NETosis, the process through which neutrophils release neutrophil extracellular traps (NETs), has emerged as a crucial mechanism in host defense and the pathogenesis of autoimmune responses. During the SARS-CoV-2 pandemic, this process received significant attention due to the central role of neutrophil recruitment and activation in infection control. However, elevated neutrophil levels and dysregulated NET formation have been linked to coagulopathy and endothelial damage, correlating with disease severity and poor prognosis in COVID-19. Moreover, it is known that SARS-CoV-2 can induce persistent low-grade systemic inflammation, known as long COVID, although the underlying causes remain unclear. It has been increasingly acknowledged that excessive NETosis and NET generation contribute to further pathophysiological abnormalities following SARS-CoV-2 infection. This review provides an updated overview of the role of NETosis in autoimmune diseases, but also the relationship between COVID-19 and long COVID with autoimmunity (e.g., latent and overt autoimmunity, molecular mimicry, epitope spreading) and NETosis (e.g., immune responses, NET markers). Finally, we discuss potential therapeutic strategies targeting dysregulated NETosis to mitigate the severe complications of COVID-19 and long COVID.

The aim of the present study was to quantify the rate of thromboembolic events (TE) in pregnant women with SARS-CoV-2 infection and to characterize risk factors to provide a basis for individualized recommendation on prophylactic measures.

CRONOS is a multicenter, prospective observational study conducted in Germany and Austria during the COVID-19 pandemic. Pregnant women with confirmed SARS-CoV-2 infection were enrolled. Data on demographics, medical history, COVID-19-related aspects, and pregnancy and birth outcomes were collected. TE was particularly queried and used as the primary outcome. A combination of "TE," "maternal or fetal death," or "severe postpartum hemorrhage" was defined as a secondary endpoint. Risk analyses were performed using univariate and multivariable logistic regression models.

Data from 8033 pregnant patients showed 40 TEs (0.5% incidence). TE rates were 10% in ICU patients, 0.2-0.4% in those with moderate-to-mild COVID-19, and < 0.1% in asymptomatic women. Pulmonary embolism occurred in 21 cases, deep vein thrombosis in 12, and 7 had atypical or arterial TE. Risk factors included advanced gestational age, COVID-19 symptoms, hospitalization or ICU admission, premature birth, cesarean section, delivery within 4 weeks of infection, higher weight gain, anemia, and chronic inflammatory bowel disease. COVID-19 vaccination reduced risk. The logistic risk model yielded an AUC of 0.87 (95% CI 0.81-0.94).

The TE rate in pregnant women is largely determined by the severity of the disease. In asymptomatic or mild cases, other factors outweigh TE risk, while severe COVID-19 requiring ICU admission poses a high TE risk despite prophylaxis.

Abnormalities in liver biochemistry are common in COVID-19 patients. Hepatic vein Doppler waveform, typically triphasic, may become biphasic or monophasic in cirrhosis, correlating with liver dysfunction, fibrosis, inflammation, and portal hypertension. This study investigates liver ultrasound (US) features in COVID-19 patients, correlating hepatic vein Doppler waveform and portal vein velocity (PVV) with inflammatory indexes and clinical outcomes.

Fifty-seven patients with SARS-CoV-2 infection participated in a crosssectional study. Bedside upper abdomen US evaluations, including B-mode and Doppler, were conducted using a convex probe. Hepatic vein Doppler waveforms were classified as triphasic, biphasic, or monophasic, and the hepatic vein waveform index (HVWI) was calculated. PVV was measured over three cardiac cycles. Tracings were blindly analyzed by three operators to ensure consistency.

Low HVWI and high PVV correlated with elevated LDH, ALT, D-dimer, and ferritin (p < 0.05). HVWI showed significant negative correlations with ferritin, D-dimer, and ALT (p < 0.05). D-Dimer and ferritin were higher in patients with biphasic/monophasic waveforms (p < 0.05). High PVV and larger spleen diameters predicted worse respiratory outcomes, including CPAP and tracheal intubation (p < 0.05). Optimal cut-off values for PVV (21.7 cm/s) and spleen diameter (9.84 cm) maximized sensitivity and specificity for predicting these outcomes. FIB-4 scores did not correlate with respiratory outcomes or hepatic hemodynamics (p > 0.05). Hemodynamic alterations were not significantly influenced by the presence of SLD (Steatotic Liver Disease).

COVID-19 patients exhibit altered intrahepatic hemodynamics, with hepatic vein waveform abnormalities potentially reflecting liver inflammation and fibrosis. PVV and spleen diameter may serve as non-invasive predictors of respiratory outcomes.

