The risk factors that modulate one's susceptibility for severe COVID-19 have been well documented. Despite this, hypercoagulability remains an often overlooked risk factor for severe disease for COVID-19. Because COVID-19 infection is a risk factor for hypercoagulability, a reasonable presumption/hypothesis is that patients with hereditary thrombophilia would be at a higher risk of thrombotic complications associated with COVID-19 infection.

This case report details two cases where previously unknown hereditary thrombophilias likely contributed to the mortality of COVID-19 patients.

The first COVID-19 patient's cause of death was pulmonary thromboemboli from deep vein thrombosis due to heterozygous MTHFR C667T and heterozygous PAI-1 4G/5G mutations. The second COVID-19 patient's cause of death was an acute myocardial infarct due to a coronary artery thrombosis in the setting of heterozygous MTHFR A1298C and homozygous PAI-1 4G/5G mutations. In each case, COVID-19 infection was also considered contributory to death.

The occurrence of these fatal thrombotic events in COVID-19 patients with hereditary thrombophilias raises questions as to whether this combination of thrombotic risk factors for hypercoagulability may have placed patients at a significant enough risk to experience these fatal thrombotic complications. Thus, while not sufficient alone to prove that SARS-CoV-2 patients with hereditary thrombophilias are at increased risk for thrombotic complications, these two cases indicate that further investigation is warranted into elucidating the relationship between thrombotic risk factors as it may identify an additional high-risk medical condition for COVID-19 and have important diagnostic and therapeutic ramifications.

The aim of this study was to analyze data on pediatric cases of COVID-19 admitted to a tertiary referral hospital in northwest Greece.

A retrospective analysis was conducted on the most common clinical manifestations and laboratory findings, stratified by age group and SARS-CoV-2 strain.

A total of 254 children were hospitalized, with a mean age of 4.5 years. Underlying conditions were present in 10.2% of cases; two children required pediatric intensive care unit (PICU) admission, and one child died. The most common hematological manifestations, in general, were neutropenia (30%) and lymphopenia (23%), whereas the findings varied when the children were stratified by age group. Eight children developed multisystem inflammatory syndrome (MIS-C), with the most common findings being anemia (75%), lymphopenia (50%), and thrombocytopenia (25%). Analysis of the SARS-CoV-2 strains revealed the proportions of the dominant strain over time. Fever was the predominant symptom across all strains, particularly in the Omicron group, which also had a high incidence of gastrointestinal symptoms. The longest hospital admission occurred in children with the Omicron strain, followed by the Wuhan, Alpha, and Delta strains.

Fever was the most consistent symptom across all age groups and virus strains. The most common hematological manifestations were neutropenia (30%) and lymphopenia (23%). The Omicron strain was associated with the longest hospital stay.

Emerging research underscores the heightened risk of vasculitis and microvascular thrombosis in COVID-19 patients, alongside concerns about prothrombotic events post-severe acute respiratory syndrome coronavirus 2 vaccination. Following the pandemic's end, we sought a comprehensive analysis to elucidate its impact on microsurgical thrombosis rates, informed by empirical and anecdotal evidence.

An institutional review board-approved retrospective review analyzed autologous breast reconstruction cases in women from January 2019 to March 2022. Data on patient history, COVID-19 infection, vaccination status, and postoperative complications were collected. Patients were categorized as prepandemic and pandemic, and based on COVID-19 influence (infection or vaccination) for statistical evaluation.

Among 527 patients, 216 underwent surgery prepandemic and 311 during the pandemic, revealing thrombotic event rates of 3.2% and 5.4%, respectively. Further comparative analysis showed no significant difference in thrombotic events among patients affected by COVID-19 through infection or vaccination during the pandemic.

Contrary to concerns, COVID-19 infection or vaccination status does not significantly increase thrombotic event rates in deep inferior epigastric perforator flap breast reconstructions. This study offers vital insights, affirming the safety and efficacy of microsurgical procedures amid the pandemic, thereby guiding microsurgeons in optimizing patient care in the post-COVID-19 era.

Background/Objectives: Stroke is a leading cause of mortality and disability worldwide, ranking as the second most common cause of death and the third in disability-adjusted life-years lost. Ischaemic stroke, which constitutes the majority of cases, poses significant public health and economic challenges. This study evaluates trends in ischaemic stroke hospitalisations in Italy from 2008 to 2022, focusing on differences before and after the COVID-19 pandemic. Methods: We analysed ischaemic stroke hospitalisations among individuals admitted through emergency services using Italian hospital discharge records from 2008 to 2022. Poisson Inverse Gaussian regression was employed to assess hospitalisation trends, accounting for age, sex, and geographic variations. Results: Among 1,689,844 ischaemic stroke hospitalisations, there was a marked age-related increase, particularly among individuals aged 74 and older, with males consistently showing higher rates. Hospitalisation trends demonstrated a 20% reduction over 15 years, suggesting improvements in stroke prevention and treatment. However, there was a slight increase in rates during the COVID-19 period, despite the overall declining trend, highlighting the potential healthcare challenges experienced during the pandemic. Multivariable analysis confirmed age and male sex as significant risk factors. Conclusions: This study underscores the age-related increase in stroke hospitalisation rates, emphasising the need for targeted prevention strategies for elderly populations. The overall reduction in stroke hospitalisation rates reflects advancements made in healthcare, although the impact of COVID-19 on access to stroke care is evident. Future policies must address the pandemic's effects on stroke care continuity and prioritise interventions tailored to age and sex.

A heightened risk for thrombosis is a hallmark of COVID-19. Expansive clinical experience and medical literature have characterized small (micro) and large (macro) vessel involvement of the venous and arterial circulatory systems. Most events occur in patients with serious or critical illness in the hyperacute (first 1-2 weeks) or acute phases (2-4 weeks) of SARS-CoV-2 infection. However, thrombosis involving the venous, arterial, and microcirculatory systems has been reported in the subacute (4-8 weeks), convalescent (> 8-12 weeks) and chronic phases (> 12 weeks) among patients with mild-to-moderate illness. The purpose of the current focused review is to highlight the distinguishing clinical features, pathological components, and potential mechanisms of venous, arterial, and microvascular thrombosis in patients with COVID-19. The overarching objective is to better understand the proclivity for thrombosis, laying a solid foundation for screening and surveillance modalities, preventive strategies, and optimal patient management.

We aimed to investigate the incidence of new acute myocardial infarction (AMI), in patients with Coronavirus disease (COVID-19) who had old MI. We hypothesized that COVID-19 increases the rate of repeated AMI in this population regardless of age and gender.

A retrospective analysis was conducted for adult patients admitted with COVID-19 and developed thromboembolic event (TEE) in 2020. Patients were categorized based on the history of old MI, new MI, age, and gender.

