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COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies
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COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 27276

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editors

Dr. Alexandru Schiopu

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Guest Editor
Department of Clinical Sciences Malmö, Lund University, 21428 Malmö, Sweden
Interests: cardiovascular research; cardiac inflammation; innate immunity; cardiology; atherosclerosis
Special Issues, Collections and Topics in MDPI journals
Dr. Emil Marian Arbănași

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Guest Editor
1. Clinic of Vascular Surgery, Mures County Emergency Hospital, 540136 Targu Mures, Romania
2. Department of Vascular Surgery, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540139 Targu Mures, Romania
Interests: vascular surgery; acute limb ischemia; vascular access; carotid endarterectomy; peripheral arterial disease
Special Issues, Collections and Topics in MDPI journals
Dr. Eliza Russu

E-Mail Website
Guest Editor
1. Department of Vascular Surgery, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540139 Targu Mures, Romania
2. Clinic of Vascular Surgery, Mures County Emergency Hospital, 540136 Targu Mures, Romania
Interests: vascular surgery; arteriovenous fistula; AVF; artery; vein; varicose veins; AAA; abdominal aortic aneurysms; carotid disease; endarterectomy; peripheral arterial disease; PAD; acute limb ischemia; critical limb ischemia; revascularization; revascularization of the lower limbs; bioengineering; biomechanical properties; aneurysmal dilatation; vascular trauma; arterial reconstruction; by-pass; angioplasty; aneurysmal rupture; adventitial collagen; photochemical crosslinking; mechanical reinforcement; proteolytic resistance; designing therapeutic strategies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

COVID-19 is a viral infection with a severe multisystemic clinical pathology. COVID-19 infection is associated with high hospitalization and intensive care unit (ICU) admission rates, and high mortality. Patients with severe Covid-19 infections display substantial immunological dysregulation including abnormal cytokine release, endothelial dysfunction, and coagulopathy. Changes in the coagulation status have been reported since the beginning of the epidemic. In the early stages of infection, D-dimer and fibrinogen levels are elevated, but activated partial prothrombin time, prothrombin time and platelet counts are frequently normal. Despite intensive worldwide efforts, the mechanisms behind COVID-19-induced coagulopathy are largely unknown and more reasearch is required to understand and treat these potentially deadly complications.

Thrombosis occurs when the primary components of the Virchow's triad exist, including stagnation of the blood circulation, damage to the endothelial and a hypercoagulable status. Among the proposed mechanisms of COVID-19-related thrombosis, COVID-19 binding to the endothelial cells through the angiotensin-converting enzyme 2 (ACE2) receptor has been shown to cause an inflammatory response that leads to endothelial damage. Angiotensin 2 can stimulate the synthesis of plasminogen activator inhibitor-1 (PAI-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) on cell surface, while P-selectin induces the synthesis of tissue factor (TF) in monocytes. In addition, patient immobilization and the increase in positive end-expiratory force due to the lung pathology and mechanical ventilation impair blood circulation and cause venous stasis.

Several COVID-19-related thrombotic consequences in both the arterial (acute limb ischemia, acute coronary syndrome, stroke, thrombosis of the thoracic and abdominal aorta, mesenteric ischemia) and the venous system (deep venous thrombosis, cerebral venous sinus thrombosis, and pulmonary embolism) have been reported, but it is unclear whether these occur through the same mechanisms.

The purpose of this Special Issue is to publish a series of relevant papers presenting some of the most important current advances in understanding the molecular pathways and the clinical manifestations of the thrombo-embolic events in COVID-19 patients. We hereby welcome researchers to contribute manuscripts focusing on the molecular pathology, diagnostics and therapeutics of COVID-19 coagulopathy.

