There are significant challenges remain in accurately categorizing the risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) patients.

We used an untargeted 1H NMR-based metabolomics to assess the metabolomic changes in serum samples from a Danish cohort of 106 COVID-19-infected patients with mild to fatal disease courses and from patients with fatal outcomes from other diseases.

In total, 240 serum samples were used for this study. We used the data for multiple analyses (1) to construct a predictive model for disease severity and outcome, (2) to identify prognostic markers for subsequent disease severity and outcome, and (3) to understand the disease consequences in the metabolome and how recovery or death is reflected in the altered biological pathways.

Our results revealed distinct alterations in the serum metabolome that could differentiate patients with COVID-19 by severity (mild or severe) or outcome (death or survival). Using receiver operating characteristic (ROC) curve analysis and four machine learning algorithms (random forest, linear support vector machine, PLS-DA, and logistic regression), we identified two biomarker sets with relevant biological functions that predict subsequent disease severity and patient outcome. The range of these severity-associated biomarkers was equally broad and included inflammatory markers, amino acids, fluid balance, ketone bodies, glycolysis-related metabolites, lipoprotein particles, and fatty acid levels.

Our data suggest the potential benefits of broader testing of these metabolites from newly diagnosed patients to predict which COVID-19 patients will progress to severe disease and which patients will manifest severe symptoms to minimize mortality.

to analyze the factors associated with mortality in patients with cardiovascular disease affected by Coronavirus Disease-2019.

this was a cross-sectional study using data from the monitoring of notifications during the pandemic. The sample included cases with cardiovascular comorbidity and clinical outcomes. The dependent variable was the progression of the case to death. Associations were tested using the binary logistic regression method, using the Odds Ratio.

the prevalence was female (50.6%), elderly (71.1%), self-declared non-white (71.0%), with multiple comorbidities associated with cardiovascular disease (60.3%), diabetes being the main one (44.8%). The study suggests that patients who were men (OR 1.13; p = 0.028), elderly (OR 2.57; p = 0.000), self-declared white (OR 1.71; p = 0.000), and had multiple comorbidities (OR 1.70; p = 0.000) were associated with a greater chance of death.

the factors associated with a higher chance of death were related to gender, age group, and the presence of comorbidities, showing the vulnerability of this population to infection.

Up to 80% of patients who develop coronavirus disease-2019 (Covid-19) infection subsequently experience long covid/post-covid syndrome. The World Health Organization (WHO) has estimated that >770 million patients have been infected with Covid-19 globally. Even if only 10% of these patients develop long covid, > 75 million patients will suffer for a long period. Among the various symptoms of post-covid syndrome, fatigue is common, affecting up to 60% of the patients. As observed in other viral infections, elevated levels of inflammatory cytokines may play a role. Transcutaneous auricular vagal nerve stimulation (taVNS) is a noninvasive method that modulates the immune system via the central nervous system and has shown promising effects in autoimmune diseases and improving fatigue. In this pilot study, we investigated the feasibility of daily taVNS in patients with long covid-related fatigue. Additionally, the effects of taVNS on fatigue and quality of life will be analyzed.

A total of 45 adult patients with long covid associated fatigue syndrome will be enrolled in this study, and will be randomized to the above-threshold-stimulation, below-threshold-stimulation, or sham-stimulation arms, after being informed that they will feel the stimulation. The above-threshold-group will receive a 4-week-long left-sided cymba conchae taVNS with 25 Hz, 250 µs pulse width 28s/32s on/off paradigm for 4 h throughout the day. The below-threshold group will receive stimulation below the sensational threshold, whereas the sham group will receive no stimulation following application of a non-functional electrode. The daily stimulation protocol will be recorded either manually or using the provided app. Three well-established questionnaires, the Multidimensional-Fatigue-Inventory-20, Short-Form-36, and Beck-Depression-Inventory, and the newly established Post-Covid-Syndrome-Score will be completed both before and after 4 weeks of stimulation.

The primary endpoint has been set as the patients' average daily stimulation time after 4 weeks, while secondary endpoints include the effects of taVNS on fatigue and Quality of Live (QoL). As a non-invasive treatment option, taVNS may be a notable alternative for patients with post-covid related fatigue.

This study was approved by the local ethics committee (23/7798) and registered (DRKS00031974) (see supporting information files).

The ethical justifiability of this study was supported by prior research demonstrating the safety of taVNS. Patients will be recruited by general practitioners, and written informed consent will be obtained. All data will be pseudonymized for collection and storage. The study results will be published in peer-reviewed journals with the aim of providing evidence of the potential of taVNS in long covid management. The study will be conducted in accordance with the principles of the Declaration of Helsinki.

Inflammation plays a fundamental role in the development and bidirectional association of di-verse diseases, such as periodontitis and type 2 diabetes mellitus (T2DM), which generates important clinical complications, where chronic exposure to high levels of blood glucose affects the repair process of periodontal tissues. Likewise, it has been observed that comorbidity, between these two diseases, influences the development of the COVID-19 disease towards a more severe course. However, there is currently very little scientific evidence on the relationship between periodontitis, T2DM and COVID-19 disease. This narrative review aims to provide an understanding of the current and most relevant aspects of the relationship between periodontitis, T2DM and COVID-19 disease. A narrative review was performed through a systematic search of published studies, without date restrictions, indexed in the electronic databases of PubMed, for the inclusion of articles in English, and LILACS for the inclusion of articles in Spanish. This review included different articles, which addressed the most important aspects to present a current perspective on the relationship and influence between periodontitis, T2DM and COVID-19 disease. Comorbidity between periodontitis and T2DM represents a greater risk of developing a more severe course of COVID-19 disease, because these three diseases share three important axes: a clinicopathological axis; an axis associated with glycemia, and an immunological axis associated with inflammation.

Severe COVID-19 is characterized by complex immunopathology that involves inflammation, endothelial dysfunction, and immunothrombosis. Neutrophil extracellular traps (NETs) have been recognized as key factors in the severity of the disease, with their emergence correlating to viral load, immmunothrombosis, and organ damage. In this study, we investigated the role of NETosis and macrophage activation in the course of severe COVID-19. We analyzed 23 autopsy samples from patients who died from COVID-19 and performed immunohistochemical staining and stereological point counting to quantify leukocyte infiltration and NET formation among other histopathological parameters. Our results showcase 2 evident immunophenotypes: lowNET and highNET. The lowNET group displayed lower NET formation, higher viral loads, and an increased incidence of secondary infections, as well as shorter survival times. In contrast, the highNET group exhibited increased neutrophil activation, pronounced endothelial damage and thrombotic complications, as well as prolonged survival times. Our data suggest a dual role of NETosis in COVID-19: initially protective, limiting viral replication, but later likely detrimental through immunothrombosis and tissue damage. These findings underline the need for tailored therapeutic actions, with early antiviral and immune-modulating interventions for lowNET patients and strategies aiming to limit excessive NETosis and coagulopathy in highNET patients. Further research is needed to define the timing of interventions based on the dynamics of NETosis.

