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| Research article summary (published 22 Jul 2006): |
Adriamycin-induced myocardial toxicity: new solutions for an old problem?
Full Abstract
Adriamycin is a potent and broad-spectrum antineoplastic agent that plays a major role in cancer chemotherapy. Unfortunately, its use has been hampered by conventional toxicities and cardiotoxicity manifested by congestive cardiomyopathy. Adriamycin is particularly toxic to heart tissue and constitutes a major cause of morbidity and mortality due to its complex pathogenesis. In this review, the different forms of cardiotoxicity produced by adriamycin as well as the biochemical changes induced by this drug are summarized. Secondly, the current hypotheses proposed to explain adriamycin-induced myocardial damage (the iron and free-radical hypothesis, the metabolic hypothesis, the "unifying hypothesis" and apoptosis) and the attempts to reduce adriamycin-induced myocardial toxicity are discussed (e.g. dose limitation, close cardiac monitoring, alteration of dosage schedules, development of new anthracycline analogs, and the administration of protective agents and liposomal encapsulation). Finally, we summarized our own experimental and clinical experience in ameliorating and or preventing adriamycin-induced cardiotoxicity and the latest attempts to prevent and/or monitor cardiac function. According to this, a combination of usual doses of calcium antagonist drugs plus vitamins A and E seems advisable.
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Author information
Author/s: Outomuro, Delia (D); Grana, Daniel R (DR); Azzato, Francisco (F); Milei, José (J);
Affiliation: Instituto de Investigaciones Cardiológicas, Universidad de Buenos Aires-Conicet, Argentina.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Review
Journal: International journal of cardiology (Int J Cardiol), published in Netherlands. (Language: eng)
Reference: 2007-Apr; vol 117 (issue 1) : pp 6-15
Dates: Created 2007/03/19; Completed 2007/05/01;
PMID: 16863672, status: MEDLINE (last retrieval date: 12/26/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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