Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/75707
Title: Mitochondrial dysfunction in fatal ventricular arrhythmias
Authors: Wachira Wongtanasarasin
Natthaphat Siri-Angkul
Borwon Wittayachamnankul
Siriporn C. Chattipakorn
Nipon Chattipakorn
Authors: Wachira Wongtanasarasin
Natthaphat Siri-Angkul
Borwon Wittayachamnankul
Siriporn C. Chattipakorn
Nipon Chattipakorn
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Apr-2021
Abstract: Ventricular fibrillation (VF) and sudden cardiac arrest (SCA) remain some of the most important public health concerns worldwide. For the past 50¬†years, the recommendation in the Advanced Cardiac Life Support (ACLS) guidelines has been that defibrillation is the only option for shockable cardiac arrest. There is growing evidence to demonstrate that mitochondria play a vital role in the outcome of postresuscitation cardiac function. Although targeting mitochondria to improve resuscitation outcome following cardiac arrest has been proposed for many years, understanding concerning the changes in mitochondria during cardiac arrest, especially in the case of VF, is still limited. In addition, despite new research initiatives and improved medical technology, the overall survival rates of patients with SCA still remain the same. Understanding cardiac mitochondrial alterations during fatal arrhythmias may help to enable the formulation of strategies to improve the outcomes of resuscitation. The attenuation of cardiac mitochondrial dysfunction during VF through pharmacological intervention as well as ischaemic postconditioning could also be a promising target for intervention and inform a new paradigm of treatments. In this review, the existing evidence available from in vitro, ex vivo and in vivo studies regarding the roles of mitochondrial dysfunction during VF is comprehensively summarized and discussed. In addition, the effects of interventions targeting cardiac mitochondria during fatal ventricular arrhythmias are presented. Since there are no clinical reports from studies targeting mitochondria to improve resuscitation outcome available, this review will provide important information to encourage further investigations in a clinical setting.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85100998897&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/75707
ISSN: 17481716
17481708
Appears in Collections:CMUL: Journal Articles

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