Evaluation of the prognostic value of the admission ECG in COVID-19 patients: a meta-analysis.

The assessment of the prognostic value of the admission electrocardiography (ECG) (specifically of the duration of the PR and QTc intervals, the QRS complex and the heart rate [HR]) in COVID-19 patients on the basis of nine observational studies (n=1,424) indicates that relatively long duration of the QTc interval and QRS complex, as well as higher HR, are linked to a severe course of COVID-19, which may be of use in risk stratification. Since there are important differences in suggested indicators of adverse prognosis between observational studies, further research is necessary to clarify high-risk criteria.

Prevalence assessment adjusted for laboratory test performance using an example of the COVID-19 serological tests

Assessment of the prevalence of the disease or condition should consider the accuracy of the diagnostic tests. In the context of the new coronavirus infection (COVID-19) pandemic, laboratory testing has been one of the most important components of the overall strategy for the control and prevention of this infection. Seroprevalence studies have been used to assess and monitor the level of population immunity to the virus. In this paper we provide detailed description of the methods to calculate and interpret the accuracy of laboratory tests as well as their sensitivity, specificity, positive-and negative prognostic values of laboratory tests using seroprevalence of COVID-19 studies as an example for better understanding of the methodological issues. The use of the laboratory tests accuracy in prevalence studies has been demonstrated. A sample syntax to calculate confidence intervals for the prevalence estimates using the bootstrap procedure with known absolute values of true positive and true negative results, false positive and false negative results for R software is also provided. Presentation of the prevalence estimates adjusted for test performance indicators with confidence intervals improves comparability of the findings obtained using different serological tests. The article is intended for undergraduate-, postgraduate-, and doctoral students in health sciences working with the assessment of the prevalence (seroprevalence) of diseases or conditions through population-based serological surveys. © 2022, Northern State Medical University. All rights reserved.

Have the number of pulmonary embolism cases increased during the COVID-19 pandemic?

Background. Coagulation disorders, endothelial dysfunction, immobility and dehydration contribute to deep vein throm-bosis (DVT) and pulmonary embolism (PE) in COVID-19 patients. While the prevalence of PE accompanying COVID-19 is high, the number of studies on its long-term effects is limited in literature. Objectives. We expanded this process and aimed to evaluate a one-year period before and during the pandemic. We sought an answer to the question: "Is there a change in the frequency and clinical course of PE?" Material and methods. Retrospectively, all patients admitted to our pulmonology clinic diagnosed with PE between October 2018-2019 (pre-pandemic) and April 2020-2021 (pandemic period) were included in the study. PE patients hospitalized due to COVID-19 infection were not included in the study. Results. The prevalence of PE cases increased by 43% in the first year of the pandemic, and there was no significant difference in terms of symptoms, localisation and extent of thrombus in the pulmonary artery, DVT frequency, systolic pulmonary artery pressure (PABs) values, right heart load, frequency of thrombolytic therapy and mortality rates. A significant decrease was observed in predisposing factors of pulmonary embolism only in the postoperative period (7 patients (77.8%) before the pandemic;2 patients (22.2%) during the pandemic;p = 0.029). Conclusions. PE cases are encountered more frequently during the pandemic process, and no significant change was seen in patient's clinical findings and mortality.

SECRETORY PHOSPHOLIPASE A2: A BIOMARKER OF INFLAMMATION IN AUTOIMMUNE, BACTERIAL AND VIRAL DISEASES.

