Outcomes of patients with decreased arterial oxyhaemoglobin saturation on pulmonary arterial hypertension drugs

Abstract

BackgroundDrugs approved for the treatment of pulmonary arterial hypertension (PAH) improve long-term outcomes. These drugs have pulmonary vasodilator properties which may potentially cause a decrease in arterial oxyhaemoglobin saturation (SaO2) in some patients. The present retrospective study of the French Pulmonary Hypertension Registry aimed to describe the clinical characteristics and outcomes of patients showing a ≥3% decrease in SaO2 while treated with PAH drugs.MethodsWe reviewed 719 PAH patients. The exclusion criteria were PAH associated with congenital heart disease and PAH with overt features of venous/capillaries involvement.Results173 (24%) patients had a ≥3% decrease in SaO2. At diagnosis, they were older with a lower diffusing capacity of the lung for carbon monoxide and a shorter 6-min walk distance compared with those who did not display a ≥3% decrease in SaO2. The percentage of patients meeting the European Society of Cardiology/European Respiratory Society (ESC/ERS) low-risk criteria at re-evaluation was significantly lower in those with a ≥3% decrease in SaO2 and more patients started long-term oxygen therapy in this group (16% versus 5%; p<0.001). A ≥3% decrease in SaO2 was associated with a poorer survival (hazard ratio 1.81, 95% CI 1.43–2.34; p<0.0001). In a multivariate Cox analysis, a ≥3% decrease in SaO2 was a prognostic factor independent of age at diagnosis and ESC/ERS risk stratification at follow-up.ConclusionsWhen treated with PAH drugs, a large subset of patients experience a ≥3% decrease in SaO2, which is associated with worse long-term outcomes and reduced survival.