Pulmonary haemodynamics in patients with OSAS or an overlap syndrome

Alveolar hypoxia is the most important mechanism leading to pulmonary arterial vasoconstriction, remodelling and pulmonary hypertension. Patients with Obstructive Sleep Apnoea Syndrome (OSAS) experience multiple short periods of alveolar hypoxia during apnoeic episodes. However, the question as to whether these hypoxic episodes are responsible for the development of permanent pulmonary hypertension is still debatable. We aimed to investigate the relationship between the episodes of nocturnal desaturation and pulmonary haemodynamics in two distinct group patients: with pure OSAS or an overlap syndrome.

We studied 67 patients with severe OSAS (means: age 45+/-8 years, AHI 62+/-22, FEV1 3.6+/-0.8 L = 97+/-16% of predicted PaO2 72+/-10 mmHg, PaCO2 40+/-4 mmHg) and 17 patients with an overlap syndrome (OS), means: age 51+/-5 years, AHI 64+/-19, FEV1 1.5+/-0.7 = 43+/-16% of predicted PaO2 57+/-9 mmHg). All subjects underwent pulmonary artery catheterisation with pressure and flow recordings and an overnight full sleep study.

On average patients with OSAS had nocturnal desaturation (mean overnight SaO2 = 87+/-5%) and normal PPA (15.8+/-4.6 mmHg). Only 11 out of 67 subjects (16%) presented with pulmonary hypertension. Patients with OS had nocturnal desaturation (mean overnight SaO2 = 80.2+/-8.5%) and mild pulmonary hypertension (PPA 24.2+/-7.4 mmHg). Only three out of 17 patients had normal pulmonary arterial pressure.

In patients with severe OSAS, pulmonary hypertension is rare (16%) and is related best to the severity of the disease and to obesity. In OS patients diurnal pulmonary hypertension is frequent but does not correlate with the severity of nocturnal desaturation.