Chest
Clinical InvestigationsPULMONARY HYPERTENSIONEffect of Orally Active Prostacyclin Analogue on Survival in Patients With Chronic Thromboembolic Pulmonary Hypertension Without Major Vessel Obstruction
Section snippets
Study Subjects
We studied 43 patients (16 men and 27 women; mean ± SD age, 54 ± 13 years) with peripheral-vessel CTEPH that was not suitable for surgical pulmonary thromboendarterectomy. The diagnosis of CTEPH was made on the basis of the previously reported procedure.14 In brief, patients with clinical symptoms suggesting CTEPH underwent ventilation/perfusion lung scanning to detect pulmonary perfusion defects. The diagnosis was confirmed by pulmonary angiography.15 When characteristic angiographic findings
Results
During a follow-up period of 2 ± 1 month, NYHA functional class significantly improved in 10 patients (50%), worsened in 1 patient (5%), and was unchanged in 9 patients (45%) in the BPS group (Fig 1). However, no significant change in NYHA functional class was observed in the conventional group.
BPS significantly lowered mean pulmonary arterial pressure by 11% (55 ± 15 to 49 ± 16 mm Hg, p < 0.05; Fig 2) and total pulmonary resistance by 18% (18 ± 6 to 15 ± 8 Wood units, p < 0.05) during a
Discussion
In the present study, we demonstrated the following: (1) oral administration of BPS improved NYHA functional class and decreased total pulmonary resistance in patients with peripheral-vessel CTEPH, for which no surgical option exists; (2) the absence of BPS therapy was significantly related to mortality in such patients; and (3) the Kaplan-Meier survival curves demonstrated that the BPS group had a significantly higher survival rate than the conventional group.
IV infusion of epoprostenol
Conclusions
This study suggest that oral administration of BPS may improve NYHA functional class, hemodynamics, and long-term prognosis in patients with peripheral-vessel CTEPH, for which no surgical option exists. Thus, BPS may be a new therapeutic approach to the treatment of inoperable CTEPH.
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This work was supported by a Research Grant for Cardiovascular Disease (12C-2) from the Ministry of Health, Labour and Welfare, the Uehara Memorial Foundation, and a grant from the Japan Cardiovascular Research Foundation.