Post-COVID-19 condition (PCC), also known as long COVID, is a complex multiple organ system condition that can develop and persist for months after acute COVID-19. PCC encompasses a wide range of symptoms, resulting in heterogeneous clinical manifestations. These manifestations likely arise from diverse underlying pathophysiological mechanisms, which, in turn, are influenced by risk factors such as age, sex, and comorbidities. To this end, characterising clinical phenotypes of PCC is essential for deepening our understanding of its (potentially) distinct pathophysiological mechanisms and for advancing diagnostic and patient-tailored management strategies. PCC is thought to result from a complex interaction of various pathophysiological mechanisms, leading to functional and structural pathological alterations across multiple organ systems. Investigating these alterations is critical to improving our currently incomplete understanding of PCC's complex pathophysiology. This review provides an overview of the main clinical phenotypes of PCC, characterises these phenotypes by examining symptoms and signs, as well as the associated risk factors. The main hypothesised pathophysiological mechanisms are discussed by outlining the current knowledge on PCC pathology, focussing on the most commonly affected organ systems. Current PCC management includes supportive care such as physiotherapy and the repurposing of existing drugs primarily targeting persistence of SARS-CoV-2 (e.g. antivirals, monoclonal antibodies) and immune dysfunction (e.g. antiinflammatory drugs, immunomodulators). To date, prevention of SARS-CoV-2 infection remains critical, which can be achieved through effective public health measures and vaccination strategies. Finally, this review highlights current knowledge gaps and proposes future research directions to advance the understanding and treatment of PCC. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Myocardial injury is a critical determinant of prognosis in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; however, its underlying mechanisms remain incompletely understood. In this study, we examined the effects of SARS-CoV-2-derived RNA fragments on human cardiomyocytes. We identified a 19-nucleotide sequence within the viral genome that shares complete sequence homology with the human F1F0 ATP synthase subunit alpha gene (ATP5A). This sequence was found to associate with Argonaute 2 (AGO2) and downregulate ATP5A expression via a mechanism analogous to RNA interference. Consequently, oxidative phosphorylation was suppressed in cardiomyocytes, leading to impaired myocardial maturation and the emergence of heart failure-like phenotypes. Notably, exosome-mimetic liposomal delivery of this RNA fragment to cardiomyocytes reproduced the ATP5A-suppressive effect. These findings suggest that SARS-CoV-2-derived RNA fragments may contribute to myocardial injury through the siRNA-like modulation of mitochondrial gene expression. Further validation in animal models and patient-derived materials is warranted.

To (1) examine considerations before and experiences with GP contact during the first COronaVIrus Disease 2019 (COVID-19) lockdown among Danish citizens; (2) analyse the associations with sex, age, chronic disease, and socioeconomic factors; and (3) explore changes in healthcare-seeking behaviour post-pandemic.

A total of 100,000 Danes aged 20 years or older, randomly selected in the general population, were invited to participate in a survey examining considerations and experiences with healthcare seeking during the first COVID-19 lockdown. Data were collected in spring 2022 and linked to register data on socioeconomic factors. Descriptive statistics and multivariable logistic regression models were applied.

Of the 27,369 eligible individuals, 18% reported a need to contact their GP. Being worried about burdening the healthcare system was most frequently reported (45%), followed by being in doubt about acceptable contact reasons (33%), and concern about infection (24%). Although 44% of those who needed to contact their GP found the digital solutions advantageous, individuals frequently found it difficult to discuss symptoms by telehealth (29%) and that they were examined less thoroughly. Generally, women, younger people, and individuals with lower socioeconomic status were more likely to be worried and report difficulties with contact to general practice. Some 86% of the respondents reported no changes in healthcare-seeking behaviour post-pandemic.

The results may assist in the organisation of healthcare in case of future lockdowns. Yet, the COVID-19 pandemic has only slightly affected the healthcare-seeking behaviour in the Danish general population.

Background: The association between Coronavirus Disease-2019 (COVID-19) and new-onset cardiomyopathy (NOC) is unclear. Objectives: We aim to assess the incidence of NOC in hospitalized COVID-19 patients and its impact on short- and long-term survival. Methods: We retrospectively studied 2219 COVID-19 patients hospitalized between March 2020 and February 2022 who underwent an in-hospital echocardiogram. NOC was defined as a left-ventricular ejection fraction (LVEF) reduction of >10%, resulting in an LVEF of <54% for females and <52% for males. The 30-day and 1-year survival outcomes in patients without and with NOC were studied. Results: Among 25,943 hospitalized COVID-19 patients, 2219 met our inclusion criteria, with 209 (9.4%) having NOC. NOC patients were more likely to be male (56.1% vs. 68.4%, p = 0.001) and have chronic kidney disease (51.4% vs. 60.3%, p = 0.018). They had a higher 30-day mortality rate (29.1% vs. 32%, p = 0.033), but the 1-year survival rate was similar between the patients without and with NOC (36.9% vs. 41.6%, p = 0.12). Multivariable regression revealed that advanced age, admission to intensive care unit, mechanical ventilation, treatment with glucocorticoids, and treatment with vasopressors were associated with higher odds of 30-day mortality in NOC patients. Only 74 (35.4%) NOC patients had follow-up echocardiograms after discharge, of which 47 showed persistent cardiomyopathy. Conclusions: NOC can affect around 1 out of 10 hospitalized COVID-19 patients undergoing echocardiography. While NOC was associated with worse short-term survival, it did not impact the long-term mortality of these patients. Persistent LVEF deficits in some patients emphasize the need for improved outpatient follow-up to identify at-risk individuals and optimize treatment.

Male sex is a well-known predictor of short-term prognosis in patients with coronavirus disease (COVID-19). Data, however, on long-term outcomes are scarce. We aimed to assess the differences in mortality between sexes and find other important predictors of survival from a long-term perspective. Data from all patients retrieved from a database of COVID-19 patients hospitalized at University Hospital in Krakow, Poland, between February 13, 2020, and May 10, 2021, were analyzed for clinical in-hospital data and after a 42 months follow-up period. Of the 4071 COVID-19 patients hospitalized, 2183 were men (53.6%). Males were on average younger and more likely to have concomitant chronic obstructive pulmonary disease, heart failure, coronary artery disease (including acute and chronic coronary syndrome) compared to women. In terms of laboratory findings, more advanced inflammatory markers and troponin I were predominantly observed in male patients than in female patients. Males were found to have a greater predisposition for relevant cardiovascular comorbidities and were more likely to have died during the 42 months follow-up. Additionally, higher levels of troponin I, N-terminal pro B-type natriuretic peptide and D-dimer were associated with a greater risk of death. Kaplan-Meier survival analyses revealed a worse 42 months survival for men up to the age of 65 years. Cardiovascular comorbidities, male sex and older age, as well as higher concentrations of markers indicating a thrombotic state and myocardial injury, were associated with poorer long-term prognosis in patients with COVID-19.

