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Digoxin therapy and left ventricular performance in premature infants with patent ductus arteriosus
Insights
Digoxin did not affect preterm infants' heart function with open ductus arteriosus. However, it shortened left ventricular ejection time after the ductus closed, indicating improved cardiac performance.
Area of Science:
- Pediatric Cardiology
- Neonatal Physiology
Background:
- Symptomatic patent ductus arteriosus (PDA) in preterm infants affects left ventricular (LV) function.
- Digoxin is used to manage cardiac conditions, but its effect on LV systolic time intervals in preterm infants with PDA is not well-defined.
Purpose of the Study:
- To evaluate the impact of digoxin therapy on left ventricular systolic time intervals in preterm infants with symptomatic left-to-right ductal shunts.
Main Methods:
- Assessed LV systolic time intervals in 16 preterm infants before, during, and after digoxin therapy.
- Measured serum digoxin concentrations and heart rate.
- Analyzed changes in systolic time intervals in relation to ductal patency and digoxin levels.
Main Results:
- An initial digoxin loading dose did not alter heart rate or LV systolic time intervals.
- Maintenance digoxin led to decreased LV ejection time, likely due to reduced ductal shunting (p<0.05).
- LV ejection time prolonged as digoxin levels decreased after ductal closure (p<0.01).
Conclusions:
- Digoxin did not influence LV systolic time intervals during persistent ductal patency.
- The observed effects on systolic time intervals occurred after ductal closure, suggesting digoxin's efficacy in improving cardiac function post-shunt reduction.
- Potential limitations include method sensitivity or the ventricle operating at maximal capacity during PDA.
Abstract:
Left ventricular systolic time intervals were assessed in 16 preterm infants with symptomatic left-to-right ductal shunts, before, during and after digoxin therapy. An intravenous loading dose of digoxin, 20 micrograms/kg, resulted in a serum digoxin concentration of 1.94 +/- 0.44 nmol/l (mean +/- 1 SD) but in no significant change in heart rate or systolic time intervals. Digoxin maintenance, 2.5 micrograms/kg/12 h, led 3-7 days later to serum concentrations of 2.57 +/- 1.06 nmol/l with an associated shortening of left ventricular ejection time (p less than 0.05) which probably reflected a reduced ductal shunt. Digoxin therapy was withdrawn after ductal closure. The terminal serum half-life was 87 +/- 17 h. Decreasing digoxin concentrations were associated with prolongation of left ventricular ejection time (p less than 0.01). Digoxin therapy did not seem to influence left ventricular systolic time intervals while ductal patency persisted. This may be attributed to limitations of the method or the left ventricle already working at its maximum.