Pathophysiological mechanisms of catecholamine and cocaine-mediated cardiotoxicity.

Details

Serval ID
serval:BIB_D9384AA22DCF
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Pathophysiological mechanisms of catecholamine and cocaine-mediated cardiotoxicity.
Journal
Heart Failure Reviews
Author(s)
Liaudet L., Calderari B., Pacher P.
ISSN
1573-7322 (Electronic)
ISSN-L
1382-4147
Publication state
Published
Issued date
2014
Peer-reviewed
Oui
Volume
19
Number
6
Pages
815-824
Language
english
Notes
Publication types: Journal Article Publication Status: ppublish
Abstract
Overactivation of the sympatho-adrenergic system is an essential mechanism providing short-term adaptation to the stressful conditions of critical illnesses. In the same way, the administration of exogenous catecholamines is mandatory to support the failing circulation in acutely ill patients. In contrast to these short-term benefits, prolonged adrenergic stress is detrimental to the cardiovascular system by initiating a series of adverse effects triggering significant cardiotoxicity, whose pathophysiological mechanisms are complex and only partially elucidated. In addition to the development of myocardial oxygen supply/demand imbalance induced by the sustained activation of adrenergic receptors, catecholamines can damage cardiomyocytes by fostering mitochondrial dysfunction, via two main mechanisms. The first one is calcium overload, consecutive to β-adrenergic receptor-mediated activation of protein kinase A and subsequent phosphorylation of multiple Ca(2+)-cycling proteins. The second one is oxidative stress, primarily related to the transformation of catecholamines into "aminochromes," which undergo redox cycling in mitochondria to generate copious amounts of oxygen-derived free radicals. In turn, calcium overload and oxidative stress promote mitochondrial permeability transition and cardiomyocyte cell death, both via the apoptotic and necrotic pathways. Comparable mechanisms of myocardial toxicity, including marked oxidative stress and mitochondrial dysfunction, have been reported with the use of cocaine, a common recreational drug with potent sympathomimetic activity. The aim of the current review is to present in detail the pathophysiological processes underlying the development of catecholamine and cocaine-induced cardiomyopathy, as such conditions may be frequently encountered in the clinical practice of cardiologists and ICU specialists.
Pubmed
Web of science
Create date
22/11/2014 9:49
Last modification date
20/08/2019 15:58
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