The United States has experienced high surge in COVID-19 cases since the dawn of 2020. Identifying the types of diagnoses that pose a risk in leading COVID-19 death casualties will enable our community to obtain a better perspective in identifying the most vulnerable populations and enable these populations to implement better precautionary measures.

To identify demographic factors and health diagnosis codes that pose a high or a low risk to COVID-19 death from individual health record data sourced from the United States.

We used logistic regression models to analyze the top 500 health diagnosis codes and demographics that have been identified as being associated with COVID-19 death.

Among 223,286 patients tested positive at least once, 218,831 (98%) patients were alive and 4,455 (2%) patients died during the duration of the study period. Through our logistic regression analysis, four demographic characteristics of patients; age, gender, race and region, were deemed to be associated with COVID-19 mortality. Patients from the West region of the United States: Alaska, Arizona, California, Colorado, Hawaii, Idaho, Montana, Nevada, New Mexico, Oregon, Utah, Washington, and Wyoming had the highest odds ratio of COVID-19 mortality across the United States. In terms of diagnoses, Complications mainly related to pregnancy (Adjusted Odds Ratio, OR:2.95; 95% Confidence Interval, CI:1.4 - 6.23) hold the highest odds ratio in influencing COVID-19 death followed by Other diseases of the respiratory system (OR:2.0; CI:1.84 - 2.18), Renal failure (OR:1.76; CI:1.61 - 1.93), Influenza and pneumonia (OR:1.53; CI:1.41 - 1.67), Other bacterial diseases (OR:1.45; CI:1.31 - 1.61), Coagulation defects, purpura and other hemorrhagic conditions(OR:1.37; CI:1.22 - 1.54), Injuries to the head (OR:1.27; CI:1.1 - 1.46), Mood [affective] disorders (OR:1.24; CI:1.12 - 1.36), Aplastic and other anemias (OR:1.22; CI:1.12 - 1.34), Chronic obstructive pulmonary disease and allied conditions (OR:1.18; CI:1.06 - 1.32), Other forms of heart disease (OR:1.18; CI:1.09 - 1.28), Infections of the skin and subcutaneous tissue (OR: 1.15; CI:1.04 - 1.27), Diabetes mellitus (OR:1.14; CI:1.03 - 1.26), and Other diseases of the urinary system (OR:1.12; CI:1.03 - 1.21).

We found demographic factors and medical conditions, including some novel ones which are associated with COVID-19 death. These findings can be used for clinical and public awareness and for future research purposes.

Patients with coronavirus disease 2019 (COVID-19)-related acute respiratory distress syndrome (ARDS) who lack clinical improvement are frequently treated with high-dose corticosteroids (HDS). Since HDS is used to reduce hyperinflammation in these patients, levels of (pro-)inflammatory biomarkers after commencing HDS treatment could be useful in predicting mortality. This study aims to evaluate biomarker levels after commencing HDS over time, along with their capacity to predict mortality.

This retrospective cohort study included patients with COVID-19 ARDS treated with HDS in the intensive care unit (ICU) at an academic hospital in the Netherlands between March 2020-March 2022. Inflammatory biomarkers (ie, C-reactive protein (CRP), D-dimer, ferritin, leukocyte count, interleukin-6 (IL-6), lactate dehydrogenase (LDH), neutrophil-to-lymphocyte ratio (NLR), and procalcitonin (PCT)) were assessed daily from start of HDS (ie baseline) until day 7. Associations between biomarker levels and all-cause-hospital-mortality were evaluated each day using logistic regression, with cut-offs identified by optimizing sensitivity (Se) and specificity (Sp).

Of the 122 patients included, 53 (43.4%) died during hospitalization. HDS was initiated for a median 7 days (IQR=1-11) after ICU admission. At baseline, a moderately high predictive capacity for mortality was observed at a ferritin level >1281 µg/L (Se=62%/Sp=64%), leukocyte count >13.7 × 109/L (Se=42%/Sp=79%), and NLR >12.1 (Se=61%/Sp=77%). During follow-up, CRP >50 mg/L on day 6 (Se=50%/Sp=75%) and >42 mg/L on day 7 (Se=50%/Sp=75%), ferritin >1082 µg/L on day 6 (Se 63%/Sp=71%) and >1852 µg/L on day 7 (Se=31%/Sp=79%), IL-6 >67 mg/L on day 7 (Se=56%/Sp=79%) and LDH >396U/L on day 6 (Se=38%/Sp=83%) and >373 U/L on day 7 (Se=47%/Sp=72%) showed moderate capacity to predict mortality. NLR was consistently associated with mortality for all days, except day 1 (Se=36-68%/Sp=72-92%).

In COVID-19 ARDS patients receiving HDS, several clinically available inflammatory biomarkers moderately predicted all-cause-hospital-mortality after the start of HDS, particularly on days 6 and 7. NLR demonstrated the most consistent association with mortality over time. The use of these markers requires validation in larger cohorts.

The effects of a concomitant infection of hepatitis B virus (HBV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are still debated, with a recognized major risk of HBV reactivation during immune-suppressive treatments. The aim of this study was to determine the prevalence and predictive factors of HBV reactivation in a cohort of hospitalized patients with coronavirus disease 2019 (COVID-19) and a current or past hepatitis B infection. In a monocentric retrospective observational study, we enrolled all consecutive hospital admitted patients with COVID-19 pneumonia and a positive HBV serology (N = 84) in our Infectious Diseases Unit from April 2021 to December 2023. We identified 18 (21%) HBsAg-positive/anti-HBc-positive, 41 (49%) HBsAg-negative/anti-HBc-positive/anti-HBs-positive, and 25 (30%) HBsAg-negative/anti-HBc-positive/anti-HBs-negative subjects. The overall rate of hepatitis flare was 10.7%, without any HBsAg seroreversion, severe HBV reactivation, and/or need for new HBV antiviral therapy introduction. Systemic corticosteroid treatment for COVID-19 and baseline anti-HBsAg status were associated with this risk of HBV reactivation. In conclusion, the overall risk of hepatitis flares in hospitalized COVID-19 was reasonably low, with higher doses of corticosteroids treatment being the major risk factor for HBV reactivation, and anti-HBs-positive serological status as a protective element.

Studies have shown an association between the clinical severity of coronavirus disease (COVID-19) and sociodemographic and clinical variables in older adults. However, few studies have described the explanatory factors of the relationship between these variables and the clinical severity of COVID-19 using structural equation modeling.

To analyze the factors directly and indirectly associated with the clinical severity of coronavirus disease (COVID-19) among older adults in Minas Gerais, Brazil.

Retrospective epidemiological study.

This study included 51,141 elderly adults with COVID-19 living in Minas Gerais, Brazil. Data were collected through the Individual Registration Form - Hospitalized Cases of Severe Acute Respiratory Syndrome from January 28, 2020, to January 27, 2022.

