Wide QRS Complex and Lateral ST-T Segment Abnormality Are Associated With Worse Clinical Outcomes in COVID-19 Patients

BackgroundThe information on electrocardiographic features of patients with coronavirus disease 2019 (COVID-19) is limited. Our aim was to determine if baseline electrocardiographic features of hospitalized COVID-19 patients are associated with markers of myocardial injury and clinical outcomes.MethodsIn this retrospective, single center cohort study, we included 223 hospitalized patients with laboratory-confirmed COVID-19. Clinical, electrocardiographic and laboratory data were collected and analyzed. Primary composite endpoint of mortality, need for invasive mechanical ventilation, or admission to the intensive care unit was assessed.ResultsForty patients (17.9%) reached the primary composite endpoint. Patients with the primary composite endpoint were more likely to have wide QRS complex (>120 ms) and lateral ST-T segment abnormality. The multivariable Cox regression showed increasing odds of the primary composite endpoint associated with acute respiratory distress syndrome (odds ratio 7.76, 95% CI 2.67–22.59; p < 0.001), acute cardiac injury (odds ratio 3.14, 95% CI 1.26–7.99; p = 0.016), high flow oxygen therapy (odds ratio 2.43, 95% CI 1.05–5.62; p = 0.037) and QRS duration longer than >120 ms (odds ratio 3.62, 95% CI 1.39–9.380; p = 0.008) Patients with a wide QRS complex (>120 ms) had significantly higher median level of troponin T and pro-BNP than those without it. Patients with abnormality of lateral ST-T segment had significantly higher median level of troponin T and pro-BNP than patients without.ConclusionsThe presence of QRS duration longer than 120 ms and lateral ST-T segment abnormality were associated with worse clinical outcomes and higher levels of myocardial injury biomarkers.     

The Impact of COVID-19 Patients With Troponin Elevation on Renal Impairment and Clinical Outcome

BackgroundCardiac involvement in coronavirus disease 2019 (COVID-19) is known, manifested by troponin elevation, and these patients have a worse prognosis than patients without myocardial injury.MethodsWe analyzed COVID-19-positive patients who presented to the MedStar Health system (11 hospitals in Washington, DC, and Maryland) during the pandemic (March 1–September 30, 2020). We compared renal function and subsequent in-hospital clinical outcomes based on the presence or absence of troponin elevation. The primary outcome was the incidence of acute kidney injury in COVID-19 patients with troponin elevation. We also evaluated in-hospital mortality, overall and based on the presence and absence of both troponin elevation and renal dysfunction.ResultsThe cohort included 3386 COVID-19-positive admitted patients for whom troponin was drawn. Of these patients, 195 had troponin elevation (defined as ≥1.0 ng/mL), mean age was 61 ± 16 years, and 51% were men. In-hospital mortality was significantly higher (53.8%) in COVID-19-positive patients with concomitant troponin elevation than in those without troponin elevation (14.5%; p < 0.001). COVID-19-positive patients with troponin elevation had a higher prevalence of renal dysfunction (58.5%) than those without troponin elevation (23.4%; p < 0.001). Further analysis demonstrated that having both troponin elevation and renal dysfunction carried the worst in-hospital prognosis (in-hospital mortality 57.9%; intensive-care-unit admission 76.8%; ventilation requirement 63.2%), as compared to the absence or presence of either.ConclusionCOVID-19 patients with troponin elevation are at higher risk for worsening renal function, and these patients subsequently have worse in-hospital clinical outcomes. Efforts should focus on early recognition, evaluation, and intensifying care of these patients.     