Background: The SARS-CoV-2 virus, identified in December 2019, led to a global pandemic resulting in over 6 million deaths. While most COVID-19 cases present mild symptoms, severe complications can develop in immunocompromised patients, including impacts on the heart. This study aimed to compare angiographic findings and hospitalization outcomes in acute coronary syndrome (ACS) patients with and without COVID-19. Methods: This retrospective study analyzed 174 ACS patients (105 men, 69 women) hospitalized in the Department of Cardiology and Internal Medicine of the Nicolaus Copernicus University in Bydgoszcz and Regional Hospital in Grudziądz (2019-2021). Forty-eight of them had COVID-19. The analyzed parameters included, inter alia, the coronary artery disease severity, the presence of thrombosis, survival rates, risk factors, and prior endovascular procedures. Results: COVID-19 patients with ACS showed a higher rate of thrombus in non-culprit vessels (6.25% vs. 0.0%, p = 0.0293), and overall survival was significantly lower (68.75% vs. 93.65%, p < 0.0001), while prior PCI rates were higher in non-COVID patients (34.13% vs. 6.25%, p = 0.0002). Procedure times were shorter for non-COVID patients, reducing catheterization lab exposure. Other procedural factors showed no significant differences. Conclusions: This study highlights significant differences in coronary angiography and hospitalization outcomes between ACS patients with and without COVID-19. The extended stay of COVID-19 patients in the catheterization lab poses an increased risk to medical staff, and the presence of thrombi underscores the need for effective antithrombotic strategies. The significant association of COVID-19 with hypercoagulability and its role in precipitating acute coronary syndromes necessitates the development of specific clinical guidelines to manage these patients effectively.

The COVID-19 pandemic, caused by SARS-CoV-2, posed a tremendous challenge to healthcare systems globally. Severe COVID-19 infection was reported to be associated with altered immunometabolism and cytokine storms, contributing to poor clinical outcomes and in many cases resulting in mortality. Despite promising preclinical results, many drugs have failed to show efficacy in clinical trials, highlighting the need for novel approaches to combat the virus and its severe manifestations. Mitochondria, crucial for aerobic respiration, play a pivotal role in modulating immunometabolism and neuronal function, making their compromised capability as central pathological mechanism contributing to the development of neurological complications in COVID-19. Dysregulated mitochondrial dynamics can lead to uncontrolled immune responses, underscoring the importance of mitochondrial regulation in shaping clinical outcomes. Aging further accelerates mitochondrial dysfunction, compounding immune dysregulation and neurodegeneration, making older adults particularly vulnerable to severe COVID-19 and its neurological sequelae. COVID-19 infection impairs mitochondrial oxidative phosphorylation, contributing to the long-term neurological complications associated with the disease. Additionally, recent reports also suggest that up to 30% of COVID-19 patients experience lingering neurological issues, thereby highlighting the critical need for further research into mitochondrial pathways to mitigate long-tern neurological consequences of Covid-19. This review examines the role of mitochondrial dysfunction in COVID-19-induced neurological complications, its connection to aging, and potential biomarkers for clinical diagnostics. It also discusses therapeutic strategies aimed at maintaining mitochondrial integrity to improve COVID-19 outcomes.

Thrombophilia, characterized by an imbalance between fibrinolysis and coagulation leading to inappropriate blood clotting, is a significant medical condition. The CDC has designated it as an underdiagnosed, serious, and potentially preventable disorder, contributing to an estimated 600,000-900,000 cases and 100,000 deaths annually in the United States. These figures surpass the combined annual mortality of AIDS, breast cancer, and motor vehicle accidents. The pathogenesis of thrombophilia involves complex interactions between genetic predispositions, such as mutations in Factor V Leiden, Factor II, MTHFR, and Serpine-1, and environmental factors, including unhealthy lifestyles, prolonged hospitalization, obesity, and cancer. Prevalence of specific genetic mutations varies across populations. Additional risk factors include age, family history, and pregnancy, with recent attention to increased susceptibility in SARS-CoV-2 infection. While molecular diagnostic techniques are available, there remains a need for robust, cost-effective, and accurate screening methods for large populations. This systematic review provides an updated overview of thrombophilia, encompassing pathophysiology, epidemiology, genetic and environmental risk factors, coagulation cascade, population-specific mutation prevalence, and diagnostic approaches. By synthesizing clinical and molecular evidence, this review aims to guide researchers, hematologists, and clinicians in the diagnosis and management of thrombophilia.