Older age (P < 0.001), male sex (P < 0.001), dyspnea (P < 0.001), change in chest X-ray examination findings (P < 0.001), greater number of risk factors/comorbidities (P < 0.001), and longer hospitalization time (P < 0.001) were directly associated with the clinical severity of COVID-19. Female sex, mediated by the greater number of risk/comorbidity factors (β = -0.02, P < 0.001), and younger age, mediated by longer hospitalization time (β = -0.01; P < 0.001), were indirectly associated with the clinical severity of COVID-19.

Demographic and clinical variables were directly associated with increased disease severity. In addition to the direct effect, a greater number of risk/comorbidity factors and longer hospitalization time mediated the association between demographic variables and outcomes.

Patients with SARS-CoV-2 infection carry an increased risk of cardiovascular disease encompassing various implications, including acute myocardial injury or infarction, myocarditis, heart failure, and arrhythmias. A growing volume of evidence correlates SARS-CoV-2 infection with myocardial injury, exposing patients to higher mortality risk. SARS-CoV-2 attacks the coronary arterial bed with various mechanisms including thrombosis/rupture of preexisting atherosclerotic plaque, de novo coronary thrombosis, endotheliitis, microvascular dysfunction, vasculitis, vasospasm, and ectasia/aneurysm formation. The angiotensin-converting enzyme 2 receptor plays pivotal role on the cardiovascular homeostasis and the unfolding of COVID-19. The activation of immune system, mediated by proinflammatory cytokines along with the dysregulation of the coagulation system, can pose an insult on the coronary artery, which usually manifests as an acute coronary syndrome (ACS). Electrocardiogram, echocardiography, cardiac biomarkers, and coronary angiography are essential tools to set the diagnosis. Revascularization is the first-line treatment in all patients with ACS and obstructed coronary arteries, whereas in type 2 myocardial infarction treatment of hypoxia, anemia and systemic inflammation are indicated. In patients presenting with coronary vasospasm, nitrates and calcium channel blockers are preferred, while treatment of coronary ectasia/aneurysm mandates the use of antiplatelets/anticoagulants, corticosteroids, immunoglobulin, and biologic agents. It is crucial to untangle the exact mechanisms of coronary involvement in COVID-19 in order to ensure timely diagnosis and appropriate treatment. We have reviewed the current literature and provide a detailed overview of the pathophysiology and clinical spectrum associated with coronary implications of SARS-COV-2 infection. Patients with SARS-CoV-2 infection carry an increased risk of cardiovascular disease encompassing various implications, including acute myocardial injury or infarction, myocarditis, heart failure, and arrhythmias. A growing volume of evidence correlates SARS-CoV-2 infection with myocardial injury, exposing patients to higher mortality risk. SARS-CoV-2 attacks the coronary arterial bed with various mechanisms including thrombosis/rupture of preexisting atherosclerotic plaque, de novo coronary thrombosis, endotheliitis, microvascular dysfunction, vasculitis, vasospasm, and ectasia/aneurysm formation. The angiotensin-converting enzyme 2 receptor plays pivotal role on the cardiovascular homeostasis and the unfolding of COVID-19. The activation of immune system, mediated by proinflammatory cytokines along with the dysregulation of the coagulation system, can pose an insult on the coronary artery, which usually manifests as an acute coronary syndrome (ACS). Electrocardiogram, echocardiography, cardiac biomarkers, and coronary angiography are essential tools to set the diagnosis. Revascularization is the first-line treatment in all patients with ACS and obstructed coronary arteries, whereas in type 2 myocardial infarction treatment of hypoxia, anemia and systemic inflammation are indicated. In patients presenting with coronary vasospasm, nitrates and calcium channel blockers are preferred, while treatment of coronary ectasia/aneurysm mandates the use of antiplatelets/anticoagulants, corticosteroids, immunoglobulin, and biologic agents. It is crucial to untangle the exact mechanisms of coronary involvement in COVID-19 in order to ensure timely diagnosis and appropriate treatment. We have reviewed the current literature and provide a detailed overview of the pathophysiology and clinical spectrum associated with coronary implications of SARS-COV-2 infection.

COVID-19 had devastating impacts worldwide. However, most research examining the impact of dementia on COVID-19 outcomes has been conducted in Europe and Asia and has not examined dementia subtypes.

A retrospective analysis of electronic health record data from 21 US health-care systems examined relationships of all-cause dementia, Alzheimer's disease (AD), and vascular dementia with in-hospital mortality, intensive care unit (ICU) admission, and hospital stay duration.

All-cause dementia, but not AD or vascular dementia independently, was associated with increased mortality risk, the inclusion of discharge to hospice as a mortality equivalent increased risk for mortality for all-cause dementia, and AD and vascular dementia. Patients with all-cause dementia and AD were less likely to be admitted to the ICU than patients without. Patients with any form of dementia had longer hospital stays than patients without.

Dementia was associated with increased mortality or hospice discharge, decreased ICU admissions, and longer hospital stays.

Only all-cause dementia was associated with increased mortality risk. This risk was lower than what has been published in previous research. Combining mortality and hospice discharge increased risk for all dementia subtypes. All-cause and Alzheimer's disease (AD) dementia were associated with decreased intensive care unit admissions. All-cause, vascular, and AD dementia were associated with longer hospital stays.

It is necessary to identify appropriate clinical, biochemical, epidemiological and genetic biomarkers to elucidate the underlying mechanisms of the coronavirus disease-2019 (COVID-19) disease. The study focused on not only the link between disease severity (non-intense unit care (non-ICU) versus intensive unit care (ICU) and genetic susceptibility in COVID-19 patients but also the connection between comorbidity and genetic susceptibility affecting the severity of COVID-19.

One hundred and sixty-two COVID-19 patients treated in the non-ICU and ICU in Kayseri City Hospital were included. All volunteers underwent a physical examination and biochemical evaluation. Angiotensin-converting enzyme (ACE p.T776T G > A(rs4343) and g.16471_16472delinsALU (also referred to as I/D polymorphism; rs1799752), angiotensin II receptor type-1 (AGTR1) c.*86A > C (also referred to as A1166C; rs5186), and plasminogen activator inhibitor-1 (PAI-1-844 G > A (rs2227631) polymorphisms were analysed as well.

To have ACE "ID" genotype did not change the severity of the disease (OR: 0.92, 95% CI: 0.41-2.1, p = 0.84), but decreased the mortality risk 2.9-fold (OR: 2.9, 95% CI: 1.1-7.0, p = 0.03). In PAI-1-844 G > A, having the "AA" genotype in the "A" recessive model increased the risk of the diabetes mellitus (DM) 2.3-fold (OR: 2.3 95%, CI: 1.16-4.66, p = 0.018). In the "G" recessive model, to have the GG genotype increased the risk of chronic kidney disease (CKD) 4.8-fold (OR:4.8, 95% CI: 1.5-15.5, p = 0.008). "GG" genotype in the DM group had a higher fibrinogen level compared to those with the "AG" genotype (AG:4847.2 mg/L (1704.3) versus GG:6444.67 mg/L (1861.62) p = 0.019) and "AA" genotype in the CKD group had lower platelet levels and those with "GG" had higher platelet levels (AA:149 µL (18-159) versus GG: 228 µL (146-357) p = 0.022).

