The effect of COVID-19 on the human vascular system

2021 ◽  
pp. 72-79
Author(s):  
Riana Shamilievna Tinaeva ◽  
Vsevolod Vladimirovich Skvortsov Vsevolod
Keyword(s):  
Arterial Thrombosis ◽  
Vascular System ◽  
Vascular Dysfunction ◽  
Multiple Organ ◽  
World Health ◽  
Large Artery ◽  
Vascular Effects ◽  
Vein Thrombosis ◽  
Organ Systems ◽  
Novel Coronavirus

The World Health Organization (WHO) as a pandemic recognized the outbreak of the novel coronavirus COVID-19, which was first reported on December 8, 2019 in Hubei Province in China, on March 11, 2020. This disease was recognized as an infection with a new beta-coronavirus. Today, the current problem is COVID-19 and its effect on blood vessels and blood. Although COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects other organ systems. COVID-19 is manifested by hypercoagulation, pulmonary intravascular coagulation, microangiopathy, and venous thromboembolism (VTE) or arterial thrombosis. Clinically, the vascular dysfunction associated with COVID-19 manifests itself outside the lungs in various ways, including deep vein thrombosis, pulmonary embolism, large artery thrombosis, and multiple organ venous and arterial thrombosis, and these manifestations are attributed to factors such as hypoxemia, viral sepsis, immobility, and sometimes vasculitis. In some cases, DIC syndrome (which is a simulator of vasculitis) can occur with the lightning-fast lung disease COVID-19, and is also characterized by diffuse thrombosis and bleeding. If you exclude DIC and large vessel thrombosis, it is clear that patients with severe COVID-19 pneumonia may also have severe changes such as skin vasculitis, suspected cerebral vasculitis, and multiple organ failure, resulting in suspected viral endothelitis, direct viral infection, or vasculitis. Understanding the vascular effects of COVID-19 is essential for comprehensive medical care.

scholarly journals SARS-CoV-2, ACE2 expression, and systemic organ invasion

2020 ◽  
Author(s):  
Usman M Ashraf ◽  
Ahmed A Abokor ◽  
Jonnelle M. Edwards ◽  
Emily W. Waigi ◽  
Rachel S. Royfman ◽  
...  
Keyword(s):  
Respiratory Illness ◽  
Normal Function ◽  
Multiple Organ ◽  
Angiotensin Converting Enzyme 2 ◽  
Multiple Organs ◽  
Global Pandemic ◽  
Organ Systems ◽  
Novel Coronavirus ◽  
Severe Respiratory Illness ◽  
Organ Invasion

A novel coronavirus disease, COVID-19, has created a global pandemic in 2020, posing an enormous challenge to healthcare systems and affected communities. COVID-19 is caused by Severe Acute Respiratory Syndrome (SARS)-CoronaVirus-2 (CoV-2) that manifests as bronchitis, pneumonia, or a severe respiratory illness. SARS-CoV-2 infects human cells via binding a "spike" protein on its surface to angiotensin-converting enzyme 2 (ACE2) within the host. ACE2 is crucial for maintaining tissue homeostasis and negatively regulates the renin-angiotensin-aldosterone system (RAAS) in the humans. The RAAS is paramount for normal function in multiple organ systems including the lungs, heart, kidney, and vasculature. Given that SARS-CoV-2 internalizes via ACE2, the resultant disruption in ACE2 expression can lead to altered tissue function and exacerbate chronic diseases. The widespread distribution and expression of ACE2 across multiple organs is critical to our understanding of the varied clinical outcomes of COVID-19. This perspective review based on the current literature was prompted to show how disruption of ACE2 by SARS-CoV-2 can affect different organ systems.

scholarly journals Characterizing Long COVID: Deep Phenotype of a Complex Condition

2021 ◽  
Author(s):  
Rachel R Deer ◽  
Madeline A Rock ◽  
Nicole Vasilevsky ◽  
Leigh C Carmody ◽  
Halie M Rando ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Clinical Manifestations ◽  
Analysis Data ◽  
Clinical Findings ◽  
Multiple Organ ◽  
Diverse Range ◽  
Human Phenotype ◽  
Organ Systems ◽  
Novel Coronavirus