Acute macular neuroretinopathy (AMN) is a rare retinal condition that predominantly affects young females. The incidence of AMN increased significantly during the COVID-19 pandemic, thereby providing a unique opportunity to elucidate the etiology of this disease. In the present study, 24 articles reporting 59 patients were reviewed. The average age of the patients was 33.51 ± 14.02 years, ranging from 16 to 75 years, with females comprising 71.19% of the cases. The average duration of ocular symptoms post-infection was 8.22 ± 10.69 days, ranging from 4 to 150 days. This study investigated the potential pathogenesis of AMN, including the impact of COVID-19 on retinal neurovascular structure and function, immune-mediated inflammatory factor production, blood-retinal barrier disruption, and retinal microvascular damage, as well as potential clinical therapeutic interventions. This research provides a theoretical framework that can inform further investigations of AMN.

Obesity is a critical risk factor for ischemic heart disease (IHD), affecting 42% of the U.S. population. This study examines trends in obesity-related IHD mortality among U.S. adults aged 25 and older from 1999 to 2020, using the CDC WONDER database.

We analyzed IHD as the primary cause and obesity as a contributing factor, calculating age-adjusted (AAMRs) and crude mortality rates (CMRs) per 100,000 individuals. Joinpoint regression assessed annual percent changes (APC), stratifying by race, sex, age, and region.

From 1999 to 2020, 139,644 obesity-related IHD deaths were recorded. AAMR rose from 1.92 to 4.69 per 100,000. Rates were higher in men (3.79) than women (2.10), with Black Americans showing the highest AAMR (4.07). Older adults (65+) had the highest CMR (5.73). Nonmetropolitan areas exhibited higher AAMRs (3.47) than metropolitan regions (2.78). States with the highest mortality included Vermont, Oklahoma, Wyoming, Wisconsin and Iowa while Alabama, Virginia, Massachusetts, Connecticut and Georgia had the lowest.

The findings indicate a 2.5-fold increase in obesity-related IHD mortality, highlighting the need for targeted public health interventions and further research to address this growing public health concern.

This study aimed to analyze the risk factors of lower extremity deep vein thrombosis (LEDVT) in emergency inpatients in the post-epidemic era, and to establish a prediction model for identifying high-risk patients of LEDVT.

Emergency inpatients admitted to our hospital from June 2022 to June 2023 were divided into two groups: the epidemic group and the post-epidemic group. The baseline characteristics, blood routine, liver and kidney function, blood coagulation function, and LE ultrasonography were compared between the two groups. Multivariate logistic analysis and receiver operating character (ROC) curve were used to establish and evaluate the effectiveness of a prediction model for LEDVT in the post-epidemic era.

A total of 967 patients were analyzed, including 388 cases in the epidemic group and 579 cases in the post-epidemic group. The portion of LEDVT cases in the post-epidemic group (33.2%) was significantly higher than that in the epidemic group (26.8%, P = 0.036). Binary Logistic regression analysis showed that age, smoking history, drinking history and glycosylated hemoglobin (HBA1c) were independent risk factors for thrombosis. The prediction model was established as P = 0.863 × age + 0.978 × smoking history + 0.702 × drinking history + 0.104 × HBA1c - 2.439. The area under the ROC curve was 0.718.

The incidence of LEDVT in emergency inpatients in the post-epidemic era was significantly higher than that in the epidemic period. Age, smoking and drinking history, and glycosylated hemoglobin are at high risk for thrombosis.

Atrial fibrillation (AF) is associated with a high burden of cardiovascular disease, which has been worsened during the coronavirus disease 2019 (COVID-19) pandemic. The purpose of this study was to assess the association between clinical markers, especially interleukin-6 (IL-6) and other inflammatory biomarkers, and the severity of COVID-19 in patients with AF.

This retrospective cohort study categorized patients based on clinical presentations and laboratory results to investigate the prognostic significance of inflammatory markers in COVID-19 outcomes among those with AF. The study included 100 hospitalized COVID-19 patients aged between 40 to 80 years and was conducted at the Chapidze Hospital in Tbilisi, Georgia. Patients were then grouped by disease severity according to computed tomography (CT) scores, clinical symptoms, respiratory rate and oxygen saturation. Levels of IL-6 were obtained at three time points during hospitalization. A broad range of laboratory tests, including C-reactive protein (CRP), ferritin, and D-dimer, were also conducted.

Patients with AF demonstrated significantly elevated levels of IL-6 (P = 0.024), CRP (P = 0.001), and ferritin (P < 0.001), suggesting a severe inflammatory response. D-dimer levels were also notably higher in the AF group (P < 0.005), indicating an increased risk of thrombotic complications. Oxygen saturation levels were significantly lower (P = 0.004) and CT scores higher in patients with AF. Furthermore, the length of hospitalization was longer among patients with AF (median duration significantly higher, P = 0.032), indicating a more severe disease course.

The proinflammatory markers such as IL-6 are independent predictive markers of COVID-19 severity in AF patients. Overall, it highlights urgent treatment approaches, such as available anti-inflammatory drugs, for COVID-19 patients with arrhythmias. Combining these biomarkers into clinical routines helps us better identify patients at risk and how to treat them.