Among 16,903 patients with COVID-19 who were admitted, 210 (1.2%) developed TEE (89% were males, 55% were <55 years old, and 80.5% had an old MI). COVID-19 was severe in 32% of cases. AMI occurred in 160 patients (42.5% STEMI and 57.5% NSTEMI). In patients with prior MI, 92.5% developed another AMI. NSTEMI was higher in patients with severe COVID-19 than STEMI (33% vs 21%). Patients with severe COVID-19 had higher mortality (39.4% vs 5.6%), fewer rates of prior MI (74% vs 83%), hypertension (40% vs 60%), and STEMI (31.8% vs 46.5%) than mild COVID-19 patients. On multivariable analysis, COVID-19 severity was an independent predictor of mortality (OR10; 95%CI 1.62-67.19) after adjustment for age, gender, diabetes mellitus, C-reactive protein, serum Ferritin, Procalcitonin, and Fibrinogen values, and prior or new MI.

Patients with old MI could develop a new AMI in 80% of COVID-19. However, the mortality was higher in patients without a history of MI due to the severity of COVID-19. Attention should be given to patients who possess thrombotic risk factors in pandemics.

The impact of COVID-19 on pregnant women and newborns continues to be a critical societal concern. However, the majority of research focuses on the disease resulting from the early pandemic variants, without sufficient study on the more recent BA.5.2/BF.7. We retrospectively recruited pregnant women giving birth during the surge of the BA.5.2/BF.7 and analysed the risk impact of COVID-19 on maternal and neonatal outcomes. Furthermore, subjects matched through propensity scores were used for the analysis of clinical laboratory tests. A total of 818 pregnant women were enrolled, among 276 (33.7%) were diagnosed with SARS-CoV-2 during childbirth. COVID-19 significantly increased the risk of a hospital length of stay equal to or greater than seven days and neonatal admission to the neonatal intensive care unit, with an aHR of 2.03 (95% CI, 1.22-3.38) and 1.51 (95% CI, 1.12-2.03), respectively. In the analysis of 462 matched subjects, it was found that subjects infected with SARS-CoV-2 tended slight leucopenia and coagulation abnormalities. We found that during the surge of the BA.5.2/BF.7, COVID-19 increased the risk of maternal and neonatal outcomes among Chinese pregnant women. This finding offers significant insights to guide clinical practices involving pregnant women infected with the recently emerged Omicron subvariants.

Although plastic surgery procedures generally demonstrate less than 2% incidence of venous thromboembolism (VTE) outcomes, the post-COVID era data remain elusive. This study sought to elucidate the relationship between COVID-19 infection and the risk of VTE outcomes across plastic surgery procedures.

Plastic surgery procedures were identified in the 2012-2022 National Surgical Quality Improvement Program databases. The outcomes of interest were the postoperative occurrence of VTE, defined as deep vein thrombosis (DVT) or pulmonary embolism (PE), and postoperative complication. Propensity score matching was used to 1) compare overall rates of VTE between the pre-pandemic era and pandemic era cohorts and 2) compare rates of VTE and overall postoperative complications in cases with and without COVID-19 diagnosis in the years 2021-2022 (p < 0.05).

Overall, 269,006 plastic surgery cases were identified, comprising general breast (76%) and trunk (9.4%) procedures. Non-breast free tissue transfer cases were associated with the highest rates of DVT (1.3%) and trunk procedures with the highest rates of PE (0.7%). After propensity score matching, the overall rate of VTE after the onset of the COVID-19 pandemic was not significantly different from the pre-pandemic era (p = 0.40). In a separately matched cohort, COVID-19 diagnosis did not significantly predict the risk for VTE (p = 0.48) but did significantly predict the risk for overall postoperative complications (p < 0.001).

Although COVID-19 diagnosis itself did not predict the risk of VTE in matched analysis, it significantly predicted the overall postoperative complications. Future studies may further investigate the effects of COVID-19 infection over longer periods of follow-up.

The incidence of postoperative complications among patients with coronavirus disease 2019 (COVID-19) positivity undergoing elective surgical operations is poorly understood. This study aimed to identify differences in postoperative complications after elective abdominal wall reconstruction (AWR) in patients diagnosed with COVID-19 compared with patients presenting prepandemic.

A single-institution, retrospective chart review was performed of patients undergoing AWR between January 2017 and September 2022. Patients were stratified by date: pre-COVID-19 (January 2017 to December 2019) and post-COVID-19 (January 2020 to September 2022). Patients confirmed as COVID-19-positive were also identified. Data collected included demographics, clinical characteristics, and complications. Univariate and multivariate analyses were performed.

We included 168 patients. The mean age was 54 years, and the mean body mass index was 33 kg/m2. Seventy-five patients underwent surgery pre-COVID-19 and 93 patients after. Of 93 patients, 16 (17%) had a positive COVID-19 test before surgery or during the perioperative period. These 2 groups were risk-matched. Patients with COVID-19 had no significant increase in postoperative complications. Major complications occurred at 13.3% in the pre-COVID-19 group and 7.5% in the post-COVID-19 group. Patients with COVID-19 were more likely to be younger (48 versus 57; P = 0.049) and more likely to have a shorter length of stay in the hospital (3 versus 5.8; P = 0.038).

In our case series, there was an associated increase in the incidence of overall pulmonary-related complications in the postpandemic group. This study is limited by its small sample size. Further investigation should be carried out on this topic.

Acute ischemic stroke (AIS) is a complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We aimed to explore neurovascular imaging patterns in patients with SARS-CoV-2-related AIS.

We retrospectively analyzed clinical and radiological data of patients hospitalized with AIS and a positive PCR test for SARS-CoV-2 prior to AIS onset. The control group comprised of AIS patients from a pre-COVID-19 pandemic period matched for gender and age.

Thirty-five SARS-CoV-2-related stroke patients, and 35 controls were included. Fifty-seven percent of SARS-CoV-2 patients had either mild or asymptomatic disease. A distinctive imaging pattern of floating arterial mural thrombus was detected in 5 patients of the SARS-CoV-2 group. In 4 patients thrombus was attached to a stenotic atherosclerotic plaque in the proximal internal carotid artery. In the 5th patient a cardiac CTA showed multiple floating thrombi in the descending aorta. In the control group, floating thrombus was only detected in one patient. Treatment with dual antiplatelet therapy was associated with thrombus dissolution and good clinical outcome. Patients with floating thrombi had a longer time from SARS-CoV-2 diagnosis to stroke onset (mean 7.4 versus 3.4 days).

Floating arterial mural thrombi attached to atherosclerotic plaques are unique characteristic source of AIS in SARS-CoV-2 patients. They may lead to ischemic stroke in patients with mild or asymptomatic infection up to 1-2 weeks from SARS-CoV-2 diagnosis. Patients with embolic AIS and SARS-CoV-2 diagnosis should perform high resolution cranio-cervical vascular imaging to evaluate floating thrombi as a potential embolic source.