Dr. Alexandru Schiopu
Dr. Emil Marian Arbănași
Dr. Eliza Russu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

Keywords

  • COVID-19
  • thrombosis
  • coagulopathy
  • coagulation factors
  • vascular inflammation
  • acute limb ischemia
  • acute coronary syndrome
  • stroke
  • mesenteric ischemia
  • deep venous thrombosis
  • pulmonary embolism
  • cerebral venous sinus thrombosis

Published Papers (15 papers)

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Editorial

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6 pages, 225 KiB  
Editorial
Special Issue “COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies”
by Eliza Russu, Emil-Marian Arbănaşi and Alexandru Șchiopu
Int. J. Mol. Sci. 2024, 25(6), 3548; https://doi.org/10.3390/ijms25063548 - 21 Mar 2024
Viewed by 561
Abstract
The Special Issue on COVID-19 coagulopathy initiated one year ago aimed to shed light on the mechanisms underlying the changes in the coagulation status making SARS-CoV-2 infection such a tough adversary for every one of the medical specialties encountering it, along with overseeing [...] Read more.
The Special Issue on COVID-19 coagulopathy initiated one year ago aimed to shed light on the mechanisms underlying the changes in the coagulation status making SARS-CoV-2 infection such a tough adversary for every one of the medical specialties encountering it, along with overseeing the therapeutic applications derived from the current understanding of these mechanisms [...] Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)