Pneumonia caused by SARS-CoV-2 is a public health problem. Older adults are vulnerable and the atypical presentation delays diagnosis and increases mortality. In this group the atypical clinical manifestations are more frequent.

To identify the clinical manifestations and mortality of COVID-19 pneumonia in hospitalized older adults.

A comparative cross-sectional observational study was carried out, from July 1, 2020, to December 31, 2021, in a general hospital of Mexico City. Patients aged 60 years or more who were hospitalized with a diagnosis of COVID-19 were included.

267 older adults participated; 53.9% were men, with a median age of 74 years. The most frequent comorbidities in this population were type 2 diabetes mellitus (T2DM), hypertension and chronic obstructive pulmonary disease (COPD). 41.2% showed atypical presentation of the disease; mortality in the studied population was 53.5%.

The atypical presentation of COVID-19 pneumonia is common in adults over 60 years of age and it increases significantly as they become older. The absence of typical symptoms of pneumonia and the ignorance of the most common signs could delay diagnosis and timely care in this age group, which may increase complications and mortality.

Patients with pre-existing Parkinson's disease (PD) face higher risks of severe acute COVID-19 outcomes than matched controls, but long-term post-COVID-19 outcomes remain largely unknown. This study investigated clinical outcomes up to 3.5 years post-infection in a Bronx inner-city PD population.

This retrospective study evaluated 3512 patients with PD in the Montefiore Health System (January 2016-July 2023), which serves a large diverse population and was an epicenter of the early COVID-19 pandemic and subsequent infection surges. Comparisons were made with PD patients without a positive SARS-CoV-2 test (defined by polymerase chain reaction test). Outcomes were post-index date all-cause mortality, major adverse cardiovascular events (MACE), altered mental status, fatigue, dyspnea, headache, psychosis, dementia, depression, anxiety, dysphagia, falls, and orthostatic hypotension. Changes in Levodopa prescriptions were also tabulated. Adjusted hazard ratios (aHR) were computed accounting for competing risks.

PD patients with COVID-19 had similar demographics but a higher prevalence of pre-existing comorbidities compared to PD patients without COVID-19. PD patients with COVID-19 had greater risk of mortality (aHR = 1.58 [95% CI: 1.03, 2.41]), MACE (aHR = 1.57 [1.19, 2.07]), dyspnea, fatigue, and fall compared to PD patients without COVID-19. Levodopa dose adjustment was higher post-infection in the COVID-19 cohort.

Among PD patients, COVID-19 was associated with a higher risk of adverse long-term outcomes. PD patients who survive COVID-19 may benefit from heightened clinical awareness and close follow-up. Findings highlight the need to improve post-COVID care for PD patients to mitigate disease progression and maintain quality of life.

The novel coronavirus disease 2019 (COVID-19) is associated with life-threatening complications. Electrocardiogram (ECG) changes associated with COVID-19 have also been reported in the majority of critically ill patients.

In this study, we aimed to investigate the prevalence of fragmented QRS (fQRS) and its prognostic value in hospitalized patients with COVID-19. In addition, we performed a systematic review and meta-analysis of the literature to evaluate the effect of fQRS on the outcomes of COVID-19 patients.

A total of 310 patients with a mean age of 65.7 ± 14.5 years were followed up for 3 months, of whom 139 (44.8%) had fQRS on their ECGs. The rates of in-hospital mortality (8.8% vs. 8.6%), rehospitalization during follow- up (13.7% vs. 12.3%), and 90-day mortality (6.5% vs. 5.3%) were comparable between the patients with and without fQRS, respectively. In the meta-analysis, 9 studies in addition to our study reported outcomes, with a total of 2928 patients with a mean age of 53.8 years, and 1431 (48.9%) were males. The rate of fQRS was 0.31 (95% confidence interval [CI], 0.23-0.38; I2 = 95.21%). In addition, the pooled proportion of in-hospital mortality reported by 5 studies was 0.31 (95% CI, 0.12-0.51; I2 = 98.36). The rate of in-hospital mortality was higher among patients with fQRS compared to those without fQRS (odds ratio, 2.33; 95% CI, 1.52-3.58; p = 0.0001; I2 = 74%).

The rate of fQRS on ECG was relatively high in COVID-19 patients, and according to the meta-analysis, it was associated with worse outcomes in hospitalized COVID-19 patients.

COronaVIrus Disease-2019 (COVID-19) is associated with a hypercoagulable state. Intracardiac thrombosis is a potentially serious complication but has seldom been evaluated in COVID-19 patients. We assessed the incidence, associated factors, and outcomes of COVID-19 patients with intracardiac thrombosis. In 2020, COVID-19 inpatients were identified from the National Inpatient Sample (NIS) database. Data on clinical characteristics, intracardiac thrombosis, and adverse outcomes were collected. Multivariable logistic regression was used to identify factors associated with intracardiac thrombosis, in-hospital mortality, and morbidities. In 2020, 1,683,785 COVID-19 inpatients (mean age 63.8 years, 32.2% females) were studied. Intracardiac thrombosis occurred in 0.10% (1830) of cases. In-hospital outcomes included 13.2% all-cause mortality, 3.5% cardiovascular mortality, 2.6% cardiac arrest, 4.4% acute coronary syndrome (ACS), 16.1% heart failure, 1.3% stroke, and 28.3% acute kidney injury (AKI). Key factors for intracardiac thrombosis were congestive heart failure history and coagulopathy. Intracardiac thrombosis independently linked to higher risks of all-cause mortality (odds ratio [OR]: 3.32 (2.42-4.54)), cardiovascular mortality (OR: 2.95 (1.96-4.44)), cardiac arrest (OR: 2.04 (1.22-3.43)), ACS (OR: 1.62 (1.17-2.22)), stroke (OR: 3.10 (2.11-4.56)), and AKI (OR: 2.13 (1.68-2.69)), but not heart failure. While rare, intracardiac thrombosis in COVID-19 patients independently raised in-hospital mortality and morbidity risks.

Personality traits involving negative affect, as well as mental disorders including depression, anxiety, and posttraumatic stress disorder, are cardiovascular risk factors. However, which of these confer risk independently is uncertain, and the implications of their overlap, combinations, and interactions are poorly understood. Potential explanatory mechanisms are being characterized with increasing detail and sophistication. Of particular interest are psychobiological processes initiated by stress. Other mechanisms involve stress-related health behaviors, and illness behaviors that delay or reduce the effectiveness of medical treatment. With some promising exceptions, findings of intervention trials are uncertain regarding the effectiveness of psychological treatments for modifying affective traits and mental disorders to reduce their impact on cardiovascular disease. Recent developments include novel conceptualizations of mental disorders; examination of the interplay between cognitive factors and emotion; and theoretical frameworks that integrate psychological stress processes with neuroscience, health behavior, and social cognition. Also promising is increased attention to the roles of gender identity and minority group membership.