Adoptive cellular therapies (ACT) are novel, promising treatments for life-threatening malignancies. In addition to the better known chimeric antigen receptor (CAR) T cells, ACTs include tumor infiltrating lymphocytes (TIL), cancer antigen-specific T cell receptors (TCRs), and CAR-NK (natural killer) cells. In key historic milestones, several adoptive therapies recently received FDA approvals, including 6 CAR-T products for the treatment of hematologic malignancies and the first TIL therapy for the treatment for metastatic melanoma. The rapid pace of clinical trials in the field and the discoveries they provide are ushering in a new era of cancer immunotherapy. However, the potential complications of these therapies are still not fully understood. In particular, patients receiving ACT may be at increased risk for severe infections due to immunocompromise resulting from their underlying malignancies, which are further compounded by the immune derangements that develop in the setting of cellular immunotherapy and/or the preconditioning treatment needed to enhance ACT efficacy. Moreover, these treatments are being readily implemented at a time following the height of the COVID-19 pandemic, and it remains unclear what additional risks these patients may face from SARS-CoV-2 and similar infections. Here, we examine the evidence for infectious complications with emerging adoptive therapies, and provide a focused review of the epidemiology, complications, and clinical management for COVID-19 in CAR-T recipients to understand the risk this disease may pose to recipients of other forms of ACT.

This study aimed to evaluate the eicosanoid and pro-resolutive parameters in patients with Post-COVID Syndrome (PCS) during a 12-week supplementation with a marine oil enriched in specialized pro-resolving mediators (SPMs).

This study was conducted on 53 adult patients with PCS. The subjects included must have had a positive COVID-19 test (PCR, fast antigen test, or serologic test) and persistent symptoms related to COVID-19 at least 12 weeks before their enrolment in the study. The following parameters were evaluated: polyunsaturated fatty acids EPA, DHA, ARA, and DPA; specialized pro-resolving mediators (SPMs), 17-HDHA, 18-HEPE, 14-HDHA, resolvins, maresins, protectins, and lipoxins. The eicosanoids group included prostaglandins, thromboxanes, and leukotrienes. The development of the clinical symptoms of fatigue and dyspnea were evaluated using the Fatigue Severity Scale (FSS) and the Modified Medical Research Council (mMRC) Dyspnea Scale. Three groups with different intake amounts were evaluated (daily use of 500 mg, 1500 mg, and 3000 mg) and compared to a control group not using the product.

In the serum from patients with PCS, an increase in 17-HDHA, 18-HEPE, and 14-HDHA could be observed, and a decrease in the ratio between the pro-inflammatory and pro-resolutive lipid mediators was detected; both differences were significant (p < 0.05). There were no differences found between the three treatment groups. Fatigue and dyspnea showed a trend of improvement after supplementation in all groups.

A clear enrichment in the serum of the three monohydroxylated SPMs could be observed at a dosage of 500 mg per day. Similarly, a clear improvement in fatigue and dyspnea was observed with this dosage.

To this date, COVID-19 remains an unresolved pandemic, and the impairment of redox homeostasis dictates the severity of clinical outcomes. Here we examined initial UCLA cohort of 440 COVID-19 patients hospitalized between March 1st and April 1st, 2020, representing the first wave of the pandemic. The mean age was 58.88 ± 21.12, among which males were significantly more than females (55.5 % vs. 44.5 %), most distinctively in age group of 50-69. The age groups of 50-69 (33.6 %) and ≥70 (34.8 %) dominated. The racial composition was in general agreement with Census data with slight under-representation of Hispanics and Asians, and over-representation of Caucasians. Smoking was a significant factor (28.8 % vs. 11.0 % in LA population), likewise for obesity (BMI ≥30) (37.4 % vs. 27.7 % in LA population). Patients suffering from obesity or BMI<18.5 checked into ICU at a significantly higher rate. A 74.5 % of the patients had comorbidities including diabetes, chronic kidney disease, chronic pulmonary disease, congestive heart failure and peripheral vascular disease. The levels of d-dimer were drastically upregulated (1159.5 ng/mL), indicating hypercoagulative state. Upregulated LDH (328 IU/L) indicated significant tissue damages. A distorted redox hemeostasis is a common trait associated with these risk factors and clinical markers. A quarter of the patients received antivirals, among which Remdesivir most prescribed (23.6 %). Majority received antithrombotics (75 %), and antibiotics. Upon admission, 67 patients were intubated or received CPR; 177 patients eventually received intensive care (40.2 %). While 290 were discharged alive, 10 remained hospitalized, 73 were transferred, and 36 died with 3 palliatively discharged. In summary, our data fully characterized a Californian cohort of COVID-19 at the breaking phase of the pandemic, indicating that population demographics, biophysical characters, comorbidities and molecular pathological parameters have significant impacts on the evolvement of a pandemic. These provide critical insights into effective management of COVID-19, and future break from another pathogen.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), that caused coronavirus disease 2019 (COVID-19), has been studied thoroughly, and several variants are revealed across the world with their corresponding mutations. Studies and vaccines development focus on the genetic mutations of the S protein due to its vital role in allowing the virus attach and fuse with the membrane of a host cell. In this perspective, we study the effects of all ionic amino acid mutations of the SARS-CoV-2 viral spike protein S1 when bound to Antibody CC12.1 within the SARS-CoV-2:CC12.1 complex model. Binding free energy calculations between SARS-CoV-2 and antibody CC12.1 are based on the Analysis of Electrostatic Similarities of Proteins (AESOP) framework, where the electrostatic potentials are calculated using Adaptive Poisson-Boltzmann Solver (APBS). The atomic radii and charges that feed into the APBS calculations are calculated using the PDB2PQR software. Our results are the first to propose in silico potential life-threatening mutations of SARS-CoV-2 beyond the present mutations found in the five common variants worldwide. We find each of the following mutations: K378A, R408A, K424A, R454A, R457A, K458A, and K462A, to play significant roles in the binding to Antibody CC12.1, since they are turned into strong inhibitors on both chains of the S1 protein, whereas the mutations D405A, D420A, and D427A, show to play important roles in this binding, as they are turned into mild inhibitors on both chains of the S1 protein.

Both diabetes and peripheral arterial disease (PAD) have complex interactions with COVID-19. PAD is one of the most important underlying factors in the development of diabetic foot. The COVID-19 pandemic has also caused an increase in cardiovascular complications in those with chronic diseases, including diabetics, due to both the thrombophilic course of the viral disease and the lockdown measures applied for prevention. Since both COVID-19 and diabetes mellitus predispose to thrombosis, PAD is likely to have a more severe course in diabetic patients with COVID-19. The aim of our study is to discuss the complications, prophylaxis, and treatment of PAD, which is a serious complication of diabetes, during the pandemic period.

Patients with colorectal cancer commonly experience disturbances in coagulation homeostasis. Activation of the coagulation system contributes to cancer-associated thrombosis as the second risk factor for death in cancer patients. This study intended to discover coagulation-related genes and construct a risk model for colorectal cancer patients' prognosis.

