PULMONARY BLOOD-FLOW REGULATES PLASMA TISSUE-PLASMINOGEN ACTIVATOR CONCENTRATIONS IN PATIENTS WITH CONGENITAL HEART-DEFECTS

Objective: The wall shear stress generated by blood flow regulates the expression of fibrinolytic proteins by endothelial cells in vitro. In the present study, the effects of pulmonary blood flow on fibrinolyti c activity were studied in patients with congenital heart defects and pulmonary hypertension. Methods: Twenty-seven patients who underwent c ardiac operation because of congenital heart defects were divided into four groups according to the severity of pulmonary hypertension. Grou p I consisted of seven patients with normal pulmonary artery pressure, group II consisted of nine patients with pulmonary hypertension cause d by increased pulmonary blood flow, group III consisted of six patien ts with pulmonary hypertension caused by increased pulmonary vascular resistance, and group IV consisted of five patients with tetralogy of Fallot. Plasma concentrations of tissue plasminogen activator, plasmin , and thrombin were assayed as the inhibitor-bound forms. Results: The preoperative concentration of tissue plasminogen activator was higher in group II than in all other groups (p = 0.0003). However, the posto perative concentration decreased only in patients in group II when com pared with the preoperative value (p = 0.01). By Pearson's correlation analysis, pulmonary blood flow was found to correlate with the preope rative concentration of tissue plasminogen activator (95% confidence i nterval = 3.99 to 10.58, p 0.0001). No definite conclusion was found f or the relationship between tissue plasminogen activator and plasmin c oncentration. Further, the preoperative thrombin concentration was sim ilar in all groups. Conclusions: These findings suggest that pulmonary blood flow may regulate the plasma concentration of tissue plasminoge n activator in patients with congenital heart defects.