Risk factors associated with indoor transmission during home quarantine of COVID-19 patients.

Purpose: The study aimed to identify potential risk factors for family transmission and to provide precautionary guidelines for the general public during novel Coronavirus disease 2019 (COVID-19) waves. Methods: A retrospective cohort study with numerous COVID-19 patients recruited was conducted in Shanghai. Epidemiological data including transmission details, demographics, vaccination status, symptoms, comorbidities, antigen test, living environment, residential ventilation, disinfection and medical treatment of each participant were collected and risk factors for family transmission were determined. Results: A total of 2,334 COVID-19 patients participated. Compared with non-cohabitation infected patients, cohabitated ones were younger (p = 0.019), more commonly unvaccinated (p = 0.048) or exposed to infections (p < 0.001), and had higher rates of symptoms (p = 0.003) or shared living room (p < 0.001). Risk factors analysis showed that the 2019-nCov antigen positive (OR = 1.86, 95%CI 1.40-2.48, p < 0.001), symptoms development (OR = 1.86, 95%CI 1.34-2.58, p < 0.001), direct contact exposure (OR = 1.47, 95%CI 1.09-1.96, p = 0.010) were independent risk factors for the cohabitant transmission of COVID-19, and a separate room with a separate toilet could reduce the risk of family transmission (OR = 0.62, 95%CI 0.41-0.92, p = 0.018). Conclusion: Patients showing negative 2019-nCov antigen tests, being asymptomatic, living in a separate room with a separate toilet, or actively avoiding direct contact with cohabitants were at low risk of family transmission, and the study recommended that avoiding direct contact and residential disinfection could reduce the risk of all cohabitants within the same house being infected with COVID-19.

Review and Thinking on Forensic Pathological Changes of Coronavirus-Infected Diseases.

Since the beginning of this century, three types of coronavirus have widely transmitted and caused severe diseases and deaths, which strongly indicates that severe infectious diseases caused by coronavirus infection are not accidental events. Coronavirus-infected diseases are mainly manifested by respiratory symptoms, with multiple organ dysfunctions. Precisely investigating the pathological process, characteristics and pathogenesis of coronavirus-infected diseases will be beneficial for us to understand clinical manifestations and provide targeted suggestions on prophylaxis and treatment. This paper briefly reviews the pathological findings of three known coronavirus-infected diseases, and attempts to construct the pathological spectrum of coronavirus-infected diseases, aiming to provide reference and thinking for autopsy, histopathological examination and animal infection model study of coronavirus-infected diseases.

Global Cold-Chain Related SARS-CoV-2 Transmission (preprint)

The COVID-19 pandemic poses a great threat to human society. SARS-CoV-2 is mainly transmitted through social contact; however, it is highly debated whether cold-chain related transmission has occurred and can be identified in the epidemic areas of COVID-19. Here, we provide a new method and distinguish two transmission routes by detecting a lineage-specific reduction of SARS-CoV-2 mutation rate. After analyzing 1,610,125 SARS-CoV-2 genomic sequences, we find that two outbreaks in Xinfadi-Beijing and Auckland are cold-chain related and respectively caused by two mutation-dormant variants. A Dalian outbreak in July 2020 and a Yingkou outbreak ten months later are epidemiologically connected and derived from a cold-chain related variant. Mutation-dormant variants are detected during the spread of spike D614G variant and the Delta Variant of Concern. Cold-chain contaminations repeatedly caused by epidemiologically connected patients are also found and have resulted in infections. Moreover, the COVID-19 outbreak in Wuhan is likely to be cold-chain related. A systematic identification reveals that the frequency of cold-chain related transmission is in the order of magnitude of 0.1-10%. Our results indicate that that cold-chain related transmission is rare but happens globally.

Association between tachyarrhythmia and mortality in a cohort of critically ill patients with coronavirus disease 2019 (COVID-19).

BACKGROUND: Cardiovascular involvement manifesting as arrhythmias has been confirmed in patients with coronavirus disease 2019 (COVID-19), so we aimed to explore the association between primary tachyarrhythmia and death in critically ill patients with COVID-19 in this retrospective study. METHODS: A total of 79 critically ill patients with COVID-19 were included. Demographic characteristics, clinical data (past history, vital signs, therapeutic management, and outcomes), and results of laboratory findings and cardiac investigations were collected. All statistical analyses were performed using SPSS 23.0 software (IBM, Armonk, NY, USA). RESULTS: The median age was 65±12 years, and 53 patients (67%) were male. A total of 57 (72%) patients died, and compared with survivors, these patients were older and had significantly higher Acute Physiology and Chronic Health Evaluation (APACHE) II score, Sequential Organ Failure Assessment (SOFA) score and fewer lymphocytes as well as higher heart rate (P<0.05). Autopsy findings did not suggest severe myocarditis. A total of 19 (24%) patients had tachyarrhythmias, including 10 (13%) with atrial fibrillation (AF) and 9 (11%) with ventricular tachycardia or fibrillation. The incidence of tachyarrhythmias in non-survivor was much higher than in survivors (P=0.04). In a Cox regression model, older patients with ventricular tachyarrhythmias (VTAs) age were at a higher risk of death, with hazard ratio (HR) of 3.302 [95% confidence interval (CI), 1.524-7.154, P=0.002] and 1.045 (95% CI, 1.020-1.071, P=0.000), respectively. The use of beta-blockers [HR, 0.219 (95% CI, 0.066-0.722); P=0.013] was associated with a lower risk of death. CONCLUSIONS: Critically ill patients with COVID-19 had a poor prognosis. VTA and older age were independent prognostic factors of death. Beta-blockers might be an effective therapy to improve survival.