Coagulation-related genes were identified by searching coagulation-related pathways in the Molecular Signatures Database. Transcriptomic data and clinical data were downloaded from the Cancer Genome Atlas and Gene Expression Omnibus datasets. Univariate Cox and backward stepwise regression were utilized to identify prognosis-related genes and construct a predictive risk model for the training cohort. Next, survival analysis determines the risk model's predictive power, correlation with clinicopathological characteristics, and nomogram. Additionally, we characterized the variances in immune cell infiltration, somatic mutations, immune checkpoint molecules, biological functions, and drug sensitivity between the high- and low-score patients.

Eight hundred forty-five genes were obtained by searching the theme term "coagulation" after de-duplication. After univariate regression analysis, 69 genes correlated with prognosis were obtained from the Cancer Genome Atlas dataset. A signature consisting of 17 coagulation-related genes was established through backward stepwise regression. The Kaplan-Meier curve indicated a worse prognosis for high-score patients. Time-dependent receiver operating characteristic curve analysis demonstrated high accuracy in predicting overall survival. Further, the results were validated by two independent datasets (GSE39582 and GSE17536). Combined with clinicopathological characteristics, the risk model was proven to be an independent prognostic factor to predict poor pathological status and worse prognosis. Furthermore, high-score patients had significantly higher stromal cell infiltration. Low-score patients were associated with high infiltration of resting memory CD4+ T cells, activated CD4+ T cells, and T follicular helper cells. The low-score patients exhibited increased expression of immune checkpoint genes, and this might be relevant to their better prognosis. High-score patients exhibited lower IC50 values of Paclitaxel, Rapamycin, Temozolomide, Cyclophosphamide, etc. The differential signaling pathways mainly involve the calcium signaling pathway and the neuroactive ligand-receptor interaction. Lastly, a nomogram was constructed and showed a good prediction.

The prognostic signature of 17 coagulation-related genes had significant prognostic value for colorectal cancer patients. We expect to improve treatment modalities and benefit more patients through research on molecular features.

COVID-19 is still a global health issue, there is limited evidence in South America regarding laboratory biomarkers associated with severe disease. The objective of our study was to identify hematological and hemostatic changes associated with severe COVID-19.

A total of 170 hospitalized patients with COVID19 were included in the study, defining their severity according to established criteria. Demographic, clinical, and laboratory (days 1, 3, 7, 15) data were obtained. We performed a statistical analysis, assuming significance with a value of p < 0.05. We analyzed the correlation between severity and biomarkers and established cut-off values for severe patients through ROC curves, estimating Odds Ratio associated with severe disease.

Day 1 was observed significant differences between moderate vs severe patients for leukocytes (WBC), Neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR) and D-dimer, establishing cut-off points for each of them. The markers we found associated to risk of severe disease were WBC (OR=3.2396; p = 0.0003), NLR (OR=5.7084; p < 0.0001), PLR (OR=4.4094; p < 0.0001), Neutrophil (OR=4.1193; p < 0.0001), D-dimer (OR=2.7827; p = 0.0124).

The results allow to establish basic laboratory biomarkers associated to severe disease, which could be used as prognostic markers.

The coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), formerly known as 2019-nCoV. Numerous cellular and biochemical issues arise after COVID-19 infection. The severe inflammation that is caused by a number of cytokines appears to be one of the key hallmarks of COVID-19. Additionally, people with severe COVID-19 have coagulopathy and fulminant thrombotic events. We briefly reviewed the COVID-19 disease at the beginning of this paper. The inflammation and coagulation markers and their alterations in COVID-19 illness are briefly discussed in the parts that follow. Next, we talked about NETosis, which is a crucial relationship between coagulation and inflammation. In the end, we mentioned the two-way relationship between inflammation and coagulation, as well as the factors involved in it. We suggest that inflammation and coagulation are integrated systems in COVID-19 that act on each other in such a way that not only inflammation can activate coagulation but also coagulation can activate inflammation.

SARS-CoV-2 infection affects and modulates serum as well as hematological parameters. However, whether it modifies these parameters in the existing disease conditions, which help in the erection of specific treatments for the disease, is under investigation. Here, we aimed to determine whether serum and hematological parameters alteration in various diseases, diabetes mellitus (DM), hypertension (HTN), ischemic heart disease (IHD) and myocardial infarction (MI) conditions correlate and signal SARS-CoV-2 infection, which could be used as a rapid diagnosis tool for SARS-CoV-2 infection in disease conditions. To assess the projected goals, we collected blood samples of 1,113 male and female patients with solo and multiple disease conditions of DM/HTN/IHD/MI with severe COVID-19, followed by biochemical analysis, including COVID-19 virus detection by RT-qPCR. Furthermore, blood was collected from age-matched disease and healthy individuals 502 and 660 and considered as negative control. In our results, we examined higher levels of serum parameters, including D-dimer, ferritin, hs-CRP, and LDH, as well as hematological parameters, including TLC in sole and multiple diseases (DM/HTN/IHD/MI) conditions compared to the control subjects. Besides, the hematological parameters, including Hb, RBC, and platelet levels, decreased in the patients. In addition, we found declined levels of leukocyte count (%), lymphocyte (%), monocyte (%), and eosinophil (%), and elevated level of neutrophil levels (%) in all the disease patients infected with SARS-CoV-2. Besides, NLR and NMR ratios were also statistically significantly (p < 0.05) high in the patients with solo and multiple disease conditions of DM/HTN/IHD/MI infected with the SARS-CoV-2 virus. In conclusion, rapid alteration of sera and hematological parameters are associated with SARS-CoV-2 infections, which could help signal COVID-19 in respective disease patients. Moreover, our results may help to improve the clinical management for the rapid diagnosis of COVID-19 concurrent with respective diseases.

The vigorous spread of SARS-CoV-2 resulted in the rapid infection of millions of people worldwide and devastation of not only public healthcare, but also social, educational, and economic infrastructures. The evolution of SARS-CoV-2 over time is due to the mutations that occurred in the genome during each replication. These mutated forms of SARS-CoV-2, otherwise known as variants, were categorized as variants of interest (VOI) or variants of concern (VOC) based on the increased risk of transmissibility, disease severity, immune escape, decreased effectiveness of current social measures, and available vaccines and therapeutics. The swift development of COVID-19 vaccines has been a great success for biomedical research, and billions of vaccine doses, including boosters, have been administered worldwide. BNT162b2 vaccine (Pfizer-BioNTech), mRNA-1273 (Moderna), ChAdOx1 nCoV-19 (AstraZeneca), and Janssen (Johnson & Johnson) are the four major COVID-19 vaccines that received early regulatory authorization based on their efficacy. However, some SARS-CoV-2 variants resulted in higher resistance to available vaccines or treatments. It has been four years since the first reported infection of SARS-CoV-2, yet the Omicron variant and its subvariants are still infecting people worldwide. Despite this, COVID-19 vaccines are still expected to be effective at preventing severe disease, hospitalization, and death from COVID. In this review, we provide a comprehensive overview of the COVID-19 pandemic focused on evolution of VOC and vaccination strategies against them.