Importance: Since late 2019, the novel coronavirus SARS-CoV-2 has given rise to a global pandemic and introduced many health challenges with economic, social, and political consequences. In addition to a complex acute presentation that can affect multiple organ systems, there is mounting evidence of various persistent long-term sequelae. The worldwide scientific community is characterizing a diverse range of seemingly common long-term outcomes associated with SARS-CoV-2 infection, but the underlying assumptions in these studies vary widely making comparisons difficult. Numerous publications describe the clinical manifestations of post-acute sequelae of SARS-CoV-2 infection (PASC or long COVID), but they are difficult to integrate because of heterogeneous methods and the lack of a standard for denoting the many phenotypic manifestations of long COVID. Observations: We identified 303 articles published before April 29, 2021, curated 59 relevant manuscripts that described clinical manifestations in 81 cohorts of individuals three weeks or more following acute COVID-19, and mapped 287 unique clinical findings to Human Phenotype Ontology (HPO) terms. Conclusions and Relevance: Patients and clinicians often use different terms to describe the same symptom or condition. Addressing the heterogeneous and inconsistent language used to describe the clinical manifestations of long COVID combined with the lack of standardized terminologies for long COVID will provide a necessary foundation for comparison and meta-analysis of different studies. Translating long COVID manifestations into computable HPO terms will improve the analysis, data capture, and classification of long COVID patients. If researchers, clinicians, and patients share a common language, then studies can be compared or pooled more effectively. Furthermore, mapping lay terminology to HPO for long COVID manifestations will help patients assist clinicians and researchers in creating phenotypic characterizations that are computationally accessible, which may improve the stratification and thereby diagnosis and treatment of long COVID.

scholarly journals COVID-19-Induced Hyperleucocytosis in Chronic Lymphocytic Leukaemia

2021 ◽  
Author(s):  
Balraj Singh ◽  
Sarah Ayad ◽  
Parminder Kaur ◽  
Ro-Jay Reid ◽  
Sachin Gupta ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Chronic Lymphocytic Leukaemia ◽  
Respiratory Symptoms ◽  
Lymphocytic Leukaemia ◽  
Wide Spectrum ◽  
Multiple Organ ◽  
Global Pandemic ◽  
Organ Systems ◽  
Wbc Count ◽  
Novel Coronavirus

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus responsible for the current global pandemic, coronavirus disease 2019 (COVID-19). COVID-19 usually presents with respiratory symptoms but can affect multiple organ systems. A wide spectrum of complications can occur depending upon the comorbidities of patients. There is limited literature available regarding the presentation and outcome of COVID-19 in chronic lymphocytic leukaemia (CLL) patients. We report 2 cases of COVID-19-induced hyperleucocytosis (WBC count >100,000/?l) in CLL patients.

scholarly journals Acute kidney injury in hospitalized patients with COVID-19 (retrospective study)

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Haitham A. Azeem ◽  
Hytham Abdallah ◽  
Mohamad M. Abdelnaser
Keyword(s):  
Acute Kidney Injury ◽  
Retrospective Study ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Multiple Organ ◽  
Hospitalized Patients ◽  
World Health ◽  
Incidence And Mortality ◽  
Novel Coronavirus ◽  
Health Organization

Abstract Background The World Health Organization (WHO) has named the virus as 2019 novel coronavirus on January 12, 2020, and has declared a public health emergency globally on January 30, 2020. The epidemic started in Wuhan, China, in December of 2019 and quickly spread to over 200 countries. COVID-19 can cause multiple organ injuries (e.g., kidney, heart, blood, and nervous system). Among them, acute kidney injury (AKI) is a critical complication due to its high incidence and mortality rate. So, it is essential to evaluate AKI in COVID-19 patients during this pandemic state. The aim of this work is to detect the occurrence of AKI in hospitalized COVID-19 patients. So, a retrospective study was conducted on hospitalized adult patients > 18 years old with confirmed SARS-CoV-2 infection admitted to the Abo Teeg Hospital at Assiut City, Egypt, from May 1, 2020, to July 1, 2020. All data were collected from medical records, patients’ follow-up, and charts. Data were verified, coded by the researcher, and analyzed using IBM-SPSS 21.0. Results Eighty-six COVID-19 patients were admitted to Abo Teeg Hospital in Assiut City, Egypt, between May and July 2020. Thirty-eight patients (33%) were of the male gender. Mean age was 58.07 ± 17.9, and 61 patients developed AKI. 32.8% of the AKI group were a stage I severity (increase in serum creatinine by 0.3 mg/dl within 48 h), 21.3% of them presented by stage II (2–2.9 times increase in serum creatinine), and 45.9% were in stage III (3 times or more increase in serum creatinine). The overall hospital mortality for the patients admitted to ICU with AKI was 6.7% (11/61), compared to 1% (4/25) in those without AKI. Conclusion Hospitalized patients with COVID-19 had a higher risk of AKI, and we recommended that those patients should be evaluated after discharge for the development of CKD.