Secretory phospholipases A2 (sPLA2) represent a large superfamily of enzymes with a molecular weight of 14-19 kDa, including 15 groups and more than 30 isoforms belonging to four types: secretory (sPLA2), cytosolic (cPLA2), calcium-independent (iPLA2) and lipoprotein-associated phospholipase A2 (LP-PLA2, PAF-AH). Eleven species of secretory sPLA2s (IB, IIA, IIC, IID, IIE, IIF, III, V, X, XIIA, and XIIB) have been found in mammals, performing versatile functions and participating in the pathogenesis of a wide range of diseases. On the one hand, sPLA2 may promote elimination of damaged, apoptotic cells by hydrolyzing membrane phospholipids, and exerts a strong bactericidal and antiviral properties, including pronounced effects against antibiotic-resistant strains of microorganisms. In this regard, the use of sPLA2 may represent a new strategy for the treatment of bacterial and viral infections. Moreover, due to the action of sPLA2 on its substrates, a number of biologically active molecules (arachidonic, lysophosphatidic acids, lysophospholipids, fatty acids, prostaglandins, leukotrienes, thromboxanes) are formed, which provide strong inflammatory, detergent, coagulating effects and increase vascular permeability. This pro-inflammatory role of sPLA2 may explain its increase levels and activity in cardiovascular, respiratory, autoimmune, metabolic, oncological, bacterial and viral disorders. The review article presents a classification of sPLA2 isoforms, their substrates, regulatory factors, biological significance, and mechanisms of their strong bactericidal, virucidal, and proinflammatory activity in the heart and lung disorders, autoimmune, metabolic, bacterial, and viral diseases. In particular, the mechanisms of the selective action of sPLA2 against Gram-positive and Gram-negative microorganisms are discussed. We consider diagnostic and prognostic significance, correlations between elevated levels and activity of sPLA2 and distinct clinical symptoms, severity and outcome in the patients with coronary heart disease (CAD), acute myocardial infarction (AMI), atherosclerosis, acute inflammatory lung injury (ALI), respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), rheumatoid arthritis, bronchial asthma, bacterial infections, septicemia and viral (COVID-19) infections. The opportunity of using sPLA2 as a biomarker of the severity and outcome of patients with chronic obstructive pulmonary disease, bacterial infections, sepsis and viral infections, including COVID-19, is also considered. (English) [ FROM AUTHOR] Секреторные фосфолипазы А2 (sPLA2) представляют собой большое суперсемейство ферментов с молекулярной массой 14-19 кДа, включающее 15 групп и более 30 изоформ, принадлежащих к четырем типам: секреторный (sPLA2), цитозольный (cPLA2), кальций-независимый (iPLA2) и липопротеин-ассоциированная фосфолипаза A2 (LP-PLA2, PAF-AH). У млекопитающих обнаружены одиннадцать секреторных sPLA2 (IB, IIA, IIC, IID, IIE, IIF, III, V, X, XIIA и XIIB), выполняющие разносторонние функции и участвующие в патогенезе широкого спектра заболеваний. С одной стороны, sPLA2, гидролизуя фосфолипиды мембран, способствуют элиминации поврежденных, апоптотических клеток и оказывают сильное бактерицидное, вируцидное действие, в том числе против антибиотикорезистентных штаммов микроорганизмов. Ð’ этом плане использование sPLA2 может представлять новую стратегию терапии бактериальных и вирусных инфекций. С другой стороны, в результате действия sPLA2 на ее субстраты образуются биологически активные молекулы (арахидоновая, лизофосфатидная кислоты, лизофосфолипиды, жирные кислоты, простагландины, лейкотриены, тромбоксаны), которые оказывают сильное воспалительное, детергирующее, коагулирующее действие и повышают проницаемость сосудов. Такая провоспалительная роль sPLA2 обуславливает повышение ее уровней и активности при сердечно-сосудистых, дыхательных, аутоиммунных, метаболических, онкологических, бактериальных и вирусных заболеваниях. Ð’ обзоре приводится классификация изоформ sPLA2, рассматриваются их субстраты, регулирующие факторы, биологическое значение и механизмы сильного бактерицидного, вируцидного действия, а также провоспалительной активности при сердечно-сосудистых, дыхательных, аутоиммунных, метаболических, бактериальных и вирусных заболеваниях. Отдельно излагаются механизмы селективного действия sPLA2 в отношении грамположительных и грамотрицательных микроорганизмов. Обсуждаются диагностическая, прогностическая значимость, корреляции повышенных уровней и активности sPLA2 с клиническими симптомами, тяжестью и исходом пациентов с ишемической болезнью сердца (CAD), острыминфарктом миокарда (AMI), атеросклерозом, острым воспалительным повреждением легких (ALI), респираторным дистресс-синдромом (ARDS), хронической обструктивной болезнью легких (COPD), ревматоидным Ð°Ñ€Ñ‚Ñ€Ð¸Ñ Ð¾Ð¼, бронхиальной астмой, бактериальными инфекциями, сепсисом и вирусными (COVID-19) инфекциями. Рассматривается возможность использования sPLA2 в качестве биомаркера тяжести и исхода пациентов с хронической обструктивной болезнью легких, бактериальными инфекциями, сепсисом и вирусными, в том числе COVID-19, инфекциями. (Russian) [ FROM AUTHOR] Copyright of Medical Immunology (1563-0625) is the property of National Electronic-Information Consortium and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

