Cardiorespiratory adaptation to low‐dose dexamethasone for lung disease in extremely preterm infants: A prospective echocardiographic study

The cardiovascular impact of dexamethasone (Dex) is not well understood. Most data are obtained from a 6 week, high‐dose regimen, and are limited to findings of hypertension and cardiac hypertrophy. The present study ascertained the impact of low‐dose Dex on cardiac indices when administered to extr...

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Published in:The Journal of physiology Vol. 600; no. 19; pp. 4361 - 4373
Main Authors: Sehgal, Arvind, Nold, Marcel F., Roberts, Calum T., Menahem, Samuel
Format: Journal Article
Language:English
Published: London Wiley Subscription Services, Inc 01-10-2022
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Summary:The cardiovascular impact of dexamethasone (Dex) is not well understood. Most data are obtained from a 6 week, high‐dose regimen, and are limited to findings of hypertension and cardiac hypertrophy. The present study ascertained the impact of low‐dose Dex on cardiac indices when administered to extremely preterm infants for lung disease. A pre–post intervention prospective echocardiographic (Echo) study was undertaken, with cardiac assessments performed before and within 24 h after completion of first course of therapy (10 day regimen, cumulative 0.89 mg kg–1). Thirty infants with a gestational age of 24.6 ± 1.1 weeks and birthweight of 612 ± 125 g, respectively, were studied. The age at Dex administration was 20 ± 9 days. Fractional inspired oxygen decreased from 0.7 ± 0.23 to 0.35 ± 0.14 (P < 0.001). Patent ductus arteriosus was noted in 20 infants at Echo1. At Echo2, the ductal diameter decreased from 2.16 ± 0.8 to 1.1 ± 0.8 mm (P = 0.0003), with complete closure in 7/20 (35%). A reduction in left pulmonary artery end‐diastolic velocity was noted (17 ± 12 to 9 ± 10 cm s–1, P < 0.001). Pulmonary vascular resistance decreased (increased time to peak velocity/right ventricular ejection time, 0.2 ± 0.03 to 0.23  ± 0.03, P = 0.0001) and right ventricular systolic performance improved (tricuspid annular plane systolic excursion, 4.9 ± 0.8 to 5.5 ± 0.9 mm, P = 0.02). No significant changes in fractional shortening and left ventricular mass were noted. A significant increase in blood pressure was noted. As a percentage of pre‐treatment baseline, the mean increase for systolic blood pressure was 20.3% (95% confidence interval = 14–26) on day 2 (P = 0.008). Low‐dose Dex influenced cardiovascular parameters related to pulmonary circulation. Key points Corticosteroid therapy is frequently used in preterm infants who are dependent on ventilator support. Echocardiographic studies in infants administered a 6 week course of steroids have noted left ventricular hypertrophy, outlet obstruction and hypertension, but no information is available on right heart indices. The cardiopulmonary effects of the current, significantly lesser cumulative dose (10 day regimen, commonly described as ‘DART’) have not been evaluated. The present study noted a significant influence on ductal and pulmonary circulation indices. Left heart architecture and function was maintained, whereas a significant but transient increase in blood pressure was noted. figure legend. Summary of the multifaceted physiological effects of dexamethasone. This illustrates how low‐dose dexamethasone influences cardiorespiratory function in extremely preterm infants. There appears to be a direct constrictive effect on the patent ductus arteriosus, alongside lowering of pulmonary vascular resistance. A drop in pulmonary vascular resistance was accompanied by improved right ventricular contractility (ventriculo‐arterial coupling). Administration of low‐dose dexamethasone (DART regimen, cumulative 0.89 mg kg–1) did not lead to cardiac hypertrophy or left ventricular outflow tract obstruction, which was commonly seen with higher doses. A transient increase in systolic blood pressure was noted, peaking at 48 h after the start of 10 day therapy.
Bibliography:The peer review history is available in the Supporting Information section of this article
Handling Editors: Laura Bennet & Janna Morrison
https://doi.org/10.1113/JP282973#support‐information‐section
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ISSN:0022-3751
1469-7793
DOI:10.1113/JP282973