Congenital heart disease (CHD) is the most common congenital anomaly worldwide and is associated with substantial infant morbidity and mortality. This narrative review synthesizes evidence linking CHD to alterations in the gut microbiome across neonatal, perioperative, and chronic stages and highlights a gut–heart–immune framework in which microbial imbalance, intestinal barrier dysfunction, and systemic inflammation may interact to influence clinical outcomes. Early infancy represents a potential window for microbiome and immune development, shaped by delivery mode and feeding, with many breastfed infants developing a Bifidobacterium-dominant community supported by human milk oligosaccharides. In CHD, abnormal splanchnic perfusion and hypoxemia, together with intensive care and perioperative exposures (fasting, delayed enteral feeding, antibiotics, acid suppression), may predispose to dysbiosis and impaired barrier function. Cardiac surgery with cardiopulmonary bypass can act as a “second hit,” with evidence of increased gut permeability, endotoxemia, inflammatory activation, and biomarker signals of enterocyte injury and tight-junction disruption. Clinically, these mechanisms align with gut-sensitive outcomes including necrotizing enterocolitis (especially in ductal-dependent lesions), feeding intolerance, and postoperative infection-risk phenotypes. Interventions show mixed evidence: human milk exposure appears protective for NEC risk, synbiotics demonstrated outcome benefits in a randomized trial of cyanotic CHD infants, while probiotics may modify dysbiosis without consistently preventing intestinal injury and require careful safety frameworks. Key research gaps include the need for longitudinal stage-based cohorts, integration of microbiome profiling with barrier injury and perfusion markers, and standardized safety monitoring in intervention trials.