Anthracycline cardiotoxicity

Menna, Pierantonio; Paz, Odalys Gonzalez; Chello, Massimo; Covino, Elvio; Salvatorelli, Emanuela; Minotti, Giorgio

doi:10.1517/14740338.2011.589834

Cited by 164 publications

(123 citation statements)

References 81 publications

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“…15 Huerta et al 18 also found an elevated risk of a first hospital admission for HF in current users of NSAIDs (adjusted RR, 1.3; 95% CI, 1.1-1.6) that occurred independently of duration of exposure but was associated with higher-dose NSAIDs (RR, 1.44; 95% CI, 1.06-1. 94). …”

Section: Prescription Medications Analgesicsmentioning

confidence: 99%

“…This produces a prolonged cellular concentration and continued damage that results in decreased contractility and subsequent cell death. 94 The anthracycline class of drugs includes older agents, doxorubicin and daunorubicin, and newer agents, epirubicin, idarubicin, and mitoxantrone. 95 Administration of anthracyclines leads to acute, earlyonset, and delayed-onset cardiotoxicity.…”

Section: Anthracyclinesmentioning

confidence: 99%

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Drugs That May Cause or Exacerbate Heart Failure

Page¹,

O’Bryant²,

Cheng³

et al. 2016

Circulation

325

170

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Heart failure is a common, costly, and debilitating syndrome that is associated with a highly complex drug regimen, a large number of comorbidities, and a large and often disparate number of healthcare providers. All of these factors conspire to increase the risk of heart failure exacerbation by direct myocardial toxicity, drug-drug interactions, or both. This scientific statement is designed to serve as a comprehensive and accessible source of drugs that may cause or exacerbate heart failure to assist healthcare providers in improving the quality of care for these patients.

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Section: Prescription Medications Analgesicsmentioning

confidence: 99%

Section: Anthracyclinesmentioning

confidence: 99%

Drugs That May Cause or Exacerbate Heart Failure

Page¹,

O’Bryant²,

Cheng³

et al. 2016

Circulation

325

170

View full text Add to dashboard Cite

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“…4,27,28 Females may produce less mitochondrial free radicals and have a higher content of antioxidant enzymes than males; these differences having been suggested as a mechanism promoting longevity and preventing cardiovascular diseases. 29 Estrogen receptors and their signaling cascades have been implicated in the control of antioxidant enzyme expression.…”

Section: Discussionmentioning

confidence: 99%

“…However, the level and importance of oxidative stress are surely time, species, and concentration dependent leading to different results according to the model of doxorubicin treatment. 4,14,27,28,31,32 Cardiomyocyte loss through various cell death signaling pathways linked to oxidative stress and DNA damage and mitochondrial alterations has been described in doxorubicin cardiotoxicity. 28,33 However, depending on in vitro and in vivo analyses, the results were not always consistent.…”

Section: Discussionmentioning

confidence: 99%

Sexual Dimorphism of Doxorubicin-Mediated Cardiotoxicity

Moulin

Piquereau

Matéo

et al. 2015

Circ: Heart Failure

107

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Background— Cardiovascular diseases are the major cause of mortality among both men and women with a lower incidence in women before menopause. The clinical use of doxorubicin, widely used as an antineoplastic agent, is markedly hampered by severe cardiotoxicity. Even if there is a significant sex difference in incidence of cardiovascular disease at the adult stage, it is not known whether a difference in doxorubicin-related cardiotoxicity between men and women also exists. The objective of this work was to explore the cardiac side effects of doxorubicin in adult rats and decipher whether signaling pathways involved in cardiac toxicity differ between sexes. Methods and Results— After 7 weeks of doxorubicin (2 mg/kg per week), males developed major signs of cardiomyopathy with cardiac atrophy, reduced left ventricular ejection fraction and 50% mortality. In contrast, no female died and their left ventricular ejection fraction was only moderately affected. Surprisingly, neither global oxidation levels nor the antioxidant response nor the apoptosis signaling pathways were altered by doxorubicin. However, the level of total adenosine monophosphate–activated protein kinase was severely decreased only in males. Moreover, markers of mitochondrial biogenesis and cardiolipin content were strongly reduced only in males. To analyze the onset of the pathology, maximal oxygen consumption rate of left ventricular permeabilized fibers after 4 weeks of treatment was reduced only in doxorubicin-treated males. Conclusions— Altogether, these results clearly evidence sex differences in doxorubicin toxicity. Cardiac mitochondrial dysfunction and adenosine monophosphate–activated protein kinase seem as critical sites of sex differences in cardiotoxicity as evidenced by significant statistical interactions between sex and treatment effects.

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“…It is important to determine not only the main compounds, but also their respective 13-Sdihydro metabolites, which are not only pharmacologically active, but also have been linked to anthracycline's cardiotoxic side effects [14,41]. Aglycones and glucuronides (in the case of epirubicin) can be measured, but are not considered to be toxicologically relevant [6].…”

Section: Analytes and Concentrations Of Interestmentioning

confidence: 99%