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Hypertrophic cardiomyopathy associated with dexamethasone therapy for bronchopulmonary dysplasia
J C Werner1, R E Sicard, T W Hansen
1Department of Pediatrics, Rhode Island Hospital, Providence 02903.
Insights
High-dose dexamethasone therapy in infants with bronchopulmonary dysplasia caused temporary cardiac effects, including myocardial hypertrophy. These changes, assessed by echocardiography, were reversible within six weeks of treatment.
Area of Science:
- Pediatric Cardiology
- Neonatology
- Pharmacology
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in infants.
- Dexamethasone is used to treat BPD, but its cardiac effects are not fully understood.
Purpose of the Study:
- To prospectively evaluate potential cardiac effects of high-dose dexamethasone therapy in infants with BPD.
Main Methods:
- Prospective evaluation of 13 respirator-dependent infants with BPD.
- Two-dimensional and M-mode echocardiography used for cardiac assessments.
- Dexamethasone administered at 500 mcg/kg/day, tapered over 6 weeks.
Main Results:
- Significant increases in interventricular septum and ventricular free wall thickness observed.
- Systolic anterior motion of the mitral valve noted in 7/13 infants.
- Cardiac effects were transient, peaking by week 3 and resolving by week 6.
Conclusions:
- Dexamethasone therapy is associated with transient myocardial hypertrophy in infants with BPD.
- The exact mechanisms and cardiopulmonary implications of these cardiac changes require further investigation.
Abstract:
The potential induction of cardiac effects by high-dose dexamethasone therapy was evaluated prospectively in 13 respirator-dependent infants with bronchopulmonary dysplasia by means of two-dimensional and M-mode echocardiography. The initial divided dose of dexamethasone was 500 micrograms/kg per day, tapered progressively for as long as 6 weeks. Evaluations were made before treatment and at 3, 7, 14, 21, 28, 35, and 42 days after the start of dexamethasone therapy. This regimen was associated with a significant (p less than 0.01) increase in thickness of the interventricular septum (2.60 +/- 0.09 to 4.00 +/- 0.16 mm), diastolic left ventricular free wall (2.80 +/- 0.13 to 4.06 +/- 0.20 mm), and diastolic right ventricular free wall (1.55 +/- 0.08 to 2.02 +/- 0.12 mm). In addition, seven dexamethasone-treated infants but no control infants had systolic anterior motion of the mitral valve (p less than 0.001). These effects were transient, reached their maximal degree by the third week of treatment, and approached pretreatment conditions by the sixth week of treatment. Ejection fraction was not affected; heart rate and mean arterial pressure were transiently increased during dexamethasone therapy. We conclude that a transient absolute myocardial hypertrophy is associated with dexamethasone therapy in infants with bronchopulmonary dysplasia. The mechanism or mechanisms through which this hypertrophy arises and the cardiopulmonary implications are unclear.
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