Research

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13 pages, 967 KiB  
Article
IL-6 and Neutrophil/Lymphocyte Ratio as Markers of ICU Admittance in SARS-CoV-2 Patients with Diabetes
by Iulia Făgărășan, Adriana Rusu, Horațiu Comșa, Tudor-Dan Simu, Damiana-Maria Vulturar and Doina-Adina Todea
Int. J. Mol. Sci. 2023, 24(19), 14908; https://doi.org/10.3390/ijms241914908 - 5 Oct 2023
Cited by 3 | Viewed by 857
Abstract
Inflammation along with coagulation disturbances has an essential role in the evolution towards a severe disease in patients with the coronavirus disease 2019 (COVID-19). This study aimed to evaluate inflammatory and coagulation biomarkers when predicting the need to visit an intensive care unit [...] Read more.
Inflammation along with coagulation disturbances has an essential role in the evolution towards a severe disease in patients with the coronavirus disease 2019 (COVID-19). This study aimed to evaluate inflammatory and coagulation biomarkers when predicting the need to visit an intensive care unit (ICU) in diabetes mellitus (DM) patients. In a retrospective study, laboratory parameters were examined for 366 participants: ICU = 90, of which 44 patients had DM and no ICU admittance = 276. The ability of inflammatory and coagulation markers to distinguish the severity of COVID-19 was determined using univariate and multivariate regression analysis. In all patients, lactate dehydrogenase was the only predictor for ICU admittance in the multivariate analysis. In the DM group, the results showed that the interleukin (IL)-6 and neutrophil/lymphocyte ratio (NLR) values at admission could predict the need for ICU admittance. Even though there were significant differences between the ICU and no ICU admittance groups regarding the coagulation markers, they could not predict the severity of the disease in DM patients. The present study showed for the first time that the IL-6 and NLR admission values could predict ICU admittance in DM patients. This finding could help clinicians manage the infection more easily if the COVID-19 pandemic strikes again. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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22 pages, 8283 KiB  
Article
SARS-CoV-2 Spike Proteins and Cell–Cell Communication Induce P-Selectin and Markers of Endothelial Injury, NETosis, and Inflammation in Human Lung Microvascular Endothelial Cells and Neutrophils: Implications for the Pathogenesis of COVID-19 Coagulopathy
by Biju Bhargavan and Georgette D. Kanmogne
Int. J. Mol. Sci. 2023, 24(16), 12585; https://doi.org/10.3390/ijms241612585 - 9 Aug 2023
Cited by 6 | Viewed by 1283
Abstract
COVID-19 progression often involves severe lung injury, inflammation, coagulopathy, and leukocyte infiltration into pulmonary tissues. The pathogenesis of these complications is unknown. Because vascular endothelium and neutrophils express angiotensin-converting enzyme-2 and spike (S)-proteins, which are present in bodily fluids and tissues of SARS-CoV-2-infected [...] Read more.
COVID-19 progression often involves severe lung injury, inflammation, coagulopathy, and leukocyte infiltration into pulmonary tissues. The pathogenesis of these complications is unknown. Because vascular endothelium and neutrophils express angiotensin-converting enzyme-2 and spike (S)-proteins, which are present in bodily fluids and tissues of SARS-CoV-2-infected patients, we investigated the effect of S-proteins and cell–cell communication on human lung microvascular endothelial cells and neutrophils expression of P-selectin, markers of coagulopathy, NETosis, and inflammation. Exposure of endothelial cells or neutrophils to S-proteins and endothelial–neutrophils co-culture induced P-selectin transcription and expression, significantly increased expression/secretion of IL-6, von Willebrand factor (vWF, pro-coagulant), and citrullinated histone H3 (cit-H3, NETosis marker). Compared to the SARS-CoV-2 Wuhan variant, Delta variant S-proteins induced 1.4–15-fold higher P-selectin and higher IL-6 and vWF. Recombinant tissue factor pathway inhibitor (rTFPI), 5,5′-dithio-bis-(2-nitrobenzoic acid) (thiol blocker), and thrombomodulin (anticoagulant) blocked S-protein-induced vWF, IL-6, and cit-H3. This suggests that following SARS-CoV-2 contact with the pulmonary endothelium or neutrophils and endothelial–neutrophil interactions, S-proteins increase adhesion molecules, induce endothelial injury, inflammation, NETosis and coagulopathy via the tissue factor pathway, mechanisms involving functional thiol groups, and/or the fibrinolysis system. Using rTFPI, effectors of the fibrinolysis system and/or thiol-based drugs could be viable therapeutic strategies against SARS-CoV-2-induced endothelial injury, inflammation, NETosis, and coagulopathy. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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13 pages, 2711 KiB  
Article
A Potential Association between Ribonuclease 1 Dynamics in the Blood and the Outcome in COVID-19 Patients
by Elisabeth Zechendorf, Christian Beckers, Nadine Frank, Sandra Kraemer, Carolina Neu, Thomas Breuer, Michael Dreher, Edgar Dahl, Gernot Marx, Lukas Martin and Tim-Philipp Simon
Int. J. Mol. Sci. 2023, 24(15), 12428; https://doi.org/10.3390/ijms241512428 - 4 Aug 2023
Viewed by 895
Abstract
The COVID-19 pandemic caused by the new SARS-CoV-2 coronavirus is the most recent and well-known outbreak of a coronavirus. RNase 1 is a small endogenous antimicrobial polypeptide that possesses antiviral activity against viral diseases. In this study, we investigated a potential association between [...] Read more.
