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Anthracycline cardiotoxicity

Anthracyclins. Table 1 Strategies for reducing anthracycline cardiotoxicity... [Pg.95]

McGhee AM, Procter DJ (2006) Radical Chemistry on Solid Support. 264 93-134 Menna P, Salvatorelli E, Gianni L, Minotti G (2008) Anthracycline Cardiotoxicity. 283 21-44 Mentel M, Breinbauer R (2007) Combinatorial Solid-Phase Natural Product Chemistry. 278 209-241... [Pg.223]

In 11 patients with anthracycline cardiotoxicity studied by heart catheterization and endomyocardial biopsy, myocytic damage correlated linearly with cumulative dose (11). There was a non-linear relation between electron microscopic changes and the extent of hemodynamic impairment. There was pronounced fibrous thickening of... [Pg.245]

Mortensen SA, Olsen HS, Baandrup U. Chronic anthracycline cardiotoxicity haemodynamic and histopathologi-cal manifestations suggesting a restrictive endomyocardial disease. Br Heart J 1986 55(3) 274-82. [Pg.251]

Drug news. Anthracycline cardiotoxicity uncovered. Drug Ther 1991 Dec 57. [Pg.252]

Rowan RA, Masek MA, Billingham ME. Ultrastructural morphometric analysis of endomyocardial biopsies. Idiopathic dilated cardiomyopathy, anthracycline cardiotoxicity, and normal myocardium. Am J Cardiovasc Pathol 1988 2(2) 137 4. [Pg.252]

Avery important mechanism of use-limiting anthracycline cardiotoxicity involves the formation of cytotoxic free radicals. A free radical is a highly reactive species with an unpaired electron. Of particular importance to the antineoplastic action of these drugs is the formation of the superoxide radical anion ( O2 ) and the hydroxyl radical ( OH), both of which are formed via reduction of the anthracyclinone quinone (ring C) to hydroquinone by NADPH/CYP450 reductase. The mechanism by which cytotoxic free radicals are generated is shown in Figure 42.18. [Pg.1800]

Hale ]P. Lewis IJ. Anthracyclines Cardiotoxicity and its prevention. Arch Dis Childhood 1994 71 457-462. [Pg.650]

As noted previously, cardiac dysfunction and heart failure are potentially common late effects of oncologic therapy (Lenihan and Cardinale 2012). The authors emphasized the importance of the latter category precisely because of the benefits of early identification and appropriate intervention. Cardinale and colleagues (2015) conducted a prospective study addressing the early detection of anthracycline cardiotoxicity and improvement with heart failure therapy. In the study, including 2,625 participants initially, individuals were followed up after the last dose of anthracy-cline-containing therapy the median follow-up period was 5.2 years (range 4 months to 19 years). Two hundred and twenty-five (9 %) participants were lost to follow-up. Of the rest, cardiotoxicity occurred in 226 (9 %). The median time between cessation of treatment and the development of cardiotoxicity was 3.5 months. [Pg.212]

Taxanes Paclitaxel (853 Da) Docetaxel (861 Da) Sinus bradycardia, ventricular arrhythmias, myocardial ischemia, LV dysfunction, enhanced anthracycline cardiotoxicity... [Pg.410]

Choi HS, Park ES, Kang HJ, Shin HY, Noh Cl, Yun YS, et al. Dexrazoxane for preventing anthracycline cardiotoxicity in children with solid trunors. J Korean Med Sci 2010 25(9) 1336--42. [Pg.691]

Lotrionte M, Biondi-Zoccai G, Abbate A, Lanzetta G, D Ascenzo F, Malavasi V, et al. Review and meta-analysis of incidence and clinical predictors of anthracycline cardiotoxicity. Am J Cardiol 2013 112(12) 1980--4. [Pg.691]


See other pages where Anthracycline cardiotoxicity is mentioned: [Pg.94]    [Pg.95]    [Pg.779]    [Pg.780]    [Pg.94]    [Pg.95]    [Pg.105]    [Pg.51]    [Pg.600]    [Pg.215]    [Pg.410]    [Pg.429]    [Pg.430]    [Pg.685]    [Pg.691]   
See also in sourсe #XX -- [ Pg.108 ]




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