By largely unknown mechanism(s), SARS-CoV-2 hijacks the host translation apparatus to promote COVID-19 pathogenesis. We report that the histone methyltransferase G9a noncanonically regulates viral hijacking of the translation machinery to bring about COVID-19 symptoms of hyperinflammation, lymphopenia, and blood coagulation. Chemoproteomic analysis of COVID-19 patient peripheral mononuclear blood cells (PBMC) identified enhanced interactions between SARS-CoV-2-upregulated G9a and distinct translation regulators, particularly the N 6 -methyladenosine (m 6 A) RNA methylase METTL3. These interactions with translation regulators implicated G9a in translational regulation of COVID-19. Inhibition of G9a activity suppressed SARS-CoV-2 replication in human alveolar epithelial cells. Accordingly, multi-omics analysis of the same alveolar cells identified SARS-CoV-2-induced changes at the transcriptional, m 6 A-epitranscriptional, translational, and post-translational (phosphorylation or secretion) levels that were reversed by inhibitor treatment. As suggested by the aforesaid chemoproteomic analysis, these multi-omics-correlated changes revealed a G9a-regulated translational mechanism of COVID-19 pathogenesis in which G9a directs translation of viral and host proteins associated with SARS-CoV-2 replication and with dysregulation of host response. Comparison of proteomic analyses of G9a inhibitor-treated, SARS-CoV-2 infected cells, or ex vivo culture of patient PBMCs, with COVID-19 patient data revealed that G9a inhibition reversed the patient proteomic landscape that correlated with COVID-19 pathology/symptoms. These data also indicated that the G9a-regulated, inhibitor-reversed, translational mechanism outperformed G9a-transcriptional suppression to ultimately determine COVID-19 pathogenesis and to define the inhibitor action, from which biomarkers of serve symptom vulnerability were mechanistically derived. This cell line-to-patient conservation of G9a-translated, COVID-19 proteome suggests that G9a inhibitors can be used to treat patients with COVID-19, particularly patients with long-lasting COVID-19 sequelae.

Although prophylactic anticoagulation therapy is suggested to be adopted in severe COVID-19 patients, its effects on the long-term cardiovascular (CV) outcomes, namely the risk of major adverse CV events(MACEs) in high-risk CV patients amid the omicron wave of the pandemic, remain unknown.

We conducted this prospective cohort study of consecutive adults hospitalized COVID-19 between 19 April and 12 June 2022, COVID-19 patients with at least two CV risk factors or pre-existing CV diseases were enrolled. A propensity score matching(PSM) method was used to evaluated the effects of prophylactic anticoagulation therapy in hospital on long-term MACEs, including CV death, non-fatal myocardial infarction, non-fatal stroke, hospitalization due to unstable angina pectoris, coronary revascularization and arterial or venous thrombosis.

Two cohorts (with or without anticoagulants during hospitalization) of each 230 patients with balanced baseline characteristics were formed using PSM. During the 15-month follow-up period, 13 patients with anticoagulants and 29 patients without anticoagulants developed MACEs. Overall, the anticoagulation group had a significantly lower risk of MACEs than the control group (hazard ratio [HR] 0.431; 95 % confidence interval [CI]: 0.224-0.830, P = 0.010). Regarding specific constituents of MACEs, the differences were mainly reflected in arterial or venous thrombosis. The significantly lower HRs of overall MACEs were significantly observed in subgroup of age > 75 years, women, higher D dimer level, unvaccinated and non-nirmatrelvir-ritonavir prescribed patients.

Prophylactic anticoagulation therapy during hospitalization was effective in reducing long-term MACEs among COVID-19 patients with CV risk factors or pre-existing CV diseases amid the omicron wave of the pandemic.

Several studies have evaluated the possible association between whole blood viscoelastic testing (VET) parameters in patients hospitalized for acute Coronavirus disease 2019 (COVID-19) pneumonia and mortality. A few studies found no significant differences between survivors and non-survivors, though other studies identified potential predictors of COVID-19-related mortality. We conducted a systematic review and meta-analysis of the literature to evaluate the possible association between standard thromboelastometry/graphy parameters and mortality in patients hospitalized for acute COVID-19 pneumonia.

Relevant studies were searched through MEDLINE, EMBASE, and Google Scholar from their inception until 15th June 2023. We aimed to identify any study including: i) adults admitted to intensive care units (ICU) or medicine wards (MW) for acute COVID-19 pneumonia; ii) viscoelastic testing; iii) mortality.

We included 13 studies: nine prospective and four retrospective, 231 (30.4 %) non-survivors and 528 (69.6 %) survivors. Mortality rates ranged from 12.8 % to 67.5 %. The studies using the TEG apparatus found a significant difference in K time in the Kaolin test among survivors vs. non-survivors (mean difference [MD] 0.20, 95 % confidence interval [CI] 0.12, 0.28, I2 0%). The studies using the rotational thromboelastometry apparatus found a significant difference in CT-INTEM (MD -17.14, 95 % CI -29.23, -5.06, I2 0%) and LI60-EXTEM (MD -1.00, 95 % CI -1.00, -1.00, I2 0%) assays among survivors vs. non-survivors.

We identified no specific hypercoagulable or hypocoagulable profile associated with mortality in patients with COVID-19-related pneumonia. Large prospective studies are needed to explore the possible prognostic role of VET in this subset of patients.

Neurological manifestations may occur in more than 80% of patients hospitalized with COVID-19 infection, including severe disruptions of the central nervous system (CNS), such as strokes, encephalitis, or seizures. Although the primary pathophysiological mechanism for the effects of COVID-19 in CNS remains unknown, evidence exists for both direct injury from neuroinvasion and indirect effects from disruptions in systemic inflammatory and coagulation pathways. In this study, we analyzed CNS tissue from living patients to better understand these processes.

With institutional review board approval and patient consent, samples that would be otherwise discarded from patients with active or recent (within 6 days of surgery) COVID-19 infection undergoing neurosurgical intervention were collected and tested for the presence of SARS-CoV-2 using immunohistochemistry, in situ hybridization, electron microscopy, and reverse transcription polymerase chain reaction.

Five patients with perioperative mild-to-moderate COVID-19 infection met inclusion criteria (2 male, 3 female; mean age 38.8 ± 13.5 years). Neurosurgical diagnoses included a glioblastoma, a ruptured arteriovenous malformation, a ruptured posterior inferior cerebellar artery aneurysm, a middle cerebral artery occlusion, and a hemorrhagic pontine cavernous malformation. Samples analyzed included the frontal lobe cortex, olfactory nerve, arteriovenous malformation/temporal lobe parenchyma, middle cerebral artery, cerebellum, and cavernous malformation/brainstem parenchyma. Testing for the presence of SARS-CoV-2 was negative in all samples.

The CNS is likely not a significant viral reservoir during mild-to-moderate COVID-19 infection, although direct neuroinvasion is not definitively excluded. Additional testing to help elucidate the relative contributions of direct and indirect pathways for CNS injury from COVID is warranted.