The COVID-19 pandemic caused by the new SARS-CoV-2 coronavirus is the most recent and well-known outbreak of a coronavirus. RNase 1 is a small endogenous antimicrobial polypeptide that possesses antiviral activity against viral diseases. In this study, we investigated a potential association between ribonuclease 1 and the outcome in COVID-19 patients and the impact of increased and decreased RNase 1 levels serum during the course of the disease. Therefore, two patient populations, Cohort A (n = 35) and B (n = 80), were subclassified into two groups, in which the RNase 1 concentration increased or decreased from time point one to time point two. We show that the RNase 1 serum levels significantly increased in the increasing group of both cohorts (p = 0.0171; p < 0.0001). We detect that patients in the increasing group who died had significantly higher RNase 1 serum levels at both time points in Cohort A (p = 0.0170; p = 0.0393) and Cohort B (p = 0.0253; p = 0.0034) than patients who survived. Additionally, we measured a significant correlation of RNase 1 serum levels with serum creatinine as well as creatinine clearance in the increasing and decreasing group at both time points of Cohort A. Based on these results, there is now good evidence that RNase 1 may play a role in renal dysfunction associated with ICU COVID-19 patients and that increasing RNase 1 serum level may be a potential biomarker to predict outcome in COVID-19 patients. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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11 pages, 1653 KiB  
Article
Elevated FAI Index of Pericoronary Inflammation on Coronary CT Identifies Increased Risk of Coronary Plaque Vulnerability after COVID-19 Infection
by Botond Barna Mátyás, Imre Benedek, Emanuel Blîndu, Renáta Gerculy, Aurelian Roșca, Nóra Rat, István Kovács, Diana Opincariu, Zsolt Parajkó, Evelin Szabó, Bianka Benedek and Theodora Benedek
Int. J. Mol. Sci. 2023, 24(8), 7398; https://doi.org/10.3390/ijms24087398 - 17 Apr 2023
Cited by 7 | Viewed by 1974
Abstract
Inflammation is a key factor in the development of atherosclerosis, a disease characterized by the buildup of plaque in the arteries. COVID-19 infection is known to cause systemic inflammation, but its impact on local plaque vulnerability is unclear. Our study aimed to investigate [...] Read more.
Inflammation is a key factor in the development of atherosclerosis, a disease characterized by the buildup of plaque in the arteries. COVID-19 infection is known to cause systemic inflammation, but its impact on local plaque vulnerability is unclear. Our study aimed to investigate the impact of COVID-19 infection on coronary artery disease (CAD) in patients who underwent computed tomography angiography (CCTA) for chest pain in the early stages after infection, using an AI-powered solution called CaRi-Heart®. The study included 158 patients (mean age was 61.63 ± 10.14 years) with angina and low to intermediate clinical likelihood of CAD, with 75 having a previous COVID-19 infection and 83 without infection. The results showed that patients who had a previous COVID-19 infection had higher levels of pericoronary inflammation than those who did not have a COVID-19 infection, suggesting that COVID-19 may increase the risk of coronary plaque destabilization. This study highlights the potential long-term impact of COVID-19 on cardiovascular health, and the importance of monitoring and managing cardiovascular risk factors in patients recovering from COVID-19 infection. The AI-powered CaRi-Heart® technology may offer a non-invasive way to detect coronary artery inflammation and plaque instability in patients with COVID-19. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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12 pages, 1607 KiB  
Article
The Long Term Residual Effects of COVID-Associated Coagulopathy
by Marco Ranucci, Ekaterina Baryshnikova, Martina Anguissola, Sara Pugliese, Mara Falco and Lorenzo Menicanti
Int. J. Mol. Sci. 2023, 24(6), 5514; https://doi.org/10.3390/ijms24065514 - 14 Mar 2023
Cited by 12 | Viewed by 1674
Abstract
During the acute phase of COVID-19, many patients experience a complex coagulopathy characterized by a procoagulant pattern. The present study investigates the persistence of hemostatic changes in post-COVID patients at a long-term follow up, and the link with the persistence of physical and [...] Read more.
During the acute phase of COVID-19, many patients experience a complex coagulopathy characterized by a procoagulant pattern. The present study investigates the persistence of hemostatic changes in post-COVID patients at a long-term follow up, and the link with the persistence of physical and neuropsychological symptoms. We completed a prospective cohort study on 102 post-COVID patients. Standard coagulation and viscoelastic tests were performed, along with an assessment of persistent symptoms and recording of acute phase details. A procoagulant state was adjudicated in the presence of fibrinogen > 400 mg/dL, or D-dimer > 500 ng/mL, or platelet count > 450,000 cells/µL, or a maxim clot lysis at viscoelastic test < 2%. A procoagulant state was identified in 75% of the patients at 3 months follow up, 50% at 6 months, and 30% at 12–18 months. Factors associated with the persistence of a procoagulant state were age, severity of the acute phase, and persistence of symptoms. Patients with major physical symptoms carry a procoagulant state relative risk of 2.8 (95% confidence interval 1.17–6.7, p = 0.019). The association between persistent symptoms and a procoagulant state raises the hypothesis that an ongoing process of thrombi formation and/or persistent microthrombosis may be responsible for the main physical symptoms in long-COVID patients. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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Review

