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Jose Milei - One of the best experts on this subject based on the ideXlab platform.

  • adriamycin induced myocardial toxicity new solutions for an old problem
    International Journal of Cardiology, 2007
    Co-Authors: Delia Outomuro, Daniel R Grana, Francisco Azzato, Jose Milei
    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.

  • adriamycin induced myocardial toxicity new solutions for an old problem
    International Journal of Cardiology, 2007
    Co-Authors: Delia Outomuro, Daniel R Grana, Francisco Azzato, Jose Milei
    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.

Delia Outomuro - One of the best experts on this subject based on the ideXlab platform.

  • adriamycin induced myocardial toxicity new solutions for an old problem
    International Journal of Cardiology, 2007
    Co-Authors: Delia Outomuro, Daniel R Grana, Francisco Azzato, Jose Milei
    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.

  • adriamycin induced myocardial toxicity new solutions for an old problem
    International Journal of Cardiology, 2007
    Co-Authors: Delia Outomuro, Daniel R Grana, Francisco Azzato, Jose Milei
    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.

Francisco Azzato - One of the best experts on this subject based on the ideXlab platform.

  • adriamycin induced myocardial toxicity new solutions for an old problem
    International Journal of Cardiology, 2007
    Co-Authors: Delia Outomuro, Daniel R Grana, Francisco Azzato, Jose Milei
    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.

  • adriamycin induced myocardial toxicity new solutions for an old problem
    International Journal of Cardiology, 2007
    Co-Authors: Delia Outomuro, Daniel R Grana, Francisco Azzato, Jose Milei
    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.

Daniel R Grana - One of the best experts on this subject based on the ideXlab platform.

  • adriamycin induced myocardial toxicity new solutions for an old problem
    International Journal of Cardiology, 2007
    Co-Authors: Delia Outomuro, Daniel R Grana, Francisco Azzato, Jose Milei
    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.

  • adriamycin induced myocardial toxicity new solutions for an old problem
    International Journal of Cardiology, 2007
    Co-Authors: Delia Outomuro, Daniel R Grana, Francisco Azzato, Jose Milei
    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.

Gabreëls F.j.m. - One of the best experts on this subject based on the ideXlab platform.

  • Nonmuscular involvement in merosin-negative congenital muscular dystrophy.
    2002
    Co-Authors: Gilhuis H.j., Donkelaar, H.j. Ten, Tanke R.b., Vingerhoets D.m., Zwarts M.j., Verrips A., Gabreëls F.j.m.
    Abstract:

    The spectrum of nonmuscular involvement in six children with merosin-negative congenital muscular dystrophy is described. In all children, biochemical, neuroradiologic, cardiac, and neurophysiologic studies were performed. Cerebral structures that were myelinated at gestation, including internal capsule, corpus callosum, brainstem, and cerebellar white matter, demonstrated no abnormalities, whereas the periventricular and subcortical white matter, which were myelinated in the first postnatal year, demonstrated signs of leukoencephalopathy. Cerebrospinal fluid analysis revealed an elevated albumin cerebrospinal fluid to serum ratio in the younger children. Electroencephalogram results were abnormal in the two elder children. One child suffered from Congestive Cardiomyopathy. The increase in nerve conduction velocity in these children over the years lagged behind those of healthy patients, pointing to a demyelinating neuropathy. We conclude that in merosin-negative congenital muscular dystrophy patients, nonmuscular involvement includes the central and peripheral nervous system and the heart. The pattern of myelination of the brain and nerve conduction slowing suggests a myelination arrest. Merosin deficiency can give rise to a Congestive Cardiomyopathy, which is of no clinical relevance in the majority of children

  • Nonmuscular involvement in merosin-negative congenital muscular dystrophy.
    'Elsevier BV', 2002
    Co-Authors: Gilhuis H.j., Donkelaar, H.j. Ten, Tanke R.b., Vingerhoets D.m., Zwarts M.j., Verrips A., Gabreëls F.j.m.
    Abstract:

    Item does not contain fulltextThe spectrum of nonmuscular involvement in six children with merosin-negative congenital muscular dystrophy is described. In all children, biochemical, neuroradiologic, cardiac, and neurophysiologic studies were performed. Cerebral structures that were myelinated at gestation, including internal capsule, corpus callosum, brainstem, and cerebellar white matter, demonstrated no abnormalities, whereas the periventricular and subcortical white matter, which were myelinated in the first postnatal year, demonstrated signs of leukoencephalopathy. Cerebrospinal fluid analysis revealed an elevated albumin cerebrospinal fluid to serum ratio in the younger children. Electroencephalogram results were abnormal in the two elder children. One child suffered from Congestive Cardiomyopathy. The increase in nerve conduction velocity in these children over the years lagged behind those of healthy patients, pointing to a demyelinating neuropathy. We conclude that in merosin-negative congenital muscular dystrophy patients, nonmuscular involvement includes the central and peripheral nervous system and the heart. The pattern of myelination of the brain and nerve conduction slowing suggests a myelination arrest. Merosin deficiency can give rise to a Congestive Cardiomyopathy, which is of no clinical relevance in the majority of children