Understanding dead space in giraffes, and its application to critically ill COVID-19 patients

Giraffes have long been a subject of study for scientists due to the physiological anomaly their anatomical design can present. The study of the species helps aid in understanding of clinically relevant processes. The long trachea of a giraffe presents the dilemma of exaggerated dead space;however, this physiological problem is surmounted by a narrow trachea when compared to mammals of similar size, thus decreasing potential dead space. As COVID-19 patients in the hospital and ICU can develop COVID-19 associated acute respiratory distress syndrome, limiting excess dead space in COVID-19 patients is favorable. Removing additional tubing for a patient with an endotracheal tube in a ventilator circuit could help lower the patient's PaCO2 and raise their pH.

The Impact of Left Ventricle Geometry Patterns on Length of Hospital Stay in COVID-19 Patients

Objective: The coronavirus disease 2019 (COVID-19) has placed huge strains on medical systems. Therefore, it is essential to determine the predictors of the long hospital stay. We sought to investigate whether alterations in left ventricular (LV) geometry in COVID-19 patients are associated with the length of stay (LoS) and a long hospital stay. Materials and Methods: 108 consecutive hospitalized COVID-19 patients were incorporated in the study and 89 patients remained for statistical analysis. All participants underwent standard two-dimensional (2D) and Doppler echocardiographic examinations. Patients were classified according to LV geometry characteristics namely normal geometry (NG), concentric remodeling, concentric hypertrophy and eccentric hypertrophy. Results: Multiple binary logistic regression model adjusted for clinical and laboratory variables yielded significant and independent association of LV mass index (LVMI) (OR: 1.12, 95% CI: 1.06-1.19, p<0.001), 10 g/m(2) increase in LVMI (OR: 3.63, 95% CI: 2.00-6.59, p<0.001), LV geometry patterns (OR: 2.92, 95% CI: 1.46-5.34, p=0.002), and altered geometric patterns compared to NG (OR: 3.97, 95% CI: 1.08-14.5, p=0.037) with long hospital stay. Correlation analysis of LVMI and LoS demonstrated significant and moderate correlation (rho=0.58, p<0.001). Conclusion: LVMI and LV geometric patterns independently predict long hospital stays in COVID-19 patients. The significant correlation between LoS and LVMI underlies the significance of LV geometry in this infection.

SARS-CoV-2 induced myocarditis: Current knowledge about its molecular and pathophysiological mechanisms

The existence of an inflammatory process in the heart muscle, related to a progressive worsening of myocardial function, different etiopathogenetic mechanisms concur and often overlap, thus making the diagnosis and the therapeutic approach complex. As the COVID-19 pandemic progresses, the effects of the disease on the organ systems and in particular on the cardiovascular system are becoming more and more profound. Cardiac involvement is a well-known event with a high percentage of findings in the heart's magnetic field, even in asymptomatic areas. There are numerous uncertainties regarding their evolution, in the long and short term, due not only to a difficult to determine the varied clinical expression and the rarely performed intramyocardial biopsy which additionally presents diagnostic problems but also in part to different clinical prognosis. Today, the new SARS-CoV-2 virus that uses the angiotensin converting enzyme 2 (ACE2) which is present at high levels in myocardial cells as its entrance it can create even severe heart injury. The pathophysiology in all of these cases can involve multiple immune and non-immune mechanisms within organs and vessels and can be occur in the clinical phases. Possible mechanisms of direct and indirect myocardial infarction in patients with COVID-19 include additional lesion and oxygen-rich and generalized inflammation response with myocardial immune hyperactivity (myocarditis). Therefore, these can occur through the excessive release of cytokines, the presence of thrombocytopenia, endocrine damage, heart failure, arrhythmias and more. Patients can show average signs of myocardial damage, and some develop spontaneous cardiac complications, such as heart failure, arrhythmias and, rarely, rare cardiogenic disorders. Pathophysiology in all of these may involve multiple mechanisms within the cytokine cephalic membrane, endocrine damage and thrombogenicity. The diagnosis of this myocardial injuri is mainly based on the myocardial enzyme troponin. This viewpoint paper explains today's knowledge on viral myocarditis, in particular that from SARS-CoV-2 infection, if there is a connection with other possible biomolecular pathogenetic factors that can influence its natural course. In fact, it is for this reason that the pathogenetic mechanisms are analyzed and described. At the same time, its possible interaction with other parameters that are documented risk factors for cardiovascular disease was examined. Although these biomolecular findings were mainly related to necrotic parts of the myocardium, it is important to recognize that myocardial damage early for a better approach and prognosis.

