BACKGROUND: Cardiac troponin I (cTnI) is currently considered to be the most sensitive and specific biochemical marker of acute coronary syndrome and acute myocardial infarction. However, few reports have described the use of cTnI assays for evaluating abnormal hemodynamic load in children with congenital heart disease (CHD). It was hypothesized that significant hemodynamic overload due to a left-to-right shunt induces myocardial injury. METHODS AND RESULTS: A highly sensitive cTnI assay was used to measure the serum cTnI levels in 30 children with atrial septal defect (ASD), 32 children with ventricular septal defect (VSD), and 350 healthy children. Cardiac catheterization was performed in the children with ASD and VSD to determine the ratio of pulmonary to systemic blood flow, the ratio of pulmonary to systemic arterial pressure (Pp/Ps), the pulmonary vascular resistance index, and the right and left ventricular end-diastolic volume. Serum cTnI levels in both the ASD and VSD children were significantly higher than those in healthy children (P<0.05 and P<0.01, respectively). Furthermore, serum cTnI levels significantly correlated with Pp/Ps (r=0.745, P<0.001) in VSD children. CONCLUSIONS: Significant volume and pressure overload due to a left-to-right shunt induce myocardial injury and might eventually cause irreversible myocardial remodeling in children with CHD. The serum cTnI level is a useful biomarker for evaluating myocardial damage associated with pulmonary hypertension in VSD children.
BACKGROUND:Cardiac troponin I (cTnI) is currently considered to be the most sensitive and specific biochemical marker of acute coronary syndrome and acute myocardial infarction. However, few reports have described the use of cTnI assays for evaluating abnormal hemodynamic load in children with congenital heart disease (CHD). It was hypothesized that significant hemodynamic overload due to a left-to-right shunt induces myocardial injury. METHODS AND RESULTS: A highly sensitive cTnI assay was used to measure the serum cTnI levels in 30 children with atrial septal defect (ASD), 32 children with ventricular septal defect (VSD), and 350 healthy children. Cardiac catheterization was performed in the children with ASD and VSD to determine the ratio of pulmonary to systemic blood flow, the ratio of pulmonary to systemic arterial pressure (Pp/Ps), the pulmonary vascular resistance index, and the right and left ventricular end-diastolic volume. Serum cTnI levels in both the ASD and VSD children were significantly higher than those in healthy children (P<0.05 and P<0.01, respectively). Furthermore, serum cTnI levels significantly correlated with Pp/Ps (r=0.745, P<0.001) in VSD children. CONCLUSIONS: Significant volume and pressure overload due to a left-to-right shunt induce myocardial injury and might eventually cause irreversible myocardial remodeling in children with CHD. The serum cTnI level is a useful biomarker for evaluating myocardial damage associated with pulmonary hypertension in VSD children.