This study was shown that genetic predispositions that causes comorbidities were also likely to affect the prognosis of COVID-19.

The coronavirus disease 2019 (COVID-19) pandemic is associated with increases in morbidity and mortality worldwide. The mechanisms of how SARS-CoV-2 may cause cardiovascular (CV) complications are under investigation. The aim of the study was to assess the impact of the COVID-19 pandemic on CV risk.

These are single-centre Bialystok PLUS (Poland) population-based and case‒control studies. The survey was conducted between 2018 and 2022 on a sample of residents (n = 1507) of a large city in central Europe and patients 6-9 months post-COVID-19 infection (n = 126). The Systematic Coronary Risk Estimation 2 (SCORE2), the Systematic Coronary Risk Estimation 2-Older Persons (SCORE2-OP), the Cardiovascular Disease Framingham Heart Study and the LIFEtime-perspective model for individualizing CardioVascular Disease prevention strategies in apparently healthy people (LIFE-CVD) were used. Subsequently, the study populations were divided into CV risk classes according to the 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice.

The study population consisted of 4 groups: a general population examined before (I, n = 691) and during the COVID-19 pandemic (II, n = 816); a group of 126 patients post-COVID-19 infection (III); and a control group matched subjects chosen from the pre-COVID-19 pandemic (IV). Group II was characterized by lower blood pressure, low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) values than group I. Group III differed from the control group in terms of lower LDL-c level. There was no effect on CV risk in the general population, but in the population post-COVID-19 infection, CV risk was lower using FS-lipids, FS-BMI and LIFE-CVD 10-year risk scores compared to the prepandemic population. In all subgroups analysed, no statistically significant difference was found in the frequency of CV risk classes.

The COVID-19 pandemic did not increase the CV risk calculated for primary prevention. Instead, it prompted people to pay attention to their health status, as evidenced by better control of some CV risk factors. As the COVID-19 pandemic has drawn people's attention to health, it is worth exploiting this opportunity to improve public health knowledge through the design of wide-ranging information campaigns.

The precise prediction of COVID-19 prognosis remains a clinical challenge. In this regard, early identification of severe cases facilitates the triage and management of COVID-19 cases. The present paper aims to explore the prognosis of COVID-19 patients based on routine laboratory tests taken when patients are admitted.

A data set including 1455 COVID-19 patients (727 male, 728 female) and their routine laboratory tests conducted upon hospital admission, age, Intensive Care Unit (ICU) admission, and outcome were gathered. The data set was randomly split into the train (75% of the data) and test data set (25% of the data). The explainable boosting machine (EBM) and extreme gradient boosting (XGBoost) were used for predicting the mortality and ICU admission of COVID-19 cases. Also, feature importance was extracted using EBM and XGBoost.

The EBM and XGBoost achieved 86.38% and 88.56% accuracy in the test data set, respectively. In addition, EBM and XGBoost predicted the ICU admission with an accuracy of 89.37%, and 79.29% in the test data set for COVID-19 patients, respectively. Also, obtained models indicated that aspartate transaminase (AST), lymphocyte, blood urea nitrogen (BUN), and age are the most significant predictors of COVID-19 mortality. Furthermore, the lymphocyte count, AST, and BUN level were the most significant ICU admission predictors of COVID-19 patients.

The current study indicated that both EBM and XGBoost could predict the ICU admission and mortality of COVID-19 cases based on routine hematological and clinical chemistry evaluation at the time of admission. Also, based on the results, AST, lymphocyte count, and BUN levels could be used as early predictors of COVID-19 prognosis.

This study aimed to investigate the utility of CT quantification of lung volume for predicting critical outcomes in COVID-19 patients.

This retrospective cohort study included 1200 hospitalised patients with COVID-19 from 4 hospitals. Lung fields were extracted using artificial intelligence-based segmentation, and the percentage of the predicted (%pred) total lung volume (TLC (%pred)) was calculated. The incidence of critical outcomes and posthospitalisation complications was compared between patients with low and high CT lung volumes classified based on the median percentage of predicted TLCct (n=600 for each). Prognostic factors for residual lung volume loss were investigated in 208 patients with COVID-19 via a follow-up CT after 3 months.

The incidence of critical outcomes was higher in the low TLCct (%pred) group than in the high TLCct (%pred) group (14.2% vs 3.3%, p<0.0001). Multivariable analysis of previously reported factors (age, sex, body mass index and comorbidities) demonstrated that CT-derived lung volume was significantly associated with critical outcomes. The low TLCct (%pred) group exhibited a higher incidence of bacterial infection, heart failure, thromboembolism, liver dysfunction and renal dysfunction than the high TLCct (%pred) group. TLCct (%pred) at 3 months was similarly divided into two groups at the median (71.8%). Among patients with follow-up CT scans, lung volumes showed a recovery trend from the time of admission to 3 months but remained lower in critical cases at 3 months.

Lower CT lung volume was associated with critical outcomes, posthospitalisation complications and slower improvement of clinical conditions in COVID-19 patients.

We describe mortality-related risk factors of inpatients with diabetes and coronavirus disease 2019 (COVID-19) in Belgium.

We conducted a multicenter retrospective study from March to May, 2020, in 8 Belgian centers. Data on admission of patients with diabetes and COVID-19 were collected. Survivors were compared to non-survivors to identify prognostic risk factors for in-hospital death using multivariate analysis in both the total population and in the subgroup of patients admitted in the intensive care unit (ICU).

The study included 375 patients. The mortality rate was 26.4% (99/375) in the total population and 40% (27/67) in the ICU. Multivariate analysis identified older age (HR 1.05 [CI 1.03-1.07], P<0.0001) and male gender (HR 2.01 [1.31-3.07], P=0.0013) as main independent risk factors for in-hospital death in the total population. Metformin (HR 0.51 [0.34-0.78], P=0.0018) and renin-angiotensin-aldosterone system blockers (HR 0.56 [0.36-0.86], P=0.0088) use before admission were independent protective factors. In the ICU, chronic kidney disease (CKD) was identified as an independent risk factor for death (HR 4.96 [2.14-11.5], P<0.001).

In-hospital mortality due to the first wave of COVID-19 pandemic in Belgium was high in patients with diabetes. We found that advanced age and male gender were independent risk factors for in-hospital death. We also showed that metformin use before admission was associated with a significant reduction of COVID-19-related in-hospital mortality. Finally, we showed that CKD is a COVID-19-related mortality risk factor in patients with diabetes admitted in the ICU.