Thrombotic complications are common in Coronavirus disease 2019 (COVID-19) patients, with pulmonary embolism (PE) being the most frequent. Randomised trials have provided inconclusive results on the optimal dosage of thromboprophylaxis in critically ill COVID-19 patients. We utilized data from the multicentre CAPACITY-COVID patient registry to assess the effect of differential application of Low Molecular Weight Heparin (LMWH) dose protocols on PE and in-hospital mortality risk in critically ill COVID-19 patients. An instrumental variable analysis was performed to estimate the intention-to-treat effect, utilizing differences in thromboprophylaxis prescribing behaviour between hospitals. We included 939 patients with PCR confirmed SARS-CoV-2 infection from 34 hospitals. Two-hundred-and-one patients (21%) developed a PE. The adjusted cause-specific HR of PE was 0.92 (95% CI: 0.73-1.16) per doubling of LMWH dose. The adjusted cause-specific HR for in-hospital mortality was 0.82 (95% CI: 0.65-1.02) per doubling of LMWH dose. This dose-response relationship was shown to be non-linear. To conclude, this study did not find evidence for an effect of LMWH dose on the risk of PE, but suggested a non-linear decreased risk of in-hospital mortality for higher doses of LMWH. However, uncertainty remains, and the dose-response relationship between LMWH dose and in-hospital mortality needs further investigation in well-designed studies.

This retrospective study aimed to investigate the effect of mild-to-moderate COVID-19 on the risk of deep vein thrombosis (DVT) in patients with hip fractures. Hip fractures are common in the elderly, and previous research has shown that they accounted for 58.3% of traumatic fractures in older inpatients during the COVID-19 pandemic in China. Meanwhile, the relationship between COVID-19 and DVT is complex. Some studies have reported that the incidence of DVT in critically ill COVID-19 patients can be as high as 46%, and 20% in those with moderate-to-severe cases. However, the impact of mild-to-moderate COVID-19 on DVT risk in hip fracture patients remains unclear.

Adult patients who underwent surgery for hip fractures between December 8, 2022, and January 9, 2023, were included in the study. All patients were tested for SARS-CoV-2 nucleic acid and were assessed for DVT preoperatively using doppler ultrasonography (DUS). Logistic regression was used to identify risk factors for DVT.

The records of 98 patients with hip fractures, were included in the analysis, of whom 63 were SARS-CoV-2 positive and 35 were SARS-CoV-2 negative. Pre-operative DUS showed that 36/98 patients (37%) had DVT, including 25/63 (40%) patients with COVID-19, and 11/35 (31%) patients without COVID-19. Multivariable logistic regression analysis showed that pre-operative leukocyte count and platelet-to-lymphocyte ratio (PLR) were independent risk factors for DVT, whereas mild-to-moderate COVID-19 was not an independent risk factor for DVT. In patients with hip fractures, COVID-19 did not significantly increase the risk of DVT.

Therefore, in patients with hip fractures, DVT prevention measures should be implemented routinely, regardless of COVID-19 status.

The aim of this study was to evaluate the association between SARS-CoV-2 vaccination and the occurrence of thrombotic complications in patients admitted to intensive care for severe COVID-19 pneumonia.

Observational, descriptive, prospective, multicentre study.

Intensive care units of five university hospitals.

A total of 255 patients admitted to the intensive care unit (ICU) with SARS-CoV-2 pneumonia, confirmed by RT-PCR in throat swab or tracheal aspirate, starting the date the first vaccinated patient against SARS-CoV-2 was admitted in one of the participating ICUs, were included in the analysis.

Vaccination status against SARS-CoV-2 and thrombotic events.

18.8% of patients had received some form of vaccination. Thrombotic events occurred in 21.2% of patients. Lack of vaccination was associated with thrombotic events (OR 5.024; 95% CI: 1.104-23.123; p = 0.0037) and death (OR 5.161; 95% CI: 1.075-24.787; p = 0.04). ICU mortality was not associated with the occurrence of thrombotic complications.

In this series of patients, vaccination against SARS-CoV-2 reduced the risk of thrombotic events and mortality in patients with severe COVID-19 admitted to the ICU. Thrombotic complications did not alter ICU mortality.

