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Vascular Damage and Coagulopathy during COVID-19 Infections
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Vascular Damage and Coagulopathy during COVID-19 Infections

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Vascular Medicine".

Deadline for manuscript submissions: closed (20 January 2021) | Viewed by 13438

Special Issue Editors

Dr. Olivier Morel

E-Mail Website
Guest Editor
Interventional Cardiology Department, University of Strasbourg, 67081 Strasbourg, France
Interests: thrombosis; acute coronary syndrome; platelet; chronic kidney disease; senescence; bleedings; aortic stenosis; TAVR; microparticles; endothelium
Special Issues, Collections and Topics in MDPI journals
Dr. Benjamin Marchandot

E-Mail Website
Guest Editor
Department of Cardiology, University Hospital of Strasbourg, 1 Place de l'Hôpital BP 426, CEDEX, 67091 Strasbourg, France
Interests: acute cardiac care; Imaging; Thrombosis; Bleeding

Special Issue Information

Dear Colleagues,

The pathogenic coronavirus has been wreaking havoc worldwide since January. Reports of thrombotic complications in patients with Covid-19 are increasingly prominent, and growing evidence strongly suggests that some of the clinical features of Covid-19 infection are driven by a localized thrombotic phenomenon. More specifically, there is increasing recognition that the Covid-19-associated hemostasis abnormality may be resulting in localized thrombosis in the lungs. Histologic analysis of pulmonary vessels in patients with Covid-19 revealed severe endothelial injury associated with intracellular SARS-CoV-2 virus and disrupted endothelial cell membranes together with widespread thrombosis and occlusion of alveolar capillaries. The Covid-19 acquired coagulopathy involves venous, arterial, and microcirculatory systems, and offers unique features in comparison with the thrombogenicity observed in previous viral or bacterial illness.
The pathophysiological mechanisms are complex and most likely involve endothelial cell activation and endothelitis, vWF release, cytokine storms and hyperinflammation, procoagulant microparticle release, lupus anticoagulant generation, platelet activation, neutrophils extracellular traps (NETs), alteration of the fibrinolytic pathways, hypoxia, hyperviscosity, and altered shear stress. On top of these proposed pro-thrombotic routes, at sites of endothelial injury, imbalance between ACE2 and ACE1 activity could contribute to unopposed angiotensin II accumulation which further exacerbates tissue injury and promotes both inflammation and thrombosis.
Several questions remain unanswered: Are we facing in situ pulmonary thrombosis or pulmonary embolism? What is the contribution of vWF, NETs, and microparticles to thrombus growth? What are the optimal antithrombotic strategies for both the prevention and treatment of venous thromboembolic events?
The development of vasculitis including the recent outbreak of Kawasaki disease still remains to be fully characterized. The impact of “host damage-control” strategies including anti-complement and anti-inflammatory approaches are appealing leads, and finally, the restoration of the ACE2/ACE1 (role of ACEi, ARB, statins) imbalance within the vascular wall is a key approach that deserves further insights.
From a more practical point of view, the definition of the optimal anticoagulant strategy (type, dose, and duration) and the role for anti-platelet therapy or combined strategies are today’s hot topics.
The present Special Issue aims to provide significant development in the management of vascular damages and coagulopathy burden during SARS-CoV-2 infection.

Prof. Dr. Olivier Morel
Dr. Benjamin Marchandot
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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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
  • Pulmonary embolism
  • Venous thromboembolism
  • Stroke
  • Myocardial infarction
  • Kidney injury
  • Lupus anticoagulant
  • Shear stress
  • Bleeding
  • Kawasaki disease
  • Neutrophils extracellular traps
  • Leukocytes
  • Endothelium

Published Papers (4 papers)