In this study, the highly risky drug Edoxaban (EDX), which can threaten life and cause bleeding, was electro analytically evaluated. The electrochemical behavior of EDX was investigated using glassy carbon electrode (GCE) and boron-doped diamond electrode (BDDE). In this study, for the first time, a simple, rapid, sensitive, and selective voltammetric technique was developed by using different electrodes for the electrochemical characterization and detection of EDX. The optimized voltammetric technique showed anodic signals of EDX at +1.09 V and +1.08 V on GCE and BDDE, respectively, in BR (pH 5.0) solution. The developed voltammetric method provided a very good analytical working range for EDX in BR (pH 5.0) solution on GCE and BDDE, covering concentration ranges from 1.84 μM to 12.88 μM and from 3.68 μM to 14.72 μM, respectively. The limits of detection for EDX on GCE and BDDE under these experimental conditions were calculated as 0.24 μM and 0.57 μM, respectively. The developed voltammetric methods on both electrodes were successfully applied to urine and tablet samples. Additionally, the obtained voltammetric results were compared with UV-Vis spectroscopy results.

Infection, a significant cause of death in multiple myeloma (MM) patients, is a common complication and is closely associated with immunoparesis. There exists no clear definition of early infection, so early infection is defined in this paper as the occurrence within 3 months after diagnosis, considering the high incidence of infections within 3 months after diagnosis. This study established a new nomogram model based on immunoparesis to identify MM patients with high-risk early infection.

A retrospective collection of 430 NDMM patients from June 2013 to June 2022 was conducted, and the patients were further divided into a training cohort and a validation cohort. In the training cohort, the least absolute shrinkage and selection operator (LASSO) was used to select the best variables that can be used to establish a new nomogram prediction model. Validation was performed in the validation and entire cohorts.

After diagnosis, 67.7 % of the patients suffered from severe infection within 1 year, and 59.5 % experienced the first severe infection within 3 months. Variables associated with an increased risk of severe infection in the first 3 months included: BMPC, D-dimer, serum β2 microglobulin, immunoparesis, albumin, and eGFR. The nomogram based on the above six factors achieved a good C-index of 0.754, 0.73, and 0.731 in predicting early infection in the training cohort, validation cohort, and entire cohort, respectively. Finally, the time-dependent receiver operating characteristic (ROC) curve and decision curve analysis (DCA) of the nomogram showed that the model provided superior diagnostic capacity and clinical net benefit.

In this study, we established a nomogram model to predict early grade ≥ 3 infection in NDMM patients. This model can assist clinicians in identifying NDMM patients with high-risk infections and improve their prognosis through early intervention.

Every novel infection requires an assessment of the host response coupled with identification of unique biomarkers for predicting disease pathogenesis, treatment targets and diagnostic utility. Studies have exposed dysregulated inflammatory response induced by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as significant predictor or cause of disease severity/prognosis and death. This study evaluated inflammatory biomarkers induced by SARS-CoV-2 in plasma of patients with varying disease phenotypes and healthy controls with prognostic or therapeutic potential. We stratified SARS-CoV-2 plasma samples based on disease status (asymptomatic, mild, severe, and healthy controls), as diagnosed by RT-PCR SARS-CoV-2. We used a solid phase sandwich and competitive Enzyme-Linked Immunosorbent Assay (ELISA) to measure levels of panels of immunological (IFN-γ, TNF-α, IL-6, and IL-10) and biochemical markers (Ferritin, Procalcitonin, C-Reactive Protein, Angiotensin II, Homocysteine, and D-dimer). Biomarker levels were compared across SARS-CoV-2 disease stratification. Plasma IFN-γ, TNF-α, IL-6, and IL-10 levels were significantly (P < 0.05) elevated in the severe SARS-CoV-2 patients as compared to mild, asymptomatic, and healthy controls. Ferritin, Homocysteine, and D-dimer plasma levels were significantly elevated in severe cases over asymptomatic and healthy controls. Plasma C-reactive protein and Angiotensin II levels were significantly (P < 0.05) higher in mild than severe cases and healthy controls. Plasma Procalcitonin levels were significantly higher in asymptomatic than in mild, severe cases and healthy controls. Our study demonstrates the role of host inflammatory biomarkers in modulating the pathogenesis of COVID-19. The study proposes a number of potential biomarkers that could be explored as SARS-CoV-2 treatment targets and possible prognostic predictors for a severe outcome. The comprehensive analysis of prognostic biomarkers may contribute to the evidence-based management of COVID-19 patients.

Background: Coronavirus disease 2019, caused by SARS-CoV-2 (SCV-2) was stated as a pandemic on March 11 2020 by World Health Organization (WHO), and since then, it has become a major health issue worldwide. It mainly attacks the respiratory system with various accompanying complications, including cardiac injury, renal failure, encephalitis and Stroke.Materials and Methods: The current systematic review has been compiled to summarize the available literature on SCV-2 induced ischemic Stroke and its subtypes. Further, the mechanisms by which the virus crosses the blood-brain barrier (BBB) to enter the brain have also been explored. The role of CRP and D-dimer as potent prognostic markers was also explored. The literature search was carried out comprehensively on Google scholar, PubMed, SCOP US, Embase and Cochrane databases by following guidelines.Results: All the studies were reviewed thoroughly by authors and disagreements were resolved by consensus and help of the senior authors. The most common subtype of the IS was found to be large artery atherosclerosis in SCV-2 induced IS. Hypertension emerged as the most significant risk factor. The mechanism resulting in elevated levels of CRP and D-dimer have also been discussed. However, there is a scarcity of definitive evidence on how SCV-2 enters the human brain. The available literature based on various studies demonstrated that SCV-2 enters through the nasopharyngeal tract via olfactory cells to olfactory neurons, astrocytes and via choroid plexus through endothelial cells. Further, disruption of gut-brain axis has been also discussed.Conclusion: Data available in the literature is not adequate to come to a conclusion. Therefore, there is a need to carry out further studies to delineate the possible association between SCV-2 induced IS.

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.

As severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) is becoming more infectious and less virulent, symptoms beyond the lungs of the Coronavirus Disease 2019 (COVID-19) patients are a growing concern. Studies have found that the severity of COVID-19 patients is associated with an increased risk of ischemic stroke (IS); however, the underlying pathogenic mechanisms remain unknown. In this study, bioinformatics approaches were utilized to explore potential pathogenic mechanisms and predict potential drugs that may be useful in the treatment of COVID-19 and IS. The GSE152418 and GSE122709 datasets were downloaded from the GEO website to obtain the common differentially expressed genes (DEGs) of the two datasets for further functional enrichment, pathway analysis, and drug candidate prediction. A total of 80 common DEGs were identified in COVID-19 and IS datasets for GO and KEGG analysis. Next, the protein-protein interaction (PPI) network was constructed and hub genes were identified. Further, transcription factor-gene interactions and DEGs-miRNAs coregulatory network were investigated to explore their regulatory roles in disease. Finally, protein-drug interactions with common DEGs were analyzed to predict potential drugs. We successfully identified the top 10 hub genes that could serve as novel targeted therapies for COVID-19 and screened out some potential drugs for the treatment of COVID-19 and IS.

