PREDICTIVE VALUE OF CARDIAC TROPONIN-T IN PEDIATRIC-PATIENTS AT RISK FOR MYOCARDIAL INJURY

Citation
Se. Lipshultz et al., PREDICTIVE VALUE OF CARDIAC TROPONIN-T IN PEDIATRIC-PATIENTS AT RISK FOR MYOCARDIAL INJURY, Circulation, 96(8), 1997, pp. 2641-2648
Citations number
33
Categorie Soggetti
Peripheal Vascular Diseas",Hematology
Journal title
ISSN journal
00097322
Volume
96
Issue
8
Year of publication
1997
Pages
2641 - 2648
Database
ISI
SICI code
0009-7322(1997)96:8<2641:PVOCTI>2.0.ZU;2-H
Abstract
Background Biochemical markers have not been routinely used in childre n at risk for myocardial damage. Yet, because of somatic growth and th e duration of survival, a low level of myocardial damage may ultimatel y be of more consequence in children than in adults. Methods and Resul ts We investigated the utility of cardiac troponin T (cTnT) blood leve ls (CARDIAC T ELISA Troponin T, Boehringer Mannheim Corp) in 51 consec utively sampled patients from 1 day to 34 years of age (median=5.7 yea rs) undergoing cardiovascular (n=19) or noncardiovascular (n=17) surge ry or who received doxorubicin for acute lymphoblastic leukemia (ALL) (n=15). Minimum detectable cTnT elevations were 0.03 ng/mL. cTnT was m easurable in children of all ages with myocyte damage. In patients who underwent cardiovascular surgery, a correlation was noted between a s core of increasing surgical severity and the mean level of postoperati ve cTnT (r =.79, P<.0001). Postoperative cTnT levels were elevated in children who completed cardiovascular surgery with an open chest compa red with those with a closed chest (P=.0083). In addition, cTnT levels before cardiovascular surgery predicted postoperative survival (P=.00 7). cTnT elevations were observed after initial doxorubicin therapy fo r ALL. The magnitude of elevation predicted left ventricular dilatatio n (r=.80 when variables were treated as continuous, P=.003) and wall t hinning (r =.61, P=.044) 9 months later. Conclusions Elevations of blo od cTnT in children relate to the severity of myocardial damage and pr edict subsequent subclinical and clinical cardiac morbidity and mortal ity.