Frequency of clinically unsuspected myocardial injury at a children's hospital☆
Received 2 May 2005; accepted 20 June 2005.
Background
Ill children are at risk but rarely screened for myocardial injury. The frequency of such injury in ill children is unknown. Elevated levels of plasma cardiac troponin I (cTnI) can detect subclinical myocardial injury.
Methods
We measured cTnI levels from 283 Children's Hospital, Boston patients (median age 2.10 years, range 0.13-22.4 years) seen in an outpatient or emergency clinic without clinically apparent cardiac disease. We took ≥0.5 ng/mL as an indication of myocardial injury. We also measured plasma creatine kinase–MB, total creatine kinase, and myoglobin, and performed a chart review.
Results
Fifteen (7.8%) of the 193 acutely ill children and 4 (4.4%) of the 90 well children had an elevated cTnI level (P = .44). Within the acutely ill group, the children with elevated cTnI were younger and had lower mean hemoglobin and hematocrit levels. Cardiac troponin I levels correlated with creatine kinase–MB (r = 0.22; P < .001) but not with creatine kinase or myoglobin. The 4 children with cTnI >0.89 ng/mL, who also had plasma cardiac troponin T measured, showed cardiac troponin T elevations that were consistent with unstable angina levels in adults. Four children had high-level cTnI elevations (>2 ng/mL) consistent with acute myocardial infarction levels in adults.
Conclusions
Elevated cTnI levels occur in children without clinically apparent cardiac disease and can be at adult unstable angina or acute myocardial infarction levels. Prospective studies to determine the clinical significance of these findings and their relationship to the development of cardiomyopathy are warranted.
aDepartment of Cardiology, Harvard Medical School, Boston, MA
bDivision of Laboratory Medicine, Children's Hospital, Harvard Medical School, Boston, MA
cHarvard School of Public Health, Harvard Medical School, Boston, MA
dDepartment of Pediatrics, Harvard Medical School, Boston, MA
eDepartment of Pathology, Harvard Medical School, Boston, MA
fDivision of Pediatric Cardiology, Golisano Children's Hospital at Strong and University of Rochester Medical Center, Rochester, NY
gDepartment of Pediatrics, University of Rochester School of Medicine and Dentistry, Rochester, NY
hDepartment of Biometry and Epidemiology, Medical University of South Carolina, Charleston, SC
iDepartment of Pediatrics, University of Miami Miller School of Medicine, Holtz Children's Hospital of the University of Miami-Jackson Memorial Medical Center, Batchelor Children's Research Institute, and the Sylvester Comprehensive Cancer Center, Miami, FL
Reprint requests: Steven E. Lipshultz, MD, Department of Pediatrics (D820), University of Miami Miller School of Medicine, P.O. Box 016820, Miami, FL 33101.
☆ This work was supported in part (financial and material) by grants CA68484, CA34183, CA79060, CA06516, HL69800, HL53392, HL59837, HL53392, and HL48012 from the National Institutes of Health, Bethesda, Md; the David B. Perini, Jr Quality of Life Program; The Laura Coulter Jones Foundation; the Parker Family Foundation; the Children's Cardiomyopathy Foundation, Dade Behring Corporation, Newark, Del; and Roche Diagnostics Corporation, Indianapolis, Ind. No funding organization played a role in the design, conduct, interpretation, or analysis of this study.
ABSTRACT