The anticoagulant drug edoxaban has a blood thinning mechanism of action. In this study, a pencil graphite electrode was electrochemically activated at + 1.4 V for 60 s. in a Britton-Robinson (pH 9.0) supporting electrolyte solution.

A simple, fast, and sensitive electrochemical procedure was developed using cyclic voltammetry and square wave voltammetry techniques. It was observed that edoxaban gave a good oxidation signal with cyclic voltammetry technique at a potential of + 0.98 V (vs. Ag/AgCl).

This procedure showed a linear response in a Britton-Robinson (pH 9.0) media within the concentration range of 0.2-1.8 µM and limit of detection (LOD) and the limit of quantification (LOQ) values were determined to be 0.073 μM (0.133 μg mL-1) and 0.243 μM (0.443 μg mL-1), respectively.

The method developed in this study was successfully applied to drug and urine samples. The developed voltammetric method was highly selective and gave satisfactory recovery results in urine and pharmaceutical samples. The results of the voltammetric method were compared with the spectroscopic method and it was determined that the results were compatible.

To evaluate long-term effects of COVID-19 on auditory and vestibular symptoms in a diverse cohort impacted by the initial 2020 COVID-19 infection in the pandemic's epicenter, before vaccine availability.

Cohort study of individuals with confirmed COVID-19 infection, diagnosed in the March-May 2020 infection wave. A randomized, retrospective chart review of 1,352 individuals was performed to identify those with documented new or worsening auditory (aural fullness, tinnitus, hyperacusis, hearing loss) or vestibular (dizziness, vertigo) symptoms. Those with documented symptoms (613 of the 1,352 initial cohort) were contacted for a follow-up telephone survey in 2021-2022 to obtain self-report of aforementioned symptoms.

Academic tertiary hospital system in Bronx, NY.

Adults 18 to 99 years old with confirmed COVID-19 infection, alive at time of review. One hundred forty-eight charts were excluded for restricted access, incomplete data, no COVID-19 swab, or deceased at time of review.

Confirmed COVID-19 infection, March to May 2020.

Auditory and vestibular symptoms documented in 2020 medical records and by self-report on 2021 to 2022 survey.

Among the 74 individuals with documented symptoms during the first 2020 COVID-19 wave who participated in the 2021 to 2022 follow-up survey, 58% had documented vestibular symptoms initially in 2020, whereas 43% reported vestibular symptoms on the 2021 to 2022 survey ( p = 0.10). In contrast, 9% had documented auditory symptoms initially in 2020 and 55% reported auditory symptoms on the 2021 to 2022 survey ( p < 0.01).

COVID-19 may impact vestibular symptoms early and persistently, whereas auditory effects may have more pronounced long-term impact, suggesting the importance of continually assessing COVID-19 patients.

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged as a global health threat in 2019. An important feature of the disease is that multiorgan symptoms of SARS-CoV-2 infection persist after recovery. Evidence indicates that people who recovered from COVID-19, even those under the age of 65 years without cardiovascular risk factors such as smoking, obesity, hypertension, and diabetes, had a significantly increased risk of cardiovascular disease for up to one year after diagnosis. Therefore, it is important to closely monitor individuals who have recovered from COVID-19 for potential cardiovascular damage that may manifest at a later stage. Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by the production of reactive oxygen species (ROS) and increased lipid peroxide levels. Several studies have demonstrated that ferroptosis plays an important role in cancer, ischemia/reperfusion injury (I/RI), and other cardiovascular diseases. Altered iron metabolism, upregulation of reactive oxygen species, and glutathione peroxidase 4 inactivation are striking features of COVID-19-related cardiovascular injury. SARS-CoV-2 can cause cardiovascular ferroptosis, leading to cardiovascular damage. Understanding the mechanism of ferroptosis in COVID-19-related cardiovascular injuries will contribute to the development of treatment regimens for preventing or reducing COVID-19-related cardiovascular complications. In this article, we go over the pathophysiological underpinnings of SARS-CoV-2-induced acute and chronic cardiovascular injury, the function of ferroptosis, and prospective treatment approaches.

Coronavirus disease 2019 (COVID-19) has been declared a new pandemic in March 2020. Although most patients are asymptomatic, those with underlying cardiovascular comorbidities may develop a more severe systemic infection which is often associated with fatal pneumonia. Nonetheless, neurological and cardiovascular manifestations could be present even without respiratory symptoms. To date, no COVID-19-specific drugs are able for preventing or treating the infection and generally, the symptoms are relieved with general anti-inflammatory drugs. Angiotensin-converting-enzyme 2 (ACE2) may function as the receptor for virus entry within the cells favoring the progression of infection in the organism. On the other hand, ACE2 is a relevant enzyme in renin angiotensin system (RAS) cascade fostering Ang1-7/Mas receptor activation which promotes protective effects in neurological and cardiovascular systems. It is known that RAS is composed by two functional countervailing axes the ACE/AngII/AT1 receptor and the ACE/AngII/AT2 receptor which counteracts the actions mediated by AngII/AT1 receptor by inducing anti-inflammatory, antioxidant and anti-growth functions. Subsequently an "alternative" ACE2/Ang1-7/Mas receptor axis has been described with functions similar to the latter protective arm. Here, we discuss the neurological and cardiovascular effects of COVID-19 highlighting the role of the stimulation of the RAS "alternative" protective arm in attenuating pulmonary, cerebral and cardiovascular damages. In conclusion, only two clinical trials are running for Mas receptor agonists but few other molecules are in preclinical phase and if successful these drugs might represent a successful strategy for the treatment of the acute phase of COVID-19 infection.