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11 pages, 879 KiB  
Article
D-Dimers Level as a Possible Marker of Extravascular Fibrinolysis in COVID-19 Patients
by Antonin Trimaille, Jecko Thachil, Benjamin Marchandot, Anaïs Curtiaud, Ian Leonard-Lorant, Adrien Carmona, Kensuke Matsushita, Chisato Sato, Laurent Sattler, Lelia Grunebaum, Yves Hansmann, Samira Fafi-Kremer, Laurence Jesel, Mickaël Ohana and Olivier Morel
J. Clin. Med. 2021, 10(1), 39; https://doi.org/10.3390/jcm10010039 - 24 Dec 2020
Cited by 17 | Viewed by 2913
Abstract
Background and Objective: Host defence mechanisms to counter virus infection include the activation of the broncho-alveolar haemostasis. Fibrin degradation products secondary to extravascular fibrin breakdown could contribute to the marked increase in D-Dimers during COVID-19. We sought to examine the prognostic value on [...] Read more.
Background and Objective: Host defence mechanisms to counter virus infection include the activation of the broncho-alveolar haemostasis. Fibrin degradation products secondary to extravascular fibrin breakdown could contribute to the marked increase in D-Dimers during COVID-19. We sought to examine the prognostic value on lung injury of D-Dimers in non-critically ill COVID-19 patients without thrombotic events. Methods: This study retrospectively analysed hospitalized COVID-19 patients classified according to a D-Dimers threshold following the COVID-19 associated haemostatic abnormalities (CAHA) classification at baseline and at peak (Stage 1: D-Dimers less than three-fold above normal; Stage 2: D-Dimers three- to six-fold above normal; Stage 3: D-Dimers six-fold above normal). The primary endpoint was the occurrence of critical lung injuries on chest computed tomography. The secondary outcome was the composite of in-hospital death or transfer to the intensive care unit (ICU). Results: Among the 123 patients included, critical lung injuries were evidenced in 8 (11.9%) patients in Stage 1, 6 (20%) in Stage 2 and 15 (57.7%) in Stage 3 (p = 0.001). D-Dimers staging at peak was an independent predictor of critical lung injuries regardless of the inflammatory burden assessed by CRP levels (OR 2.70, 95% CI (1.50–4.86); p < 0.001) and was significantly associated with increased in-hospital death or ICU transfer (14.9 % in Stage 1, 50.0% in Stage 2 and 57.7% in Stage 3 (p < 0.001)). D-Dimers staging at peak was an independent predictor of in-hospital death or ICU transfer (OR 2.50, CI 95% (1.27–4.93); p = 0.008). Conclusions: In the absence of overt thrombotic events, D-Dimers quantification is a relevant marker of critical lung injuries and dismal patient outcome. Full article
(This article belongs to the Special Issue Vascular Damage and Coagulopathy during COVID-19 Infections)
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12 pages, 1314 KiB  
Article
Risk and Severity of COVID-19 and ABO Blood Group in Transcatheter Aortic Valve Patients
by Marion Kibler, Laurent Dietrich, Mohamad Kanso, Adrien Carmona, Benjamin Marchandot, Kensuke Matsushita, Antonin Trimaille, Cécile How-Choong, Albane Odier, Gabrielle Gennesseaux, Ophélie Schramm, Antje Reydel, Sébastien Hess, Chisato Sato, Sophie Caillard, Laurence Jesel, Olivier Morel and Patrick Ohlmann
J. Clin. Med. 2020, 9(11), 3769; https://doi.org/10.3390/jcm9113769 - 22 Nov 2020
Cited by 17 | Viewed by 3093
Abstract
While cardiovascular disease has been associated with an increased risk of coronavirus disease 2019 (COVID-19), no studies have described its clinical course in patients with aortic stenosis who had undergone transcatheter aortic valve replacement (TAVR). Numerous observational studies have reported an association between [...] Read more.
While cardiovascular disease has been associated with an increased risk of coronavirus disease 2019 (COVID-19), no studies have described its clinical course in patients with aortic stenosis who had undergone transcatheter aortic valve replacement (TAVR). Numerous observational studies have reported an association between the A blood group and an increased susceptibility to SARS-CoV-2 infection. Our objective was to investigate the frequency and clinical course of COVID-19 in a large sample of patients who had undergone TAVR and to determine the associations of the ABO blood group with disease occurrence and outcomes. Patients who had undergone TAVR between 2010 and 2019 were included in this study and followed-up through the recent COVID-19 outbreak. The occurrence and severity (hospitalization and/or death) of COVID-19 and their associations with the ABO blood group served as the main outcome measures. Of the 1125 patients who had undergone TAVR, 403 (36%) died before 1 January 2020, and 20 (1.8%) were lost to follow-up. The study sample therefore consisted of 702 patients. Of them, we identified 22 cases (3.1%) with COVID-19. Fourteen patients (63.6%) were hospitalized or died of disease. Multivariable analysis identified the A blood group (vs. others) as the only independent predictor of COVID-19 in patients who had undergone TAVR (odds ratio (OR) = 6.32; 95% confidence interval (CI) = 2.11−18.92; p = 0.001). The A blood group (vs. others; OR = 8.27; 95% CI = 1.83−37.43, p = 0.006) and a history of cancer (OR = 4.99; 95% CI = 1.64−15.27, p = 0.005) were significantly and independently associated with disease severity (hospitalization and/or death). We conclude that patients who have undergone TAVR frequently have a number of cardiovascular comorbidities that may work to increase the risk of COVID-19. The subgroup with the A blood group was especially prone to developing the disease and showed unfavorable outcomes. Full article
