Evaluation of early doxorubicin-induced cardiotoxicity by means of systolic time intervals

Villani, F; Beretta, G; Guindani, A

doi:10.1007/bf00254740

Cited by 18 publications

(5 citation statements)

References 3 publications

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“…Furthermore, a significant incidence of cardiovascular side effects namely hypotension, tachycardia, arrhythmias, and ultimately congestive heart failure were also described . Acute DOX side effects, including pericarditis‐myocarditis or arrhythmias, are generally reversible and clinically manageable . However, the mortality of patients that develop congestive heart failure after DOX chronic treatment can be as high as 50%, increasing significantly when cumulative doses higher than 500 mg/m 2 …”

Section: Introduction: Doxorubicin As a Cardiotoxic Anticancer Agentmentioning

confidence: 99%

Doxorubicin‐Induced Cardiotoxicity: From Bioenergetic Failure and Cell Death to Cardiomyopathy

Carvalho

Burgeiro

Garcia

et al. 2013

Medicinal Research Reviews

462

354

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Doxorubicin (DOX) is an anticancer anthracycline that presents a dose-dependent and cumulative cardiotoxicity as one of the most serious side effects. Several hypotheses have been advanced to explain DOX cardiac side effects, which culminate in the development of life-threatening cardiomyopathy. One of the most studied mechanisms involves the activation of DOX molecule into a more reactive semiquinone by mitochondrial Complex I, resulting in increased oxidative stress. The present review describes and critically discusses what is known about some of the potential mechanisms of DOX-induced cardiotoxicity including mitochondrial oxidative damage and loss of cardiomyocytes. We also discuss alterations of mitochondrial metabolism and the unique characteristics of DOX delayed toxicity, which can also interfere on how the cardiac muscle handles a "second-hit stress." We also present pharmaceutical and nonpharmaceutical approaches that may decrease DOX cardiac alterations in animal models and humans and discuss the limitations of each strategy.C 2013 Wiley Periodicals, Inc. Med. Res. Rev., 34, No. 1, 106-135, 2014

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Section: Introduction: Doxorubicin As a Cardiotoxic Anticancer Agentmentioning

confidence: 99%

Doxorubicin‐Induced Cardiotoxicity: From Bioenergetic Failure and Cell Death to Cardiomyopathy

Carvalho

Burgeiro

Garcia

et al. 2013

Medicinal Research Reviews

462

354

View full text Add to dashboard Cite

show abstract

“…Doxorubicin (DOX) is a leading therapeutic in clinical oncology, having a broad range of activity against both “liquid” and solid tumors, including lung cancers. ,, Since the discovery of DOX, thousands of other anthracyclines have been screened for their anticancer properties, but only few have emerged as clinically relevant . In spite of its immense acceptability, however, DOX causes a series of side effects, of particular relevance being its toxicity to the cardiac tissue. − While DOX-induced cardiomyopathy is clinically manageable, it is associated with 50% mortality in those patients that develop congestive heart failure during treatment, , thus limiting the range of applicability of this powerful therapeutic. The ability to efficiently deliver DOX locally to the lungs and to improve DOX’s biodistribution by minimizing its concentration in the cardiac tissue may, therefore, represent an important step forward in the use of such a relevant anticancer therapeutic in the treatment of lung cancers.…”

Section: Introductionmentioning

confidence: 99%

Poly(amidoamine) Dendrimer–Doxorubicin Conjugates: In Vitro Characteristics and Pseudosolution Formulation in Pressurized Metered-Dose Inhalers

Zhong

Rocha

2016

Mol. Pharmaceutics

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Lung cancers are the leading cause of cancer death for both men and women. A series of PEGylated poly(amidoamine) dendrimer-based doxorubicin (DOX) nanocarriers (G3NH2-mPEG-nDOX) were synthesized and their chemistry tailored for the development of novel pseudosolution formulations in propellant-based metered-dose inhalers (pMDIs) with enhanced aerosol characteristics. A pH-labile bond was used to conjugate DOX to dendrimer for controlled intracellular release. We employed a two-step PEGylation strategy to cover a range of DOX loading and PEGylation density. We investigated the impact of pH, PEGylation density, and DOX payload on the release of DOX from the conjugate. We also determined the cellular internalization of the conjugate, the intracellular release kinetics of DOX from the conjugate, and their ability to kill human alveolar carcinoma cells (A549). The acid-labile conjugates sustained the release of DOX in acidic medium, and also intracellularly, as determined by nuclear colocalization studies with confocal microscopy. Meanwhile, DOX was retained in the conjugate at extracellular physiological conditions, indicating their potential to achieve spatial and temporal controlled release profiles. We also observed that the kinetics of cellular entry of the conjugates with DOX increased significantly compared to free DOX. Due to controlled release, the G3NH2-mPEG-nDOX conjugates showed time-dependent cell kill, but their cell kill ability was comparable to free DOX, which suggests their potential in vivo as compared to free DOX. The conjugates were formulated in pMDIs as pseudosolution formulations, with the help of a minimum amount of cosolvent (ethanol; <0.4%; v/v). The physical stability and aerosol characteristics of the conjugates were controlled by the PEGylation density of the carriers: the higher the PEG density, the better the dispersibility and the better the deep lung deposition of the conjugates (fine particle fraction up to ca. 80%).

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“…In spite of its potent anticancer efficacy, the clinical use of DOX is hampered by cardiotoxicity, which manifests as either acute or chronic heart injury. Acute cardiotoxicity, including pericarditis, myocarditis, arrhythmias, and acute heart failure, occurs after receiving high doses of DOX and is clinically manageable (3,4). However, chronic DOX-induced cardiotoxicity is irreversible and more serious and may even develop to cardiomyopathy (5,6).…”

Section: Introductionmentioning

confidence: 99%

The Protective Role of Phenolic Compounds Against Doxorubicin-induced Cardiotoxicity: A Comprehensive Review

Razavi-Azarkhiavi

Iranshahy

Sahebkar

et al. 2016

Nutrition and Cancer

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Although doxorubicin (DOX) is among the most widely used anticancer agents, its clinical application is hampered owing to its cardiotoxicity. Adjuvant therapy with an antioxidant has been suggested as a promising strategy to reduce DOX-induced adverse effects. In this context, many phenolic compounds have been reported to protect against DOX-induced cardiotoxicity. The cardioprotective effects of phenolic compounds are exerted via multiple mechanisms including inhibition of reactive oxygen species generation, apoptosis, NF-κB, p53, mitochondrial dysfunction, and DNA damage. In this review, we present a summary of the in vitro, in vivo, and clinical findings on the protective mechanisms of phenolic compounds against DOX-induced cardiotoxicity.

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Evaluation of early doxorubicin-induced cardiotoxicity by means of systolic time intervals

Cited by 18 publications

References 3 publications

Doxorubicin‐Induced Cardiotoxicity: From Bioenergetic Failure and Cell Death to Cardiomyopathy

Doxorubicin‐Induced Cardiotoxicity: From Bioenergetic Failure and Cell Death to Cardiomyopathy

Poly(amidoamine) Dendrimer–Doxorubicin Conjugates: In Vitro Characteristics and Pseudosolution Formulation in Pressurized Metered-Dose Inhalers

The Protective Role of Phenolic Compounds Against Doxorubicin-induced Cardiotoxicity: A Comprehensive Review

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