It remains unclear about the association between stroke and Coronavirus disease 2019 (COVID-19). Therefore, a Mendelian randomization (MR) analysis was conducted to explore the relationship between them.

In this study, the most recent large-scale genome-wide association studies (GWASs) were selected from the publicly available COVID-19 GWAS meta-analysis (Round 7) as the exposure. Data from a recent original stroke GWAS were used as the outcome for the experimental group, while the stroke GWAS data from the IEU GWAS database were used as the validation group. In addition, an MR analysis was conducted to explore the causal relationships of susceptibility, hospitalization, and severity of COVID-19 with stroke and its subtypes. In addition, the results of the experimental and validation groups were integrated to perform a meta-analysis.

The MR analysis results corroborated that there was a positively causal relationship between the hospitalization (OR, 1.11; p = 0.015) (ORmeta, 1.11; p < 0.001), and severity (OR, 1.06; p = 0.043) (ORmeta, 1.07; p = 0.002) of COVID-19 and cardioembolic stroke (CES). This result is supported by the validation group and sensitivity analysis.

This study demonstrates for the first time that COVID-19 hospitalization and COVID-19 severity are risk factors for CES.

This study evaluates the pathogenesis of COVID-19 and the therapeutic efficacy of sitagliptin in diabetic and obese mice. Using a novel double-transgenic mouse model (db/db and K18-hACE2), the findings demonstrates that SARS-CoV-2 infection (Delta variant) causes severe multi-organ damage, glucose metabolism abnormalities, insulin resistance, and pancreatic islet cell damage in diabetic mice. Infected diabetic mice displayed higher mortality, inflammation (elevated TNF-α, IL-6, IL-1β), and fibrinolytic activity (PAI-1), alongside dysregulated diabetes-related hormones (GLP-1, leptin, ghrelin, resistin) compared to non-diabetic controls. Sitagliptin treatment reduced organ injury, hyperglycemia, inflammation, and fibrinolytic activity while improving insulin resistance and glucose metabolism. This was evidenced by decreased fasting blood glucose levels, improved insulin sensitivity, and elevated insulin and GLP-1 levels. These findings suggest sitagliptin is a promising therapeutic strategy to mitigate the severity of COVID-19 in experimental diabetes by modulating inflammation and improving metabolic syndrome. Further mechanistic investigations revealed that the level of hACE2 expression, along with the activation of NF-κB and IRS-1, play critical roles in the development of SARS-CoV-2-induced diabetes, the exacerbation of pre-existing diabetes, and the therapeutic efficacy of sitagliptin.

Background/Objectives: COVID-19 is associated with multiple systemic effects, including cardiovascular complications. However, its interplay with cardiac conduction abnormalities remains underexplored. We compared the clinical profile of COVID-19 patients with pre-existing left bundle branch block (LBBB) or right bundle branch block (RBBB) at hospital admission. Methods: This study included 100 COVID-19 patients with antecedent BBB (50 LBBB, 50 RBBB). Critical cardiometabolic, renal, hematological, and inflammatory markers were measured. Logistic regression was used to identify key predictors differentiating COVID-19 patients with LBBB and RBBB. Spearman's correlations were applied to assess intra-strata associations for these variables. Results: COVID-19 patients with LBBB patients were significantly more likely to display lower systolic blood pressure (p = 0.012) but greater left atrial size (p = 0.008), left ventricular diameter (p = 0.001), and interventricular septal thickness (p = 0.023). Hematological and inflammatory markers differed, with LBBB patients being prone to exhibit higher red cell distribution width (p = 0.005), lymphocyte count (p < 0.001), neutrophil count (p = 0.045), and C-reactive protein (p < 0.001). This group also tended to show lower erythrocyte sedimentation rate (p = 0.013) and glycated hemoglobin (p = 0.045) but higher random glucose (p = 0.014). Absolute lymphocyte count, C-reactive protein, and left ventricular diameter were the most robust predictors distinguishing LBBB from RBBB. Significant associations were found exclusively for LBBB, all of them being weak. These predominantly negative relationships indicated an inflammatory origin, and most of them occurred for lymphocyte count. Conclusions: COVID-19 patients with LBBB and RBBB present distinct clinical profiles at hospital admission. The former group demonstrates a more adverse baseline clinical profile, particularly in terms of cardiac and inflammatory markers. These findings suggest that pre-existing BBB type may influence disease progression, potentially helping in risk stratification for COVID-19 patients.

Cardiovascular diseases, including stroke driven by atherosclerosis, remain a leading global health concern. Current diagnostic imaging modalities such as magnetic resonance imaging fail to characterize oxidative stress within atherosclerotic plaques. Here, we introduce difuranfluoreno-dithiophen-based polymers designed for afterglow imaging, offering ultrabright luminescence, ultralow-power excitation (0.087 milliwatts per square centimeter), and ultrashort acquisition times (0.01 seconds). Through a molecular engineering strategy, we have optimized polymers for enhanced reactive oxygen species (ROS) generation capability, ROS capturing capability, and fluorescence quantum yield, resulting in an increase in afterglow intensity (~130-fold) compared to commonly used 2-methoxy-5-(2'-ethylhexyloxy)-1,4-phenylenevinylene polymer (MEHPPV). Additionally, we have developed ratiometric afterglow nanoparticles doped with oxidative stress-responsive molecules, enabling imaging of oxidative stress markers in atherosclerotic plaque. This approach provides a tool for cardiovascular imaging and diagnostics, which is conducive to the auxiliary diagnosis and risk stratification of atherosclerosis.

Inflammatory cardiomyopathy is a condition that is characterised by the presence of inflammatory cells in the myocardium, which can lead to a significant deterioration in cardiac function. The etiology of this condition involves multiple factors, both infectious and non-infectious causes. While it is primarily associated with viral infections, other potential causes include bacterial, protozoal, or fungal infections, as well as a wide variety of toxic substances and drugs, and systemic immune-mediated pathological conditions. In spite of comprehensive investigation, the presence of inflammatory cardiomyopathy accompanied by left ventricular dysfunction, heart failure or arrhythmia is indicative of an unfavourable outcome. The reasons for the occurrence of either favourable outcomes, characterised by the absence of residual myocardial injury, or unfavourable outcomes, marked by the development of dilated cardiomyopathy, in patients afflicted by the condition remain to be elucidated. The relative contributions of pathogenic agents, genomic profiles of the host, and environmental factors in disease progression and resolution remain subjects of ongoing discourse. This includes the determination of which viruses function as active inducers and which merely play a bystander role. It remains unknown which changes in the host immune profile are critical in determining the outcome of myocarditis caused by various viruses, including coxsackievirus B3 (CVB3), adenoviruses, parvoviruses B19 and SARS-CoV-2. The objective of this review is unambiguous: to provide a concise summary and comprehensive assessment of the extant evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy. Its focus is exclusively on virus-induced and virus-associated myocarditis. In addition, the extant lacunae of knowledge in this field are identified and the extant experimental models are evaluated, with the aim of proposing future directions for the research domain. This includes differential gene expression that regulates iron and lipid and metabolic remodelling. Furthermore, the current state of knowledge regarding the cardiovascular implications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is also discussed, along with the open questions that remain to be addressed.

