Abstract
Sudden death associated with ischemic heart disease is primarily a result of an abnormality in cardiac rhythm leading to ventricular tachycardia and fibrillation [1]. A multitude of studies has carefully characterized the electrophysiologic abnormalities underlying these lethal arrhythmias in the ischemic heart. However, until the last decade little effort has been directed at characterizing the discrete, yet critical, alterations in the plasma membrane that elicit the alterations in electrophysiologic function. Although several antiarrhythmic agents are available and have been proposed for the prevention of sudden cardiac death in patients with ischemic heart disease, results of studies to date have been disappointing, probably because currently available agents are, for the most part, nonspecific membrane depressants. More specific and therefore more effective agents are likely to be available only through a thorough understanding of the specific biochemical events underlying the electrophysiologic alterations in the ischemic heart. For reasons outlined in this chapter, we have concentrated our efforts on two amphipathic metabolites, long-chain acylcarnitines and lysophosphatides. Recent data would suggest that manipulation of the activity of the enzymes controlling the synthesis and/or catabolism of these moieties can influence markedly the electrophysiologic alterations and resulting lethal arrhythmias in the ischemic heart.
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© 1989 Kluwer Academic Publishers, Boston/Dordrecht/London
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Corr, P.B., Dobmeyer, D.J. (1989). Amphipathic Lipid Metabolites and Arrhythmogenesis: A Perspective. In: Rosen, M.R., Palti, Y. (eds) Lethal Arrhythmias Resulting from Myocardial Ischemia and Infarction. Developments in Cardiovascular Medicine, vol 94. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1649-7_7
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DOI: https://doi.org/10.1007/978-1-4613-1649-7_7
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