PLASMA THROMBOXANE B-2 CONCENTRATION IN PULMONARY-HYPERTENSION ASSOCIATED WITH CONGENITAL HEART-DISEASE

Background We investigated the plasma concentration of thromboxane B-2 (TXB(2)), a stable metabolite of thromboxane A(2) (TXA(2)), to assess platelet activation in 78 patients who had pulmonary hypertension associated with congenital heart disease (PH group) and 16 patients with almost normal hemodynamics (control group). Methods and Results The PH group was divided into two subgroups: pulmonary vascular resistance (Rp) less than or equal to 10 U/m(2) (Rp less than or equal to 10 group) and >10 U/m(2) (Rp>10 group). In addition, the Rp less than or equal to 10 group was divided on the basis of clinical symptoms into groups with dyspnea (dyspnea[+] group) and without dyspnea (dyspnea[-] group). Plasma TXB(2) levels were measured by radioimmunoassay. Plasma TXB(2) levels in the three groups (control, Rp less than or equal to 10, and Rp>10) were significantly different (P<.005); the TXB(2) levels in the Rp less than or equal to 10 group were significantly higher than the others. Among the Rp less than or equal to 10 patients, the plasma TXB(2) levels were significantly higher in the dyspnea(+) group than in the dyspnea(-) group (P<.0001). In addition, the pulmonary-to-systemic flow ratio and pulmonary blood flow divided by body surface area were significantly higher in the dyspnea(+) group than in the dyspnea(-) group (P<.02 and P<.002, respectively). Conclusions These findings suggest that platelet activation led to increased TXA(2) release in patients with pulmonary hypertension, especially those with dyspnea and Rp less than or equal to 10. TXA(2) release from platelets probably caused constriction of the pulmonary arterioles and the bronchi, thus worsening pulmonary hypertension and dyspnea in these patients. In the patients with high Rp values, it was considered that the number of pulmonary arterioles where platelets could be activated had been reduced.