Biomarcadores de Lesão Miocárdica e Complicações Cardíacas Associadas à Mortalidade em Pacientes com COVID-19

BackgroundSARS-CoV-2 is an emerging RNA virus associated with a severe acute respiratory disease known as COVID-19. Although COVID-19 is predominantly a pulmonary disease, some patients have severe cardiovascular damage. We performed a quantitative evidence synthesis of clinical data, myocardial injury biomarkers, and cardiac complications associated with in-hospital death in patients with COVID-19.MethodsWe searched the databases PubMed, Embase, and Google Scholar to identify studies comparing clinical data, myocardial injury biomarkers, and cardiac complications between non-survivors and survivors of COVID-19. Effect sizes were reported as mean difference or standardized mean difference for continuous variables and risk ratio for dichotomous variables with 95% confidence intervals. A random effects model was used to pool the results.ResultsSix retrospective studies reporting data from 1,141 patients (832 survivors and 309 non-survivors) were included. We found that underlying cardiovascular conditions; elevation of high-sensitivity cardiac troponin I, N-terminal pro-B-type natriuretic peptide, and creatine kinase-MB; and cardiac complications were associated with increased risk of death for patients with SARS-CoV-2 infection.ConclusionsThe confirmation that underlying cardiovascular conditions, elevation of myocardial injury biomarkers during COVID-19 infection, and acute cardiovascular decompensation are predictors for mortality in SARS-CoV-2 infection must encourage new research to clarify potential mechanisms and test appropriate treatments. (Arq Bras Cardiol. 2020; 115(2):273-277)     

Single-center experience of patients with interstitial lung diseases during the early days of the COVID-19 pandemic

IntroductionPatients with interstitial lung diseases (ILD) can be suspected to be at risk of experiencing a rapid flare-up due to COVID-19. However, no specific data are currently available for these patients.MethodsWe retrospectively analyzed a cohort of 401 patients with ILD and determined the proportion of patients hospitalized for proven severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and specific symptoms of COVID-19.ResultsWe found that 1% of patients (n = 4) were hospitalized (1 in ICU) for COVID-19. In total, 310 of the 401 patients answered the phone call. Only 33 patients (0.08%) experienced specific symptoms of SARS-CoV-2 infection.ConclusionOur study did not demonstrate any increased occurrence of severe COVID-19 in ILD patients compared to the global population. Based on our findings, we could not make any conclusion on the incidence rate of SARS-CoV-2 infection in patients with ILDs, or on the overall outcome of immunocompromised patients affected by COVID-19.     

COVID-19 in immunocompromised patients: A systematic review of cancer,hematopoietic cell and solid organ transplant patients

BackgroundThe clinical impact of severe coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), in immunocompromised patients has not been systematically evaluated.MethodsWe reviewed current literature reporting on COVID-19 in cancer (CA), hematopoietic cell (HCT), and solid organ transplant (SOT) patients and compared their clinical data and outcomes to the general population. For adult CA, HCT and SOT patients, an extensive search strategy retrieved all articles published until July 20, 2020 by combining the terms coronavirus, coronavirus infection, COVID-19, and SARS-CoV-2 in PubMed, Cochrane, and Web of Science, and following the Preferred Reporting Items for Systematic Reviews and Meta-analysis guidelines. For the pediatric CA cohort, a global COVID-19 registry was used. For the general population cohort, a large meta-analysis was used to compare pooled prevalence estimates, and two large meta-analyses were utilized to serve as pooled comparators for hospitalized COVID-19 patients.FindingsCompared to the general population, adult CA and SOT patients with COVID-19 had higher comorbidities, greater levels of inflammatory markers at diagnosis, and higher rates of intensive care and hospital mortality. Pediatric CA patients and HCT patients with COVID-19 tended to have clinical presentations and outcomes similar to the general population.InterpretationTo our knowledge, this is the first systematic review evaluating COVID-19 phenotype and outcomes in immunocompromised patients and comparing them to the general population, which shows that hospital outcomes appear to be worse in adult CA and SOT patients, potentially due to their higher co-morbidity burden.FundingNone     

Structural Cardiac Abnormalities in Patients with Atrial Fibrillation/Flutter and Myocardial Injury

