Cardiotoxicity of Non-Cardiovascular Drugs by Giorgio Minotti

By Giorgio Minotti

Content material:
Chapter 1 Mitochondrial disorder in mobile harm and Cardiotoxicity (pages 1–23): Fabio Di Lisa, Martina Semenzato, Andrea Carpi, Sara Menazza, Nina Kaludercic, Roberta Menabo and Marcella Canton
Chapter 2 Cardiovascular Liabilities of gear: Regulatory facets (pages 25–45): Claudio Arrigoni
Chapter three mobile Mechanisms, Molecular objectives, and Structure–Function Relationships in Drug?Induced Arrhythmias: Antihistamines, Psychoactive medicines, and Antimicrobial brokers (pages 47–96): Maria Virginia Soldovieri and Maurizio Taglialatela
Chapter four Cardiovascular Toxicity of Antitumor medicinal drugs: Dimensions of the matter in kids (pages 97–126): Rebecca Scully and Steven E. Lipshultz
Chapter five Cardiovascular Toxicity of Antitumor medications: size of the matter in grownup Settings (pages 127–199): Joseph R. Carver and Chaitali J. Desai
Chapter 6 Diagnostic facets of Cardiovascular Toxicity of Antitumor medicines (pages 201–221): Michael S. Ewer and Thomas M. Suter
Chapter 7 Cardiovascular Toxicity of Antitumor medicines: Translating Molecular Mechanisms into medical proof (pages 223–256): Pierantonio Menna, Emanuela Salvatorelli, Carlo Salsano, Luca Gianni and Giorgio Minotti
Chapter eight NSAID motion and the rules for Cardiovascular Toxicity (pages 257–285): Anna L. Blobaum and Lawrence J. Marnett
Chapter nine Cardiovascular Toxicities of NSAIDS: Epidemiologic facets (pages 287–312): Antonio Gonzalez?Perez and Luis Alberto Garcia Rodriguez
Chapter 10 Cardiovascular Toxicities of Life?Saving medicinal drugs: Antiviral remedy (pages 313–332): James J. Kohler and William Lewis

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Extra info for Cardiotoxicity of Non-Cardiovascular Drugs

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This is especially true for children: the incidence of cardiac dysfunction among pediatric patients receiving anthracyclines may be as high as 57% about 6 years after treatment [51]. The histomorphology of anthracycline-induced cardiotoxicity has been well characterized in several animal species [52–55] and closely resembles that in humans [56]. Animal models have been developed which can predict the cardiotoxicity of this class of compounds [57–59]. Although not specifically mentioned in any guideline, these models could be useful in the definition of cardiotoxic liabilities of new anthracyclines under development, allowing definition of possible advantages over existing drugs.

Shih, K. J. Ridd, Monoamine oxidase: from genes to behavior, Annu. Rev. , 22, 197–217 (1999). 53. E. J. Davies, Mitochondrial free radical generation, oxidative stress, and aging, Free Radic. Biol. , 29, 222–230 (2000). 54. P. Bianchi, O. Kunduzova, E. , Oxidative stress by monoamine oxidase mediates receptor-independent cardiomyocyte apoptosis by serotonin and postischemic myocardial injury, Circulation, 112, 3297–3305 (2005). 55. A. Carpi, R. Menabo`, N. , The cardioprotective effects elicited by p66(Shc) ablation demonstrate the crucial role of mitochondrial ROS formation in ischemia/reperfusion injury, Biochim.

In a retrospective study on the causes of drug failure, Schuster et al. [1] found that, of 16 drugs withdrawn from the market from 1992 to 2002, seven (>43%) were withdrawn because of cardiovascular adverse reactions. Cardiovascular diseases are the number one cause of death globally. int/ cardiovascular_diseases/en/). Given this high incidence of cardiovascular disease and the prevalence of recognized cardiovascular risk factors in the population, it is sometimes difficult to clearly ascribe an individual patient’s cardiovascular condition to the use (or abuse) of a particular drug.

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