Pre-existing coronary artery disease (CAD), and thrombotic, inflammatory, or virus infectivity response phenomena have been associated with COVID-19 disease severity. However, the association of candidate single nucleotide variants (SNVs) related to mechanisms of COVID-19 complications has been seldom analysed. Our aim was to test and validate the effect of candidate SNVs on COVID-19 severity. CARGENCORS (CARdiovascular GENetic risk score for Risk Stratification of patients positive for SARS-CoV-2 [COVID-19] virus) is an age- and sex-matched case-control study with 818 COVID-19 cases hospitalized with hypoxemia, and 1636 controls with COVID-19 treated at home. The association between severity and SNVs related to CAD (n = 32), inflammation (n = 19), thrombosis (n = 14), virus infectivity (n = 11), and two published to be related to COVID-19 severity was tested with adjusted logistic regression models. Two external independent cohorts were used for meta-analysis (SCOURGE and UK Biobank). After adjustment for potential confounders, 14 new SNVs were associated with COVID-19 severity in the CARGENCORS Study. These SNVs were related to CAD (n = 10), thrombosis (n = 2), and inflammation (n = 2). We also confirmed eight SNVs previously related to severe COVID-19 and virus infectivity. The meta-analysis showed five SNVs associated with severe COVID-19 in adjusted analyses (rs11385942, rs1561198, rs6632704, rs6629110, and rs12329760). We identified 14 novel SNVs and confirmed eight previously related to COVID-19 severity in the CARGENCORS data. In the meta-analysis, five SNVs were significantly associated to COVID-19 severity, one of them previously related to CAD.

During the first wave of COVID-19, three-quarters of Canadian deaths were among those age 80 and older. We examined whether age, chronic disease load, sex, or place was the strongest predictor of such deaths. A cross-sectional analysis of administrative data from 1 January 2020 to 30 October 2020 for the population of Ontario (n = 15,023,174) was performed. Using logistic regression analysis, we determined whether place of residence (community dwelling, community dwelling with formal home care, or long-term care facility), age group, sex, or chronic disease burden was most strongly associated with the outcome of death within 60 days of a positive SARS-CoV-2 PCR test. Overall, there were 2766 deaths attributed to COVID-19. The age-related odds of dying increased from 6.1 (age 65-74) to 13.4 (age 85 or older) relative to those aged <65 years. This age effect was dwarfed by an odds ratio of 117.1 for those living in long-term care versus independently in the community, adjusted for age, sex, and chronic disease burden. The risk of death from COVID-19 aligned much more with social realities than individual risks. The disproportionate mortality arising specifically from institutional residence demands action to identify sources and ameliorate the harms of living in such facilities.

Pre-existing neurological diseases have been identified as risk factors for severe COVID-19 infection and death. There is a lack of comprehensive literature review assessing the relationship between pre-existing neurological conditions and COVID-19 outcomes. Identification of high risk groups is critical for optimal treatment and care.

A literature review was conducted for systematic reviews, meta-analyses, and scoping reviews published between January 1, 2020 and January 1, 2023. Literature assessing individuals with pre-existing neurological diseases and COVID-19 infection was included. Information regarding infection severity was extracted, and potential limitations were identified.

Thirty-nine articles met inclusion criteria, with data assessing >3 million patients from 51 countries. 26/51 (50.9%) of countries analyzed were classified as high income, while the remaining represented middle-low income countries (25/51; 49.0%). A majority of evidence focused on the impact of cerebrovascular disease (17/39; 43.5%) and dementia (5/39; 12.8%) on COVID-19 severity and mortality. 92.3% of the articles (36/39) suggested a significant association between neurological conditions and increased risk of severe COVID-19 and mortality. Cerebrovascular disease, dementia, Parkinson's disease, and epilepsy were associated with increased COVID severity and mortality.

Pre-existing neurological diseases including cerebrovascular disease, Alzheimer's disease and other dementias, epilepsy, and Parkinson's disease are significant risk factors for severity of COVID-19 infection and mortality in the acute infectious period. Given that 61.5% (24/39) of the current evidence only includes data from 2020, further updated literature is crucial to identify the relationship between chronic neurological conditions and clinical characteristics of COVID-19 variants.

Patients diagnosed with coronavirus disease (CVD) who experience cardiovascular complications or have pre-existing cardiovascular disease are at an increased risk of death. The primary heart-related consequences associated with COVID-19 encompass venous thromboembolism, shock, heart failure, arrhythmias, myocarditis, acute myocardial infarction, and acute cardiac damage. The coronavirus has the potential to induce cardiovascular complications or exacerbate pre-existing CVD through various mechanisms. These mechanisms include dysregulation of the renin-angiotensin-aldosterone system; direct viral toxicity; damage to endothelial cells; formation of blood clots and subsequent inflammation, a phenomenon known as thromboinflammation; an excessive immune response known as cytokine storm; and an imbalance between the demand and supply of oxygen in the body. In this study, we comprehensively analyze the cardiovascular symptoms, histology, and underlying mechanisms associated with COVID-19. Our aim is to contribute to the identification of future research objectives and aid in the advancement of therapeutic management approaches.

Evidence increasingly shows that the risk of thrombotic complications in COVID-19 is associated with a hypercoagulable state. Several organizations have released guidelines for the management of COVID-19-related coagulopathy and prevention of VTE. However, an urgent need exists for practical guidance on the management of arterial thrombosis and thromboembolism in this setting.

What is the current available evidence informing the prevention and management of arterial thrombosis and thromboembolism in patients with COVID-19?

A group of approved panelists developed key clinical questions by using the Population, Intervention, Comparator, and Outcome (PICO) format that address urgent clinical questions regarding prevention and management of arterial thrombosis and thromboembolism in patients with COVID-19. Using MEDLINE via PubMed, a literature search was conducted and references were screened for inclusion. Data from included studies were summarized and reviewed by the panel. Consensus for the direction and strength of recommendations was achieved using a modified Delphi survey.

The review and analysis of the literature based on 11 PICO questions resulted in 11 recommendations. Overall, a low quality of evidence specific to the population with COVID-19 was found. Consequently, many of the recommendations were based on indirect evidence and prior guidelines in similar populations without COVID-19.

The existing evidence and panel consensus do not suggest a major departure from the management of arterial thrombosis according to recommendations predating the COVID-19 pandemic. Data on the optimal strategies for prevention and management of arterial thrombosis and thromboembolism in patients with COVID-19 are sparse. More high-quality evidence is needed to inform management strategies in these patients.

The establishment of Alternate Care Sites (ACS) helped the most severely impacted countries expand their response capability. The aim of this study was to evaluate the clinical characteristics and risk factors associated with the mortality of hospitalized COVID-19 patients at Alternate Care Site in Mexico City.

A monocentric cohort study was conducted at Mexico City's Temporary Unit COVID-19 (UTC-19). Sociodemographic, clinical, laboratory and treatment variables were included in the analysis.