BackgroundHigh-sensitivity cardiac troponin (hs-cTnT) is often increased in patients with atrial fibrillation/flutter, portending a poor prognosis. The etiologies for these increases have not been systematically investigated. Our aim was to define prevalence/significance of structural cardiac abnormalities in patients with atrial fibrillation/flutter and high-sensitivity cardiac troponin T (hs-cTnT) increases.MethodsThis is a retrospective observational cohort study of patients with atrial fibrillation/flutter diagnosis with hs-cTnT measurements, echocardiograms, and coronary angiograms. Myocardial injury was defined as hs-cTnT >10 ng/L for women and >15 ng/L for men. Cases with myocardial injury were adjudicated according to the Fourth Universal Definition of Myocardial Infarction.ResultsPatients with definite causes for increased hs-cTnT (n = 875) were tabulated but not evaluated further; common diagnoses were type 1 myocardial infarction, critical illness, and known heart failure. Of the remaining 401, increased hs-cTnT was present in 336 (84%) patients. Of those, 78% had nonischemic myocardial injury, the remaining (n = 75, 22%) had type 2 myocardial infarction. Patients with elevated hs-cTnT had greater left ventricular mass index, left ventricular filling pressures, and right ventricular systolic pressure. They more frequently had significant coronary artery disease (47% vs 31%, P = .016), especially in type 2 myocardial infarction. With logistic regression, age, sex (F), diabetes, left ventricular mass index, e′ medial velocity, and right ventricular systolic pressure were independent determinants of myocardial injury. One-year mortality was higher in patients with myocardial injury.ConclusionsStructural heart abnormalities are common in patients with atrial fibrillation/flutter and increased hs-cTnT. Causes of myocardial injury should be elucidated in each patient to craft appropriate therapies.     

Clinical Impact and Predictors of Troponin Elevation in Patients With COVID-19

BackgroundCardiac involvement in coronavirus disease 2019 (COVID-19) is known, manifested by troponin elevation. Studies in the initial phase of the pandemic demonstrated that these patients tended to have a worse prognosis than patients without myocardial injury. We sought to evaluate the clinical impact of significant troponin elevation in COVID-19-positive patients, along with predictors of poor outcomes, over the span of the pandemic to date.MethodsWe analyzed COVID-19-positive patients who presented to the MedStar Health system (11 hospitals in Washington, DC, and Maryland) during the pandemic (March 1–June 30, 2020). We compared clinical course and outcomes based on the presence of troponin elevation and identified predictors of mortality.ResultsThe cohort included 2716 COVID-19-positive admitted patients for whom troponin was drawn. Of these patients, 250 had troponin elevation (≥1.0 ng/mL). In the troponin-elevation arm, the minimum troponin level was 1.9 ± 8.82 ng/mL; maximum elevation was 10.23 ± 31.07 ng/mL. The cohort's mean age was 68.0 ± 15.0 years; 52.8% were men. Most (68.5%) COVID-19-positive patients with troponin elevation were African American. Patients with troponin elevation tended to be older, with more co-morbidities, and most required mechanical ventilation. In-hospital mortality was significantly higher (48.4%) in COVID-19-positive patients with concomitant troponin elevation than without troponin elevation (12.2%; p < 0.001).ConclusionCOVID-19 patients with troponin elevation are at higher risk for mechanical ventilation and mortality. Efforts should focus on early recognition, evaluation, and intensifying care of these patients.     

