Copyright © 2004 by the European Society of Cardiology.
Editorial
Metabolic therapy for heart failure
Department of Medicine, Faculty of Health Sciences, Hatter Institute for Cardiology Research, University of Cape Town Medical School, Observatory 7925, Cape Town, South Africa
* Corresponding author. Tel.: +27 21 406 6358; fax: +27 21 447 8789 (E-mail: opie@capeheart.uct.ac.za).
| The first 10% of the full text of this article appears below. |
This editorial refers to "Trimetazidine improves left
ventricular function and quality of life in elderly patients with
coronary artery disease"
by C. Vitale et
al. on
page 1814
The concept that high blood free fatty acids (FFA) can be damaging to the ischaemic myocardium, especially in the presence of raised circulating catecholamines, is well entrenched.1 Furthermore, when the myocardial metabolism of FFA is limited and that of glucose enhanced by a variety of procedures, such as decreasing blood levels of FFA by insulin and/or glucose, or by anti-adrenergic therapy, or by inhibitors of the entry of activated fatty acids into the mitochondria, or by partial inhibitors of fatty acid oxidation by agents such as trimetazidine (TMZ) or ranolazine, markers of ischaemia generally improve. Clinical applications of these ideas include the use of glucose–insulin–potassium (GIK) or glucagon-like peptide for acute myocardial infarction and TMZ or ranolazine as anti-anginal agents.
Indirectly increased glucose oxidation
Decreased fatty acid-induced oxygen wastage
Mitochondrial mechanisms and uncoupling proteins
Fatty acid metabolism and impaired myocardial contractility
Effects of trimetazidine in heart failure
A new approach to the therapy of heart failure
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Related articles in EHJ:
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- Cristiana Vitale, Mauricio Wajngaten, Barbara Sposato, Otavio Gebara, Paola Rossini, Massimo Fini, Maurizio Volterrani, and Giuseppe M.C. Rosano
EHJ 2004 25: 1814-1821.[Abstract] [FREE Full Text]
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