Myocardial Injury on Admission as a Risk in Critically Ill COVID-19 Patients: A Retrospective in-ICU Study.

OBJECTIVE: The aim of this study was to investigate the incidence, clinical presentation, cardiovascular (CV) complications, and mortality risk of myocardial injury on admission in critically ill intensive care unit (ICU) inpatients with COVID-19. DESIGN: A single-center, retrospective, observational study. SETTING: A newly built ICU in Tongji hospital (Sino-French new city campus), Huazhong University of Science and Technology, Wuhan, China. PARTICIPANTS: Seventy-seven critical COVID-19 patients. INTERVENTIONS: Patients were divided into a myocardial injury group and nonmyocardial injury group according to the on-admission levels of high-sensitivity cardiac troponin I. MEASUREMENTS AND MAIN RESULTS: Demographic data, clinical characteristics, laboratory tests, treatment, and clinical outcome were evaluated, stratified by the presence of myocardial injury on admission. Compared with nonmyocardial injury patients, patients with myocardial injury were older (68.4 ± 10.1 v 62.1 ± 13.5 years; p = 0.02), had higher prevalence of underlying CV disease (34.1% v 11.1%; p = 0.02), and in-ICU CV complications (41.5% v 13.9%; p = 0.008), higher Acute Physiology and Chronic Health Evaluation II scores (20.3 ± 7.3 v 14.4 ± 7.4; p = 0.001), and Sequential Organ Failure Assessment scores (7, interquartile range (IQR) 5-10 v 5, IQR 3-6; p < 0.001). Myocardial injury on admission increased the risk of 28-day mortality (hazard ratio [HR], 2.200; 95% confidence interval [CI] 1.29 to 3.74; p = 0.004). Age ≥75 years was another risk factor for mortality (HR, 2.882; 95% CI 1.51-5.50; p = 0.002). CONCLUSION: Critically ill patients with COVID-19 had a high risk of CV complications. Myocardial injury on admission may be a common comorbidity and is associated with severity and a high risk of mortality in this population.

Coronavirus GenBrowser for monitoring adaptive evolution and transmission of SARS-CoV-2 (preprint)

COVID-19 has widely spread across the world, and much research is being conducted on the causative virus SARS-CoV-2. To help control the infection, we developed the Coronavirus GenBrowser (CGB) to monitor the pandemic. CGB allows visualization and analysis of the latest viral genomic data. Distributed genome alignments and an evolutionary tree built on the existing subtree are implemented for easy and frequent updates. The tree-based data are compressed at a ratio of 2,760:1, enabling fast access and analysis of SARS-CoV-2 variants. CGB can effectively detect adaptive evolution of specific alleles, such as D614G of the spike protein, in their early stage of spreading. By lineage tracing, the most recent common ancestor, dated in early March 2020, of nine strains collected from six different regions in three continents was found to cause the outbreak in Xinfadi, Beijing, China in June 2020. CGB also revealed that the first COVID-19 outbreak in Washington State was caused by multiple introductions of SARS-CoV-2. To encourage data sharing, CGB credits the person who first discovers any SARS-CoV-2 variant. As CGB is developed with eight different languages, it allows the general public in many regions of the world to easily access pre-analyzed results of more than 132,000 SARS-CoV-2 genomes. CGB is an efficient platform to monitor adaptive evolution and transmission of SARS-CoV-2.

Clinical characteristics and survival analysis in critical and non-critical patients with COVID-19 in Wuhan, China: a single-center retrospective case control study.

Since the outbreak of COVID-19 in China at the end of 2019, the world has experienced a large-scale epidemic caused by the SARS-CoV-2. The epidemiological and clinical course of COVID-19 patients has been reported, but there have been few analyses about the characteristics, predictive risk factors, and outcomes of critical patients. In this single-center retrospective case-control study, 90 adult inpatients hospitalized at Tongji Hospital (Wuhan, China) were included. Demographic, clinical, laboratory tests, and treatment data were obtained and compared between critical and non-critical patients. We found that compared with non-critical patients, the critical patients had higher SOFA score and qSOFA scores. Critical patients had lower lymphocyte and platelet count, elevated D-dimer, decreased fibrinogen, and elevated high-sensitivity C-reactive protein (hsCRP), and interleukin-6(IL-6). More critical patients received treatment including antibiotics, anticoagulation, corticosteroid, and oxygen therapy than non-critical ones. Multivariable regression showed higher qSOFA score and elevation of IL-6 were related to critical patients. Antibiotic usage and anticoagulation were associated with decreased in-hospital mortality. And critical grouping contributed greatly to in-hospital death. Critical COVID-19 patients have a more severe clinical course. qSOFA score and elevation of IL-6 are risk factors for critical condition. Non-critical grouping, positive antibiotic application, and anticoagulation may be beneficial for patient survival.

