ISSN: 2767-3774
editor@ijmsphr.com
Articles 2026-02-10 Peer Reviewed

The Role Of Oxidative Stress In The Development And Maintenance Of Pulmonary Hypertension In Children With Congenital Heart Disease

Ashurova Dilfuza Tashpulatovna • Turaeva Yulduz Shukhrat qizi
C R
DOI registered with Crossref
https://doi.org/10.37547/ijmsphr/Volume07Issue02-04
Dimensions Research discovery

Authors

Keywords

Congenital heart disease Pulmonary hypertension Oxidative stress

Abstract

Background: Pulmonary hypertension is a severe and prognostically unfavorable complication of congenital heart disease in children, characterized by progressive pulmonary vascular remodeling and increased perioperative risk. Increasing evidence suggests that oxidative stress plays a significant role in pulmonary vascular dysfunction; however, its contribution to the development and persistence of pulmonary hypertension in pediatric congenital heart disease remains insufficiently defined.

Objective: To investigate the role of oxidative stress in the development and maintenance of pulmonary hypertension in children with congenital heart disease by evaluating key antioxidant defense markers and their association with pulmonary hemodynamic parameters.

Methods: This observational study included children with congenital heart disease stratified according to the presence or absence of pulmonary hypertension based on echocardiographic assessment. Superoxide dismutase activity and total antioxidant status were measured in peripheral blood serum using spectrophotometric methods. Echocardiographic parameters reflecting pulmonary vascular involvement were analyzed in parallel. Intergroup comparisons and correlation analyses were performed using appropriate statistical methods.

Results: Children with pulmonary hypertension demonstrated significantly reduced superoxide dismutase activity compared with patients without pulmonary hypertension. Total antioxidant status was also lower in the pulmonary hypertension group, indicating depletion of overall antioxidant capacity. Oxidative stress markers were inversely associated with pulmonary artery pressure, suggesting a relationship between impaired antioxidant defense and pulmonary hemodynamic severity. Partial postoperative recovery of antioxidant parameters did not result in complete normalization, indicating persistent redox imbalance.

Conclusion: Oxidative stress, manifested by reduced enzymatic and total antioxidant defense, represents a stable pathogenic component of pulmonary hypertension in children with congenital heart disease. Assessment of antioxidant markers may provide additional insight into pulmonary vascular vulnerability and contribute to improved risk stratification and targeted management strategies in this patient population.

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