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16 pages, 536 KiB  
Review
COVID-19 and Antipsychotic Therapy: Unraveling the Thrombosis Risk
by Eszter-Anna Dho-Nagy, Attila Brassai, Patrick Lechsner, Corina Ureche and Erika-Gyöngyi Bán
Int. J. Mol. Sci. 2024, 25(2), 818; https://doi.org/10.3390/ijms25020818 - 9 Jan 2024
Viewed by 794
Abstract
In the context of the COVID-19 pandemic, this study investigates the potential correlation between the increased use of antipsychotic medications and the rising incidence of venous thromboembolism (VTE). As psychiatric disorders surged, the consequential escalation in antipsychotic drug use raised concerns about thrombotic [...] Read more.
In the context of the COVID-19 pandemic, this study investigates the potential correlation between the increased use of antipsychotic medications and the rising incidence of venous thromboembolism (VTE). As psychiatric disorders surged, the consequential escalation in antipsychotic drug use raised concerns about thrombotic risks. We conducted a comprehensive literature review using PubMed, focusing on articles that intersected COVID-19, antipsychotic medication, and thrombosis. This approach allowed for a nuanced examination of the historical and recent data on antipsychotic drugs and their association with thrombotic events. Our findings reveal a notable link between the use of antipsychotic medications, particularly second-generation antipsychotics, and an increased risk of VTE, including pulmonary embolism and deep vein thrombosis. This association was evident, despite variations in study designs and populations. The study underscores the need for cautious medication management in psychiatric care, especially during pandemic conditions like COVID-19, to mitigate thrombotic risks. It advocates a personalized approach to prescribing antipsychotics, considering individual patient factors and comorbidities, to balance the benefits against potential thrombotic complications. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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35 pages, 3673 KiB  
Review
Sialylated Glycan Bindings from SARS-CoV-2 Spike Protein to Blood and Endothelial Cells Govern the Severe Morbidities of COVID-19
by David E. Scheim, Paola Vottero, Alessandro D. Santin and Allen G. Hirsh
Int. J. Mol. Sci. 2023, 24(23), 17039; https://doi.org/10.3390/ijms242317039 - 1 Dec 2023
Cited by 3 | Viewed by 5816
Abstract
Consistent with well-established biochemical properties of coronaviruses, sialylated glycan attachments between SARS-CoV-2 spike protein (SP) and host cells are key to the virus’s pathology. SARS-CoV-2 SP attaches to and aggregates red blood cells (RBCs), as shown in many pre-clinical and clinical studies, causing [...] Read more.
Consistent with well-established biochemical properties of coronaviruses, sialylated glycan attachments between SARS-CoV-2 spike protein (SP) and host cells are key to the virus’s pathology. SARS-CoV-2 SP attaches to and aggregates red blood cells (RBCs), as shown in many pre-clinical and clinical studies, causing pulmonary and extrapulmonary microthrombi and hypoxia in severe COVID-19 patients. SARS-CoV-2 SP attachments to the heavily sialylated surfaces of platelets (which, like RBCs, have no ACE2) and endothelial cells (having minimal ACE2) compound this vascular damage. Notably, experimentally induced RBC aggregation in vivo causes the same key morbidities as for severe COVID-19, including microvascular occlusion, blood clots, hypoxia and myocarditis. Key risk factors for COVID-19 morbidity, including older age, diabetes and obesity, are all characterized by markedly increased propensity to RBC clumping. For mammalian species, the degree of clinical susceptibility to COVID-19 correlates to RBC aggregability with p = 0.033. Notably, of the five human betacoronaviruses, the two common cold strains express an enzyme that releases glycan attachments, while the deadly SARS, SARS-CoV-2 and MERS do not, although viral loads for COVID-19 and the two common cold infections are similar. These biochemical insights also explain the previously puzzling clinical efficacy of certain generics against COVID-19 and may support the development of future therapeutic strategies for COVID-19 and long COVID patients. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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Graphical abstract

