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Captopril in treatment of infant heart failure: a preliminary report
A M Scammell1, R Arnold, J L Wilkinson
1Institute of Child Health, University of Liverpool, Royal Liverpool Children's Hospital, U.K.
Insights
Captopril shows promise in treating severe infant heart failure from left-to-right shunts and pulmonary hypertension. This medication improved weight gain and vital signs, with manageable side effects.
Area of Science:
- Pediatric Cardiology
- Pharmacology
Background:
- Severe heart failure in infants, often due to left-to-right shunts and pulmonary hypertension, presents significant management challenges.
- Current treatments may have limitations, necessitating exploration of novel therapeutic agents.
Purpose of the Study:
- To evaluate the efficacy and safety of captopril in infants with severe heart failure.
- To assess captopril's impact on clinical parameters including weight gain, heart rate, respiratory rate, and feeding scores.
Main Methods:
- Retrospective study of 18 infants with severe heart failure receiving captopril (up to 3.5 mg/kg/day).
- Concomitant treatment with digoxin and frusemide was maintained; potassium-sparing diuretics were discontinued.
- Assessment period included 19 days pre-captopril and 27 days post-captopril initiation.
Main Results:
- Significant improvement in mean daily weight gain (from -7 g to +13 g, P < 0.001).
- Statistically significant reductions in mean heart rate (P < 0.05) and respiratory rate (P < 0.05).
- Notable increases in plasma sodium concentration and feeding scores were observed.
Conclusions:
- Captopril demonstrated potential benefits in managing severe heart failure in infants.
- Adverse events, including hypotension and renal function changes, were noted in two patients, potentially linked to hyponatremia.
- Further investigation is warranted to confirm captopril's role in pediatric heart failure management.
Abstract:
We have studied retrospectively 18 infants who have received captopril for treatment of severe heart failure due to left-to-right shunts with pulmonary hypertension. Captopril has been administered in doses of up to 3.5 mg/kg/day (mean 2.47 mg/kg/day). Maintenance treatment with digoxin and frusemide was continued but potassium-sparing diuretics were stopped in most patients. The mean period of assessment was 19 days before and 27 days after commencing captopril. The mean daily weight gain before captopril was -7 g and after its introduction was + 13 g (P less than 0.001). There were statistically significant (P less than 0.05) falls in mean heart rate and respiratory rate and rises in plasma sodium concentration and feeding score. Plasma urea concentration fell but this did not reach statistical significance. Two patients suffered hypotension after increments in captopril dosage and subsequently had a rise in plasma urea and creatinine values. This adverse reaction may be linked to the presence of hyponatraemia. This preliminary report shows captopril may be useful in the control of severe heart failure in infancy.