2005
DOI: 10.1056/nejm200506093522321
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Acute Doxorubicin Cardiotoxicity

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Cited by 73 publications
(42 citation statements)
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“…The proposed mechanisms of arrhythmia generally focus on the inhibition of Na + -Ca 2+ exchange with prolongation of the myocyte action potential, damage from reactive oxygen species, or myocardial necrosis [4,12]. Animal studies suggest that β-blockade may prevent these electrophysiological changes, with limited evidence in humans suggesting a role of β-blockers in patients undergoing therapy with anthracyclines [13,14].…”
Section: Discussionmentioning
confidence: 99%
“…The proposed mechanisms of arrhythmia generally focus on the inhibition of Na + -Ca 2+ exchange with prolongation of the myocyte action potential, damage from reactive oxygen species, or myocardial necrosis [4,12]. Animal studies suggest that β-blockade may prevent these electrophysiological changes, with limited evidence in humans suggesting a role of β-blockers in patients undergoing therapy with anthracyclines [13,14].…”
Section: Discussionmentioning
confidence: 99%
“…Their main adverse effect is cardiotoxicity. [110][111][112][113][114] Acute toxicity are usually reversible and nonfatal, such as hypotension, tachycardia, and arrhythmias. However, late-onset cardiotoxicity causes lethal congestive heart failure.…”
Section: Liposomesmentioning
confidence: 99%
“…Its major cumulative dose-limiting toxicity is congestive heart failure, typically insidious in onset after chronic anthracycline treatment, particularly with cumulative doses in excess of 500 mg/m 2 [2]. Rarely, acute left ventricular failure has been described within a week of anthracycline administration and is usually fatal [3][4][5]. The development of acute heart failure does not appear to be dose related, however, the total dose administered during a day or course of treatment may affect late cardiotoxicity [6].…”
Section: Introductionmentioning
confidence: 99%