Postnatal Steroids in Preterm Infants: A Narrative Review Series—Part 2: Cardiovascular Impacts

Abstract

Highlights: What are the main findings? Systemic postnatal corticosteroid use in extremely preterm infants with evolving lung disease can impact cardiovascular structure and function. Current evidence suggests it can lead to reactive myocardial hypertrophy, potentially accelerated closure of the patent ductus arteriosus and alterations in autonomic regulation and vascular resistance. Emerging diagnostic tools provide real-time monitoring capabilities: advanced techniques such as speckle tracking echocardiography, heart rate variability analysis, and biofluid markers (e.g., BNP) can detect subclinical cardiovascular changes and steroid-induced stress. What are the implications of the main findings? Routine cardiovascular surveillance is essential during steroid therapy to identify and manage potential adverse effects, such as left ventricular outflow tract obstruction or systemic hypertension, which may complicate the clinical course of infants with evolving bronchopulmonary dysplasia. Physiological data should guide a shift toward precision-based medicine, where the integration of longitudinal imaging and biomarker monitoring enables individualized steroid timing and dosing to optimize therapeutic benefits while minimizing unintended cardiovascular harm. Postnatal corticosteroids are frequently administered to extremely preterm infants to support respiratory management, yet their effects on the immature cardiovascular system are complex and underexplored. As the second installment in a series on physiology-informed steroid use, this narrative review focuses on the cardiovascular consequences of systemic corticosteroid therapy in preterm neonates. We examine how corticosteroids influence key aspects of cardiovascular physiology, including ductal closure, systemic and pulmonary vascular resistance, myocardial remodeling, and autonomic regulation. Attention is given to the hemodynamic transition of early postnatal life and how steroid exposure may interact with patency of the ductus arteriosus and vascular development. The potential for corticosteroids to contribute to reactive myocardial hypertrophy, systemic hypertension, and pulmonary hypertension is also reviewed in the context of both short- and long-term outcomes. Emerging diagnostic and monitoring tools are discussed for their potential to guide individualized therapy. These include targeted neonatal echocardiography (TnECHO) to assess cardiac function and structure, electrocardiography (ECG) for rhythm and conduction abnormalities, heart rate variability analysis for autonomic function, and circulating biomarkers to evaluate myocardial stress and inflammation. Together, these tools may inform tailored steroid timing and dosing, especially in the research context, while monitoring for signs of cardiovascular side effects in real time. By synthesizing mechanistic insights with evolving clinical evidence, this review highlights the need for a more nuanced understanding of how corticosteroids affect the developing cardiovascular system. It underscores the importance of integrating cardiovascular monitoring into routine care to optimize therapeutic benefit while minimizing unintended harm. Alongside companion reviews addressing respiratory and growth impacts, this installment contributes to a broader framework for individualized, physiology-driven steroid use in extremely preterm infants.