N-acetylcysteine (NAC) can take part in the treatment of chronic respiratory diseases because of the potent mucolytic, antioxidant, and anti-inflammatory effects of NAC. However, less is known about its use in the treatment of acute lung injury. Nowadays, an increasing number of studies indicates that early administration of NAC may reduce markers of oxidative stress and alleviate inflammation in animal models of acute lung injury (ALI) and in patients suffering from distinct forms of acute respiratory distress syndrome (ARDS) or pulmonary infections including community-acquired pneumonia or Coronavirus Disease (COVID)-19. Besides low costs, easy accessibility, low toxicity, and rare side effects, NAC can also be combined with other drugs. This article provides a review of knowledge on the mechanisms of inflammation and oxidative stress in various forms of ALI/ARDS and critically discusses experience with the use of NAC in these disorders. For preparing the review, articles published in the English language from the PubMed database were used.

The COVID-19 pandemic has underscored the importance of understanding the interplay between the cardiovascular and immune systems during viral infections. SARS-CoV-2 enters human cells via the ACE-2 enzyme, initiating a cascade of immune responses. This study presents a coupled mathematical model that integrates the cardiovascular system (CVS) and immune system (IS), capturing their complex interactions during infection. The CVS model, based on ordinary differential equations, describes heart dynamics and pulmonary and systemic circulation, while the IS model simulates immune responses to SARS-CoV-2, including immune cell interactions and cytokine production. A coupling strategy transfers information from the IS to the CVS at specific intervals, enabling the exploration of immune-driven cardiovascular effects. Numerical simulations examined how these interactions influence infection severity and recovery. The coupled model accurately replicated the evolution of cardiac function in survivors and non-survivors of COVID-19. Survivors exhibited a left ventricular ejection fraction (LVEF) reduction of up to 25% while remaining within normal limits, whereas non-survivors showed a severe 4-fold decline, indicative of myocardial dysfunction. Similarly, the right ventricular ejection fraction (RV EF) decreased by approximately 50% in survivors but underwent a drastic 5-fold reduction in non-survivors. These findings highlight the model's capacity to distinguish differential cardiac dysfunction across clinical outcomes and its potential to enhance our understanding of COVID-19 pathophysiology.

COVID-19 is associated with increased risk of post-acute cardiovascular outcomes. Population-based evidence for long periods of observation is still limited.

This population-based cohort study was conducted using data (2020-2021) from the British Columbia COVID-19 Cohort. The exposure of interest was severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, identified through reverse transcription-polymerase chain reaction (RT-PCR) assay. Individuals who tested positive (exposed) on RT-PCR were matched to negative controls (unexposed) on sex, age, and RT-PCR collection date in a 1:4 ratio. Outcomes of interest were incident major adverse cardiovascular events and acute myocardial infarction, identified more than 30 days after RT-PCR collection date. The association between SARS-CoV-2 infection and cardiovascular risk was assessed through multivariable survival models. Population attributable fractions were computed from Cox models.

We included 649,320 individuals: 129,864 exposed and 519,456 unexposed. The median duration of follow-up was 260 days; 1,786 events (0.34%) took place among the unexposed, and 702 (0.54%) in the exposed. The risk of major adverse cardiovascular events was higher in the exposed (adjusted hazard ratio [aHR] 1.34; 95% confidence interval [CI], 1.22-1.46), with greater risk observed in those who were hospitalized (aHR 3.81; 95% CI, 3.12-4.65) or required intensive care unit admission (aHR 6.25; 95% CI, 4.59-8.52) compared with the unexposed group. The fraction of cardiovascular events attributable to SARS-CoV-2 was 7.04% (95% CI, 4.67-9.41%). Comparable results were observed for acute myocardial infarction.

SARS-CoV-2 infection was associated with higher cardiovascular risk, with graded increase across the acute COVID-19 severity, contributing to 7% of incident major adverse cardiovascular events. These findings suggest that long-term monitoring of cardiovascular risk is required in COVID-19 survivors.

Coronavirus 2019 (COVID-19) has spread throughout the world and the current COVID-19 vaccines have shown to be the most effective means of combating the COVID-19. This study focused to examine the status of serum biomarkers in individuals infected and non-infected with SARS-CoV-2, both before and after COVID-19 pandemic and vaccination.

This study comprised 133 adults aged 35 and older including both academic and non-academic personnel associated with Shahjalal University of Science and Technology in Sylhet, Bangladesh. Participants were evaluated before and after COVID-19 pandemic, as well as following two doses of vaccination. Blood samples were collected to measure different serum biomarkers, including fasting blood sugar (FBS), serum creatinine, serum alanine transaminase (ALT), total cholesterol (TC), triglyceride (TG), Low density lipoprotein-cholesterol (LDL-C), and High density lipoprotein-cholesterol (HDL-C). Statistical analysis was performed using SPSS software.

In all participants, serum creatinine, FBS and TC levels significantly increased after two doses of vaccination (p = 0.022, 0.006, 0.05) compared to pre-vaccination levels. Notably, all serum biomarkers showed a significant elevation (p ≤ 0.05) in the self-reported SARS-CoV-2 infected group (n = 44). Additionally, 31% of participants were newly diagnosed with hyperglycemia after receiving the COVID-19 vaccine.

The findings indicate that both self-reported SARS-CoV-2 infection and COVID-19 vaccination could influence different serum biomarker levels. However, further comprehensive research is necessary to discern the precise factors contributing to the alterations observed in the serum biomarker levels for future health management strategy.

Viral infection by SARS-CoV2 is a pandemic affecting over 600 million people worldwide. One of five hospitalized patients may present myocardial injury, strongly associated with disease severity and mortality.

Retrospective cross-sectional study of hospitalized COVID-19 patients diagnosed between May 01, 2020, and June 30, 2021, from the database of the Registro Latinoamericano de Enfermedad Cardiovascular y COVID-19 (CARDIO COVID 19-20) with a troponin value recorded during hospitalization. A descriptive analysis of sociodemographic and clinical characteristics was performed. Bivariate analysis was conducted according to the presence or absence of myocardial injury. Survival analysis was made using Kaplan-Meier curves, by the presence of myocardial injury. A multivariate Poisson regression model was performed to determine factors associated with mortality. Statistical analyses were performed using the RStudio V.1.4.1717 package.

