TY - JOUR
T1 - Vascular consequences of inflammation
T2 - A position statement from the ESH Working Group on Vascular Structure and Function and the ARTERY Society
AU - Zanoli, Luca
AU - Briet, Marie
AU - Empana, Jean P.
AU - Cunha, Pedro G.
AU - Maki-Petaja, Kaisa M.
AU - Protogerou, Athanase D.
AU - Tedgui, Alain
AU - Touyz, Rhian M.
AU - Schiffrin, Ernesto L.
AU - Spronck, Bart
AU - Bouchard, Philippe
AU - Vlachopoulos, Charalambos
AU - Bruno, Rosa M.
AU - Boutouyrie, Pierre
AU - Association for Research into Arterial Structure, Physiology (ARTERY) Society
AU - European Society of Hypertension
N1 - Funding Information:
L.Z. was supported by 2016/2018 Department Research Plan of University of Catania, Department of Clinical and Experimental Medicine (Project #A). R.M.T. was supported by grants from the British Heart Foundation (CH/4/29762, RE/13/5/30177). The Antoine Caillon, Pierre Paradis and Ernesto L. Schiffrin work was supported by Canadian Institutes of Health Research (CIHR) grants 102606 and 123465, CIHR First Pilot Foundation Grant 143348, a Canada Research Chair (CRC) on Hypertension and Vascular Research by the CRC Government of Canada/CIHR Program, and by the Canada Fund for Innovation (all to ELS). B.S. was supported by grants from the Netherlands Organisation for Scientific Research (Rubicon 452172006) and from the European Union’s Horizon 2020 research and innovation program (no. 793805).
Publisher Copyright:
© 2020 Lippincott Williams and Wilkins. All rights reserved.
PY - 2020/9
Y1 - 2020/9
N2 - 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.
AB - 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.
KW - ACUTE MYOCARDIAL-INFARCTION
KW - C-REACTIVE PROTEIN
KW - CORONARY-HEART-DISEASE
KW - FLOW-MEDIATED DILATATION
KW - II-INDUCED HYPERTENSION
KW - INDUCED ENDOTHELIAL DYSFUNCTION
KW - NECROSIS-FACTOR-ALPHA
KW - PULSE-WAVE VELOCITY
KW - SYSTEMIC-LUPUS-ERYTHEMATOSUS
KW - T-CELLS
KW - arterial stiffness
KW - cardiovascular disease
KW - inflammation
KW - large arteries
KW - pulse wave velocity
U2 - 10.1097/HJH.0000000000002508
DO - 10.1097/HJH.0000000000002508
M3 - Article
C2 - 32649623
SN - 0263-6352
VL - 38
SP - 1682
EP - 1698
JO - Journal of Hypertension
JF - Journal of Hypertension
IS - 9
ER -