Pathophysiological correlations between SARS-CoV-2 and arrhythmogenesis: a literature review.

Introduction: SARS-CoV-2 represents one of the most extensively researched pathogens in the last decade due to its major impact on humanity. Not only does this viral infection cause respiratory disturbances, but it also generates cardiovascular injury. Cardiac arrhythmias represent one of the main consequences of SARS-CoV-2 infection, but they can also occur in the context of antiviral treatment. Furthermore, arrhythmias do not always seem to be correlated with the severity of the lung injury. However, they represent a poor prognostic factor in terms of mortality, increasing the need for intensive care and the length of hospitalization. Methods: In accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 Statement, from September 2022 to October 2023, we conducted this study by examining the literature through the PubMed database using the following keywords: COVID-19, cardiac arrhythmias, and, in terms of study design, observational studies. Results: We initially identified 266 studies across PubMed. After applying the inclusion/exclusion criteria, we managed to include 22 studies in our review. Conclusions: Deducing the pathophysiological mechanisms behind SARS-CoV-2's ability to disrupt the electrical activity of the heart, as well as identifying associated risk factors in patients with SARS-CoV-2 infection, could allow targeted therapeutic interventions to decrease the risk of mortality in hospitalized patients.

Predictors of Liver Injury in Hospitalized Patients with SARS-CoV-2 Infection.

Background and Objectives: SARS-CoV-2 infection is frequently associated with pneumonia but has a broad tissue tropism also leading to systemic complications (hematologic, gastro-intestinal, cardiac, neurologic, etc.). In this study, we aim to evaluate the impact of COVID-19 infection on the liver and to identify the risk factors/predictors for liver injury at admission to the hospital. Materials and Methods: We performed a retrospective cohort study on 249 patients, divided into two Group A (157 patients with liver involvement) and Group B (92 patients without liver involvement). We recorded demographic and lifestyle parameters, anthropometric parameters, comorbidities, clinical parameters, inflammation markers, complete blood count, coagulation, and biochemical parameters. Lung parenchyma, liver dimensions, and morphology were evaluated by computer tomography (CT) scans. Results: Patients with liver involvement had higher heart and respiratory rates, lower oxygen saturation (SO2), and necessitated higher oxygen flow at admittance. We found higher serum levels of C-reactive protein, fibrinogen, ferritin, creatine kinase, lactate dehydrogenase (LDH), serum triglycerides, and lower values for serum albumin in Group A patients. The patients with liver involvement presented more extensive lung injury with higher percentages of alveolar, mixed, and interstitial lesions, an increase in liver dimensions, and lower density ranges for the liver parenchyma. The patients presented hepatocytolytic involvement in 26 cases (10.4% from the entire study population), cholestatic involvement in 63 cases (37.7% from the entire study population), and mixed liver involvement in 68 cases (37.7% from the entire study population). Conclusions: Liver involvement in COVID-19 patients is frequent, usually mild, and occurs mostly in male patients over 50 years old. Cholestatic and mixed liver injuries are more frequent than hepatocytolytic injuries. The severity of lung injury evaluated by CT scan, increased values of inflammatory markers, LDH, and low values of SO2 can be considered risk factors/predictors for liver injury at admission to the hospital.

Evaluation of Drug-Induced Liver Injury in Hospitalized Patients with SARS-CoV-2 Infection.