A total of 2,134 patients were included, 64.2% were male, and 911 patients had myocardial injury. The median age of the total population was 61 years. Individuals with myocardial injury had a higher prevalence of hypertension, diabetes, and dyslipidemia. Survival probability was lower in this subgroup. Patients with myocardial injury had a 1.95 times higher risk of death. Age, male sex, chronic kidney disease, arrhythmias, decompensated heart failure, requirement of inotropic/vasopressor, and invasive mechanical ventilation were related to higher mortality risk in patients with myocardial injury.

Patients with COVID-19 and myocardial injury exhibit a broad spectrum of cardiac abnormalities. Myocardial injury is associated with a higher disease severity and risk of in-hospital mortality. This multicenter study uniquely represents data from 13 Latin American countries, offering regional insights into the impact of myocardial injury during the COVID-19 pandemic.

Epicardial adipose tissue (EAT), a unique fat depot surrounding the heart, plays a multifaceted role in glucose and lipid metabolism, thermogenesis, and the secretion of bioactive molecules that influence cardiac structure and function. Its proximity to the myocardium allows it to contribute directly to CVDs, including coronary artery disease, arrhythmias, and heart failure. In particular, excessive EAT has emerged as a significant factor in heart failure with preserved ejection fraction (HFpEF), the most common form of heart failure, especially in individuals with obesity and diabetes. Traditional metrics like body mass index (BMI) fail to capture the complexities of visceral fat, as patients with similar BMIs can exhibit varying CVD risks. EAT accumulation induces mechanical stress and fosters a pro-inflammatory and fibrotic environment, driving cardiac remodeling and dysfunction. Pharmacological modulation of EAT has shown promise in delivering cardiometabolic benefits. Recent advancements in diabetes therapies, such as SGLT2 inhibitors and GLP-1 receptor agonists, and antilipidemic drugs have demonstrated their potential in reducing pro-inflammatory cytokine production and improving glucose regulation, which directly influences EAT. These discoveries suggest that EAT could be a significant therapeutic target, though further investigation is necessary to elucidate its role in HFpEF and other CVDs. Recent advances have identified the prokineticin/PKR1 signaling pathway as pivotal in EAT development and remodeling. This pathway regulates epicardial progenitor cells (EPDCs), promoting angiogenesis while reducing EAT accumulation and metabolic stress on the heart, particularly under high-calorie conditions. Prokineticin, acting through its receptor PKR1, limits visceral adipose tissue growth, enhances insulin sensitivity, and offers cardioprotection by reducing oxidative stress and activating cellular survival pathways. In this review, we provide a comprehensive analysis of EAT's role in CVDs, explore novel therapeutic strategies targeting EAT, and highlight the potential of prokineticin signaling as a promising treatment for HFpEF, obesity, and diabetes.

Since its emergence in 2019, COVID-19 has continued to pose significant threats to both the physical and mental health of the global population, as well as to healthcare systems worldwide (Raman et al., Eur Heart J 43:1157-1172, 2022). Emerging evidence indicates that COVID-19 may lead to post-acute COVID-19 syndrome (PACS) with cardiovascular implications, potentially driven by factors such as ACE2 interaction with viruses, systemic inflammation, and endothelial dysfunction. However, there remains a limited amount of research on the cardiovascular manifestations of PACS, which may delay the development of optimal treatment strategies for affected patients. Therefore, it is crucial to investigate the prevalence of cardiovascular sequelae in COVID-19 patients and to determine whether COVID-19 infection acts as an independent risk factor for these outcomes.

This meta-analysis adhered to PRISMA guidelines and was registered in PROSPERO (CRD42024524290). A systematic search of PubMed, Embase, and the Cochrane Library was conducted up to March 17, 2024. The primary outcomes included hypertension, palpitations, and chest pain, with pooled effect estimate reported as proportions and odds ratios (ORs) with 95% confidence intervals (CIs). Sensitivity and subgroup analysis were performed to assess the robustness of the results and to identify sources of heterogeneity.

A total of 37 studies, encompassing 2,965,467 patients, were included in the analysis. Pooled results from case-control studies revealed that, compared to the control group, the ORs of chest pain in the COVID-19 group was 4.0 (95% CI: 1.6, 10.0). The ORs for palpitation and hypertension were 3.4 (95% CI: 1.1, 10.2) and 1.7 (95% CI: 1.6, 1.8), respectively. The proportions of PACS patients experiencing chest pain, palpitation, and hypertension as sequelae were 22% (95% CI: 14%, 33%), 18% (95% CI: 13%, 24%), and 19% (95% CI: 12%, 31%), respectively.

Our findings indicate that 15% of COVID-19 patients experience cardiovascular sequelae. Furthermore, COVID-19 infection significantly increases the likelihood of developing these sequelae compared to uninfected individuals. Future research should prioritize investigating the underlying pathological mechanisms and developing targeted preventive and management strategies.

CRD42024524290.

We test the robustness of the self-controlled risk interval (SCRI) design in a setting where time between doses may introduce time-varying confounding, using both negative control outcomes (NCOs) and quantitative bias analysis (QBA). All vaccinated cases identified from 5 European databases between September 1, 2020, and end of data availability were included. Exposures were doses 1-3 of the Pfizer, Moderna, AstraZeneca, and Janssen COVID-19 vaccines; outcomes were myocarditis and, as the NCO, otitis externa. The SCRI used a 60-day control window and dose-specific 28-day risk windows, stratified by vaccine brand and adjusted for calendar time. The QBA included two scenarios: (1) baseline probability of the confounder was higher in the control window and (2) vice versa. The NCO was not associated with any of the COVID-19 vaccine types or doses except Moderna dose 1 (IRR = 1.09; 95% CI 1.01-1.09). The QBA suggested that even the strongest literature-reported confounder (COVID-19; RR for myocarditis = 18.3) could only explain away part of the observed effect, from IRR = 3 to IRR = 1.40. The SCRI seems robust to unmeasured confounding in the COVID-19 setting, although a strong unmeasured confounder could bias the observed effect upward. Replication of our findings for other safety signals would strengthen this conclusion. This article is part of a Special Collection on Pharmacoepidemiology.

The molecular mechanisms regulating coronavirus pathogenesis are complex, including virus-host interactions associated with replication and innate immune control. However, some genetic and epigenetic conditions associated with comorbidities increase the risk of hospitalization and can prove fatal in infected patients. This systematic review will provide insight into host genetic and epigenetic factors that interfere with COVID-19 expression in light of available evidence.

