease MESHD (COVID-19) in the US are unknown. Objectives: To describe the degree of myocardial injury MESHD and associated outcomes in a large hospitalized cohort with laboratory-confirmed COVID-19. Methods: Patients with COVID-19 admitted to one of five Mount Sinai Health System hospitals in New York City between February 27th and April 12th, 2020 with troponin-I (normal value <0.03ng/mL) measured within 24 hours of admission were included (n=2,736). Demographics, medical history, admission labs, and outcomes were captured from the hospital EHR. Results: The median age TRANS was 66.4 years, with 59.6% men. Cardiovascular disease MESHD ( CVD MESHD) including coronary artery disease MESHD, atrial fibrillation HP atrial fibrillation MESHD, and heart failure MESHD, was more prevalent in patients with higher troponin concentrations, as were hypertension HP hypertension MESHD and diabetes MESHD. A total of 506 (18.5%) patients died during hospitalization. Even small amounts of myocardial injury MESHD (e.g. troponin I 0.03-0.09ng/mL, n=455, 16.6%) were associated with death MESHD (adjusted HR: 1.77, 95% CI 1.39-2.26; P<0.001) while greater amounts (e.g. troponin I>0.09 ng/dL, n=530, 19.4%) were associated with more pronounced risk (adjusted HR 3.23, 95% CI 2.59-4.02). Conclusions: Myocardial injury MESHD is prevalent among patients hospitalized with COVID-19, and is associated with higher risk of mortality. Patients with CVD MESHD are more likely to have myocardial injury MESHD than patients without CVD MESHD. Troponin elevation likely reflects non- ischemic MESHD or secondary myocardial injury MESHD.

    Clinical and radiographic features of cardiac injury MESHD in patients with 2019 novel coronavirus pneumonia MESHD pneumonia HP

    Authors: Hui Hui; Yingqian Zhang; Xin Yang; Xi Wang; Bingxi He; Li Li; Hongjun Li; Jie Tian; Yundai Chen

    doi:10.1101/2020.02.24.20027052 Date: 2020-02-27 Source: medRxiv

    Objective: To investigate the correlation between clinical characteristics and cardiac injury MESHD of COVID-2019 pneumonia HP pneumonia MESHD. Methods: In this retrospective, single-center study, 41 consecutive corona virus disease 2019 (COVID-2019) patients (including 2 deaths) of COVID-2019 in Beijing Youan Hospital, China Jan 21 to Feb 03, 2020, were involved in this study. The high risk factors of cardiac injury MESHD in different COVID-2019 patients were analyzed. Computed tomographic (CT) imaging of epicardial adipose tissue (EAT) has been used to demonstrate the cardiac inflammation MESHD of COVID-2019. ResultsOf the 41 COVID-2019 patients, 2 (4.88%), 32 (78.05%), 4 (9.75%) and 3 (7.32%) patients were clinically diagnosed as light, mild, severe and critical cases, according to the 6th guidance issued by the National Health Commission of China. 10 (24.4%) patients had underlying complications, such as hypertension HP hypertension MESHD, CAD, type 2 diabetes mellites MESHD and tumor MESHD. The peak value of TnI in critical patients is 40-fold more than normal value. 2 patients in the critical group had the onset of atrial fibrillation HP atrial fibrillation MESHD, and the peak heart rates reached up to 160 bpm. CT scan showed low EAT density in severe and critical patients. Conclusion: Our results indicated that cardiac injury MESHD of COVID-2019 was rare in light and mild patients, while common in severe and critical patients. Therefore, the monitoring of the heart functions of COVID-2019 patients and applying potential interventions for those with abnormal cardiac injury MESHD related characteristics, is vital to prevent the fatality.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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