Objective: To investigate effects of 6 years of domiciliary oxygen therapy on pulmonary hemodynamics in a large group of COPD patients.
Design: Prospective longitudinal study with serial measurements.
Setting: Research institute of pulmonary diseases.
Patients: Ninety-five patients (72 men, 23 women), mean age 58+/-9 years, had COPD but were free of any other serious disease. Functional characteristics at entry, mean+/-SD, were as follows: FVC=2.24+/-0.51 L; FEV1=0.84+/-0.31 L; PaO2=55+/-6 mm Hg; PaCO2=48+/-9 mm Hg; mean pulmonary arterial pressure (PAP)=28+/-11 mm Hg; and pulmonary vascular resistance (PVR)=353+/-172 dynexsxcm(-5).
Methods: Pulmonary hemodynamics were investigated using Swan-Ganz thermodilution catheters. After initial assessment, all patients were started on a regimen of long-term oxygen therapy (LTOT). Follow-up consisted of medical examination, spirometry, and arterial blood gas analysis every 3 months. Pulmonary artery catheterization was repeated every 2 years.
Results: Seventy-three subjects survived 2 years of LTOT. In 39 subjects catheterized after 2 years, PAP fell from 25+/-8 to 23+/-6 mm Hg (not significant [NS]). From 31 patients who completed 4 years of LTOT, hemodynamic data were obtained in 20. In these 20 patients, PAP averaged 24+/-7 mm Hg at entry, and 23+/-5 and 26+/-6 mm Hg after 2 and 4 years, respectively (NS). In 12 patients who completed 6 years of LTOT, PAP was 25+/-7 at entry, and 21+/-4, 26+/-7, and 26+/-6 mm Hg at 2, 4, and 6 years, respectively (p < 0.01 for 2 vs 6 years). PVR was 313+/-159 dynexsxcm(-5) at entry, and 268+/-110, 344+/-82, and 332+/-205 dynexsxcm(-5) at 2, 4, and 6 years, respectively (NS). During 6 years of follow-up, PaO2 decreased from 61+/-3 to 46+/-9 mm Hg (p < 0.001) and PaCO2 increased from 44+/-13 to 49+/-9 mm Hg (p < 0.01).
Conclusion: LTOT for 14 to 15 h/d resulted in a small reduction in pulmonary hypertension after the first 2 years followed by a return to initial values and subsequent stabilization of PAP over 6 years. The long-term stabilization of pulmonary hypertension occurred despite progression of the airflow limitation and of hypoxemia.