We aimed to determine the predictive accuracy of elevated soluble thrombomodulin (sTM) and angiopoietin-2 (Ang2) for thrombotic events (TE) in hospitalized COVID-19 patients. We conducted a nested case-control study within a cohort of people admitted to hospital with COVID-19 from March 2020 to August 2022. The cases (people with TE within 28 days after hospital admission) were matched by propensity score to comparable patients without TE. We determined plasma levels of sTM and Ang2 in all available frozen samples, prioritizing the earliest post-admission samples, using an automated immunoassay technique. Among 2,524 hospitalized COVID-19 patients (43% females; median age 67 years), 73 had TE (incidence 1.15 events per 1000 patient-days of follow-up). Frozen plasma samples were available for 43 cases and 176 controls. Elevated plasma concentration of sTM was significantly associated with TE (2.8 [1.8, 4] vs. 1.52 [1.1, 2.65] ng/mL; p =  0.001) and mortality (median [Q1, Q3], 3.32 [2.16, 4.65] vs. 1.58 [1.11, 2.73] ng/mL; p =  0.001), while D-dimer showed a specific association with TE (2.3 [0.8, 7.4] vs. 0.75 [0.4, 1.6] mcg/mL; p =  0.001). In contrast, Ang2 was not associated with any of these events. The association with thrombotic events remained in adjusted models (HR [95%CI] per unit increase, 1.24 [1.04-1.47] for sTM; 1.07 [1.03-1.10] for D-dimer). The adjusted regression model that included both biomarkers, sTM and D-dimer, improved (AUC 73%, sensitivity 77% and specificity 65% for TE diagnosis; p =  0.007) the predictive capacity of the same model without sTM. In conclusion, determination of soluble thrombomodulin along with D-dimer enhances thrombotic risk assessment in hospitalized COVID-19 patients.

Early antibody therapy can prevent severe SARS-CoV-2 infection (COVID-19). However, the effectiveness of COVID-19 convalescent plasma (CCP) therapy in treating severe COVID-19 remains inconclusive. To test a hypothesis that some CCP units are associated with a coagulopathy hazard in severe disease that offsets its benefits, we tracked 304 CCP units administered to 414 hospitalized COVID-19 patients to assess their association with the onset of unfavorable post-transfusion D-dimer trends. CCP recipients with increasing or persistently elevated D-dimer trajectories after transfusion experienced higher mortality than those whose D-dimer levels were persistently low or decreasing after transfusion. Within the CCP donor-recipient network, recipients with increasing or persistently high D-dimer trajectories were skewed toward association with a minority of CCP units. In in vitro assays, CCP from "higher-risk" units had higher cross-reactivity with the spike protein of human seasonal betacoronavirus OC43. "Higher-risk" CCP units also mediated greater Fcγ receptor IIa signaling against cells expressing SARS-CoV-2 spike compared with "lower-risk" units. This study finds that post-transfusion activation of coagulation pathways during severe COVID-19 is associated with specific CCP antibody profiles and supports a potential mechanism of immune complex-activated coagulopathy.

Introduction: Severely ill COVID-19 patients receiving prophylactic-dose anticoagulation exhibit high rates of thrombosis and mortality. The escalation of anticoagulation also does not reduce mortality and has an uncertain impact on thrombosis rates. The reasons why escalated doses fail to outperform prophylactic doses in reducing risks of thrombosis and death in severely ill COVID-19 patients remain unclear. We hypothesized that escalated anticoagulation would not effectively prevent hypercoagulability and, consequently, would not reduce the risk of thrombosis and death in some severely ill patients. Methods: We conducted a prospective multicenter study that enrolled 3860 COVID-19 patients, including 1654 severely ill. They received different doses of low-molecular-weight or unfractionated heparin, and their blood coagulation was monitored with activated partial thromboplastin time, D-dimer, and Thrombodynamics. A primary outcome was hypercoagulability detected by Thrombodynamics. Blood samples were collected at the trough level of anticoagulation. Results: We found that escalated anticoagulation did not prevent hypercoagulability in 28.3% of severely ill patients at the trough level of the pharmacological activity. Severely ill patients with such hypercoagulability had higher levels of inflammation markers and better creatinine clearance compared to severely ill patients without it. Hypercoagulability detected by Thrombodynamics was associated with a 1.68-fold higher hazard rate for death and a 3.19-fold higher hazard rate for thrombosis. Elevated D-dimer levels were also associated with higher hazard rates for thrombosis and death, while shortened APTTs were not. The simultaneous use of Thrombodynamics and D-dimer data enhanced the accuracy for predicting thrombotic events and fatal outcomes in severely ill patients. Conclusions: Thrombodynamics reliably detects hypercoagulability in COVID-19 patients and can be used in conjunction with D-dimer to assess the risk of thrombosis and death in severely ill patients. The pharmacological effect of LMWH at the trough level might be too low to prevent thrombosis in some severely ill patients with severe inflammation and better creatinine clearance, even if escalated doses are used.

