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Copyright ©ERS Journals Ltd 2001
Angiotensin converting enzyme in patients with sleep apnoea syndrome: plasma activity and gene polymorphisms
1 The Servei de Pneumologia and Anàlisis Cliniques and 2 Unitat d'Investigació (REUNI), Hospital Universitari Son Dureta
CORRESPONDENCE: A.G.N. Agustí, Servei de Pneumología, Hospital Universitari Son Dureta, C/Andrea Doria 55, 07014, Palma de Mallorca, Spain. Fax: 34 971175228
Keywords: ACE, atherosclerosis, cardiovascular diseases, genetics, sleep apnoea
Received: June 6, 2000
Accepted December 22, 2000
This work was supported, in part, by ABEMAR, FUCAP 1995, Fondo de Investigaciones Sanitarias (FIS 96/1718), Academia de Ciencias Médicas de Catal
a y Baleares (1995) and Carburos Metálicos
The prevalence of several cardiovascular diseases is increased with obstructive sleep apnoea syndrome (OSAS), due to, as yet, unclear reasons. Angiotensin converting enzyme (ACE) abnormalities have been implicated in the pathogenesis of various cardiovascular diseases. In this study, plasma ACE activity and the distribution of an insertion (I)/deletion (D) polymorphism of the ACE gene were determined in OSAS patients and in healthy controls.
A total of 63 patients with OSAS (mean±sem 54.5±2.5 apnoea/hypopnoeas·h-1) and 32 healthy subjects were studied. To avoid potential confounding factors, patients treated with ACE inhibitors or continuous positive airway pressure were excluded, as well as controls in whom a blood sample was not obtained early in the morning. ACE activity was determined spectrophotometrically in 46 OSAS patients and 25 controls. The I/D ACE polymorphism was determined by polymerase chain reaction in 44 patients and 32 controls.
ACE activity was higher in OSAS patients (53.9±2.5 IU·L-1) than in healthy controls (42.4±3.1 IU·L-1, p<0.01). This was independent of the presence of arterial hypertension. The frequency distribution of the DD, II and ID genotypes in OSAS patients (30%, 16%, 54%, respectively) was not significantly different from that seen in healthy subjects (31%, 28%, 41%, respectively, p=0.356).
These results indicate that ACE plasma activity is increased in untreated OSAS patients. This increased activity may contribute to the pathogenesis of the cardiovascular disease in these patients.
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