Thrombo-Inflammation in Cardiovascular Disease: An Expert Consensus Document from the Third Maastricht Consensus Conference on Thrombosis

D’Alessandro, Elisa; Becker, Christian; Bergmeier, Wolfgang; Bode, Christoph; Bourne, Joshua H.; Brown, Helena; Büller, Harry R.; Cate‐Hoek, Arina J. ten; Cate, Vincent ten; Cauteren, Yvonne J. M. van; Cheung, Hilaire Yam Fung; Cleuren, Audrey C. A.; Coenen, Daniëlle M.; Crijns, Harry J.G.M.; Simone, Ilaria De; Dólleman, Sophie; Klein, Christine Espinola; Fernández, Delia I.; Granneman, Lianne; Hof, Arnoud van ’t; Henke, Peter K.; Henskens, Yvonne; Huang, Jingnan; Jennings, Lisa K.; Jooss, Natalie J.; Karel, Mieke F.A.; Kerkhof, Danique van den; Klok, Frederikus A.; Kremers, Bram; Lämmle, Bernhard; Leader, Avi; Lundström, Annika; Mackman, Nigel; Mannucci, Pier Mannuccio; Maqsood, Zahra; Meijden, Paola E. J. van der; Moorsel, Marc van; Morán, Luis A.; Morser, John; Mourik, Manouk van; Navarro, Stefano; Neagoe, Raluca A. I.; Olie, Renske H.; Paridon, Pauline van; Posma, Jens; Provenzale, Isabella; Reitsma, Pieter H.; Scaf, Billy; Schurgers, Leon J.; Seelig, Jaap; Siegbahn, Agneta; Siegerink, Bob; Soehnlein, Oliver; Soriano, Eva Maria; Sowa, Marcin A.; Spronk, Henri M. H.; Storey, Robert F.; Tantiwong, Chukiat; Veninga, Alicia; Wang, Xueqing; Watson, Steve P.; Weitz, J.; Zeerleder, Sacha; Cate, Hugo Ten

doi:10.1055/s-0040-1708035

Cited by 68 publications

(53 citation statements)

References 270 publications

(266 reference statements)

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“…The normal endothelial surface owes its remarkable haemocompatibility to a tightly orchestrated set of functions. 6 Heparan sulfate proteoglycans decorate the surface of the endothelium. These molecules bind antithrombin III, as do heparinoids that we use daily in practice as an anticoagulant.…”

Section: The Endothelium Participates Pivotally In Thrombosis and Fibmentioning

confidence: 99%

COVID-19 is, in the end, an endothelial disease

Libby

Lüscher

2020

European Heart Journal

835

805

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The vascular endothelium provides the crucial interface between the blood compartment and tissues, and displays a series of remarkable properties that normally maintain homeostasis. This tightly regulated palette of functions includes control of haemostasis, fibrinolysis, vasomotion, inflammation, oxidative stress, vascular permeability, and structure. While these functions participate in the moment-to-moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions over-reach and turn against the host. SARS-CoV-2, the aetiological agent of COVID-19, causes the current pandemic. It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and vasculature. This essay explores the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease. Cytokines, protein pro-inflammatory mediators, serve as key danger signals that shift endothelial functions from the homeostatic into the defensive mode. The endgame of COVID-19 usually involves a cytokine storm, a phlogistic phenomenon fed by well-understood positive feedback loops that govern cytokine production and overwhelm counter-regulatory mechanisms. The concept of COVID-19 as an endothelial disease provides a unifying pathophysiological picture of this raging infection, and also provides a framework for a rational treatment strategy at a time when we possess an indeed modest evidence base to guide our therapeutic attempts to confront this novel pandemic.

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Section: The Endothelium Participates Pivotally In Thrombosis and Fibmentioning

confidence: 99%

COVID-19 is, in the end, an endothelial disease

Libby

Lüscher

2020

European Heart Journal

835

805

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“… 92 However, further data are needed to define the role of viscoelastic testing in the management of patients with thrombo-inflammation and severe COVID-19. 93 …”

Section: What Are the Knowledge Gaps?mentioning

confidence: 99%

COVID-19–Associated Coagulopathy and Inflammatory Response: What Do We Know Already and What Are the Knowledge Gaps?

Görlinger

Dirkmann

Gandhi³

et al. 2020

Anesthesia &Amp; Analgesia

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Patients with COVID-19 frequently experience a coagulopathy associated with a high incidence of thrombotic events leading to poor outcomes. Here, biomarkers of coagulation (such as D-dimer, fibrinogen, platelet count), inflammation (such as interleukin-6) and immunity (such as lymphocyte count) as well as clinical scoring systems (such as SOFA, ISTH DIC and SIC score) can be helpful in predicting clinical course, need for hospital resources (such as ICU beds, intubation and ventilator therapy, and ECMO) and patient’s outcome in patients with COVID-19. However, therapeutic options are actually limited to unspecific supportive therapy. Whether viscoelastic testing can provide additional value in predicting clinical course, need for hospital resources and patient’s outcome or in guiding anticoagulation in COVID-19 associated coagulopathy is still incompletely understood and currently under investigation (eg, in the ROHOCO study). This paper summarizes what we know already about COVID-19 associated coagulopathy and – perhaps even more importantly – characterizes important knowledge gaps.

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“…36 Circulating extracellular vesicles may also play a key role in AF pathophysiological process including inflammation, coagulation and angiogenesis. 37 Together, inflammation is strongly linked to the presence of AF. Recent evidence suggests a significant association between infection (inflammatory response) severity and AF progression and adverse events.…”

Section: Inflammationmentioning

confidence: 99%

“…Furthermore, Von Willebrand factor (vWF; a marker of endothelial dysfunction) initiates platelet adhesion upon vascular damage, leads to activation of the thrombo‐inflammatory pathways stimulating thromboembolism and has an increased expression in AF patients 36 . Circulating extracellular vesicles may also play a key role in AF pathophysiological process including inflammation, coagulation and angiogenesis 37 . Together, inflammation is strongly linked to the presence of AF.…”

Section: Endothelial Dysfunction and Vascular Maladaptation In Primary Prevention Of Afmentioning

confidence: 99%

Endothelial dysfunction and vascular maladaptation in atrial fibrillation

Qin

Boidin

Buckley

et al. 2021

Eur J Clin Investigation

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Atrial fibrillation (AF) is the most common clinically significant arrhythmia. 1 The clinical consequences of AF relate to an increased risk of mortality and morbidity from stroke, heart failure and death. 2 Even short episodes of AF are associated with atrial myocardial damage, expression of prothrombotic factors, activation of platelets and inflammatory cells, collectively contributing to a generalised prothrombotic state and, subsequently, increased risk for clinical events. 3 Several studies have examined the complex and, most likely, multi-faceted aetiology of AF, with a likely central role for inflammation. 4 The presence of a systemic inflammatory, prothrombotic state may also contribute to the higher risk for comorbidities. 5 Interestingly, the presence of cardiovascular risk factors, but also inflammation, has previously been related to the presence of vascular dysfunction. 6 Hence, this review poses that endothelial dysfunction may contribute to

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Thrombo-Inflammation in Cardiovascular Disease: An Expert Consensus Document from the Third Maastricht Consensus Conference on Thrombosis

Cited by 68 publications

References 270 publications

COVID-19 is, in the end, an endothelial disease

COVID-19 is, in the end, an endothelial disease

COVID-19–Associated Coagulopathy and Inflammatory Response: What Do We Know Already and What Are the Knowledge Gaps?

Endothelial dysfunction and vascular maladaptation in atrial fibrillation

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