Background/Objectives: The association between past coronavirus disease-19 (COVID-19) infection and pulmonary thromboembolism (PTE) is a potential research topic. We aimed to research the prevalence of previous COVID-19 infection in patients with PTE and to determine whether there is a difference in embolism severity in these cases. Methods: Study design: Multicenter, observational, cross-sectional. Patients diagnosed with PTE between 11 March 2022 and 11 March 2023 were prospectively included in this study, excluding cases with PTE along with active COVID-19, patients under the age of 18, and pregnant patients. Group 1 consisted of PTE cases with previous COVID-19, and Group 2 consisted of PTE cases without previous COVID-19. Key variables are D-Dimer level, right ventricle/left ventricle (RV/LV) ratio, simplified pulmonary embolism severity score, and treatment type. Results: A total of 1185 patients (Group 1; n = 360, Group 2; n = 825) were included in this study. The proportion of patients with RV/LV ratio > 1 on computed tomography pulmonary angiography (CTPA) was significantly high in Group 2 compared to Group 1 (27.9% vs. 19.7%, p = 0.003). In multivariate logistic regression analysis, the absence of any identifiable risk factor for PTE was found to be a 0.46-fold protective factor in the presence of previous COVID-19 (OR: 0.456 95% CI: 0.274-0.760, Wald = 9.070, df = 1, p = 0.003) and an RV/LV ratio > 1 on CTPA was found to be a 0.60-fold protective factor (OR: 0.603, 95% CI: 0.365-0.998, Wald = 3.874, df = 1, p = 0.049). Conclusions: The prevalence of previous COVID-19 infection in PTE cases was 30.4%, and 26.3% of idiopathic cases had previous COVID-19 infection. Although the parameters related to embolism severity were higher in the non-COVID-19 group, multivariate analyses revealed a 2.2-fold increased risk for idiopathic PTE and a 1.7-fold increased risk for RV/LV ratio > 1 on CTPA in patients without COVID-19 compared to those with prior COVID-19.

The global impact of SARS-CoV-2 and its associated coronavirus disease (COVID-19) has necessitated urgent characterization of prognostic biomarkers. This study aimed to delineate the epidemiological and clinical predictors of mortality among hospitalized COVID-19 patients.

A retrospective cohort study was conducted on 123 patients with laboratory-confirmed COVID-19 admitted to Huoshenshan Hospital (Wuhan, China) from 1 February 2020 to 30 April 2020. Kaplan-Meier curve and multivariate Cox regression were used to assess the independent factors with survival time. Statistical significance was set at a p-value of <0.05.

The cohort exhibited a mortality rate of 49.6% (61/123), with the critical clinical type (HR = 7.970, p = 0.009), leukocytosis (HR = 3.408, p = 0.006), and lymphopenia (HR = 0.817, p = 0.038) emerging as independent predictors of reduced survival. Critical-type patients demonstrated significantly elevated inflammatory markers (neutrophils: 10.41 ± 6.23 × 109/L; CRP: 104.47 ± 29.18 mg/L) and coagulopathy (D-dimer: 5.21 ± 2.34 μg/ml) compared to non-critical cases. Deceased patients exhibited pronounced metabolic derangements, including hyperglycemia (9.81 ± 2.07 mmol/L) and hepatic dysfunction (ALP: 174.03 ± 30.13 U/L).

We revealed the epidemiological and clinical features of different clinical types of SARS-CoV-2 as summarized in this paper. We found that critical type, leukocyte, and lymphocyte are risk factors that affect survival time, which could be an early and helpful marker to improve management of COVID-19 patients.

In the face of the global COVID-19 pandemic, the need arose to investigate potential complications associated with SARS-CoV-2, including the risk of stroke.ObjectiveThis study aimed to verify the association between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the risk of stroke on the basis of systematic reviews and meta-analyses to assess the inclusion of the virus as a new risk factor for cerebrovascular diseases.MethodsA metaumbrella study was conducted, which included 34 systematic reviews, of which 4 were selected for the final analysis on the basis of methodological quality and consistency. The analysis aggregated the results of 70 primary studies, considering different stroke subtypes and outcomes associated with COVID-19. Study heterogeneity was assessed via the I2 index, and significance bias was verified via Egger's test.ResultsCOVID-19 severity was significantly associated with an increased risk of stroke (eOR = 2.48; 95% CI: 1.55-3.95), particularly ischemic stroke (eOR = 1.76; 95% CI: 1.11-2.80) and hemorrhagic stroke (eOR = 3.86; 95% CI: 1.79-8.33). Additionally, patients with cerebrovascular comorbidities had higher mortality (eOR = 2.48; 95% CI: 2.48-19.63), as did those who had previously suffered a stroke (eOR = 6.08; 95% CI: 3.73-9.91).ConclusionThe association between SARS-CoV-2 and stroke incidence was consistent and significant, suggesting that COVID-19 should be considered a new risk factor for cerebrovascular diseases. However, the high heterogeneity among the studies analyzed reinforces the need for further research to consolidate this relationship.

