Key result
Combined direct bilirubin and uric acid identifies severe PAH in ASD patients with ~0.87 AUC.
Why the study?
Severe pulmonary arterial hypertension frequently affects ASD patients with poor prognosis, but the potential of serum bilirubin levels to differentiate SPAH in ASD patients remained unestablished.
Does the combination of serum direct bilirubin and uric acid predict severe pulmonary artery hypertension in patients with atrial septal defect?
Cross-Sectional (n=102)
No
Does the combination of serum direct bilirubin and uric acid predict severe pulmonary artery hypertension in patients with atrial septal defect?
The combination of serum direct bilirubin and uric acid serves as a strong noninvasive predictor for severe pulmonary artery hypertension in patients with atrial septal defect.
May support noninvasive PAH risk stratification in ASD; hypothesis-generating and requires prospective validation before practice change.
Background: Atrial septal defect (ASD) patients commonly experience severe pulmonary arterial hypertension (SPAH), which is frequently associated with a poor prognosis. While serum bilirubin levels, indicative of liver function, are known predictors of right heart failure (RHF), their potential to differentiate SPAH in ASD patients is yet to be ascertained. The purpose of this study was to discover the potential correlations between serum bilirubin levels and ASD patients with SPAH. Methods: In this cross-sectional study, 102 ASD patients admitted from December 2019 to November 2020 were enrolled and divided into two cohorts: those with SPAH and those without. Blood tests were conducted to measure serum direct bilirubin (DBIL), total bilirubin (TBIL), alanine aminotransferase (ALT), aspartate aminotransferase (AST), uric acid (UA) and N-terminal pro B-type natriuretic peptide (NT-proBNP). Additionally, all participants underwent transthoracic echocardiography, and invasive hemodynamic data were gathered through right heart catheterization. Results: ASD patients with SPAH exhibited significantly elevated serum DBIL (5.2 ± 3.0 vs. 2.4 ± 1.5 µmol/L, p < 0.001) and TBIL (24.6 ± 20.7 vs. 10.1 ± 4.8 µmol/L, p < 0.001) levels in comparison to those without SPAH. However, ALT and AST levels remained comparable between the cohorts. Additionally, the SPAH cohort displayed higher serum UA (403.5 ± 131.6 vs. 317.8 ± 67.9 µmol/L, p < 0.001) and NT-proBNP levels. Serum DBIL levels, when analyzed independently of other variables, correlated with an increased risk of mean pulmonary arterial pressure (mPAP) in ASD patients (β = 1.620, p = 0.010). A DBIL concentration of 2.15 mg/dL effectively differentiated ASD patients with SPAH from those without, with a sensitivity of 92.9% and a specificity of 51.4% (area under the curve [AUC]: 0.794, 95% confidence interval [CI]: 0.701–0.886, p < 0.001). Notably, the combination of DBIL and UA had a higher sensitivity of 92.9% and specificity of 71.6% (AUC: 0.874, 95% CI: 0.799–0.949, p < 0.001). Conclusions: Elevated serum DBIL and TBIL levels in ASD patients with SPAH were correlated with poor cardiac function and heightened pulmonary artery pressure. The combination of DBIL and UA has emerged as a strong noninvasive predictor for SPAH in ASD patients, presenting a potentially novel therapeutic biomarker.
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Zhang et al. (2024) conducted a cross-sectional in Atrial septal defect (ASD) with or without severe pulmonary arterial hypertension (SPAH) (n=102). Serum direct bilirubin (DBIL) and uric acid (UA) vs. ASD patients without SPAH was evaluated on Differentiation of SPAH in ASD patients using combined DBIL and UA (AUC 0.874, 95% CI 0.799-0.949, p=<0.001). The combination of serum direct bilirubin and uric acid effectively differentiated atrial septal defect patients with severe pulmonary arterial hypertension from those without, achieving an AUC of 0.874.
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