Prognostic value of circulating calprotectin levels on the clinical course of COVID-19 differs between serum, heparin, EDTA and citrate sample types.

INTRODUCTION: During the recent SARS-CoV-2 pandemic, circulating calprotectin (cCLP) gained interest as biomarker to predict the severity of COVID-19. We aimed to investigate the prognostic value of cCLP measured in serum, heparin, EDTA and citrate plasma. MATERIALS AND METHODS: COVID-19 patients were prospectively included, in parallel with two SARS-CoV-2 negative control populations. The prognostic value of cCLP was compared with IL-6, CRP, LDH, procalcitonin, and the 4C-mortality score by AUROC analysis. RESULTS: For the 136 COVID-19 patients, cCLP levels were higher compared to the respective control populations, with significantly higher cCLP levels in serum and heparin than in EDTA or citrate. Higher cCLP levels were obtained for COVID-19 patients with i) severe/critical illness (n = 70), ii) ICU admission (n = 66) and iii) need for mechanical ventilation/ECMO (n = 25), but iv) not in patients who deceased within 30 days (n = 41). The highest discriminatory power (AUC [95% CI]) for each defined outcome was i) CRP (0.835 [0.755-0.914]); ii) EDTA cCLP (0.780 [0.688-0.873]); iii) EDTA cCLP (0.842 [0.758-0.925]) and iv) the 4C-mortality score (0.713 [0.608-0.818]). CONCLUSION: Measuring cCLP in COVID-19 patients helps the clinician to predict the clinical course of COVID-19. The discriminatory power of EDTA and citrate plasma cCLP levels often outperforms heparin plasma cCLP levels.

Cardiac Biomarker Levels and Their Prognostic Values in COVID-19 Patients With or Without Concomitant Cardiac Disease.

The coronavirus disease 2019 (COVID-19) pandemic has become a global threat. Increases in cardiac biomarkers are common and are associated with adverse outcomes in patients with COVID-19. Although these increases are more likely to occur in cases with concomitant cardiac disease, the differences in cardiac biomarker levels between patients with and without cardiac disease and their associations with in-hospital mortality are largely unknown. A consecutive serial of laboratory-confirmed COVID-19 cases was retrospectively enrolled. Clinical characteristics, laboratory results, and outcome data were collected. The levels of cardiac biomarkers were evaluated and compared by stratifying patients according to concomitant cardiac conditions and clinical classifications. The prognostic efficacy of cardiac biomarker levels on admission was also assessed. Among the overall study population and survived patients, the cardiac biomarker levels at both the early and late stages in cardiac patients were significantly higher than those in non-cardiac patients. However, their concentrations in cardiac patients were comparable to non-cardiac ones among non-survivors. The cardiac biomarker levels at the late stage of the disease were significantly decreased compared to those at the early stage among patients who were alive. Whereas, the late-stage biomarker levels were significantly increased in patients who ultimately died. Subgroup analysis illustrated that increases in cardiac biomarkers were closely related to the severity of the disease, and were prognostic for high risks of in-hospital mortality in non-cardiac, rather than in cardiac patients. Myo and NT-proBNP, rather than Hs-TnI and CK-MB, were independently associated with in-hospital mortality in the overall population and non-cardiac patients. However, these associations were not significant among cardiac patients. In conclusion, our results helped better understand the release pattern and prognostic performance of cardiac biomarkers in patients with COVID-19. Increased levels of Myo and NT-proBNP on admission could be useful markers for early identifying high-risk patients. However, special attention must be paid when implementing the prognostic function for cardiac patients.

Liver injury predicts overall mortality in severe COVID-19: a prospective multicenter study in Brazil.