This study conducted a systematic review to examine the genetic and epigenetic susceptibility to COVID-19 using a comprehensive approach. Through systematic searches and applying relevant keywords across prominent online databases, including Scopus, PubMed, Web of Science, and Science Direct, we compiled all pertinent papers and reports published in English between December 2019 and June 2023.

The findings reveal that the host's HLA genotype plays a substantial role in determining how viral protein antigens are showcased and the subsequent immune system reaction to these antigens. Within females, genes responsible for immune system regulation are found on the X chromosome, resulting in reduced viral load and inflammation levels when contrasted with males. Possessing blood group A may contribute to an increased susceptibility to contracting COVID-19 as well as a heightened risk of mortality associated with the disease. The capacity of SARS-CoV-2 involves inhibiting the antiviral interferon (IFN) reactions, resulting in uncontrolled viral multiplication.

There is a notable absence of research into the gender-related predisposition to infection, necessitating a thorough examination. According to the available literature, a significant portion of individuals affected by the ailment or displaying severe ramifications already had suppressed immune systems, categorizing them as a group with elevated risk.

As the coronavirus disease 2019 (COVID-19) pandemic persists, the exploration of adjunct therapies to mitigate disease severity remains a priority. Statins, known for their pleiotropic effects, have been under investigation for their potential role in managing COVID-19 complications. The study was conducted in a single referral hospital and adhered to Consolidated Standards of Reporting Trials guidelines. Eligible participants were randomized in a 1:1 ratio into either the rosuvastatin group or the control group. Outcome measures included vital signs, laboratory data, clinical outcomes, and patient symptoms. Statistical analysis was performed using SPSS software (version 26.0, IBM Corp., Armonk, New York). A total of 100 patients were enrolled. No significant differences were observed between the rosuvastatin and control groups in terms of baseline characteristics and laboratory parameters, except for the fact that rosuvastatin-treated patients showed lower levels of C-reactive protein in comparison with the controls on both the 1st and 5th days (38.1 ± 16.3 vs 50.5 ± 25.3) compared to the control group. Clinical outcomes, including hospital length of stay, intensive care unit admission, need for intubation, and 1-month mortality, did not differ significantly between the two groups. Symptom scales, as assessed by the Borg Rating of Perceived Exertion and Leicester Cough Questionnaire, showed significant improvement in the rosuvastatin group compared to controls. Our study provides insights into the short-term efficacy of moderate-intensity rosuvastatin in COVID-19 patients. Further research is warranted to elucidate the long-term effects and optimal dosing of statins in COVID-19 management.

Coronavirus disease 2019 (COVID-19) was declared a global pandemic in 2019. It remains uncertain to what extent COVID-19 effects the heart in heathy individuals. To evaluate the effect of the COVID-19 on cardiac structure and function in middle-aged and older individuals.

A single-centre prospective observational study enroled a total of 124 participants (84 with history of COVID-19 [COVID-19 group] and 40 without a history of COVID-19 [non-COVID group]). All participants underwent echocardiography with speckle tracking to assess cardiac structure and function at rest and during peak exercise.

There were no differences in left and right ventricular diastolic function (p ≥ 0.05) between the COVID-19 and non-COVID-19 groups. Participants in COVID-19 group demonstrated higher left ventricular mass (130 ± 39.8 vs. 113 ± 27.2 g, p = 0.008) and relative wall thickness (0.38 ± 0.07 vs. 0.36 ± 0.13, p = 0.049). Left ventricular global longitudinal strain was reduced in the COVID-19 group at rest and at peak-exercise (rest: 18.3 ± 2.01 vs. 19.3 ± 1.53%, p = 0.004; peak exercise: 19.1 ± 2.20 vs. 21.0 ± 1.58%, p ≤ 0.001). However, no difference was seen in resting left ventricular ejection fraction (58 ± 2.89 vs. 59 ± 2.51%, p = 0.565) between groups. Right ventricular fractional area change was reduced in the COVID-19 group (p = 0.012).

Cardiac structural and functional remodelling was observed in middle-aged and older otherwise healthy individuals with a history of COVID-19.

Epidemiological studies link COVID-19 to increased cardiac arrest (CA) risk, but causality remains unclear due to potential confounding factors in observational studies . We conducted a Mendelian randomization (MR) analysis using genome-wide association study (GWAS) data, employing COVID-19-associated single nucleotide polymorphisms (SNPs) with significance values smaller than 5 × 10⁻⁸. We calculated inverse-variance weighted (IVW) MR estimates and performed sensitivity analyses using MR methods robust to horizontal pleiotropy. Additionally, a reverse MR analysis was conducted using CA-associated SNPs with significance values smaller than 1 × 10⁻⁵. Results indicated that infected COVID-19 (OR = 1.12, 95% CI = 0.47-2.67, p = 0.79), hospitalized COVID-19 (OR = 1.02, 95% CI = 0.70-1.49, p = 0.920), and severe respiratory COVID-19 (OR = 0.99, 95% CI = 0.81-1.21, p = 0.945) did not causally influence CA risk. Reverse MR analysis also did not support a causal effect of CA on COVID-19. Thus, associations in observational studies may stem from shared biological factors or environmental confounding.

Background and Objectives: Fever in patients who have suffered an out-of-hospital cardiac arrest (OHCA) has been linked to poor clinical outcomes, as a fever can exacerbate neurological damage, increase metabolic demands, and trigger inflammatory responses. This study evaluates the impact of the COVID-19 outbreak and associated fevers on OHCA outcomes and examines how they can worsen patient prognosis. Materials and Methods: Our retrospective observational analysis used data from the National Emergency Department Information System (NEDIS), comprising adult OHCA patients at 402 EDs in Korea between 27 January and 31 December 2020 (COVID-19 pandemic period) and the corresponding period in 2019 (pre-COVID-19). The primary outcome was in-hospital mortality, with the COVID-19 outbreak as the main exposure variable and fever as an important interaction variable. We employed multilevel multivariate logistic regression with an interaction term (year of visit × fever) to examine the effects of COVID-19 and fever on mortality. Risk-adjusted mortality rates were calculated, and a difference-in-difference analysis evaluated the impact of COVID-19 on excess mortality by fever status. Results: During COVID-19, in-hospital mortality was higher among OHCA patients compared to the pre-pandemic period (adjusted OR 1.22, 95% CI 1.11-1.34), particularly among febrile patients (adjusted OR 1.40, 95% CI 1.24-1.59). Interaction analysis revealed that COVID-19 disproportionately increased mortality in febrile OHCA patients compared with non-febrile patients (difference-in-difference: 0.8%, 95% CI 0.2-1.5). Conclusions: Our study found that the COVID-19 pandemic significantly increased mortality among OHCA patients, with febrile patients experiencing disproportionately worse outcomes due to systemic delays and pandemic-related disruptions.