Peripheral Plasma Cells Associated with Mortality Benefit in Severe COVID-19: A Marker of Disease Resolution

BackgroundCytokines seen in severe coronavirus disease 2019 (COVID-19) are associated with proliferation, differentiation, and survival of plasma cells. Plasma cells are not routinely found in peripheral blood, though may produce virus-neutralizing antibodies in COVID-19 later in the course of an infection.MethodsUsing the Johns Hopkins COVID-19 Precision Medicine Analytics Platform Registry, we identified hospitalized adult patients with confirmed severe acute respiratory coronavirus 2 (SARS-CoV-2) infection and stratified by presence of plasma cells and World Health Organization (WHO) disease severity. To identify plasma cells, we employed a sensitive flow cytometric screening method for highly fluorescent lymphocytes and confirmed these microscopically. Cox regression models were used to evaluate time to death and time to clinical improvement by the presence of plasma cells in patients with severe disease.ResultsOf 2301 hospitalized patients with confirmed infection, 371 had plasma cells identified. Patients with plasma cells were more likely to have severe disease, though 86.6% developed plasma cells after onset of severe disease. In patients with severe disease, after adjusting for age, sex, body mass index, race, and other covariates associated with disease severity, patients with plasma cells had a reduced hazard of death (adjusted hazard ratio: 0.57; 95% confidence interval: 0.38-0.87; P value: .008). There was no significant association with the presence of plasma cells and time to clinical improvement.ConclusionsPatients with severe disease who have detectable plasma cells in the peripheral blood have improved mortality despite adjusting for known covariates associated with disease severity in COVID-19. Further investigation is warranted to understand the role of plasma cells in the immune response to COVID-19.     

COVID-19 and liver injury: An ongoing challenge

The new coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was identified in December 2019, in Wuhan, China. The virus was rapidly spread worldwide, causing coronavirus disease 2019 (COVID-19) pandemic. Although COVID-19 is presented, usually, with typical respiratory symptoms (i.e., dyspnea, cough) and fever, extrapulmonary manifestations are also encountered. Liver injury is a common feature in patients with COVID-19 and ranges from mild and temporary elevation of liver enzymes to severe liver injury and, even, acute liver failure. The pathogenesis of liver damage is not clearly defined; multiple mechanisms contribute to liver disorder, including direct cytopathic viral effect, cytokine storm and immune-mediated hepatitis, hypoxic injury, and drug-induced liver toxicity. Patients with underlying chronic liver disease (i.e., cirrhosis, non-alcoholic fatty liver disease, alcohol-related liver disease, hepatocellular carcinoma, etc.) may have greater risk to develop both severe COVID-19 and further liver deterioration, and, as a consequence, certain issues should be considered during disease management. The aim of this review is to present the prevalence, clinical manifestation and pathophysiological mechanisms of liver injury in patients with SARS-CoV-2 infection. Moreover, we overview the association between chronic liver disease and SARS-CoV-2 infection and we briefly discuss the management of liver injury during COVID-19.     

The impact of coronavirus disease 2019 (COVID-19) on liver injury in China: A systematic review and meta-analysis

Introduction:The evidence for the incidence and severity of liver injury in Chinese patients with coronavirus disease 2019 (COVID-19) is still controversial. The purpose of this study was to summarize the incidence of liver injury and the differences between liver injury markers among different patients with COVID-19 in China.Methods:Computer searches of PubMed, Embase, China National Knowledge Infrastructure (CNKI) and medRxiv were used to obtain reports on the incidence and markers of liver injury in Chinese patients with COVID-19, from January 1, 2020 to April 10, 2020. (No. CRD42020181350)Results:A total of 57 reports from China were included, including 9889 confirmed cases of COVID-19 infection. The results of the meta-analysis showed that among the patients with early COVID-19 infection in China, the incidence of liver injury events was 24.7% (95% CI, 23.4%–26.4%). Liver injury in severe patients was more common than that in non-severe patients, with a risk ratio of 2.07 (95% CI, 1.77–2.43). Quantitative analysis showed that the severe the coronavirus infection, the higher the level of alanine aminotransferase (ALT), aspertate aminotransferase (AST), total bilirubin (TB), alkaline phosphatase (ALP), γ-glutamyl transpeptidase (GGT), and the lower the level of albumin (ALB).Conclusion:There is a certain risk of liver injury in Chinese patients with COVID-19, and the risk and degree of liver injury are related to the severity of COVID-19.     