The overwhelming majority of SARS-CoV-2 epidemiological studies cover a narrow time period, making general knowledge about the COVID-19 pandemic difficult. To assess COVID-19-related host aspects in the overall pandemic, we analyzed COVID-19 cases during the first two years of SARS-CoV-2 circulation in southern Brazil. Herein, 390 patients admitted in 2020-2022 to a Brazilian public referral hospital were allocated into two groups according to the COVID-19 outcome: hospital discharge (n=237) or death (n=153). In the univariate analysis, several variables, including sociodemographic, clinical and laboratory aspects (primary data), were significantly different between the analyzed groups. In multivariate logistic regression, eight of these factors remained associated with the COVID-19 outcome. In particular, we report oxygen supplementation and the need for hemodialysis as predictors of hospital discharge and death from COVID-19, respectively. To the best of our knowledge, none of these findings have been previously reported in the Brazilian or world population. In conclusion, our results contribute to current knowledge by demonstrating that factors described at different times may remain associated with COVID-19 over the pandemic and by identifying novel predictors of COVID-19 outcome.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is known to provoke a state of hypercoagulability that may lead to devastating consequences. This has been well established since the onset of the coronavirus pandemic in 2019; however, the specific relationship between COVID-19 and thrombus formation remains poorly understood. There has been increasing documentation of gastrointestinal (GI) complications in patients infected with the virus, including potentially lethal acute mesenteric ischemia (AMI), regardless of prior history of GI disease or risk factors for hypercoagulable states. Not only is mesenteric ischemia difficult to diagnose but it is also associated with high rates of morbidity and mortality, warranting prompt identification and treatment to improve clinical outcomes. We herein present a case of diffuse intestinal necrosis secondary to mesenteric thrombus formation in a previously healthy female five days after the resolution of her COVID-19 symptoms. The high rates of morbidity and mortality linked to AMI underpin the need for clinicians to maintain a high index of suspicion for thrombotic complications of COVID, even in healthy patients. This case emphasizes the importance of a thorough history-taking, physical examination, and laboratory workup even in patients without a current COVID-19 infection or predisposing thrombotic risk factors. Additionally, it suggests that the hypercoagulable state associated with a COVID-19 infection may persist after the primary COVID-19 symptoms have resolved.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and SARS-CoV-2 variants, has become a global pandemic resulting in significant morbidity and mortality. Severe cases of COVID-19 are characterized by hypoxemia, hyper-inflammation, cytokine storm in lung. Clinical studies have reported an association between COVID-19 and cardiovascular disease (CVD). Patients with CVD tend to develop severe symptoms and mortality if contracted COVID-19 with further elevations of cardiac injury biomarkers. Furthermore, COVID-19 itself can induce and promoted CVD development, including myocarditis, arrhythmia, acute coronary syndrome, cardiogenic shock, and venous thromboembolism. Although the direct etiology of SARS-CoV-2 induced cardiac injury remains unknown and under-investigated, it is suspected that it is related to myocarditis, cytokine-mediated injury, microvascular injury, and stress-related cardiomyopathy. Despite vaccinations having provided the most effective approach to reducing mortality overall, an adapted treatment paradigm and regular monitoring of cardiac injury biomarkers is critical for improving outcomes in vulnerable populations at risk for severe COVID-19. In this review, we focus on the latest progress in clinic and research on the cardiovascular complications of COVID-19 and provide a perspective of treating cardiac complications deriving from COVID-19 in Emergency Medicine.

The SARS coronavirus 2 (SARS-CoV-2) is the causative agent of the 2019 coronavirus disease (COVID-19) pandemic that has claimed the lives of 6.9 million people and infected over 765 million. It has become a major worldwide health problem and is also known to cause abnormalities in various systems, including the hematologic system. COVID-19 infection primarily affects the lower respiratory tract and can lead to a cascade of events, including a cytokine storm, intravascular thrombosis, and subsequent complications such as arterial and venous thromboses. COVID-19 can cause thrombocytopenia, lymphopenia, and neutrophilia, which are associated with worse outcomes. Prophylactic anticoagulation is essential to prevent complications and death rates associated with the virus's effect on the coagulation system. It is crucial to recognize these complications early and promptly start therapeutic anticoagulation to improve patient outcomes. While rare, COVID-19-induced disseminated intravascular coagulation (DIC) exhibits some similarities to DIC induced by sepsis. Lactate dehydrogenase (LDH), D-dimer, ferritin, and C-reactive protein (CRP) biomarkers often increase in serious COVID-19 cases and poor prognosis. Understanding the pathophysiology of the disease and identifying risk factors for adverse outcomes is critical for effective management of COVID-19.

Deep venous thrombosis (DVT) is a part of venous thromboembolism (VTE) that clinically manifests as swelling and pain in the lower limbs. The most serious clinical complication of DVT is pulmonary embolism (PE), which has a high mortality rate. To date, its underlying mechanisms are not fully understood, and patients usually present with clinical symptoms only after the formation of the thrombus. Thus, it is essential to understand the underlying mechanisms of deep vein thrombosis for an early diagnosis and treatment of DVT. In recent years, many studies have concluded that Neutrophil Extracellular Traps (NETs) are closely associated with DVT. These are released by neutrophils and, in addition to trapping pathogens, can mediate the formation of deep vein thrombi, thereby blocking blood vessels and leading to the development of disease. Therefore, this paper describes the occurrence and development of NETs and discusses the mechanism of action of NETs on deep vein thrombosis. It aims to provide a direction for improved diagnosis and treatment of deep vein thrombosis in the near future.

Patients with COVID-19 have a higher risk of thrombosis and thromboembolism, but the underlying mechanism(s) remain to be fully elucidated. In patients with COVID-19, high lipoprotein(a) (Lp(a)) is positively associated with the risk of ischemic heart disease. Lp(a), composed of an apoB-containing particle and apolipoprotein(a) (apo(a)), inhibits the key fibrinolytic enzyme, tissue-type plasminogen activator (tPA). However, whether the higher Lp(a) associates with lower tPA activity, the longitudinal changes of these parameters in hospitalized patients with COVID-19, and their correlation with clinical outcomes are unknown.

To assess if Lp(a) associates with lower tPA activity in COVID-19 patients, and how in COVID-19 populations Lp(a) and tPA change post infection.

Endogenous tPA enzymatic activity, tPA or Lp(a) concentration were measured in plasma from hospitalized patients with and without COVID-19. The association between plasma tPA and adverse clinical outcomes was assessed.

In hospitalized patients with COVID-19, we found lower tPA enzymatic activity and higher plasma Lp(a) than that in non-COVID-19 controls. During hospitalization, Lp(a) increased and tPA activity decreased, which associates with mortality. Among those who survived, Lp(a) decreased and tPA enzymatic activity increased during recovery. In patients with COVID-19, tPA activity is inversely correlated with tPA concentrations, thus, in another larger COVID-19 cohort, we utilized plasma tPA concentration as a surrogate to inversely reflect tPA activity. The tPA concentration was positively associated with death, disease severity, plasma inflammatory, and prothrombotic markers, and with length of hospitalization among those who were discharged.

High Lp(a) concentration provides a possible explanation for low endogenous tPA enzymatic activity, and poor clinical outcomes in patients with COVID-19.

The potentially fatal COVID-19 pandemic has been associated with a largespectrum of clinical presentations. Beyond the classical pulmonary manifestations, gastrointestinal tract-related symptoms suchas nausea, diarrhea, abdominal distention and pain have been observed in patients, as a consequence of the binding of SARS-CoV-19 to Angiotensin-converting Enzyme 2 (ACE2) receptors in the gastrointestinal (GI) tract. The early recognition ofspecific imaging features, including hepatobiliary involvement, pancreatic involvement, development of solid organ infarcts, ischemic bowel changes and vascular occlusion, plays a key role through the course of the disease. Also, suspicious symptoms, especially in critically ill patients with clinical and biochemical markers of hypovolemia, necessitate timely imaging for bleeding complications. The aim of this pictorial review is to illustrate the spectrum of the GIimaging findings in patients with COVID-19. Awareness of diagnostic imaging hallmarks is crucial to optimize the management of these patients.