title: Is there a potential role for serum cardiac troponin I as a marker for myocardial dysfunction in pediatric patients receiving anthracycline-based therapy? A pilot study.
abstract: Serum cardiac troponin I (cTnI) levels have been reported to have high specificity and sensitivity to acute myocardial infarction and coronary ischemic syndromes in adult patients. Our goal was to evaluate the usefulness of serum cTnI in the early diagnosis of cardiac injury from anthracyclines, and to compare these values with echocardiographic findings of cardiac dysfunction. In this prospective study, children being treated on several Children's Cancer Group protocols underwent measurement of shortening fraction (SF), ejection fraction (EF), and serum cTnI levels prior to anthracycline therapy. Sequential serum cTnI levels were then measured along with regularly scheduled echocardiograms with progressively increasing doses of anthracyclines. Fifteen children with median age of 5.75 years (range, 15 months to 15.5 years) at diagnosis were evaluated. Anthracycline doses ranged from 11.72 mg/kg (in patients < 3 years of age) to 375 mg/m2. All but one patient had normal cTnI levels. His level measured at 1.7 ng/ml after 315 mg/m2, but was normal on follow-up testing. Initial SF ranged from 32 to 48%, and EF from 60 to 80%. On follow-up, SF and EF ranged from 30 to 41% and 55 to 70%, respectively. Both SF and EF were significantly lower (p < 0.001) as compared to the initial values. Despite this, all patients remained clinically asymptomatic from the cardiac standpoint. We did not observe elevations of serum cTnI levels in clinically asymptomatic children who received anthracycline therapy up to doses of 375 mg/m2. Does this mean that cardiac injury has not occurred? The possibility of assay sensitivity and the timing of serum sampling and echocardiograms may be important. In addition, larger sample size or longer follow-up may be helpful to determine if higher doses or symptomatic patients potentially have elevations in cTnI levels.
authors.affiliation: Division of Hematology/Oncology, Department of Pediatrics, University of New Mexico, ACC 3rd Floor, 2211 Lomas Blvd., NE, Albuquerque, NM 87131-5311, USA. pmathew@salud.unm.edu
authors.forename: P
authors.initials: P
authors.lastname: Mathew
authors.forename: W
authors.initials: W
authors.lastname: Suarez
authors.forename: K
authors.initials: K
authors.lastname: Kip
authors.forename: E
authors.initials: E
authors.lastname: Bayar
authors.forename: R
authors.initials: R
authors.lastname: Jasty
authors.forename: Y
authors.initials: Y
authors.lastname: Matloub
authors.forename: D
authors.initials: D
authors.lastname: Raisch
mesh_terms: D000293:Adolescent; D000903:Antibiotics, Antineoplastic / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D015415:Biomarkers; D009202:Cardiomyopathies / Q000097:blood / Q000139:chemically induced* / Q000000981:diagnostic imaging; D002648:Child; D002675:Child, Preschool; D004305:Dose-Response Relationship, Drug; D004452:Echocardiography; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D009369:Neoplasms / Q000097:blood / Q000188:drug therapy; D010865:Pilot Projects; D011446:Prospective Studies; D020033:Protein Isoforms / Q000097:blood*; D012680:Sensitivity and Specificity; D013318:Stroke Volume; D019210:Troponin I / Q000097:blood*; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000139:chemically induced / Q000175:diagnosis / Q000503:physiopathology
chemical_list: D000903:Antibiotics, Antineoplastic; D015415:Biomarkers; D020033:Protein Isoforms; D019210:Troponin I