Distribution of spreading viruses during COVID-19 pandemic: Effect of mitigation strategies

BackgroundThe study aimed to evaluate the distribution of circulating respiratory viral pathogens other than severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) during the first year of the coronavirus disease-2019 (COVID-19) pandemic with especially focusing on the effects of the national-based mitigation strategies.MethodsThis single-center study was conducted between March 11, 2020-March 11, 2021. All children who were tested by polymerase chain reaction on nasopharyngeal swabs for SARS-CoV-2 and other common respiratory viral pathogens were included in the study.ResultsA total of 995 children with suspected COVID-19 admitted to the study center. Of these, 513 patients who were tested by polymerase chain reaction for both SARS-CoV-2 and common respiratory viral pathogens were included in the final analysis. Two hundred ninety-five patients were (57.5%) male. The median age was 3 years of age (27 days-17 years). A total of 321 viral pathogens identified in 310 (n: 310/513, 60.4%) patients, and 11 of them (n: 11/310, 3.5%) had co-detection with more than 1 virus. The most common detected virus was rhinovirus (n: 156/513, 30.4%), and SARS-CoV-2 (n: 122/513, 23.8%) followed by respiratory syncytial virus (n: 18/513, 3.5%). The influenza virus was detected in 2 patients (0.4%). A total of 193 patients were negative for both SARS-CoV-2 and other pathogens.ConclusionsThere is a decline in the frequency of all viral pathogens like SARS-CoV-2 in correlation with the national-based mitigation strategies against COVID-19 during the pandemic.     

High fecal calprotectin levels are associated with SARS-CoV-2 intestinal shedding in COVID-19 patients: A proof-of-concept study

BACKGROUNDOne third of coronavirus disease 2019 (COVID-19) patients have gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA has been detected in stool samples of approximately 50% of COVID-19 individuals. Fecal calprotectin is a marker of gastrointestinal inflammation in the general population.AIMTo investigate if fecal calprotectin correlates with SARS-CoV-2 intestinal shedding in COVID-19 patients with pneumonia.METHODSPatients with SARS-CoV-2 pneumonia admitted to the Infectious Disease Unit (University Hospital of Trieste, Italy) from September to November 2020 were consecutively enrolled in the study. Fecal samples were collected and analyzed for quantification of fecal calprotectin (normal value < 50 mg/kg) and SARS-CoV-2 RNA presence by polymerase chain reaction (PCR). Inter-group differences were determined between patients with and without diarrhea and patients with and without detection of fecal SARS-CoV-2.RESULTSWe enrolled 51 adults (40 males) with SARS-CoV-2 pneumonia. Ten patients (20%) presented with diarrhea. Real-time-PCR of SARS-CoV-2 in stools was positive in 39 patients (76%), in all patients with diarrhea (100%) and in more than two thirds (29/41, 71%) of patients without diarrhea. Obesity was one of the most common comorbidities (13 patients, 25%); all obese patients (100%) (P = 0.021) tested positive for fecal SARS-CoV-2. Median fecal calprotectin levels were 60 mg/kg [interquartile range (IQR) 21; 108]; higher fecal calprotectin levels were found in the group with SARS-CoV-2 in stools (74 mg/kg, IQR 29; 132.5) compared to the group without SARS-CoV-2 (39 mg/kg, IQR 14; 71) (P < 0.001).CONCLUSIONHigh fecal calprotectin levels among COVID-19 patients correlate with SARS-CoV-2 detection in stools supporting the hypothesis that this virus can lead to bowel inflammation and potentially to the ‘leaky gut’ syndrome.     