A total of 4865 patients were included, with a mean age of 49.33 years ± SD 15.28 years (IQR 38 to 60 years); 50.53% were women. 63.53% of the patients presented at least one comorbidity, the most frequent being: obesity (39.94%), systemic arterial hypertension (25.14%), and diabetes mellitus (21.52%). A total of 4549 patients (93.50%) were discharged due to improvement, 64 patients (1.31%) requested voluntary discharge, 39 patients (0.80%) were referred to another unit, and 213 patients (4.37%) died. Factors that were independently and significantly associated with death included male gender (odds ratio [OR], 1.60), age ≥ 50 years (OR 14.75), null or low schooling (OR 3.47), have at least one comorbidity (OR 3.26), atrial fibrillation (OR 22.14). In the multivariate analysis, the lymphopenia ≤ 1 × 103/μL (OR 1.91), and having required steroid treatment (OR 2.85), supplemental oxygen with high-flow nasal cannula (OR 3.12) or invasive mechanical ventilation (OR 42.52), was significantly associated with an increased risk of death.

This study identified the clinical characteristics and risk factors for mortality of hospitalized COVID-19 patients at ACS in Mexico City.KEY MESSAGESAn Alternate Care Site (ACS) is any building or structure that is temporarily converted or constructed for healthcare use during a public health emergency.Factors associated with death included male gender, age over 50 years, and lower educational attainment (elementary school or less).The findings corroborate the utility of the CALL score as a predictor of mortality; lymphopenia ≤1 × 103/μL was the most relevant biomarker.

This study examined the impact of multimorbidity on severe COVID-19 outcomes in community and long-term care (LTC) settings, alone and in interaction with age and sex.

We conducted a retrospective cohort study of all Ontarians who tested positive for COVID-19 between January-2020 and May-2021 with follow-up until June 2021. We used cox regression to evaluate the adjusted impact of multimorbidity, individual characteristics, and interactions on time to hospitalization and death (any cause).

24.5% of the cohort had 2 or more pre-existing conditions. Multimorbidity was associated with 28% to 170% shorter time to hospitalization and death, respectively. However, predictors of hospitalization and death differed for people living in community and LTC. In community, increasing multimorbidity and age predicted shortened time to hospitalization and death. In LTC, we found none of the predictors examined were associated with time to hospitalization, except for increasing age that predicted reduced time to death up to 40.6 times. Sex was a predictor across all settings and outcomes: among male the risk of hospitalization or death was higher shortly after infection (e.g. HR for males at 14 days = 30.3) while among female risk was higher for both outcome in the longer term (e.g. HR for males at 150 days = 0.16). Age and sex modified the impact of multimorbidity in the community.

Community-focused public health measures should be targeted and consider sociodemographic and clinical characteristics such as multimorbidity. In LTC settings, further research is needed to identify factors that may contribute to improved outcomes.

To evaluate the relationship between the in-hospital mortality of patients with COVID-19 and the history of cardiovascular disease (CVD) using data from the Russian registry of patients with COVID-19.

This study included 758 patients with COVID-19 (403 men, 355 women) aged from 18 to 95 years (median, 61 years), successively hospitalized in the COVID hospital of the Chazov National Medical Research Center of Cardiology from April through June 2020. Death predictors were studied using single- and multivariate regression analyses with the SPSS Statistics, Version 23.0 software.

During the stay in the hospital, 59 (7.8 %) patients with COVID-19 died, 677 (89.3 %) were discharged, and 22 (2.9 %) were transferred to other hospitals. The univariate regression analysis showed that the increase in age per decade was associated with a 92% increase in the risk of death [relative risk (RR), 1.92; 95% confidence interval (CI), 1.58-2.34; p <0.001], and an increase in the number of CVDs increases the risk of death by 71% (RR 1.71; 95% CI 1.42-2.07; p<0.001). The presence of one or more CVDs or specific diseases [atrial fibrillation, chronic heart failure (CHF), ischemic heart disease, myocardial infarction, history of cerebrovascular accidents], as well as diabetes mellitus were associated with a higher risk of fatal outcome during the hospitalization for COVID-19. The presence of any CVD increased the risk of in-hospital death by 3.2 times. However, when the model was adjusted for age and sex, this association lost its strength, and only the presence of CHF was associated with a 3-fold increase in the risk of death (RR, 3.16; 95 % CI, 1.64-6.09; p=0.001). Age was another independent predictor of death (RR, 1.05; 95 % CI, 1.03-1.08; p < 0.001).

A history of CVD and the CVD number and severity are associated with a higher risk of death during the hospitalization for COVID-19; the independent predictors of in-hospital death are an age of 80 years and older and CHF.

Background The emergence of the less virulent COVID-19 strains such as Omicron and its subvariants shifted the paradigm of COVID-19 treatment from inpatient treatment to regular outpatient care. The individual health determinants affecting COVID-19 disease severity among vulnerable adults treated in outpatient settings are an under-researched area. Methods This study conducted in an outpatient COVID-19 antibody infusion center employed a cross-sectional survey design to explore the impact of comorbidities, general health status, and self-care self-efficacy on COVID-19 symptom severity. We recruited 120 COVID-19-positive participants over 40 years of age, of which 117 completed the study with 87 providing complete data. After the screening and consenting process, the participants completed the following surveys in a secure REDCap survey software (Vanderbilt University, Nashville, USA) on an iPad (Apple Inc., Cupertino, USA): 1) sociodemographic questionnaire, 2) Charlson Comorbidity Index (CCI) to capture comorbidities, 3) Medical Outcomes Study Short-Form (SF-12) to assess general health including physical (PCS) and mental (MCS) health subscales, 4) Self-Care Self-Efficacy Scale (SCSES) to measure self-care self-efficacy, and 5) the COVID-19 Symptom rating scale (COVID-19 SRS). Statistical analysis used were Chi-square and Pearson correlations.  Results As evidenced by CCI, the top five comorbidities were hypertension (42%), diabetes mellitus (31%), pulmonary disease (19%), depression (14%), and solid tumors (11%). Age was statistically significantly correlated to comorbidity burden (p<0.0001). Severe COVID-19 symptoms reported were fatigue, myalgia, cough, runny nose, and sore throat. The general health status measure (SF-12) subscales showed that the patient's mental component summary (MCS) was more statistically significant to COVID-19 symptom severity than the physical component summary (PCS). The MCS demonstrated a statistically significant correlation with fatigue and myalgia (p<0.0001), headache and breathing difficulties (p<0.001), nausea/vomiting (p<0.01), and abdominal pain/diarrhea (p<0.05). The PCS showed a lesser statistically significant correlation with fatigue, myalgia, headaches (p<0.01), fever/chills, cough, congestion/runny nose, night sweats, breathing difficulties, nausea/vomiting, and abdominal pain/diarrhea (p<0.05). Interestingly, the 'loss of smell' which is the hallmark symptom of COVID-19 was the only symptom that showed a statically significant correlation with the Charlson Comorbidity Index (p<0.05), and it did not show any association with either mental (SF-12 MCS) or physical (SF-12 PCS) health status. The SF-12 MCS also showed a statistically significant correlation with a diagnosis of depression (p< 0.01), validating it as a true measure of mental health among vulnerable adults. The SCSES was not correlated with any of the COVID-19 symptoms. Conclusions The patient's general health status, especially mental health was more statistically significant to COVID-19 symptoms. The COVID-19 hallmark symptom of 'loss of smell' was the only symptom that showed statistical significance with comorbidities. Within the limitations of a cross-sectional survey design and convenient sampling methods, this study calls to tailor general health status, especially mental health, and cumulative comorbidity burden to risk assessment/risk stratification of COVID-19 care.

