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Assessing Anthracycline Cardiotoxicity In The 1990s

I. Carrió, M. Estorch, A. López-Pousa
Published 2005 · Medicine

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Anthracycline cardiotoxicity is caused by stimulated reactive oxygen metabolism. Augmented reactive oxygen flux, mediated by free radicals, causes myocyte cell damage at specific sites. In addition, anthracyclines or their metabolites may trigger release of endogenous substances such as histamine, arachidonic acid metabolites, platelet-activating factor, calcium and other compounds potentially deleterious to the myocardium [1-4]. From a clinical point of view, acute cardiotoxicity following a single anthracycline dose appears different from the chronic cardiomyopathy resulting from cumulative anthracycline administration [5-7]. Acute toxicity is often subclinical with acute and reversible electrocardiographic changes without clinical evidence of myocardial dysfunction. This can be observed in about 30% of patients within hours of doxorubicin infusion. Exceptionally, acute cardiotoxicity may present after a single dose of doxorubicin as pancarditis with overt biventricular failure. More meaningfully from a clinical viewpoint, chronic anthracycline cardiomyopathy is a congestive cardiomyopathy characterized by a non-dilated tachycardic heart with low output secondary to progressive hypocontractility which is usually unresponsive to cardiotonic agents. Chronic cardiomyopathy, unlike acute cardiomyopathy, has a delayed clinical expression, this expression occurring weeks or months after the last doxorubicin dose. Cardiotoxicity presenting well after chemotherapy had not been seriously considered until recent reports indicated an unexpectedly high incidence of late permanent cardiac functional abnormalities in patients with prolonged survival [8, 9]. More than half of children with acute lymphoblastic leukaemia in whom complete clinical remission is induced by anthracycline-containing chemotherapy may have abnormalities in contractility or in ventricular wall thickness many years after completion of therapy [8]. Prevention of this type of late cardiotoxicity in long-term survivors poses a new challenge to all medical professions involved in cancer treatment. The merely functional definition of cardiotoxicity has, of course, several drawbacks. Functional impairment is a consequence of myocardial cell damage caused by administration of the drug. Therefore, using a purely functional approach, cell damage below this threshold is not considered as cardiotoxicity. In addition, other neurohumoral factors besides myocyte cell damage may contribute to deterioration of function. Alteration of these neurohumoral mechanisms may also precede functional impairment and is part of the spectrum of cardiotoxic effects of anthracycline administration [10]. The definition of cardiotoxicity therefore has to be reviewed in the light of our improved knowledge of the natural history of the disease, and of the pathophysiological and neurohumoral interactions which result in this complex cardiomyopathy. Understanding of the underlying tissular mechanisms at a molecular level should lead to earlier diagnosis and facilitate the prevention of long-term deleterious effects.
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