Metabolic syndrome and the risk of COVID-19 infection: A nationwide population-based case-control study

Background and aimsMetabolic syndrome (MetS) is a chronic, low-grade inflammatory disease. This study aimed to investigate the impact of MetS on the risk and severity of COVID-19.Methods and resultsWe investigated a nationwide cohort with COVID-19 including all patients who underwent the test for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in Korea. The COVID-19 group included 4070 patients with positive SARS-CoV-2 test results, and the age- and sex-matched control group included 27,618 subjects with negative SARS-CoV-2 test results. The endpoints were SARS-CoV-2 positivity and the severity of COVID-19. The prevalence of MetS was 24.7% and 24.5% in the COVID-19 and control groups, respectively. The presence of MetS was not associated with the risk of developing COVID-19. Among the components of MetS, central obesity was associated with a higher risk of COVID-19 infection (adjusted odds ratio [aOR], 1.17; 95% confidence interval [CI], 1.06–1.28, P = 0.001). The presence of MetS was significantly associated with severe COVID-19 (aOR, 1.25; 95% CI, 0.78–2.00, P = 0.352). Among the individual components of MetS, prediabetes/diabetes mellitus was associated with a higher risk of severe COVID-19 (aOR, 1.61; 95% CI, 1.21–2.13, P = 0.001). The risk of severe COVID-19 linearly increased according to the number of metabolic components (P for trend = 0.005).ConclusionIn this nationwide cohort study, the individuals with MetS had a significant increase in the risk of severe COVID-19 infection. These patients, particularly those with central obesity and insulin resistance, deserve special attention amid the COVID-19 pandemic.     

Epidemiology of Acute Heart Failure in Critically Ill Patients With COVID-19: An Analysis From the Critical Care Cardiology Trials Network

BackgroundAcute heart failure (HF) is an important complication of coronavirus disease 2019 (COVID-19) and has been hypothesized to relate to inflammatory activation.MethodsWe evaluated consecutive intensive care unit (ICU) admissions for COVID-19 across 6 centers in the Critical Care Cardiology Trials Network, identifying patients with vs without acute HF. Acute HF was subclassified as de novo vs acute-on-chronic, based on the absence or presence of prior HF. Clinical features, biomarker profiles and outcomes were compared.ResultsOf 901 admissions to an ICU due to COVID-19, 80 (8.9%) had acute HF, including 18 (2.0%) with classic cardiogenic shock (CS) and 37 (4.1%) with vasodilatory CS. The majority (n = 45) were de novo HF presentations. Compared to patients without acute HF, those with acute HF had higher cardiac troponin and natriuretic peptide levels and similar inflammatory biomarkers; patients with de novo HF had the highest cardiac troponin levels. Notably, among patients critically ill with COVID-19, illness severity (median Sequential Organ Failure Assessment, 8 [IQR, 5–10] vs 6 [4–9]; P = 0.025) and mortality rates (43.8% vs 32.4%; P = 0.040) were modestly higher in patients with vs those without acute HF.ConclusionsAmong patients critically ill with COVID-19, acute HF is distinguished more by biomarkers of myocardial injury and hemodynamic stress than by biomarkers of inflammation.     

Hepatocellular injury and the mortality risk among patients with COVID-19: A retrospective cohort study