scholarly journals SARS-CoV-2 infection of circulating immune cells is not responsible for virus dissemination in severe COVID-19 patients

2021 ◽  
Author(s):  
Nicole L. Rosin ◽  
Arzina Jaffer ◽  
Sarthak Sinha ◽  
Rory P. Mulloy ◽  
Carolyn Robinson ◽  
...  
Keyword(s):  
Immune Cells ◽  
Multiple Organ ◽  
Trojan Horse ◽  
Viral Dissemination ◽  
Circulating Cells ◽  
Virus Dissemination ◽  
Global Pandemic ◽  
Organ Systems ◽  
Novel Coronavirus

SummaryIn late 2019 a novel coronavirus (SARS-CoV-2) emerged, and has since caused a global pandemic. Understanding the pathogenesis of COVID-19 disease is necessary to inform development of therapeutics, and management of infected patients. Using scRNAseq of blood drawn from SARS-CoV-2 patients, we asked whether SARS-CoV-2 may exploit immune cells as a ‘Trojan Horse’ to disseminate and access multiple organ systems. Our data suggests that circulating cells are not actively infected with SARS-CoV-2, and do not appear to be a source of viral dissemination.

scholarly journals Challenges in defining Long COVID: Striking differences across literature, Electronic Health Records, and patient-reported information

2021 ◽  
Author(s):  
Halie M. Rando ◽  
Tellen D. Bennett ◽  
James Brian Byrd ◽  
Carolyn Bramante ◽  
Tiffany J. Callahan ◽  
...  
Keyword(s):  
Electronic Health Records ◽  
Multiple Organ ◽  
Health Records ◽  
Health Crisis ◽  
Organ Systems ◽  
Wide Range ◽  
Patient Reported ◽  
Electronic Health ◽  
Novel Coronavirus

Since late 2019, the novel coronavirus SARS-CoV-2 has introduced a wide array of health challenges globally. In addition to a complex acute presentation that can affect multiple organ systems, increasing evidence points to long-term sequelae being common and impactful. As the worldwide scientific community forges ahead with efforts to characterize a wide range of outcomes associated with SARS-CoV-2 infection, the proliferation of available data has made it clear that formal definitions are needed in order to design robust and consistent studies of Long COVID that consistently capture variation in long-term outcomes. In the present study, we investigate the definitions used in the literature published to date and compare them against data available from electronic health records and patient-reported information collected via surveys. Long COVID holds the potential to produce a second public health crisis on the heels of the pandemic. Proactive efforts to identify the characteristics of this heterogeneous condition are imperative for a rigorous scientific effort to investigate and mitigate this threat.

scholarly journals A Simplified Understanding of the Black Swan: Anti-phospholipid Antibody Syndrome

2019 ◽  
Vol 57 (216) ◽  
Author(s):  
Binit Vaidya ◽  
Shweta Nakarmi ◽  
Rakshya Joshi ◽  
Rikesh Baral
Keyword(s):  
Venous Thrombosis ◽  
Multiple Organ ◽  
Thrombin Inhibitors ◽  
Moderate Intensity ◽  
Direct Thrombin Inhibitors ◽  
Acute Thrombosis ◽  
Vein Thrombosis ◽  
Asymptomatic Patients ◽  
Organ Systems ◽  
Diagnostic Clue

