title: Cardiac troponin T and creatine kinase MB mass concentrations in children receiving anthracycline chemotherapy.
abstract: Anthracyclines (doxorubicin, daunorubicin, and derivatives) are among the most effective antineoplastic drugs for pediatric cancer with dose-limiting acute and long-term cardiotoxicity. The exact mechanism of the development of cardiomyopathy is still not clear. Anthracyclines may induce subclinical acute myocardial injury leading to lysis of a limited number of myocytes. Alternatively, myocytes may experience a transient loss of cytoplasmic membrane integrity. Both conditions may lead to a transient efflux of small amounts of cytoplasmic enzymes and other proteins specific to the heart muscle fibers. To test these hypotheses we assayed plasma creatine kinase (CK) MB mass and cardiac specific troponin T (TnT). CKMB may be released even in case of reversible cell membrane injury, while prolonged elevation of TnT is the most sensitive and specific marker of limited myocardial necrosis. Thirty-five anthracycline-containing chemotherapy courses in 22 children with cancer were analyzed. CKMB mass and TnT concentrations were within the normal range in all children before anthracycline therapy. Within 72 hours from anthracycline therapy no increment of one of these two marker proteins was detected (ANOVA for repeated measures, P = 0.94 [TnT] and 0.25 [CKMB]). We conclude that only minimal if any acute necroses of cardiac myocytes occur after anthracycline therapy. Even membrane integrity appears to be maintained within the first 3 days after anthracycline therapy, in the absence of electrocardiographic or echocardiographic signs of acute cardiotoxicity.
authors.affiliation: Department of Pediatrics, University of Innsbruck, Austria.
authors.forename: F M
authors.initials: FM
authors.lastname: Fink
authors.forename: N
authors.initials: N
authors.lastname: Genser
authors.forename: C
authors.initials: C
authors.lastname: Fink
authors.forename: M
authors.initials: M
authors.lastname: Falk
authors.forename: J
authors.initials: J
authors.lastname: Mair
authors.forename: K
authors.initials: K
authors.lastname: Maurer-Dengg
authors.forename: I
authors.initials: I
authors.lastname: Hammerer
authors.forename: B
authors.initials: B
authors.lastname: Puschendorf
mesh_terms: D000293:Adolescent; D000704:Analysis of Variance; D000903:Antibiotics, Antineoplastic / Q000009:adverse effects / Q000627:therapeutic use*; D002648:Child; D002675:Child, Preschool; D003402:Creatine Kinase / Q000097:blood*; D005260:Female; D006331:Heart Diseases / Q000097:blood / Q000139:chemically induced*; D006801:Humans; D007223:Infant; D007527:Isoenzymes; D008297:Male; D009369:Neoplasms / Q000097:blood / Q000188:drug therapy*; D011446:Prospective Studies; D014336:Troponin / Q000097:blood*; D020107:Troponin T
chemical_list: D000903:Antibiotics, Antineoplastic; D007527:Isoenzymes; D014336:Troponin; D020107:Troponin T; D003402:Creatine Kinase