Sepsis, characterized as life-threatening organ dysfunction resulting from dysregulated host responses to infection, remains a significant challenge in clinical practice. Despite advancements in understanding host-bacterial interactions, molecular responses, and therapeutic approaches, the mortality rate associated with sepsis has consistently ranged between 10 and 16%. This elevated mortality highlights critical gaps in our comprehension of sepsis etiology. Traditionally linked to bacterial and fungal pathogens, recent outbreaks of acute viral infections, including Middle East respiratory syndrome coronavirus (MERS-CoV), influenza virus, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), among other regional epidemics, have underscored the role of viral pathogenesis in sepsis, particularly when critically ill patients exhibit classic symptoms indicative of sepsis. However, many cases of viral-induced sepsis are frequently underdiagnosed because standard evaluations typically exclude viral panels. Moreover, these viruses not only activate conventional pattern recognition receptors (PRRs) and retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) but also initiate primary antiviral pathways such as cyclic guanosine monophosphate adenosine monophosphate (GMP-AMP) synthase (cGAS)-stimulator of interferon genes (STING) signaling and interferon response mechanisms. Such activations lead to cellular stress, metabolic disturbances, and extensive cell damage that exacerbate tissue injury while leading to a spectrum of clinical manifestations. This complexity poses substantial challenges for the clinical management of affected cases. In this review, we elucidate the definition and diagnosis criteria for viral sepsis while synthesizing current knowledge regarding its etiology, epidemiology, and pathophysiology, molecular mechanisms involved therein as well as their impact on immune-mediated organ damage. Additionally, we discuss clinical considerations related to both existing therapies and advanced treatment interventions, aiming to enhance the comprehensive understanding surrounding viral sepsis.

Although COVID-19 has been linked to worse outcomes in patients with neurological disorders, its impact on those with essential tremor (ET) remains unclear. To investigate clinical outcomes of ET patients with and without COVID-19 three and a half years post-pandemic.

1074 ET patients were evaluated in this retrospective study in the Montefiore Health System from January 2016 to July 2023. Comparisons between ET patients with and without a positive SARS-CoV-2 polymerase chain reaction test were made. Outcomes included post-index date major adverse cardiovascular events (MACEs), new-onset sleep disturbances, fatigue, dyspnea, first-time fall, new-onset anxiety, new-onset depression, headache, new-onset imbalance, new-onset mild cognitive impairment, and all-cause mortality, adjusted hazard ratios (aHR) adjusting for covariates were calculated.

ET patients with COVID-19 had higher prevalence of pre-existing type-2 diabetes, depression, and anxiety compared to ET patients without COVID-19. COVID-19 was significantly associated with higher risk of MACEs, (aHR = 2.39 [1.49, 3.82]), new-onset sleep disturbance, (aHR = 2.12 [1.44, 3.13]), fatigue, (aHR = 1.83 [1.27, 2.65]), dyspnea, (aHR = 1.98 [1.40, 2.80]), first-time fall, (aHR = 4.76 [2.24, 10.14]), new-onset anxiety, (aHR = 3.66 [2.02, 6.64]), and new-onset depression, (aHR = 2.38 [1.20, 4.70]). COVID-19 was not associated with all-cause mortality.

In patients with ET, COVID-19 significantly increases the risk of several long-term adverse health outcomes, but not mortality.

Background: Understanding the interactions between age and comorbidities is crucial for assessing COVID-19 mortality, particularly in patients with cardiac and pulmonary conditions. This study investigates the relationship between comorbidities and mortality outcomes in a cohort of hospitalized COVID-19 patients, emphasizing the interplay of age, cardiac, and pulmonary conditions. Methods: We analyzed a cohort of 3005 patients hospitalized with COVID-19 between 2020 and 2022. Key variables included age, comorbidities (diabetes, cardiac, pulmonary, and neoplasms), and clinical outcomes. Chi-square tests and logistic regression models were used to assess the association between comorbidities and mortality. Stratified analyses by age, diabetes, and pulmonary conditions were conducted to explore interaction effects. Additionally, interaction terms were included in multivariable logistic regression models to evaluate the combined impact of age, comorbidities, and mortality. Results: Cardiac conditions such as hypertension, ischemic cardiopathy, and myocardial infarction showed significant protective effects against mortality in younger patients and in those without pulmonary conditions (p < 0.001). However, these protective effects were diminished in older patients and those with pulmonary comorbidities. Age was found to be a significant modifier of the relationship between cardiac conditions and mortality, with a stronger protective effect observed in patients under the median age (p < 0.001). Pulmonary comorbidities significantly increased the risk of mortality, particularly when co-occurring with cardiac conditions (p < 0.001). Diabetes did not significantly modify the relationship between cardiac conditions and mortality. Conclusions: The findings highlight the complex interactions between age, cardiac conditions, and pulmonary conditions in predicting COVID-19 mortality. Younger patients with cardiac comorbidities show a protective effect against mortality, while pulmonary conditions increase mortality risk, especially in older patients. These insights suggest that individualized risk assessments incorporating age and comorbidities are essential for managing COVID-19 outcomes.

Risk of cardiovascular events is increased after COVID-19. However, information on cardiovascular risk trends after COVID-19 infection is lacking and estimates by sex are inconsistent. Our aim was to examine cardiovascular outcomes and mortality in a large cohort (164,346 participants) of SARS-CoV-2 positive individuals compared to non-positive individuals, stratified by sex. Data were obtained from the Spanish Health System's electronic medical records. Selected individuals were ≥ 45 years old with/without a positive SARS-CoV-2 test in the period March-May 2020. Follow-up was obtained until January 31, 2021, for cardiovascular events (angina/myocardial infarction, arrhythmias, bypass/revascularization, heart failure, peripheral artery disease, stroke/transient ischemic attack, and thrombosis), and until March 31, 2021, for mortality. Individuals were matched by propensity score. Incidence of cardiovascular events and mortality was compared with accelerated failure time models. The effect of matching and of COVID-19 severity was assessed with sensitivity analyses. In the first 3 months of follow-up, SARS-CoV-2 positive individuals had a higher risk of mortality and of all cardiovascular events. From 4-12 months, there was increased risk of mortality in SARS-CoV-2 positive individuals overall, of heart failure in SARS-CoV-2 positive females (HR= 1.26 [1.11-1.42]), and of arrhythmias and thrombosis in SARS-CoV-2 positive males (HR= 1.29 [1.14-1.47] and HR= 1.35 [1.03-1.77], respectively). When COVID-19 patients admitted to the ICU were excluded, incidence of thrombosis was similar in males regardless of positive/non-positive SARS-CoV-2 status. In the full year of follow-up, increased incidence of heart failure and of arrhythmias and thrombosis was observed in SARS-CoV-2 positive females and males, respectively.

