Hematological Adaptation Without Differences in Systemic Inflammatory Indices in Cyanotic and Acyanotic Congenital...

Background: Chronic hypoxemia in cyanotic congenital heart disease triggers well-recognized hematological adaptation; however, whether hypoxemia also drives systemic inflammatory activation remains uncertain. This study aimed to evaluate hematological parameters and inflammatory indices in cyanotic and acyanotic congenital heart disease (CHD) to better characterize the relationship between hypoxemia and systemic inflammatory status. Methods: In this single-center retrospective study, 260 children with congenital heart disease were classified as cyanotic (n = 158) or acyanotic (n = 102). Preoperative clinical data and laboratory parameters were analyzed, including oxygen saturation, hemoglobin, hematocrit, leukocyte indices, C-reactive protein (CRP), and procalcitonin (PCT). Inflammatory indices derived from complete blood counts were calculated, including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII). Results: Oxygen saturation was significantly lower in cyanotic patients than in acyanotic patients (75 ± 9% vs. 95 ± 4%, p < 0.001). Consistent with hypoxemia-driven hematological adaptation, hemoglobin and hematocrit levels were significantly higher in the cyanotic group (16.1 ± 2.9 g/dL vs. 13.1 ± 2.0 g/dL and 50.8 ± 9.7% vs. 39.7 ± 5.5%, respectively; p < 0.001). In contrast, inflammatory indices (NLR, PLR, and SII) were similar between cyanotic and acyanotic patients, and no significant associations were observed between oxygen saturation and these inflammatory indices. Conclusions: While cyanotic congenital heart disease demonstrates marked hematological adaptation secondary to chronic hypoxemia, systemic inflammatory indices appear similar in cyanotic and acyanotic patients. These findings suggest a relative dissociation between hypoxemia-driven hematological responses and the evaluated systemic inflammatory indices, indicating that inflammatory burden in congenital heart disease may not be solely explained by cyanosis and may reflect additional underlying mechanisms not captured by these markers.