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Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Cardiol. May 26, 2016; 8(5): 333-339
Published online May 26, 2016. doi: 10.4330/wjc.v8.i5.333
Mitochondrial vasculopathy
Josef Finsterer, Sinda Zarrouk-Mahjoub
Josef Finsterer, Krankenanstalt Rudolfstiftung, 1030 Vienna, Austria
Sinda Zarrouk-Mahjoub, Genomics Platform, Pasteur Institute of Tunis, Tunis 1002, Tunisia
Author contributions: Both authors contributed equally.
Conflict-of-interest statement: There are no conflicts of interest.
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/
Correspondence to: Josef Finsterer, MD, PhD, Krankenanstalt Rudolfstiftung, Postfach 20, 1030 Vienna, Austria. fifigs1@yahoo.de
Telephone: +43-1-7116592085 Fax: +43-1-4781711
Received: December 27, 2015
Peer-review started: December 27, 2015
First decision: January 15, 2016
Revised: February 19, 2016
Accepted: March 9, 2016
Article in press: March 14, 2016
Published online: May 26, 2016
Core Tip

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.