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Vascular consequences of inflammation: a position statement from the ESH Working Group on Vascular Structure and Function and the ARTERY Society.
Zanoli, Luca; Briet, Marie; Empana, Jean P; Cunha, Pedro G; Mäki-Petäjä, Kaisa M; Protogerou, Athanase D; Tedgui, Alain; Touyz, Rhian M; Schiffrin, Ernesto L; Spronck, Bart; Bouchard, Philippe; Vlachopoulos, Charalambos; Bruno, Rosa M; Boutouyrie, Pierre.
Afiliação
  • Zanoli L; Division of Nephrology, Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
  • Briet M; INSERM U1083, CNRS UMR 6214, Centre Hospitalo-Universitaire d'Angers, Université d'Angers, Angers.
  • Empana JP; Faculté de Médecine, Université Paris Descartes, Sorbonne Paris Cité.
  • Cunha PG; INSERM U970, Cardiovascular Epidemiology and Sudden Cardiac Death, Paris, France.
  • Mäki-Petäjä KM; Internal Medicine Department, Center for the Research and Treatment of Arterial Hypertension and Cardiovascular Risk, Hospital Senhora da Oliveira.
  • Protogerou AD; Life and Health Science Research Institute (ICVS), School of Medicine, University of Minho.
  • Tedgui A; ICVS/3B's - PT Government Associate Laboratory, Guimarães, Portugal.
  • Touyz RM; Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, Cambridge, UK.
  • Schiffrin EL; Cardiovascular Prevention & Research Unit, Department of Pathophysiology Medical School, National and Kapodistrian University of Athens, Athens, Greece.
  • Spronck B; INSERM U970, Paris, France.
  • Bouchard P; Institute of Cardiovascular & Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK.
  • Vlachopoulos C; Department of Medicine, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, Quebec, Canada.
  • Bruno RM; Department of Biomedical Engineering, School of Engineering & Applied Science, Yale University, New Haven, Connecticut, USA.
  • Boutouyrie P; Department of Biomedical Engineering, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
J Hypertens ; 38(9): 1682-1698, 2020 09.
Article em En | MEDLINE | ID: mdl-32649623
ABSTRACT
Inflammation is a physiological response to aggression of pathogenic agents aimed at eliminating the aggressor agent and promoting healing. Excessive inflammation, however, may contribute to tissue damage and an alteration of arterial structure and function. Increased arterial stiffness is a well recognized cardiovascular risk factor independent of blood pressure levels and an intermediate endpoint for cardiovascular events. In the present review, we discuss immune-mediated mechanisms by which inflammation can influence arterial physiology and lead to vascular dysfunction such as atherosclerosis and arterial stiffening. We also show that acute inflammation predisposes the vasculature to arterial dysfunction and stiffening, and alteration of endothelial function and that chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease and psoriasis are accompanied by profound arterial dysfunction which is proportional to the severity of inflammation. Current findings suggest that treatment of inflammation by targeted drugs leads to regression of arterial dysfunction. There is hope that these treatments will improve outcomes for patients.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Artérias / Doenças Vasculares / Inflamação Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Artérias / Doenças Vasculares / Inflamação Idioma: En Ano de publicação: 2020 Tipo de documento: Article