Elevated liver enzymes are frequently reported in SARS-CoV-2-infected patients. Several mechanisms of liver injury have been proposed, but no clear conclusions were drawn. We aimed to evaluate hepatocellular and cholestatic injury in relation to the administration of potentially hepatotoxic drugs included in the current COVID-19 therapeutic guidelines in a retrospective cohort of 396 hospitalized COVID-19 patients. The main findings of our study are: (1) Significant increase in aminotransferases level was observed during hospitalization, suggesting drug-related hepatotoxicity. (2) Tocilizumab was correlated with hepatocellular injury, including ALT values greater than five times the upper limit of normal. (3) Anakinra was correlated with ALT values greater than three times the upper limit of normal. (4) Younger patients receiving tocilizumab or anakinra had a higher risk of hepatocellular injury. (5) The combination of favipiravir with tocilizumab was associated with AST values greater than three times the upper limit of normal and with an increase in direct bilirubin. (6) The administration of at least three potentially hepatotoxic drugs was correlated with hepatocellular injury, including ALT values greater than five times the upper limit of normal, and with the increase in indirect bilirubin. (7) Remdesivir and favipiravir by themselves did not correlate with hepatocellular or cholestatic injury in our study cohort.

Interstitial Lung Fibrosis Following COVID-19 Pneumonia.

Background and Objectives: Pulmonary fibrosis represents a stage of normal physiologic response to inflammatory aggression, mostly self-limiting and reversible; however, numerous patients treated for SARS-CoV-2 pneumonia present after release from hospital residual lung fibrosis. In this article, we aim to present an optimization method for evaluating pulmonary fibrosis by quantitative analysis, to identify the risk factors/predictors for pulmonary fibrosis in patients with SARS-CoV-2 infection, and to characterize the impact of pulmonary fibrosis on the symptomatology of patients after release from the hospital. Materials and Methods: We performed a prospective observational study on 100 patients with severe forms of pneumonia, with a control group of 61 non-COVID normal patients. Results: We found persistent interstitial changes consistent with fibrotic changes in 69% of patients. The risk of fibrosis was proportional to the values of erythrocyte sedimentation rate (ESR), C reactive protein (CRP), and lactate dehydrogenase (LDH), and to the duration of hospitalization. The imaging parameters correlated with increased risk for interstitial fibrosis were the number of affected pulmonary lobes and the percent of interstitial pulmonary fibrosis. Conclusions: The main risk factors for pulmonary fibrosis post-COVID-19 identified in our study are increased ESR, CRP, LDH, duration of hospitalization and the severity of pneumonia.

Diagnosing HIV-associated cerebral diseases - the importance of Neuropathology in understanding HIV.

The study aims to compare two aspects concerning the diagnosis of acquired immune deficiency syndrome (AIDS)-associated central nervous system (CNS) pathology (neuroAIDS): clinical diagnoses issued ante mortem with pathology results issued post mortem. The group of 39 human immunodeficiency virus (HIV)-positive patients was created over 23 years and is limited by marked heterogeneity. The enrolled cases were treated at the "Prof. Dr. Matei Bals" National Institute for Infectious Diseases, Bucharest, Romania, deceased due to AIDS-related complications and underwent brain necropsies performed in the Pathology Laboratory at the "Colentina" Clinical Hospital, Bucharest. The level of superposition between clinical and the necroptic diagnoses of neurological AIDS-associated diseases was: 60% for progressive multifocal leukoencephalopathy (PML), 50% for cerebral cryptococcosis, 33% for cerebral toxoplasmosis, 20% for cerebral lymphoma, null for cerebral tuberculosis, HIV encephalopathy (HIVE), neurosyphilis and cytomegalovirus cerebral infection. Half of the cases without an AIDS-associated CNS lesion were previously clinically overdiagnosed. We observed that the rate of overdiagnosis concerning an AIDS-associated cerebral illness has risen from 36% in 1993 to 124% in 2015, an elevation with statistical relevance [p=0.037, confidence interval (CI) 95%]. The rate of underdiagnosis has slowly risen from 24% in 1993 to 40% in 2015, however, with no statistical relevance. The rate of clinical confirmation has been stagnant in linear regression from 1993 to 2015. The results of our study reveal a gap between ante mortem and post mortem diagnoses, with many instances of overdiagnosis and underdiagnosis of several major AIDS-associated CNS illnesses, highlighting the need for a more detailed, multidisciplinary approach of neuroAIDS.