SARS-CoV-2 disease (COVID-19) has had an enormous health and economic impact globally. Although primarily a respiratory illness, multi-organ involvement is common in COVID-19, with evidence of vascular-mediated damage in the heart, liver, kidneys and brain in a substantial proportion of patients following moderate-to-severe infection. The pathophysiology and long-term clinical implications of multi-organ injury remain to be fully elucidated. Age, gender, ethnicity, frailty and deprivation are key determinants of infection severity, and both morbidity and mortality appear higher in patients with underlying comorbidities such as ischaemic heart disease, hypertension and diabetes. Our aim is to gain mechanistic insights into the pathophysiology of multiorgan dysfunction in people with COVID-19 and maximise the impact of national COVID-19 studies with a comparison group of COVID-negative controls.

COmorbidities and Sociodemographic factors on Multiorgan Injury following COVID-19 (COSMIC) is a prospective, multicentre UK study which will recruit 200 subjects without clinical evidence of prior COVID-19 and perform extensive phenotyping with multiorgan imaging, biobank serum storage, functional assessment and patient reported outcome measures, providing a robust control population to facilitate current work and serve as an invaluable bioresource for future observational studies.

Approved by the National Research Ethics Service Committee East Midlands (REC reference 19/EM/0295). Results will be disseminated via peer-reviewed journals and scientific meetings.

COSMIC is registered as an extension of C-MORE (Capturing Multi-ORgan Effects of COVID-19) on ClinicalTrials.gov (NCT04510025).

The COVID-19 pandemic has significantly impacted global healthcare systems, revealed vulnerabilities and prompted a re-evaluation of medical practices. Acute complications from the virus, including cardiovascular and neurological issues, have underscored the necessity for timely medical interventions. Advances in diagnostic methods and personalized therapies have been pivotal in mitigating severe outcomes. Additionally, Long COVID has emerged as a complex challenge, affecting various body systems and leading to respiratory, cardiovascular, neurological, psychological, and musculoskeletal problems. This broad spectrum of complications highlights the importance of multidisciplinary management approaches that prioritize therapy, rehabilitation, and patient-centered care. Vulnerable populations such as paediatric patients, pregnant women, and immunocompromised individuals face unique risks and complications, necessitating continuous monitoring and tailored management strategies to reduce morbidity and mortality associated with COVID-19.

This study aimed to assess the impact of SARS-CoV-2 therapies on the risk of venous thromboembolism (VTE) and other cardiovascular events. A retrospective, multicenter, observational study included hospitalized patients in Spain due to acute SARS-CoV-2 infection from March 2020 to March 2022. A total of 184,324 hospitalized COVID-19 patients were included, with a mean age of 67.5 (± 16) years of whom 58.4% were male. Among the comorbidities, arterial hypertension was the most common, affecting 52.5% (9618 patients), followed by dyslipidemia in 39.5% (7237 patients), diabetes mellitus in 23.7% (1748 patients), and atrial fibrillation in 10.6% (1948 patients). The overall mortality rate was 17.4% (3183 patients) and 9.9% (1819 patients) required admission to an intensive care unit. Cardiovascular events occurred in 4.08% (748 patients), with VTE occurring in 2.78% (510 patients), myocardial infarction in 0.75% (137 patients), and ischemic stroke in 0.55% (101 patients). Among therapies, beta-lactams were used in 66.7% (12,228 patients), systemic corticosteroids in 56.9% (10,424 patients), and tocilizumab in 11.6% (2128 patients). Multivariate analysis revealed an independent association between VTE and the use of tocilizumab (adjusted OR 2.07; p < 0.01), corticosteroids (adjusted OR 1.44; p = 0.02), and macrolides (adjusted OR 0.58; p < 0.01). None of the therapies were associated with the risk of myocardial infarction or ischemic stroke. In this large national cohort, tocilizumab and corticosteroids exhibited an independent association for the risk of VTE, but not for myocardial infarction or ischemic stroke.

Limited knowledge exists about prophylactic anticoagulation patterns in patients hospitalized for COVID-19.