18 pages, 887 KiB  
Review
The Management of COVID-19-Related Coagulopathy: A Focus on the Challenges of Metabolic and Vascular Diseases
by Mónika Szilveszter, Sándor Pál, Zsuzsánna Simon-Szabó, Orsolya-Zsuzsa Akácsos-Szász, Mihály Moldován, Barbara Réger, Lóránd Dénes, Zsuzsanna Faust, Mariana Cornelia Tilinca and Enikő Nemes-Nagy
Int. J. Mol. Sci. 2023, 24(16), 12782; https://doi.org/10.3390/ijms241612782 - 14 Aug 2023
Cited by 2 | Viewed by 1487
Abstract
The course of COVID-19 is highly dependent on the associated cardiometabolic comorbidities of the patient, which worsen the prognosis of coronavirus infection, mainly due to systemic inflammation, endothelium dysfunction, and thrombosis. A search on the recent medical literature was performed in five languages, [...] Read more.
The course of COVID-19 is highly dependent on the associated cardiometabolic comorbidities of the patient, which worsen the prognosis of coronavirus infection, mainly due to systemic inflammation, endothelium dysfunction, and thrombosis. A search on the recent medical literature was performed in five languages, using the PubMed, Embase, Cochrane, and Google Scholar databases, for the review of data regarding the management of patients with a high risk for severe COVID-19, focusing on the associated coagulopathy. Special features of COVID-19 management are presented, based on the underlying conditions (obesity, diabetes mellitus, and cardiovascular diseases), emphasizing the necessity of a modern, holistic approach to thromboembolic states. The latest findings regarding the most efficient therapeutic approaches are included in the article, offering guidance for medical professionals in severe, complicated cases of SARS-CoV-2 infection. We can conclude that severe COVID-19 is closely related to vascular inflammation and intense cytokine release leading to hemostasis disorders. Overweight, hyperglycemia, cardiovascular diseases, and old age are important risk factors for severe outcomes of coronavirus infection, involving a hypercoagulable state. Early diagnosis and proper therapy in complicated SARS-CoV-2-infected cases could reduce mortality and the need for intensive care during hospitalization in patients with cardiometabolic comorbidities. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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21 pages, 1556 KiB  
Review
Interrelationship between COVID-19 and Coagulopathy: Pathophysiological and Clinical Evidence
by Beatrice Ragnoli, Beatrice Da Re, Alessandra Galantino, Stefano Kette, Andrea Salotti and Mario Malerba
Int. J. Mol. Sci. 2023, 24(10), 8945; https://doi.org/10.3390/ijms24108945 - 18 May 2023
Cited by 4 | Viewed by 1562
Abstract
Since the first description of COVID-19 infection, among clinical manifestations of the disease, including fever, dyspnea, cough, and fatigue, it was observed a high incidence of thromboembolic events potentially evolving towards acute respiratory distress syndrome (ARDS) and COVID-19-associated-coagulopathy (CAC). The hypercoagulation state is [...] Read more.
Since the first description of COVID-19 infection, among clinical manifestations of the disease, including fever, dyspnea, cough, and fatigue, it was observed a high incidence of thromboembolic events potentially evolving towards acute respiratory distress syndrome (ARDS) and COVID-19-associated-coagulopathy (CAC). The hypercoagulation state is based on an interaction between thrombosis and inflammation. The so-called CAC represents a key aspect in the genesis of organ damage from SARS-CoV-2. The prothrombotic status of COVID-19 can be explained by the increase in coagulation levels of D-dimer, lymphocytes, fibrinogen, interleukin 6 (IL-6), and prothrombin time. Several mechanisms have been hypothesized to explain this hypercoagulable process such as inflammatory cytokine storm, platelet activation, endothelial dysfunction, and stasis for a long time. The purpose of this narrative review is to provide an overview of the current knowledge on the pathogenic mechanisms of coagulopathy that may characterize COVID-19 infection and inform on new areas of research. New vascular therapeutic strategies are also reviewed. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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16 pages, 600 KiB  
Review
Determinants of COVID-19 Disease Severity–Lessons from Primary and Secondary Immune Disorders including Cancer
by Antonio G. Solimando, Max Bittrich, Endrit Shahini, Federica Albanese, Georg Fritz and Markus Krebs
Int. J. Mol. Sci. 2023, 24(10), 8746; https://doi.org/10.3390/ijms24108746 - 14 May 2023
Viewed by 1499
Abstract
At the beginning of the COVID-19 pandemic, patients with primary and secondary immune disorders—including patients suffering from cancer—were generally regarded as a high-risk population in terms of COVID-19 disease severity and mortality. By now, scientific evidence indicates that there is substantial heterogeneity regarding [...] Read more.
