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Impaired endothelial function in patients with cryptogenic stroke and patent foramen ovale is not affected by closure

Impaired endothelial function in patients with cryptogenic stroke and patent foramen ovale is not... INTRODUCTIONPatent foramen ovale (PFO) is present in approximately 25% of the general population. It is more prevalent in patients with cryptogenic stroke (CS), and is considered to be a source of paradoxical embolism. Prevalence of PFO is 40‐60% in patients with migraine with aura (MA) , and MA is also more prevalent in patients with PFO; 15‐50% compared to 4‐5% in the general population. Hypotheses are that micro emboli through a PFO can trigger migraine attacks, and also that higher levels of vasoactive substances in the systemic circulation, normally degraded in the lungs, can trigger migraine attacks.Endothelial dysfunction (ED) has been linked to both migraine and stroke. The main features of ED are impaired endothelium‐dependent vasodilatation and endothelial activation, where release of cytokines and chemokines cause a pro‐inflammatory and pro‐thrombotic environment. ED can be assessed either by measuring changes in vascular tone in response to shear stress, using different techniques like flow‐mediated dilatation (FMD) or peripheral arterial tonometry, or analysing biomarkers of endothelial activation. ED is associated with development of atherosclerosis and future cardiovascular disease, but might also be involved in migraine pathophysiology, both as a cause and a consequence of migraine attacks. Several studies have shown increased levels http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Interventional Cardiology Wiley

Impaired endothelial function in patients with cryptogenic stroke and patent foramen ovale is not affected by closure

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References (50)

Publisher
Wiley
Copyright
© 2017 Wiley Periodicals, Inc.
ISSN
0896-4327
eISSN
1540-8183
DOI
10.1111/joic.12383
pmid
28439982
Publisher site
See Article on Publisher Site

Abstract

INTRODUCTIONPatent foramen ovale (PFO) is present in approximately 25% of the general population. It is more prevalent in patients with cryptogenic stroke (CS), and is considered to be a source of paradoxical embolism. Prevalence of PFO is 40‐60% in patients with migraine with aura (MA) , and MA is also more prevalent in patients with PFO; 15‐50% compared to 4‐5% in the general population. Hypotheses are that micro emboli through a PFO can trigger migraine attacks, and also that higher levels of vasoactive substances in the systemic circulation, normally degraded in the lungs, can trigger migraine attacks.Endothelial dysfunction (ED) has been linked to both migraine and stroke. The main features of ED are impaired endothelium‐dependent vasodilatation and endothelial activation, where release of cytokines and chemokines cause a pro‐inflammatory and pro‐thrombotic environment. ED can be assessed either by measuring changes in vascular tone in response to shear stress, using different techniques like flow‐mediated dilatation (FMD) or peripheral arterial tonometry, or analysing biomarkers of endothelial activation. ED is associated with development of atherosclerosis and future cardiovascular disease, but might also be involved in migraine pathophysiology, both as a cause and a consequence of migraine attacks. Several studies have shown increased levels

Journal

Journal of Interventional CardiologyWiley

Published: Jun 1, 2017

Keywords: ; ; ;

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