Anti-phospholipid antibody syndrome is caused by the presence of specific antibodies against phospholipid-binding plasma proteins in serum of patient, with or without underlying autoimmune diseases, that causes prolongation of tests of coagulation. High index of clinical suspicion is required for diagnosis. Stroke or myocardial infarction in young, unprovoked recurrent deep vein thrombosis and recurrent pregnancy loss are typical scenarios where it should be suspected. Presence of non-criteria manifestations like livedoreticularis, skin ulcers, nephropathy, valvular-heart disease and thrombocytopenia adds to diagnostic clue for presence of the syndrome. Therapeutic anti-coagulation with heparin followed by warfarin is required for patients with acute thrombosis. Those with venous thrombosis are given moderate-intensity warfarin(INR 2-3), whereas those with arterial thrombosis or recurrent venous thrombosis even on warfarin are treated with high intensity warfarin (INR 3-4). Similarly, anticoagulation with heparin is advised throughout pregnancy and up to six weeks postpartum. Treatment recommendations are still not clear for asymptomatic patients and in those with non-criteria manifestations of the disease. Steroids, intravenous immunoglobulin and immunosuppressant are reported to be effective in catastrophic cases characterized by rapid small vessel thrombotic involvement of multiple organ systems. Studies are evaluating the efficacy of direct thrombin inhibitors in the management of refractory cases.

scholarly journals Prerequisites for the creation of an atlas of postcovid inflammation as a way of personalized pharmacotherapy, as well as predicting and preventing organ and systemic dysfunctions

2021 ◽  
pp. 72-88
Author(s):  
I. V. Kukes ◽  
J. M. Salmasi ◽  
K. S. Ternovoy ◽  
A. N. Kazimirskii ◽  
T. E. Obodzinskaya ◽  
...  
Keyword(s):  
Vascular Dysfunction ◽  
Clinical Status ◽  
Cellular Tissue ◽  
Multiple Organ ◽  
Metabolic Dysfunction ◽  
Persistent Symptoms ◽  
Metabolism Disorder ◽  
Number Of Patients ◽  
Aromatic Amino Acid Metabolism ◽  
Novel Coronavirus

SARS-CoV-2 is a novel coronavirus that has been identified as the cause of the 2019 coronavirus infection (COVID-19), which originated at Wuhan city of PRC in late 2019 and widespread worldwide. As the number of patients recovering from COVID-19 continue to grow, it’s very important to understand what health issues they may keep experiencing. COVID-19 is now recognized as an infectious disease that can cause multiple organ diseases of various localization. It is against this background that a new term was introduced: post-acute post-COVID-19 syndrome characterized by several persistent symptoms inherent in the acute phase of the disease, as well as the occurrence of delayed and (or) long-term complications beyond 4 weeks from the onset of the disease. The work reflected in this article revealed a portrait of a patient with post-COVID-19 syndrome, the most common complications of this period, as well as the mechanisms of their development and the resulting metabolic, cellular, tissue disorders leading to the tissue and organ dysfunctions. A comprehensive biochemical and immunological screening was carried out using the example of three clinical cases to identify the most significant disorders in these patients and to correlate with their clinical status over time. In point of fact, such patients were diagnosed with vascular dysfunction factors (development of endothelial dysfunction), metabolic dysfunction factors (metabolic acidosis, mitochondrial dysfunction, carbohydrate metabolism disorder, insulin resistance, altered branched-chain and aromatic amino acid metabolism), neurological disorder factors (neurotoxicity of the resulting metabolites), immunological disorder factors (decreased efficiency of detoxification systems, secondary immunodeficiency, risk of secondary bacterial infection). 

Risk Factors for Thrombosis in WHO-Defined Early/Prefibrotic Myelofibrosis: An International Study of 264 Patients,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3846-3846
Author(s):  
Veronika Buxhofer-Ausch ◽  
Heinz Gisslinger ◽  
Juergen Thiele ◽  
Bettina Gisslinger ◽  
Hans-Michael Kvasnicka ◽  
...  
Keyword(s):  
Risk Factors ◽  
Venous Thrombosis ◽  
Arterial Thrombosis ◽  
Risk Profile ◽  
World Health ◽  
Vascular Events ◽  
Cox Regression Analysis ◽  
Vein Thrombosis ◽  
Specific Risk