The COVID-19 pandemic has evolved since the publication of the initial American Society of Echocardiography (ASE) statements providing guidance to echocardiography laboratories. In light of new developments, the ASE convened a diverse, expert writing group to address the current state of the COVID-19 pandemic and to apply lessons learned to echocardiography laboratory operations in future pandemics. This statement addresses important areas specifically impacted by the current and future pandemics: (1) indications for echocardiography, (2) application of echocardiographic services in a pandemic, (3) infection/transmission mitigation strategies, (4) role of cardiac point-of-care ultrasound/critical care echocardiography, and (5) training in echocardiography.

Although the severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) causing coronavirus disease 2019 (COVID-19) primarily affects the respiratory system, the disease entity has been associated with cardiovascular complications. This study sought to assess the effect of concomitant SARS-COV-2 infection on clinical outcomes of patients hospitalized primarily for acute cardiac conditions on cardiology wards in Switzerland.

In this prospective, observational study conducted in 5 Swiss cardiology centers during the COVID-19 pandemic, patients hospitalized due to acute cardiac conditions underwent a reverse-transcriptase polymerase chain reaction test at the time of admission and were categorized as SARS-COV-2 positive (cases) or negative (controls). Patients hospitalized on cardiology wards underwent treatment for the principal acute cardiac condition according to local practice. Clinical outcomes were recorded in-hospital, at 30 days, and after 1 year and compared between cases and controls. To adjust for imbalanced baseline characteristics, a subgroup of patients derived by propensity matching was analyzed.

Between March 2020 and February 2022, 538 patients were enrolled including 122 cases and 416 controls. Mean age was 68.0 ± 14.7 years, and 75% were men. Compared with controls, SARS-COV-2-positive patients more commonly presented with acute heart failure (35% vs. 17%) or major arrhythmia (31% vs. 9%), but less commonly with acute coronary syndrome (26% vs. 53%) or severe aortic stenosis (4% vs. 18%). Mortality was significantly higher in cases vs. controls in-hospital (16% vs. 1%), at 30 days (19.0% vs. 2.2%), and at 1 year (28.7% vs. 7.6%: p < 0.001 for all); this was driven primarily (up to 30 days) and exclusively (at one-year follow-up) by higher non-cardiovascular mortality, and was accompanied by a greater incidence of worsening renal function in cases vs. controls. These findings were maintained in a propensity-matched subgroup of 186 patients (93 cases and 93 controls) with balanced clinical presentation and baseline characteristics.

In this observational study of patients hospitalized for acute cardiac conditions, SARS-COV-2 infection at index hospitalization was associated with markedly higher all-cause and non-cardiovascular mortality throughout one-year follow-up. These findings highlight the need for effective, multifaceted management of both cardiac and non-cardiac morbidities and prolonged surveillance in patients with acute cardiac conditions complicated by SARS-COV-2 infection.

Acute kidney injury is a complication of COVID-19 and is associated with severity. Despite no specific antiviral treatment strategy, lopinavir/ritonavir and remdesivir have been used. Data on the association between AKI and receiving antiviral agents with outcomes in hospitalized patients with COVID-19 is scarce. We aimed to determine the incidence of AKI and its outcomes in COVID-19 patients with and without antiviral medications.

We conducted a retrospective study on hospitalized adult patients with SARS-CoV-2 infection in a tertiary center. The primary endpoint was determining mortality, intensive care unit (ICU) admission, and length of hospitalization affected by AKI development using antiviral agents. The logistic regression method was used to explore the predictive effects of AKI and antiviral therapy on composite outcomes (i.e., mortality, ICU admission, and prolonged hospitalization) in four defined groups by AKI development/not and utilizing antivirals/not. We used IBM SPSS version 24.0 software for statistical analysis.

Out of 833 COVID-19 patients who were included, 75 patients were treated with antiviral agents and developed AKI. There was a significant difference in the occurrence of AKI and using antiviral medications (p = 0.001). Also, the group using antiviral agents and the development of AKI had the highest rate of preexisting hypertension (p = 0.002). Of note, the group of patients who used antiviral agents and also developed AKI had the most remarkable association with our composite outcome (p<0.0001), especially ICU admission (OR = 15.22; 95% CI: 8.06-27.32).

The presence of AKI among COVID-19 patients treated with antiviral agents is linked to increased severity and mortality. Therefore, it is imperative to explore preventive measures for AKI development in patients receiving antiviral therapy. Larger-scale randomized controlled trials may be warranted to provide a more comprehensive understanding of these associations.

Cardiovascular (CV) disease is a known complication of SARS-CoV-2 infection. A clear benefit of COVID-19 vaccination is a reduction mortality; however, COVID-19 vaccination may also prevent cardiovascular disease (CVD). We aim to describe CV pathology associated with SARS-CoV-2 infection and describe how COVID-19 vaccination is a strategy for CVD prevention.

The risks and benefits of COVID-19 vaccination have been widely studied. Analysis of individuals with and without pre-existing CVD has shown that COVID-19 vaccination can prevent morbidity associated with SARS-CoV-2 infection and reduce mortality. COVID-19 vaccination is effective in preventing myocardial infarction, cerebrovascular events, myopericarditis, and long COVID, all associated with CVD risk factors. Vaccination reduces mortality in patients with pre-existing CVD. Further study investigating ideal vaccination schedules for individuals with CVD should be undertaken to protect this vulnerable group and address new risks from variants of concern.

Molnupiravir is an oral antiviral agent authorized for emergency use to treat mild to moderate cases of coronavirus disease 2019 (COVID-19) in adults at high risk for progression to severe clinical outcomes. This study aimed to describe patient characteristics and health outcomes in a cohort of adult patients treated with molnupiravir in an outpatient setting in the United States.

This was a retrospective cohort study of adults identified in the HealthVerity database with a pharmacy claim for molnupiravir between December 24, 2021, and April 14, 2022. Hospitalization and health care use were assessed over the 28 days after the molnupiravir pharmacy claim.

