Demographic and histopathological evaluation of thymus in 1173 cases of cyanotic and acyanotic congenital heart diseases.

BACKGROUND

The thymus is central to T-cell development and immune tolerance. In congenital heart disease (CHD), especially cyanotic types, chronic hypoxia may alter thymic morphology with potential immune consequences. To assess histopathological thymic changes in pediatric CHD patients and their associations with age, sex, genetic syndromes, and cyanotic status.

METHODS

Thymic samples from 1173 patients (0-2 years) undergoing cardiac surgery (2020-2025) were retrospectively analyzed. Histological features-including Hassall's corpuscles (HCs), keratinization, calcification, cystic changes, cortical atrophy, corticomedullary blurring, eosinophil infiltration, starry-sky pattern, and involution-were semi-quantitatively graded (0-3). Statistical analyses used Chi-square and Spearman tests (P < 0.05).

RESULTS

Cyanotic CHD patients showed significantly more frequent HCs increase, keratinization, calcification, cortical atrophy, corticomedullary blurring, and eosinophil expansion (P < 0.05). HCs increase correlated strongly with degenerative changes, suggesting remodeling rather than reduction. Down syndrome cases exhibited higher rates of calcification, keratinization, cystic changes, cortical atrophy, and eosinophil infiltration. Age correlated positively with keratinization, calcification, and involution, but inversely with cortical atrophy and eosinophil expansion. Male patients more often had HCs and eosinophil increases, whereas females more frequently exhibited HCs reduction.

CONCLUSIONS

Cyanotic and acyanotic CHDs impose distinct effects on thymic histology. Chronic hypoxia accelerates involution and degenerative processes in HCs, cortex, and eosinophil distribution. Age, sex, and genetic background further influence these changes. The thymus thus emerges as a circulation-sensitive organ, and recognition of its pathology may guide strategies to preserve thymic integrity and mitigate long-term immune dysfunction in CHD patients.