The Journal of pediatrics · 2008
Influence of a patent ductus arteriosus on cardiac troponin T levels in preterm infants.
Сравнительное исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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El-Khuffash Afif F, Molloy Eleanor J
Аннотация
OBJECTIVE: To evaluate the effect of patent ductus arteriosus (PDA) on the myocardium by measuring levels of cardiac troponin T (cTnT), a marker of ischemic myocardial damage.
STUDY DESIGN: Eighty infants with a median gestation of 28 weeks (interquartile range ([IQR] = 26.1 to 29.5 weeks) and median birth weight of 1.06 kg (IQR = 0.87 to 1.21 kg) underwent echocardiographic and cTnT assessments at 12 and 48 hours of life. The infants with PDA were treated with ibuprofen or surgical ligation. Follow-up echocardiography and cTnT assay was performed after treatment.
RESULTS: The median 12-hour cTnT level was 0.20 microg/L (IQR = 0.11 to 0.40 microg/L). At 48 hours, median cTnT level was significantly higher in the PDA group (n = 45) than in the spontaneous closure group (n = 35) (0.43 vs 0.13 microg/L; P < .001). Following successful treatment, cTnT levels decreased significantly, to 0.10 microg/L (P < .001). cTnT levels correlated significantly with ductal diameter, left atrial-to-aortic diameter ratio, and descending aortic end-diastolic velocity. The receiver operating characteristics curve for detection of PDA through cTnT values had an area under the curve of 0.78 (95% confidence interval = 0.66 to 0.90; P < .001).
CONCLUSIONS: cTnT may be a useful marker of ductal significance and treatment response, because it correlates with echocardiographic markers of PDA. Elevated cTnT level may reflect the potential myocardial damage caused by a PDA.
STUDY DESIGN: Eighty infants with a median gestation of 28 weeks (interquartile range ([IQR] = 26.1 to 29.5 weeks) and median birth weight of 1.06 kg (IQR = 0.87 to 1.21 kg) underwent echocardiographic and cTnT assessments at 12 and 48 hours of life. The infants with PDA were treated with ibuprofen or surgical ligation. Follow-up echocardiography and cTnT assay was performed after treatment.
RESULTS: The median 12-hour cTnT level was 0.20 microg/L (IQR = 0.11 to 0.40 microg/L). At 48 hours, median cTnT level was significantly higher in the PDA group (n = 45) than in the spontaneous closure group (n = 35) (0.43 vs 0.13 microg/L; P < .001). Following successful treatment, cTnT levels decreased significantly, to 0.10 microg/L (P < .001). cTnT levels correlated significantly with ductal diameter, left atrial-to-aortic diameter ratio, and descending aortic end-diastolic velocity. The receiver operating characteristics curve for detection of PDA through cTnT values had an area under the curve of 0.78 (95% confidence interval = 0.66 to 0.90; P < .001).
CONCLUSIONS: cTnT may be a useful marker of ductal significance and treatment response, because it correlates with echocardiographic markers of PDA. Elevated cTnT level may reflect the potential myocardial damage caused by a PDA.