At the beginning of the COVID-19 pandemic, patients with primary and secondary immune disorders—including patients suffering from cancer—were generally regarded as a high-risk population in terms of COVID-19 disease severity and mortality. By now, scientific evidence indicates that there is substantial heterogeneity regarding the vulnerability towards COVID-19 in patients with immune disorders. In this review, we aimed to summarize the current knowledge about the effect of coexistent immune disorders on COVID-19 disease severity and vaccination response. In this context, we also regarded cancer as a secondary immune disorder. While patients with hematological malignancies displayed lower seroconversion rates after vaccination in some studies, a majority of cancer patients’ risk factors for severe COVID-19 disease were either inherent (such as metastatic or progressive disease) or comparable to the general population (age, male gender and comorbidities such as kidney or liver disease). A deeper understanding is needed to better define patient subgroups at a higher risk for severe COVID-19 disease courses. At the same time, immune disorders as functional disease models offer further insights into the role of specific immune cells and cytokines when orchestrating the immune response towards SARS-CoV-2 infection. Longitudinal serological studies are urgently needed to determine the extent and the duration of SARS-CoV-2 immunity in the general population, as well as immune-compromised and oncological patients. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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16 pages, 2342 KiB  
Review
Thrombotic Mechanism Involving Platelet Activation, Hypercoagulability and Hypofibrinolysis in Coronavirus Disease 2019
by Hideo Wada, Katsuya Shiraki, Hideto Shimpo, Motomu Shimaoka, Toshiaki Iba and Katsue Suzuki-Inoue
Int. J. Mol. Sci. 2023, 24(9), 7975; https://doi.org/10.3390/ijms24097975 - 28 Apr 2023
Cited by 9 | Viewed by 1493
Abstract
Coronavirus disease 2019 (COVID-19) has spread, with thrombotic complications being increasingly frequently reported. Although thrombosis is frequently complicated in septic patients, there are some differences in the thrombosis noted with COVID-19 and that noted with bacterial infections. The incidence (6–26%) of thrombosis varied [...] Read more.
Coronavirus disease 2019 (COVID-19) has spread, with thrombotic complications being increasingly frequently reported. Although thrombosis is frequently complicated in septic patients, there are some differences in the thrombosis noted with COVID-19 and that noted with bacterial infections. The incidence (6–26%) of thrombosis varied among reports in patients with COVID-19; the incidences of venous thromboembolism and acute arterial thrombosis were 4.8–21.0% and 0.7–3.7%, respectively. Although disseminated intravascular coagulation (DIC) is frequently associated with bacterial infections, a few cases of DIC have been reported in association with COVID-19. Fibrin-related markers, such as D-dimer levels, are extremely high in bacterial infections, whereas soluble C-type lectin-like receptor 2 (sCLEC-2) levels are high in COVID-19, suggesting that hypercoagulable and hyperfibrinolytic states are predominant in bacterial infections, whereas hypercoagulable and hypofibrinolytic states with platelet activation are predominant in COVID-19. Marked platelet activation, hypercoagulability and hypofibrinolytic states may cause thrombosis in patients with COVID-19. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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16 pages, 705 KiB  
Review
Pathways of Coagulopathy and Inflammatory Response in SARS-CoV-2 Infection among Type 2 Diabetic Patients
by Orsolya-Zsuzsa Akácsos-Szász, Sándor Pál, Kinga-Ilona Nyulas, Enikő Nemes-Nagy, Ana-Maria Fárr, Lóránd Dénes, Mónika Szilveszter, Erika-Gyöngyi Bán, Mariana Cornelia Tilinca and Zsuzsánna Simon-Szabó
Int. J. Mol. Sci. 2023, 24(5), 4319; https://doi.org/10.3390/ijms24054319 - 21 Feb 2023
Cited by 6 | Viewed by 1743
Abstract
Chronic inflammation and endothelium dysfunction are present in diabetic patients. COVID-19 has a high mortality rate in association with diabetes, partially due to the development of thromboembolic events in the context of coronavirus infection. The purpose of this review is to present the [...] Read more.