BACKGROUNDClearly, infection with severe acute respiratory syndrome coronavirus 2 is not limited to the lung but also affects other organs. We need predictive models to determine patients’ prognoses and to improve health care resource allocation during the coronavirus disease 2019 (COVID-19) pandemic. While treating COVID-19, we observed differential outcome prediction weights for markers of hepatocellular injury among hospitalized patients.AIMTo investigate the association between hepatocellular injury and all-cause in-hospital mortality among patients with COVID-19.METHODSThis multicentre study employed a retrospective cohort design. All adult patients admitted to Al-Azhar University Hospital, Assiut, Egypt and Abo Teeg General Hospital, Assiut, Egypt with confirmed COVID-19 from June 1, 2020, to July 30, 2020 were eligible. We categorized our cohort into three groups of (1) patients with COVID-19 presenting normal aminotransferase levels; (2) patients with COVID-19 presenting one-fold higher aminotransferase levels; and (3) patients with COVID-19 presenting two-fold higher aminotransferase levels. We analysed the association between elevated aminotransferase levels and all-cause in-hospital mortality. The survival analysis was performed using the Kaplan–Meier method and tested by log-rank analysis.RESULTSIn total, 376 of 419 patients met the inclusion criteria, while 29 (8%) patients in our cohort died during the hospital stay. The median age was 40 years (range: 28-56 years), and 51% were males (n = 194). At admission, 54% of the study cohort had liver injury. The pattern of liver injury was hepatocellular injury with an aspartate aminotransferase (AST) predominance. Admission AST levels were independently associated with all-cause in-hospital mortality in the logistic regression analysis. A one-fold increase in serum AST levels among patients with COVID-19 led to an eleven-fold increase in in-hospital mortality (P < 0.001). Admission AST levels correlated with C-reactive protein (r = 0.2; P < 0.003) and serum ferritin (r = 0.2; P < 0.0002) levels. Admission alanine aminotransferase levels correlated with serum ferritin levels (r = 0.1; P < 0.04). Serum total bilirubin levels were independently associated with in-hospital mortality in the binary logistic regression analysis after adjusting for age and sex but lost its statistical significance in the fully adjusted model. Serum ferritin levels were significantly associated with in-hospital mortality (P < 0.01). The probability of survival was significantly different between the AST groups and showed the following order: a two-fold increase in AST levels > a one-fold increase in in AST levels > normal AST levels (P < 0.0001).CONCLUSIONLiver injury with an AST-dominant pattern predicts the severity of COVID-19. Elevated serum ferritin levels are associated with fatal outcomes.     

Marcadores de daño miocárdico en la predicción del pronóstico a corto plazo de los pacientes con COVID-19

Introduction and objectivesCOVID-19 is currently causing high mortality and morbidity worldwide. Information on cardiac injury is scarce. We aimed to evaluate cardiovascular damage in patients with COVID-19 and determine the correlation of high-sensitivity cardiac-specific troponin T (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) with the severity of COVID-19.MethodsWe included 872 consecutive patients with confirmed COVID-19 from February to April 2020. We tested 651 patients for high-sensitivity troponin T (hs-TnT) and 506 for NT-proBNP on admission. Cardiac injury was defined as hs-TnT > 14 ng/L, the upper 99th percentile. Levels of NT-proBNP > 300 pg/mL were considered related to some extent of cardiac injury. The primary composite endpoint was 30-day mortality or mechanical ventilation (MV).ResultsCardiac injury by hs-TnT was observed in 34.6% of our COVID-19 patients. Mortality or MV were higher in cardiac injury than noncardiac injury patients (39.1% vs 9.1%). Hs-TnT and NT-proBNP levels were independent predictors of death or MV (HR, 2.18; 95%CI, 1.23-3.83 and 1.87 (95%CI, 1.05-3.36), respectively) and of mortality alone (HR, 2.91; 95%CI, 1.211-7.04 and 5.47; 95%CI, 2.10-14.26, respectively). NT-ProBNP significantly improved the troponin model discrimination of mortality or MV (C-index 0.83 to 0.84), and of mortality alone (C-index 0.85 to 0.87).ConclusionsMyocardial injury measured at admission was a common finding in patients with COVID-19. It reliably predicted the occurrence of mortality and need of MV, the most severe complications of the disease. NT-proBNP improved the prognostic accuracy of hs-TnT.     

