Childhood systemic glucocorticoid exposure and subsequent alterations in myocardial structure and cardiac function: a narrative review of clinical evidence

Background Systemic glucocorticoids (GCs) remain indispensable in pediatric care, yet their potential long-term cardiovascular sequelae—particularly after exposure during developmental windows—are incompletely defined. Objective To synthesize representative clinical evidence linking childhood/adolescent systemic GC exposure with cardiac structure remodeling, subclinical functional alterations, and longer-term cardiovascular outcomes, and to contextualize plausibly mediating pathophysiologic pathways. Evidence synthesis Across pediatric conditions with repeated or prolonged systemic GC use, the most consistent structural signal is a time-locked, reversible myocardial hypertrophy phenotype in neonates/young infants—often observed during or shortly after dexamethasone exposure and regressing after dose reduction or discontinuation. In older children and adolescents, evidence for persistent, overt structural damage is sparse and confounded by underlying disease and treatment context. Conventional systolic indices (e.g., EF) are frequently preserved, while more sensitive metrics (tissue Doppler–derived parameters, myocardial performance index, strain) can reveal mild, subclinical systolic–diastolic impairment in selected populations (e.g., congenital adrenal hyperplasia). For “hard” adult outcomes (heart failure, coronary events, atrial fibrillation), direct longitudinal pediatric-to-adult data remain limited; however, pediatric GC exposure shows clearer dose–time associations with intermediate cardiometabolic risk factors and thromboembolic events, supporting a plausible mediated pathway to later cardiovascular disease. Conclusions Current pediatric evidence more strongly supports transient remodeling and risk-factor clustering than definitive, irreversible cardiomyopathy. Future studies need long-horizon, indication-aware cohorts with harmonized imaging and event endpoints to quantify exposure–response relationships and identify actionable mediators.