Chronic inflammation and endothelium dysfunction are present in diabetic patients. COVID-19 has a high mortality rate in association with diabetes, partially due to the development of thromboembolic events in the context of coronavirus infection. The purpose of this review is to present the most important underlying pathomechanisms in the development of COVID-19-related coagulopathy in diabetic patients. The methodology consisted of data collection and synthesis from the recent scientific literature by accessing different databases (Cochrane, PubMed, Embase). The main results are the comprehensive and detailed presentation of the very complex interrelations between different factors and pathways involved in the development of arteriopathy and thrombosis in COVID-19-infected diabetic patients. Several genetic and metabolic factors influence the course of COVID-19 within the background of diabetes mellitus. Extensive knowledge of the underlying pathomechanisms of SARS-CoV-2-related vasculopathy and coagulopathy in diabetic subjects contributes to a better understanding of the manifestations in this highly vulnerable group of patients; thus, they can benefit from a modern, more efficient approach regarding diagnostic and therapeutic management. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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21 pages, 1758 KiB  
Review
Monocytic HLA-DR Expression in Immune Responses of Acute Pancreatitis and COVID-19
by Shiyu Liu, Wenjuan Luo, Peter Szatmary, Xiaoying Zhang, Jing-Wen Lin, Lu Chen, Dan Liu, Robert Sutton, Qing Xia, Tao Jin, Tingting Liu and Wei Huang
Int. J. Mol. Sci. 2023, 24(4), 3246; https://doi.org/10.3390/ijms24043246 - 7 Feb 2023
Cited by 6 | Viewed by 2367
Abstract
Acute pancreatitis is a common gastrointestinal disease with increasing incidence worldwide. COVID-19 is a potentially life-threatening contagious disease spread throughout the world, caused by severe acute respiratory syndrome coronavirus 2. More severe forms of both diseases exhibit commonalities with dysregulated immune responses resulting [...] Read more.
Acute pancreatitis is a common gastrointestinal disease with increasing incidence worldwide. COVID-19 is a potentially life-threatening contagious disease spread throughout the world, caused by severe acute respiratory syndrome coronavirus 2. More severe forms of both diseases exhibit commonalities with dysregulated immune responses resulting in amplified inflammation and susceptibility to infection. Human leucocyte antigen (HLA)-DR, expressed on antigen-presenting cells, acts as an indicator of immune function. Research advances have highlighted the predictive values of monocytic HLA-DR (mHLA-DR) expression for disease severity and infectious complications in both acute pancreatitis and COVID-19 patients. While the regulatory mechanism of altered mHLA-DR expression remains unclear, HLA-DR−/low monocytic myeloid-derived suppressor cells are potent drivers of immunosuppression and poor outcomes in these diseases. Future studies with mHLA-DR-guided enrollment or targeted immunotherapy are warranted in more severe cases of patients with acute pancreatitis and COVID-19. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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9 pages, 3362 KiB  
Case Report
Prenatal and Neonatal Pulmonary Thrombosis as a Potential Complication of SARS-CoV-2 Infection in Late Pregnancy
by Gazala Abdulaziz-Opiela, Anna Sobieraj, Greta Sibrecht, Julia Bajdor, Bartłomiej Mroziński, Zuzanna Kozłowska, Rafał Iciek, Katarzyna Wróblewska-Seniuk, Ewa Wender-Ożegowska and Tomasz Szczapa
Int. J. Mol. Sci. 2023, 24(8), 7629; https://doi.org/10.3390/ijms24087629 - 21 Apr 2023
Cited by 1 | Viewed by 1764
Abstract
Neonatal venous thrombosis is a rare condition that can be iatrogenic or occur due to viral infections or genetic mutations. Thromboembolic complications are also commonly observed as a result of SARS-CoV-2 infections. They can affect pediatric patients, especially the ones suffering from multisystem [...] Read more.
Neonatal venous thrombosis is a rare condition that can be iatrogenic or occur due to viral infections or genetic mutations. Thromboembolic complications are also commonly observed as a result of SARS-CoV-2 infections. They can affect pediatric patients, especially the ones suffering from multisystem inflammatory syndrome in children (MIS-C) or multisystem inflammatory syndrome in neonates (MIS-N). The question remains whether the maternal SARS-CoV-2 infection during pregnancy can lead to thromboembolic complications in fetuses and neonates. We report on a patient born with an embolism in the arterial duct, left pulmonary artery, and pulmonary trunk, who presented several characteristic features of MIS-N, suspecting that the cause might have been the maternal SARS-CoV2 infection in late pregnancy. Multiple genetic and laboratory tests were performed. The neonate presented only with a positive result of IgG antibodies against SARS-CoV-2. He was treated with low molecular weight heparin. Subsequent echocardiographic tests showed that the embolism dissolved. More research is necessary to evaluate the possible neonatal complications of maternal SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies)
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