Statins and SARS-CoV-2 disease: Current concepts and possible benefits

Background and aimsInflammation-mediated tissue injury is the major mechanism involved in the pathogenesis of coronavirus disease 2019 (COVID-2019), caused by Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2). Statins have well-established anti-inflammatory, anti-thrombotic and immuno-modulatory effects. They may also influence viral entry into human cells.MethodsA literature search was done using PubMed and Google search engines to prepare a narrative review on this topic.ResultsStatins interact with several different signaling pathways to exert their anti-inflammatory and vasculoprotective effects. They also variably affect cholesterol content of cell membranes and interfere with certain coronavirus enzymes involved in receptor-binding. Both these actions may influence SARS-CoV-2 entry into human cells. Statins also upregulate expression of angiotensin-converting enzyme 2 receptors on cell surfaces which may promote viral entry into the cells but at the same time, may minimize tissue injury through production of angiotensin [1-7]. The net impact of these different effects on COVID-19 pathogenesis is not clear. However, the retrospective clinical studies have shown that statin use is potentially associated with lower risk of developing severe illness and mortality and a faster time to recovery in patients with COVID-19.ConclusionsEarly observations suggest beneficial effect of statin use on the clinical outcomes in COVID-19. Prospective randomized studies as well as well-designed laboratory studies are required to confirm these observations and to elucidate the mechanisms of such benefits, if proven.     

SARS-CoV-2 infection in pregnant women and newborns in two maternity hospitals in Salvador-Bahia,Brazil

The outbreak of the new coronavirus (SARS-CoV-2) causing the coronavirus disease (COVID-19) has spread globally. As of June 18, 2020, a high maternal mortality rate due to SARS-CoV-2 infections was identified in Brazil, representing most of the world cases at that time. An observational, cross-sectional study was performed with pregnant women admitted in two maternity hospitals located in Salvador/Bahia and their newborns, from May 24^th up to July 17^th of 2020. Among 329 pregnant women enrolled at hospital admission, a high prevalence (n=28; 8.5%) of pregnant women with COVID-19 was observed, as well as a high proportion of asymptomatic cases (n=19; 67.9%). Two newborns had detectable SARS-CoV-2 but evolved without abnormalities. This data highlight the importance of identifying pregnant women with COVID-19 for proper isolation measures to prevent in-hospital transmission.     

Liver diseases in COVID-19:Etiology,treatment and prognosis

In December 2019, a novel coronavirus named severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) was identified in Wuhan, China causing coronavirus disease-2019(COVID-19). Numerous studies have shown varying degrees of liver damage in patients infected with SARS-CoV-2. However, in previous case studies of COVID-19, the exact cause of liver injury has not been clearly elucidated, nor is there clear evidence of the interaction between liver injury and COVID-19. This study will analyze the causes of liver injury in COVID-19 and the influence of liver-related complications on the treatment and prognosis of COVID-19.     

The role of androgens in COVID-19

Background and aimThe coronavirus disease 2019 (COVID-19) pandemic is a global health emergency. According to the findings, male patients with COVID-19 infection are at an increased risk for severe complications than females. The causes of this issue are unknown and are most probably multifactorial. Sexual hormones affect the immune system, so estrogen strengthens the immune system, and testosterone suppresses it. Due to the reports of the high prevalence of androgenic alopecia in hospitalized patients with COVID-19 and a higher risk of respiratory disease and increased use of allergy/asthma medications among patients with polycystic ovary syndrome (PCOS) as a hyperandrogenism condition compared with non-PCOS women, this review aimed to evaluate androgens role in COVID-19.Methods42 related articles from 2008 to 2020 were reviewed with the keywords of androgens, hormonal factors, and hair loss in combination with COVID-19 in medical research databases.ResultsThe evidence of transmembrane protease, serine 2 (TMPRSS2) expression in lung tissue, which is an androgen-regulated gene and expressed mainly in the adult prostate may interpret the increased susceptibility of the male gender to severe COVID-19 complications. Moreover, angiotensin-converting enzyme 2 (ACE-2) acts as a functional receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and male hormones are effective in the ACE-2 passageway and simplify SARS-CoV-2 entry into host cells.ConclusionFurther studies on the severity of symptoms in patients with COVID-19 in other hyperandrogenism conditions compared to the control group are recommended.