Among 26,554 patients identified, 71.1% were aged ≥50 years and 58.9% were female. A total of 8794 patients (33.1%) had received at least 1 dose of the COVID-19 vaccine. The most prevalent risk factors for severe COVID-19 identified were hypertension (45.1%), steroid and/or immunosuppressant use (39.6%), and being obese or overweight (24.6%), with 79.1% of patients having ≥1 risk factor. The majority (61.0%) of patients were prescribed comedications contraindicated with or had the potential for major drug-drug interactions with ritonavir-containing regimens. Within 28 days after initiating molnupiravir, 3.3% of patients were hospitalized for any cause and 1.7% for COVID-19-related reasons. Among all hospitalized patients, 9.2% were admitted to an intensive care unit, 3.9% received oxygen, and 3.8% required mechanical ventilation.

The majority of patients treated with molnupiravir in early 2022 had at least one risk factor for severe COVID-19 and had comedications that could require treatment modification or monitoring if given a ritonavir-containing regimen. Hospitalization was uncommon after treatment with molnupiravir, with COVID-19-related inpatient admission in <2% of patients. Among those hospitalized, patient use of intensive care and oxygen-based resources was infrequent. The study design, however, does not permit any conclusions regarding the effectiveness of molnupiravir.

Molnupiravir (MOV) was introduced in Israel in January 2022 during the SARS-CoV-2 Omicron surge for high-risk patients contraindicated for nirmatrelvir/ritonavir. This retrospective cohort study aimed to describe characteristics of patients offered COVID-19 antiviral treatment in Maccabi Healthcare Services (antiviral treatment-eligible cohort; n = 5596) between 12 January and 28 February 2022, and the subset of these who were dispensed MOV (MOV-treated cohort; n = 1147), as well as outcomes following MOV dispensation. Median (interquartile range) age in the antiviral treatment-eligible and MOV-treated cohorts were 70.5 (61.1, 77.3) and 74.1 (64.3, 81.7) years, respectively. The MOV-treated cohort (male: 53.2%) had high rates of COVID-19 vaccination (91.4%) and comorbidities, including immunosuppression (40.0%) and chronic kidney disease (67.0%; eGFR < 30 mL/min/1.73 m2: 28.8%), and most used comedications either contraindicated or with major potential for drug-drug interactions with nirmatrelvir/ritonavir (87.3%). At 28 days post-MOV dispensation, the cumulative incidence (95% CI) of COVID-19-related hospitalization and/or all-cause mortality was 3.6% (2.5%, 4.6%), with similar rates across sexes and age groups (18-64 vs. ≥65 years), and lower rates among recently vaccinated and/or recently SARS-CoV-2-infected patients. These data describe the characteristics and outcomes for MOV-treated patients in Israel, whose clinical characteristics may preclude the use of nirmatrelvir/ritonavir to treat their COVID-19 infection.

There are limited data on precision medicine in infectious diseases and vaccines; however, precise management of infectious diseases plays a critical role in trust for government, health-care organizations, science, and pharma. The improvement in biomedical technologies, availability of large clinical and -omic data and appropriate application of artificial intelligence may allow precision in vaccines and public health and restore trust. This is an invited editorial on the role of precision medicine in infectious diseases and vaccines.

Myocardial injury is a prevalent complication observed in patients hospitalized with COVID-19 and is strongly associated with severe illness and in-hospital mortality. However, the long-term consequences of myocardial injury on clinical outcomes remain poorly understood. This study aimed to assess the impact of myocardial injury on both acute-phase and long-term prognosis in COVID-19 patients.

A retrospective, observational study was conducted on all patients who received treatment at the Intensive Care Center for COVID-19 patient, University Medical Center Ho Chi Minh City (UCICC), from August 3rd, 2021, to October 28th, 2021.

A total of 582 patients were enrolled in the study, of which 55.3% were female. The mean age of participants was 63.3 ± 16.2. Out of these patients, 330 cases (56.8%) showed myocardial injury. Compared to patients without myocardial injury, those with myocardial injury were older and had a higher incidence of chronic diseases including hypertension, ischemic heart disease, atrial fibrillation, heart failure, diabetes mellitus, chronic kidney disease. They also presented with more severe respiratory failure upon admission and showed a more pronounced abnormality in inflammation and kidney function tests. Furthermore, the in-hospital mortality rate was significantly higher in the group with myocardial injury (49.7% vs 14.3%, p < 0.001). After adjusting for age, gender, comorbidities, renal function, and disease severity at admission, myocardial injury emerged as an independent risk factor for in-hospital mortality (OR = 3.758, 95% CI 1.854-7.678, p < 0.001). Among successfully discharged COVID-19 patients, the all-cause mortality rate after a median follow-up of 18.4 months was 7.9%. Patients with myocardial injury had a significantly higher long-term mortality rate compared to those without myocardial injury (14.0% vs. 3.2%, p < 0.001). However, multivariable Cox regression analysis did not find myocardial injury to be a significant predictor of long-term mortality (HR = 2.128, 95% CI 0.792-5.712, p = 0.134).

Myocardial injury is a common and serious complication in hospitalized COVID-19 patients, associated with increased in-hospital mortality. However, it does not significantly impact long-term mortality in successfully discharged COVID-19 patients.

Coronavirus disease 2019 (COVID-19), caused by a novel coronavirus, manifests as a respiratory illness primarily and symptoms range from asymptomatic to severe respiratory syndrome and even death. During the pandemic, due to overcrowding of medical facilities, clinical assessment to triage patients for home care or in-hospital treatment was an essential element of management.

Study the demographic features, comorbidities and bio-markers that predict severe illness and mortality from COVID-19 infection.

Retrospective observational SETTING: Single tertiary care center PATIENTS AND METHODS: The study included all patients admitted with a positive PCR test for COVID-19 during the period from March 2020 to September 2020 (7 months). Data on demographics, clinical data and laboratory parameters was collected from medical records every 3 days during hospital stay or up until transfer to ICU.

Demographic, comorbidities and biochemical features that might predict severe COVID-19 disease.

372 RESULTS: Of the 372 patients, 72 (19.4%) had severe disease requiring admission to intensive care unit (ICU); 6 (1.6%) died. Individuals over 62 years were more likely to be admitted to the ICU (P=.0001, while a BMI of 40 and higher increased the odds of severe disease (P=.032). Male gender (P=.042), hypertension (P=.006) and diabetes (P=.001) conferred a statistically significant increased risk of admission to ICU, while coexisting COPD, and ischemic heart disease did not. Laboratory features related to severe COVID-19 infection were: leukocytosis (P=.015), thrombocytopenia (P=.001), high levels of C-reactive protein (P=.0001), lactic dehydrogenase (P=.0001), D-dimer (P=.0001) and ferritin (P=.001). With the multivariate analysis, diabetes, high lac-tate dehydrogenase, C-reactive protein and thrombocytopenia were associated with severity of illness.

Particular demographic and clinical parameters may predict severe illness and need for ICU care.

Single referral center, several cases of severe COVID-19 could not be included due to lack of consent and or data.

None.