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Neonatal glucocorticosteroid treatment causes systolic dysfunction and compensatory dilation in early life: studies
Miriam P Bal1, Willem B de Vries, Feike R van der Leij
1Department of Cardiology, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
Insights
Neonatal dexamethasone treatment, used to prevent lung disease in premature infants, impairs cardiac function in young rats. This early cardiac dysfunction may precede severe heart problems and reduced lifespan later in life.
Area of Science:
- Cardiology
- Neonatal Medicine
- Pharmacology
Background:
- Glucocorticosteroids like dexamethasone are used to prevent chronic lung disease in premature infants.
- Previous studies in adult rats showed negative long-term cardiac effects and reduced lifespan after neonatal dexamethasone exposure.
- Early cardiac alterations in young animals may predict later-life dysfunction.
Purpose of the Study:
- To investigate if neonatal dexamethasone treatment causes detectable cardiac function alterations in prepubertal rats.
- To assess systolic and diastolic cardiac function in young rats exposed to dexamethasone.
Main Methods:
- Neonatal male rats received intraperitoneal injections of dexamethasone or saline over the first three days of life.
- Cardiac function was evaluated at 4 weeks of age using pressure-conductance catheterization to measure pressure-volume loops.
- Histological examination of heart tissue was performed.
Main Results:
- Dexamethasone-treated rats exhibited reduced ventricular weight and impaired systolic function (reduced end-systolic elastance).
- Cardiac output was maintained, but end-diastolic volume increased, suggesting compensatory dilatation.
- Heart rate, diastolic function, and systemic vascular resistance remained unchanged.
Conclusions:
- Neonatal dexamethasone exposure induces cardiac alterations detectable in the prepubertal period.
- These early changes may precede severe cardiac dysfunction and reduced life expectancy.
- Findings suggest potential need for cardiac screening in human infants treated with dexamethasone for secondary prevention.
Abstract:
Glucocorticosteroid treatment is widely used to prevent chronic lung disease in premature infants. Recent studies in adult rats, treated with dexamethasone in the neonatal period, report negative long-term effects on the heart and severely reduced life expectancy. We treated neonatal rats with dexamethasone and studied cardiac function after 4 wk (prepubertal age) to investigate whether the late effects as previously described are preceded by detectable alterations in cardiac function at a younger age. Male rat pups (n = 12) were injected intraperitoneally with dexamethasone on d 1, 2, and 3 (0.5, 0.3, and 0.1 mug/g) of life. Control pups (n = 10) received saline. At 4 wk the animals were anesthetized, and a pressure-conductance catheter was introduced into the left ventricle to measure pressure-volume loops. Cardiac function was measured and pressure-volume relations were determined to quantify intrinsic systolic and diastolic function. Subsequently, hearts were excised for histologic examination. Compared with saline-treated animals, dexamethasone-treated rats had a reduced ventricular weight (270 +/- 40 versus 371 +/- 23 mg, p < 0.001) and reduced systolic function (end-systolic elastance: 1.24 +/- 0.43 versus 2.50 +/- 1.39 mm Hg/muL, p = 0.028). Cardiac output was maintained and end-diastolic volume was increased (84 +/- 23 versus 59 +/- 19 microL, p = 0.012) indicating a state of compensatory dilatation. Heart rate, diastolic function, and systemic vascular resistance were unchanged. Neonatal dexamethasone treatment causes cardiac alterations that can be detected in the prepubertal period and that may precede severe cardiac dysfunction later in life. If our findings are confirmed in humans, this may have consequences for a large patient population and cardiac screening at young age may be indicated to enable secondary prevention.