Swollen heart in COVID-19 patients who progress to critical illness: a perspective from echo-cardiologists.

AIMS: Cardiac complications are common and associated with mortality in critically ill patients with COVID-19; however, the diagnostic and prognostic implications of critical care echocardiography (CCE) have not been studied. METHODS AND RESULTS: A cohort of 43 patients with COVID-19 who were in the intensive care unit (ICU) underwent bedside CCE during their disease course. Demographic, clinical, and survival data were collected. The echocardiographic analyses revealed high frequencies of pericardial effusion (90.7%), increased left ventricular mass index (60.5%), elevated relative wall thickness (76.7%), and reduced left ventricular stroke volume index (LVSVi; 53.5%) and cardiac index (51.2%). Twenty-two (51.2%) patients died in the ICU. In multivariate Cox regression, the strongest predictor of in-ICU death was decreased cardiac index [hazard ratio (HR), 0.67, 95% confidence interval (CI), 0.45-0.98; P = 0.041], after adjusting for male sex, shock status, high-sensitivity cardiac troponin I, and N-terminal pro-B-type natriuretic peptide. Negative associations with mortality were observed for LVSVi (HR, 0.91, 95% CI 0.85-0.96; P = 0.002), tricuspid annular plane systolic excursion (HR, 0.74, 95% CI 0.64-0.84; P < 0.001), and S' (HR, 0.78, 95% CI 0.69-0.88; P < 0.001). Kaplan-Meier analyses indicated that reductions in LVSVi, cardiac index, TAPSE, and S' were associated with a shorter survival time. CONCLUSIONS: Pericardial effusion and increased ventricular mass in COVID-19 might indicate a swollen heart. Both left and right heart dysfunction and a reduced cardiac index may lead to an increased risk of mortality. Clinicians should pay special attention to cardiac haemodynamic disorders in critical patients with COVID-19.

High Inflammatory Burden: A Potential Cause of Myocardial Injury in Critically Ill Patients With COVID-19.

Background: Myocardial injury is a severe complication of novel coronavirus disease (COVID-19), and inflammation has been suggested as a potential cause of myocardial injury. However, the correlation of myocardial injury with inflammation in COVID-19 patients has not been revealed so far. Method: This retrospective single-center cohort study enrolled 64 critically ill patients with COVID-19. Patients were categorized into two groups by the presence of myocardial injury on admission. Demographic data, clinical characteristics, laboratory tests, treatments, and outcomes were analyzed in this study. Result: Of these patients, the mean age was 64.8 ± 12.2 years old, and 34 (53.1%) were diagnosed with myocardial injury. Compared with non-myocardial injury patients, myocardial injury patients were older (67.8 ± 10.3 vs. 61.3 ± 13.3 years; P = 0.033), had more cardiovascular (CV) risk factors such as smoking (16 [47.06%] vs. 7 [23.33%]; P = 0.048) and were more likely to develop CV comorbidities (13 [38.2%] vs. 2 [6.7%]; P = 0.003). Scores on the Acute Physiology and Chronic Health Evaluation II (median [interquartile range (IQR)] 19.0 [13.25-25.0] vs. 13.0 [9.25-18.75]; P = 0.005) and Sequential Organ Failure Assessment systems (7.0 [5.0-10.0] vs. 4.5 [3.0-6.0]; P < 0.001) were significantly higher in the myocardial injury group. In addition, patients with myocardial injury had higher mortality than those without myocardial injury (29 [85.29%] vs. 18 [60.00%]; P = 0.022). Cox regression suggested that myocardial injury was an independent risk factor for high mortality during the time from admission to death (hazard ratio [HR], 2.06 [95% confidence interval (CI), 1.10-3.83]; P = 0.023). Plasma levels of high-sensitivity C-reactive protein (hs-CRP), interleukin (IL)-1ß, interleukin-2 receptor (IL-2R), IL-6, IL-8, IL-10, and tumor necrosis factor-α (TNF-α) exceeded the normal limits, and levels of hs-CRP, IL-2R, IL-6, IL-8, and TNF-α were statistically higher in the myocardial injury group than in the non-myocardial injury group. Multiple-variate logistic regression showed that plasma levels of hs-CRP (odds ratio [OR] 6.23, [95% CI, 1.93-20.12], P = 0.002), IL-6 (OR 13.63, [95% CI, 3.33-55.71]; P < 0.001) and TNF-α (OR 19.95, [95% CI, 4.93-80.78]; P < 0.001) were positively correlated with the incidence of myocardial injury. Conclusion: Myocardial injury is a common complication that serves as an independent risk factor for a high mortality rate among in-ICU patients with COVID-19. A high inflammatory burden may play a potential role in the occurrence of myocardial injury.