Serum level of soluble intercellular adhesion molecule-1 correlates with pulmonary arterial pressure in children with congenital heart disease.

BACKGROUND: Endothelial activation and vascular inflammation are thought to be the mechanisms of pulmonary hypertension. Increased expression of the intercellular adhesion molecule (ICAM-1) and raised serum level of its soluble form (sICAM-1) are found in various conditions associated with endothelial activation. METHODS: Serum samples from 31 children (14 boys and 17 girls; age, 4.9 +/- 4.6 years) with congenital heart disease (CHD) collected at the time of cardiac catheterization were analyzed for sICAM-1 level. Uni- and multivariable stepwise linear regression analyses were performed for the following variables against the sICAM-1 level: age, hemoglobin, serum creatinine, systemic arterial pressure (SAP), pulmonary arterial pressure (PAP), pulmonary blood flow (Qp) and resistance (Rp), systemic blood flow (Qs) and resistance (Rs), Qp/Qs, Rp/Rs, and pulmonary and systemic oxygen saturation. RESULTS: The sICAM-1 levels in children who had CHD with and without pulmonary hypertension were 411 +/- 110 and 344 +/- 81 ng/ml, respectively (p = 0.11). In the univariable models, age, serum creatinine, systolic PAP, mean PAP, diastolic PAP, Rp, and Rp/Rs were significantly correlated with sICAM-1 level. In the multiple stepwise regression model, only mean PAP remained as an independent predictor of sICAM-1 level (r = 0.55; p = 0.002). CONCLUSION: Children with CHD and pulmonary hypertension had a trend toward elevated sICAM-1 compared with CHD children who had no pulmonary hypertension. A linear correlation was found between mean pulmonary arterial pressure and sICAM-1 level.

Plasma levels of nitric oxide in children with congenital heart disease and increased pulmonary blood flow.

BACKGROUND: Development of pulmonary hypertension commonly accompanies congenital heart disease; nitric oxide (NO) is evidently an important mediator of pulmonary vascular reactivity. OBJECTIVE: Investigate the effect of pulmonary hypertension (PH) associated with congenital heart disease on NO production. MATERIAL AND METHOD: The authors measured plasma levels of nitric oxide-related compounds in 28 patients, aged 3 months to 12 years with congenital heart disease (CHD) and increased pulmonary blood flow. Blood samples were obtained during their cardiac catheterization. The subjects were subsequently divided into two groups, namely: group 1 CHD were those with left-to-right shunt; and group 2, CHD with right-to-left shunt. RESULTS: Four patients had severe pulmonary hypertension (mean pulmonary arterial pressure > 60 mmHg). The total levels of NO-related compounds between the two groups were not statistically different as well as the levels in pre- and post-pulmonary artery. In patients with left-to-right shunt with mild to moderate pulmonary hypertension, the levels of total NO-related compounds were directly correlated with the level of pulmonary arterial pressure and pulmonary vascular resistance (r = 0.67; p-value < 0.05, and r = 0.75; p-value < 0.05). Additionally, in patients with severe pulmonary hypertension, the levels of total NO-related compounds decreased when compared to the levels in patients with mild to moderate pulmonary hypertension. CONCLUSION: The present results suggested that the hemodynamic status of the pulmonary circulation in congenital heart defect is at least partly correlated with the blood levels of nitric oxide.