We conducted a retrospective cohort study using American Heart Association COVID-19 Cardiovascular Disease Registry data from May 2020 to March 2022. We included patients without preexisting indications for or contraindications to anticoagulation, excluding those with missing anticoagulation data. Patients were categorized by the highest anticoagulation dose received. Multilevel logistic regression was used to assess the relationship between anticoagulation use/dose, patient demographics, clinical presentation, in-hospital course, institutional characteristics, and admission date, accounting for hospital clustering. Among 26 775 patients, 4157 (16%) received no anticoagulation, 15 617 (58%) low-dose, 3071 (11%) intermediate-dose, and 3930 (15%) full-dose anticoagulation. Significant hospital-level variability occurred for any anticoagulation use (range, 0%-98%; P<0.0001) and by dose (full anticoagulation range, 0%-85%; P<0.0001). Controlling for hospital variability, older age, male sex, non-White race, higher body mass index, higher platelets, corticosteroid use, and intensive care unit admission were positively associated with any anticoagulation use. Older age, male sex, higher body mass index, higher platelets, corticosteroid use, intensive care unit admission, mechanical ventilation, and admission before October 2020 were associated with higher anticoagulation dose (full versus low dose). Rates of no anticoagulation significantly increased in both intensive care unit and non-intensive care unit strata over time (P trend=0.01 and <0.0001, respectively).

In this large real-world analysis, nearly 1 in 6 patients hospitalized for COVID-19 received no prophylactic anticoagulation. Patient and disease characteristics associated with thrombotic risk and COVID-19 severity correlated with anticoagulation strategy. Importantly, substantial institutional differences emerged, highlighting gaps between clinical practice and guideline recommendations.

ObjectiveThe objective of this study is to examine the lifespan of red blood cells (RBCs) in individuals with systemic lupus erythematosus (SLE), explore the factors influencing this lifespan, and assess its significance in clinical contexts.MethodsThe experimental group comprised of 182 patients with SLE, while the control group consisted of 90 healthy participants. By using a non-invasive breath test, we measured the RBC lifespan in both groups. Subsequently, we conducted a comparative analysis of general clinical data and laboratory findings to explore the correlation between RBC lifespan in patients with SLE and various parameters associated with RBC characteristics, inflammatory markers, and immunological indicators. Furthermore, we examined the impact of COVID-19 infection on RBC lifespan among patients with SLE and assessed the diagnostic efficacy of RBC lifespan.ResultsRBC lifespan was notably reduced in the SLE group in comparison to the healthy control group (P = 0.002). A positive correlation was observed between RBC lifespan and hemoglobin (HB), complement 3, and complement 4, whereas a negative correlation was noted with IgG, erythrocyte sedimentation rate (ESR), C-reactive protein, and anti-dsDNA levels (all P < 0.05). Noteworthy independent contributors to the reduction in RBC lifespan among patients with SLE included disease activity and presence of anemia. While RBC lifespan remained unchanged in the control group before and after COVID-19 infection (P > 0.05), a reduction in RBC lifespan post-COVID-19 infection was observed among patients with SLE (P < 0.05). Also, RBC lifespan was notably shorter during the active disease phase of SLE compared to the stable phase, with post-COVID-19 active patients with SLE exhibiting even shorter RBC lifespan compared to the pre-COVID-19 active group (all P < 0.05). An optimal cutoff for the prediction of anemia in patients with SLE on the day of assessment was determined to be 93.5 days (AUC 0.792, P < 0.05).ConclusionPatients with SLE exhibited shorter RBC lifespan in contrast to the healthy population, which is notably linked with levels of inflammatory and immune markers, as well as the incidence of COVID-19 infection. This discovery holds crucial significance for both the diagnosis of anemia and the comprehension of its underlying pathogenic mechanisms within the context of SLE.

Thromboembolic events of COVID-19 are due to hyperinflammatory process associated with hypercoagulable state. The aim of the study was to determine characteristics and clinical outcomes of patients with COVID-19 who presented with aortic thrombus.

We retrospectively conducted a single-center, descriptive study over a period of 1 year and 7 months, between June 2021 and December 2022, involving eight patients with documented SARS-CoV-2 infection associated with aortic thrombus revealed by acute limb ischemia.

The mean age of patients was 67 years with a median of 64, 5 ± 14. Of the eight included patients, six were men and two were women. Aortic thrombus was diagnosed in all cases. Six patients developed one episode of acute limb ischemia and one patient had recurrent upper and lower ischemia despite full anticoagulation whereas one patient had distal embolization with palpable pulses. In six patients, the thrombi were located in descending and abdominal aorta, while two patients presented with ascending aorta floating thrombus. Seven patients required urgent revascularization whereas medical treatment was recommended for one patient. The primary outcomes were successful in five cases, one patient had to be amputated above elbow, whereas two patients died due to a rapid deterioration of respiratory condition.

Aortic thrombosis is a rare clinical presentation in SARS-CoV-2 infection but with potentially fatal embolic complication. Physicians should maintain a high degree of clinical suspicion to diagnose thromboembolic consequences of SARS-CoV-2 infection for timely management and avoiding morbidities like ischemic stroke and major amputations.