We measured serial cardiac troponin T in babies with respiratory distress syndrome and in “healthy”controls (no cardiorespiratory support required). We investigated relationships between cardiac troponin T and myoca...We measured serial cardiac troponin T in babies with respiratory distress syndrome and in “healthy”controls (no cardiorespiratory support required). We investigated relationships between cardiac troponin T and myocardial performance in respiratory distress syndrome. This was a prospective observational study at a large tertiary maternity unit that recruited 104 “healthy”babies from whom individual samples were collected. A further 24 infants with respiratory distress syndrome and 14 “healthy”preterm infants had serial sampling over the first three days. We measured fractional shortening in 14 of the infants with respiratory distress syndrome. Cardiac troponin T rose from a median (interquartile range) of 10 (10-11) pgmL on day one to 34 (22-46) pgmL by day three, p=0.005, in “healthy”babies. In respiratory distress syndrome levels were higher, 91 (46-135) pgmL at 6 (5-7) hours of age, P< 0.001, and remained so for all three days. In babies with respiratory distress syndrome on day one cardiac troponin T correlated negatively with fractional shortening, Rho=-0.831, P < 0.001, but this correlation did not persist. In “healthy”babies there is a minimal rise of cardiac troponin T by day 3. In respiratory distress syndrome there is an early and sustained elevation of cardiac troponin T, with a negative relationship with fraction shortening, suggesting significant myocardial damage of antenatalintrapartum origin, giving rise to measurable dysfunction.展开更多
文摘We measured serial cardiac troponin T in babies with respiratory distress syndrome and in “healthy”controls (no cardiorespiratory support required). We investigated relationships between cardiac troponin T and myocardial performance in respiratory distress syndrome. This was a prospective observational study at a large tertiary maternity unit that recruited 104 “healthy”babies from whom individual samples were collected. A further 24 infants with respiratory distress syndrome and 14 “healthy”preterm infants had serial sampling over the first three days. We measured fractional shortening in 14 of the infants with respiratory distress syndrome. Cardiac troponin T rose from a median (interquartile range) of 10 (10-11) pgmL on day one to 34 (22-46) pgmL by day three, p=0.005, in “healthy”babies. In respiratory distress syndrome levels were higher, 91 (46-135) pgmL at 6 (5-7) hours of age, P< 0.001, and remained so for all three days. In babies with respiratory distress syndrome on day one cardiac troponin T correlated negatively with fractional shortening, Rho=-0.831, P < 0.001, but this correlation did not persist. In “healthy”babies there is a minimal rise of cardiac troponin T by day 3. In respiratory distress syndrome there is an early and sustained elevation of cardiac troponin T, with a negative relationship with fraction shortening, suggesting significant myocardial damage of antenatalintrapartum origin, giving rise to measurable dysfunction.
