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Pathophysiological mechanisms of catecholamine and cocaine-mediated cardiotoxicity

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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 Ca2+-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.

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Acknowledgments

This work was supported, in part, by a grant from the Swiss National Fund for Scientific Research (No. 320000/118174) to LL and by the Intramural Program of the NIH/NIAAA to PP.

Conflict of interest

Drs. Lucas LIAUDET, Belinda CALDERARI and Pal PACHER have no conflicts of interest or financial ties to disclose with respect to this work.

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Authors and Affiliations

  1. Department of Intensive Care Medicine and Burn Center, Faculty of Biology and Medicine, University Hospital Medical Center, BH 08-621, 1010, Lausanne, Switzerland

    Lucas Liaudet & Belinda Calderari

  2. The Laboratory of Physiologic Studies, NIH/NIAA, Bethesda, MD, 20892-9413, USA

    Pal Pacher

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Correspondence to Lucas Liaudet.

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Liaudet, L., Calderari, B. & Pacher, P. Pathophysiological mechanisms of catecholamine and cocaine-mediated cardiotoxicity. Heart Fail Rev 19, 815–824 (2014). https://doi.org/10.1007/s10741-014-9418-y

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