BACKGROUND/PURPOSE: The relationship between liver injury and mortality remains unclear in patients with COVID-19. We aimed to evaluate the prognostic value of aminotransferases levels at hospital admission to predict mortality in patients with COVID-19. METHODS AND RESULTS: This prospective study included 406 patients [57% male, aged 56 years] with COVID-19 hospitalized in 26 centers in Brazil. Overall, 36.7% (95% CI 32.1-41.5) presented at admission with severe disease requiring respiratory support. The prevalence of elevated ALT and AST levels at admission [> 2 × ULN] was 14.0% (95% CI 11.0-17.8) and 12.9% (95% CI 10.0-16.6), respectively. Sixty-two patients [15.3% (95% CI 12.1-19.1)] died during hospitalization and the overall mortality rate was 13.4 (10.5-17.2) deaths per 1000 persons-years. The 15-day-overall survival (95% CI) was significantly lower in patients with ALT levels ≥ 2 × ULN compared to those with ALT < 2 × ULN [67.1% (48.4-80.2) vs 83.4% (76.1-88.6), p = 0.001] and in those with AST levels ≥ 2 × ULN compared to those with AST < 2 × ULN [61.5% (44.7-74.6) vs 84.2% (76.5-89.5), p < 0.001]. The presence of elevated aminotransferases levels at hospital admission significantly increased the risk of in-hospital all-cause mortality adjusted for age-and-sex. Those findings were present in the subgroup of critically ill patients already admitted in need of respiratory support (n = 149), but not in patients without that requirement at admission (n = 257). CONCLUSIONS: Elevated aminotransferases at hospital admission predicted in-hospital all-cause mortality in patients with COVID-19, especially in those with severe disease. Measurement of transaminases levels at hospital admission should be integrated to the care of patients with COVID-19 as an auxiliary strategy to identify patients at higher death risk.

[IRM et myocardite infectieuse]. / IRM et myocardite infectieuse.

Over the past ten years, cardiac MRI has become an indispensable tool for acute myocarditis diagnosis. Under appropriate conditions, cardiac MRI may allow postponement of initial coronary angiography in many instances. The 2020 ESC guidelines give a class I recommendation to its use in the setting of MINOCA for differential diagnosis between acute myocardial infarction, myocarditis, Tako-Tsubo and other cardiac pathologies, in order to improve therapeutic management and follow-up. This article describes the technical characteristics of MRI in myocarditis (Lake Louise diagnostic criteria and criteria based on myocardial tissue mapping), the main differential diagnoses, the prognostic value and addresses the issue of myocarditis in the setting of COVID-19.

Prognostic value of lactate dehydrogenase for in-hospital mortality in severe and critically ill patients with COVID-19.

Background: Lactate dehydrogenase (LDH) has been proved to be a prognostic factor for the severity and poor outcomes of coronavirus disease 2019 (COVID-19). In most studies, patients with various levels of COVID-19 severity were pooled and analyzed which may prevent accurate evaluation of the relationship between LDH and disease progression and in-hospital death. In this study, we aimed to evaluate the association of LDH with in-hospital mortality in severe and critically ill patients with COVID-19. Methods: This single-center retrospective study enrolled 119 patients. Survival curves were plotted using Kaplan-Meier method and compared by log-rank test. Multivariate Cox regression models were used to determine the independent risk factors for in-hospital mortality. Receiver-operator curves (ROCs) were constructed to evaluate the predictive accuracy of LDH and other prognostic biomarkers. Results: Compared to the survival group, LDH levels in the dead group were significantly higher [559.5 (172, 7575) U/L vs 228 (117, 490) U/L, (P < 0.001)]. In Multivariate Cox regression, it remained an independent risk factor for in-hospital mortality (Hazard ratio 5.985, 95.0%CI: 1.498-23.905; P=0.011). A cutoff value of 353.5 U/L predicted the in-hospital mortality with a sensitivity of 94.4% and a specificity of 89.2% respectively. Conclusion: LDH is a favorable prognostic biomarker with high accuracy for predicting in-hospital mortality in severe and critically ill patients with COVID-19. This may direct physicians worldwide to effectively prioritize resources for patients at high risk of death and to implement more aggressive treatments at an earlier phase to save patients' lives.