Publication Name	World Journal of Cardiology
Manuscript ID	23941
Country	Australia

Received	2015-12-27 14:00
Peer-Review Started	2015-12-27 16:03
To Make the First Decision	2016-01-14 17:15
Return for Revision	2016-01-15 18:07
Revised	2016-01-16 07:48
Second Decision	2016-02-25 17:01
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2016-03-14 12:10
Articles in Press	2016-03-14 12:10
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2016-05-05 16:22
Publish the Manuscript Online	2016-05-20 11:59

ISSN	1949-8462 (online)
Open Access	This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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Category	Neurosciences
Manuscript Type	Minireviews
Article Title	Mitochondrial vasculopathy
Manuscript Source	Invited Manuscript
All Author List	Josef Finsterer and Sinda Zarrouk-Mahjoub
Funding Agency and Grant Number
Corresponding Author	Josef Finsterer, MD, PhD, Krankenanstalt Rudolfstiftung, Postfach 20, 1030 Vienna, Austria. fifigs1@yahoo.de
Key Words	Mitochondrial disorder; Multisystem; MtDNA; Phenotype; Vasculopathy; Arteriopathy; Angiopathy; Genotype
Core Tip	Recently, it has been shown that rarely also the arteries may be affected in mitochondrial disorders, known as mitochondrial vasculopathy. Mitochondrial vasculopathy manifests as either microangiopathy or macroangiopathy. Clinical manifestations of mitochondrial microangiopathy include leukoencephalopathy, migraine-like headache, stroke-like episodes, or peripheral retinopathy. Mitochondrial macroangiopathy manifests as atherosclerosis, ectasia of arteries, aneurysm formation, dissection, or spontaneous rupture of arteries. The diagnosis relies on the documentation and confirmation of the mitochondrial metabolic defect or the genetic cause after exclusion of non-mitochondrial causes. Treatment is not at variance compared to treatment of vasculopathy due to non-mitochondrial causes.
Publish Date	2016-05-20 11:59
Citation	Finsterer J, Zarrouk-Mahjoub S. Mitochondrial vasculopathy. World J Cardiol 2016; 8(5): 333-339
URL	http://www.wjgnet.com/1949-8462/full/v8/i5/333.htm
DOI	http://dx.doi.org/10.4330/wjc.v8.i5.333

Full Article (PDF)	WJC-8-333.pdf
Full Article (Word)	WJC-8-333.doc
Manuscript File	23941-Review.docx
Answering Reviewers	23941-Answering reviewers.pdf
Audio Core Tip	23941-Audio core tip.mp3
Conflict-of-Interest Disclosure Form	23941-Conflict-of-interest statement.pdf
Copyright License Agreement	23941-Copyright assignment.pdf
Peer-review Report	23941-Peer-review(s).pdf
Scientific Misconduct Check	23941-Scientific misconduct check.pdf
Scientific Editor Work List	23941-Scientific editor work list.pdf