Abstract Abstract 3846 INTRODUCTION There is strong evidence indicating that the clear-cut separation of prefibrotic primary myelofibrosis (PMF) from essential thrombocythemia (ET) by consequent application of the World Health Organization (WHO) 2008 criteria is reflected in different, well defined clinical pictures and divergent prognoses (Barbui et al, JCO 2011,Thiele et al, Blood 2011). Very recently the specific risk profile for arterial and venous thrombosis in WHO- diagnosed ET was published (Carobbio et al, Blood 2011). In PMF so far all published data on vascular events were exclusively based on overt disease manifestations until now there are no data available regarding prefibrotic stages. Consequently, we aimed to evaluate the corresponding risk profile of patients with WHO-diagnosed prefibrotic PMF. METHODS A total number of 264 patients with WHO-defined prefibrotic PMF derived from either the Medical University of Vienna or an International Database (Barbui et al, JCO 2011) were studied. Nonfatal thrombotic events considered in this study were reported as rates per 100 patient-years and included transient ischemic attacks, thrombotic cerebrovascular accidents, coronary artery disease, myocardial infarction, peripheral arterial disease, deep vein thrombosis of peripheral vasculature, pulmonary embolism, and abdominal large vein thrombosis. Cardiovascular risks factors considered, comprised of arterial hypertension, diabetes mellitus and tobacco use. To evaluate risk factors for total thrombosis and for arterial and venous events in particular multivariate Cox- regression analysis including the co-variables sex, age, previous thrombotic event, laboratory parameters measured at diagnosis and need for cytoreductive and/or antiplatelet therapy during follow-up was calculated. P values less than 0.05 were considered as statistically significant. RESULTS After a median follow- up of 5.8 years (range0.0 – 27.2), the total rate of non fatal thrombotic events was 2.1% patient-years (95% CI, 1.5–2.8); the incidence of arterial events was higher (1.7% patient- years) than of venous events (0.6% patient-years).Considering thrombosis in general a higher white blood cell (WBC) count enhances the risk significantly (p=0.005; HR 1.15). This is also true in arterial events in particular (p=0.047; HR 1.12). A lower platelet count is associated with a higher risk for thrombotic events; for thrombosis in general this association is of borderline significance (p=0.056; HR 0.99), for arterial thrombosis in particular of significance (p= 0.042; HR 0.99). A lower hemoglobin level is associated with a higher risk for venous thrombosis (p=0.007; HR 0.59). CONCLUSION Leukocytosis appears as a risk factor for thrombosis in general and also for arterial thrombosis in particular in WHO-diagnosed prefibrotic PMF. Moreover, higher platelet counts seem to decrease significantly the risk for thrombotic events in general and arterial thrombosis in particular. Anemia is associated with a higher risk for venous thrombosis. These observations are partly in line with recently published findings in WHO-diagnosed ET (Carobbio et al,2011) and might indicate the existence of a specific risk profile for thrombotic events in prefibrotic PMF. This is the first study reporting data on the risk profile for thrombosis in WHO-diagnosed prefibrotic PMF. Certainly these findings ask for validation in a larger patient population. Disclosures: Gisslinger: Novartis: Speakers Bureau; Celgene Austria: Research Funding, Speakers Bureau; AOP-Orphan Pharmaceuticals AG: Speakers Bureau. Vannucchi:Novartis: Honoraria.

scholarly journals Histopathology and Pathogenesis of Coronavirus disease 2019 (COVID-19)

2020 ◽  
Vol 2 (3) ◽  
pp. 230-234
Author(s):  
Nikolaos Chrysanthakopoulos ◽  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Immune Responses ◽  
Good Prognosis ◽  
Multiple Organ ◽  
World Health ◽  
The Novel ◽  
Angiotensin Converting Enzyme 2 ◽  
Corona Virus ◽  
Novel Coronavirus ◽  
Health Organization

A severe pandemic of CoronaVirus disease 2019 (COVID-19), according to World Health Organization (WHO), appeared in China in December 2019, and spread rapidly. The majority of the patients had mild symptoms and good prognosis after recovery; however some patients developed severe inflammatory reaction and passed away from multiple organ complications. The novel coronavirus, Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2) is a beta-coronavirus and is similar with the Severe Acute Respiratory Syndrome Corona Virus 1 (SARS-CoV-1) and the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). SARS-CoV-2 and -1 have the same host receptor, the angiotensin-converting enzyme 2 (ACE2). The pathogenesis of SARS-CoV-2 infection in humans remains unclear. The immune response is essential to control and reduce SARS-CoV-1 and -2 infections, however, irregular and exaggerated immune responses may lead to the immunopathology of the disease and the lung lesions. This article presents the immunological features of SARS-CoV-2 infection and its potential pathogenesis based on the recent observations of the International literature.

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