Serum angiotensin converting enzyme and the obstructive sleep apnea hypopnea syndrome

We wanted to see if the obstructive sleep apnea hypopnea syndrome (OSAHS) causes hypertension and endothelial dysfunction through activation of the angiotensin-converting enzyme (ACE).

A cross-sectional followed by a prospective, interventional study in a sleep disordered breathing clinic in a UK Hospital. We measured baseline serum ACE activity and ACE allele frequencies in 26 consecutive (untreated) OSAHS patients, 26 consecutive Sleepy Snorers, and 26 healthy (non-sleepy) controls. The OSAHS and Sleepy Snorers had serum ACE repeated after 6 months, with the OSAHS group receiving CPAP in the interim.

There was no difference in baseline mean serum ACE among OSAHS (33 lU/L), sleepy snorers (36 IU/L), and healthy controls (32 IU/L), p = 0.63. There was no difference in serum ACE activity between OSAHS and sleepy snorers after 6 months (p = 0.9) and no change in serum ACE from baseline in either group. In particular, there was no change in ACE activity in the OSAHS group on an intention to treat basis or when limiting analysis was limited to only "good" CPAP users (n = 16, p = 0.68), despite significant improvements in their Epworth scores and blood pressure and normalization of the 4% dip-rate.

Changes in serum ACE activity do not occur in OSAHS; therefore it is unlikely to be associated with the hypertension and other cardiovascular dysfunction often reported in OSAHS.