(This article belongs to the Special Issue Vascular Damage and Coagulopathy during COVID-19 Infections)
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11 pages, 3136 KiB  
Article
Coagulation Parameters: An Efficient Measure for Predicting the Prognosis and Clinical Management of Patients with COVID-19
by Manuel Quintana-Díaz, Eva María Andrés-Esteban, Karen Lizzette Ramírez-Cervantes, Bárbara Olivan-Blázquez, Raúl Juárez-Vela and Vicente Gea-Caballero
J. Clin. Med. 2020, 9(11), 3482; https://doi.org/10.3390/jcm9113482 - 28 Oct 2020
Cited by 13 | Viewed by 2950
Abstract
Background. COVID-19 is an ongoing global pandemic. Since the detection of the first cases of coronavirus disease 2019 (COVID-19) in Wuhan, China, the current pandemic has affected more than 25.3 million people worldwide. The aim of this study was to evaluate the relationship [...] Read more.
Background. COVID-19 is an ongoing global pandemic. Since the detection of the first cases of coronavirus disease 2019 (COVID-19) in Wuhan, China, the current pandemic has affected more than 25.3 million people worldwide. The aim of this study was to evaluate the relationship between coagulation abnormalities and prognosis in a cohort of patients with COVID-19. Methods. We performed a retrospective cohort study of 3581 patients admitted to Hospital La Paz (Madrid, Spain) due to respiratory infection by severe acute respiratory syndrome coronavirus from the beginning of the current pandemic to 15 July 2020. Results. Of the 3581 study patients, 48.94% were men, and 19.80% were healthcare workers. The median age was 62 years. Compared with the survivors, the non-survivors had lower prothrombin activity (82.5 (Interquartile range—IQR, 67–95) vs. 95.25 (IQR, 87–104) for non-survivors and survivors, respectively; p < 0.001), higher fibrinogen levels (748.5—IQR, 557–960) vs. 572.75 (IQR, 417–758; p < 0.001), and notably higher D-dimer levels (2329—IQR, 1086.12–5670.40) vs. 635.5 (IQR, 325.5–1194.8); p < 0.001). Conclusions. The evaluation of coagulation parameters could be an efficient measure for predicting the prognosis and improving the clinical management of patients with COVID-19. Full article
(This article belongs to the Special Issue Vascular Damage and Coagulopathy during COVID-19 Infections)
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7 pages, 403 KiB  
Brief Report
Reduced Flow-Mediated Dilatation Is Not Related to COVID-19 Severity Three Months after Hospitalization for SARS-CoV-2 Infection
by Marianne Riou, Walid Oulehri, Cedric Momas, Olivier Rouyer, Fabienne Lebourg, Alain Meyer, Irina Enache, Cristina Pistea, Anne Charloux, Christophe Marcot, Frederic de Blay, Olivier Collange, Michel Mertes, Emmanuel Andrès, Samy Talha and Bernard Geny
J. Clin. Med. 2021, 10(6), 1318; https://doi.org/10.3390/jcm10061318 - 23 Mar 2021
Cited by 21 | Viewed by 3667
Abstract
The coronavirus disease 2019 (COVID-19) pandemic has spread rapidly worldwide, with more than two million deaths. Evidence indicates the critical role of the vascular endothelium in its pathophysiology but, like potential changes in functional vasodilation, the vascular effect of SARS-CoV-2 at a given [...] Read more.
The coronavirus disease 2019 (COVID-19) pandemic has spread rapidly worldwide, with more than two million deaths. Evidence indicates the critical role of the vascular endothelium in its pathophysiology but, like potential changes in functional vasodilation, the vascular effect of SARS-CoV-2 at a given distance from the acute infection is largely unknown. We assessed brachial artery flow-mediated dilatation (FMD) in 27 COVID-19 patients needing conventional or intensive care unit hospitalization, three months after SARS-CoV-2 infection diagnosis and in nine age- and sex- matched control subjects. Interestingly, the FMD was lower in COVID-19 patients as compared to controls (8.2 (7.2–8.9) vs. 10.3 (9.1–11.7)); p = 0.002, and half of the hospitalized COVID-19 survivors presented with a reduced FMD < 8% at three months of COVID-19 onset. Impaired FMD was not associated with severe or critical SARS-CoV-2 infection, reflected by ICU hospitalization, total hospitalization duration, or severity of lung damage. In conclusion, reduced FMD is often observed even three months after hospitalization for SARS-CoV-2 infection, but such alteration predominantly appears to not be related to COVID-19 severity. Longer and larger follow-up studies will help to clarify the potential prognosis value of FMD among COVID-19 patients, as well as to further determine the mechanisms involved. Full article
(This article belongs to the Special Issue Vascular Damage and Coagulopathy during COVID-19 Infections)
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