The pandemic COVID-19 (coronavirus disease 2019) is caused by the severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), which devastated the global economy and healthcare system. The infection caused an unforeseen rise in COVID-19 patients and increased the mortality rate globally. This study gives an overall idea about host-pathogen interaction, immune responses to COVID-19, recovery status of infection, targeted organs and complications associated, and comparison of post-infection immunity in convalescent subjects and non-infected individuals. The emergence of the variants and episodes of COVID-19 infections made the situation worsen. The timely introduction of vaccines and precautionary measures helped control the infection's severity. Later, the population that recovered from COVID-19 grew significantly. However, understanding the impact of healthcare issues resulting after infection is paramount for improving an individual's health status. It is now recognised that COVID-19 infection affects multiple organs and exhibits a broad range of clinical manifestations. So, post COVID-19 infection creates a high risk in individuals with already prevailing health complications. The identification of post-COVID-19-related health issues and their appropriate management is of greater importance to improving patient's quality of life. The persistence, sequelae and other medical complications that normally last from weeks to months after the recovery of the initial infection are involved with COVID-19. A multi-disciplinary approach is necessary for the development of preventive measures, techniques for rehabilitation and strategies for clinical management when it comes to long-term care.

This editorial article is intended to perform a discussion on the manuscript entitled "Simultaneous portal vein thrombosis and splenic vein thrombosis in a COVID-19 patient: A case report and review of literature" written by Abramowitz et al. The article focuses on the diagnostic processes in a 77-year-old-male patient with a simultaneous portal vein and splenic artery thrombosis accompanying coronavirus disease 2019 (COVID-19). The authors postulated that splanchnic thrombosis should be on the list of differential diagnoses in a patient presenting with abdominal pain in presence of a COVID-19 infection. The tendency for venous and arterial thrombosis in COVID-19 patients is encountered, largely attributed to hypercoagulopathy. In general, venous thromboembolism mostly manifest as deep vein thrombosis (DVT), pulmonary embolism (PE) or catheter-related thromboembolic events. Acute PE, DVT, cerebrovascular events and myocardial infarction are seen as the most common thromboembolic complications in COVID-19 patients. COVID-19-associated hemostatic abnormalities include mild thrombocytopenia and increased D-dimer level. Similar to other coagulopathies, the treatment of the underlying condition is the mainstay. Addition of antiplatelet agents can be considered in critically ill patients at low bleeding risk, not on therapeutic anticoagulation, and receiving gastric acid suppression Early administration of antithrombotic drugs will have a beneficial effect in both the prevention and treatment of thrombotic events, especially in non-ambulatory patients. Low molecular weight heparin (LMWH) should be started if there is no contraindication, including in non-critical patients who are at risk of hospitalization LMWH (enoxaparin) is preferred to standard heparin.

Introduction. Post-coronavirus disease-2019 (COVID-19) patients may develop cardiac symptoms. We hypothesized that cardiovascular magnetic resonance (CMR) can assess the background of post-COVID-19 cardiac symptoms using multi-parametric evaluation. We aimed to conduct an investigation of symptomatic patients with post-COVID-19 syndrome using CMR (INSPIRE-CMR). Methods. INSIPRE-CMR is a retrospective multicenter study including 174 patients from five centers referred for CMR due to cardiac symptoms. CMR was performed using 3.0 T/1.5 T system (24%/76%, respectively). Myocardial inflammation was determined by the updated Lake Louise criteria. Results. Further, 174 patients with median age of 40 years (IQR: 26-54), 72 (41%) were women, and 17 (9.7%) had a history of autoimmune disease, muscular dystrophy, or cancer. In total, 149 (86%) patients were late gadolinium enhanced (LGE)-positive with a non-ischemic pattern, and of those evaluated with the updated Lake Louise criteria, 141/145 (97%) had ≥1 pathologic T1 index. Based on the T2-criterion, 62/173 (36%) patients had ≥1 pathologic T2 index. Collectively, 48/145 (33%) patients had both positive T1- and T2-criterion. A positive T2-criterion or a combination of a positive T1- and T2-criterion were significantly more common amongst patients with severe COVID-19 [45 (31%) vs. 17 (65%), p = 0.001 and 32 (27%) vs. 16 (64%), p < 0.001, respectively]. During the one-year evaluation, available for 65/174 patients, shortness of breath, chest pain, and arrhythmia were identified in 7 (4%), 15 (8.6%), and 43 (24.7%), respectively. CMR evaluation, available in a minority of them, showed mildly reduced LVEF, while nat T1 mapping and EVC remained at levels higher than the normal values of the local MRI units. Conclusions. The majority of post-COVID-19 patients with cardiac symptoms presented non-ischemic LGE and abnormalities in T1 and T2-based indices. Multi-parametric CMR reveals important information on post-COVID-19 patients, supporting its role in short/long-term evaluation.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) not only posed major health and economic burdens to international societies but also threatens patients with comorbidities and underlying autoimmune disorders, including Crohn's disease (CD) patients. As the vaccinated population is gradually relieved from the stress of the latest omicron variant of SARS-CoV-2 due to competent immune responses, the anxiety of CD patients, especially those on immunosuppressive treatment, has not subsided. Whether the use of immunosuppressants for remission of CD outweighs the potential risk of severe coronavirus disease 2019 (COVID-19) has long been discussed. Thus, for the best benefit of CD patients, our primary goal in this study was to navigate the clinical management of CD during the COVID pandemic. Herein, we summarized COVID-19 outcomes of CD patients treated with immunosuppressive agents from multiple cohort studies and also investigated possible mechanisms of how SARS-CoV-2 impacts the host immunity with special consideration of CD patients. We first looked into the SARS-CoV-2-related immunopathology, including lymphocytopenia, T-cell exhaustion, cytokine storms, and their possible molecular interactions, and then focused on mechanistic actions of gastrointestinal systems, including interruption of tryptophan absorption, development of dysbiosis, and consequent local and systemic inflammation. Given challenges in managing CD, we summarized up-to-date clinical and molecular evidence to help physicians adjust therapeutic strategies to achieve the best clinical outcomes for CD patients.

This review discusses the pivotal role of microcirculation in maintaining tissue oxygenation and waste removal and highlights its significance in various pathological conditions. It delves into the cellular mechanisms underlying hemodynamic coherence, elucidating the roles of the endothelium, glycocalyx, and erythrocytes in sustaining microcirculatory integrity. Furthermore, the review gives comprehensive information about microcirculatory changes observed in cardiac surgery, sepsis, shock, and COVID-19 disease. Through comprehensive exploration, the review underscores the intricate relationship between microcirculation, disease states, and clinical outcomes, emphasizing the importance of understanding and monitoring microvascular dynamics in critical care settings.