Introduction and aims. There is evidence of endothelial dysfunction and a lower rate of NO production in obstructive sleep apnoea (OSA) so that increased homocysteine plasma levels can be expected in this pathology. The prothrombotic activity of HC should represent one of the mechanisms by which OSA predisposes to cardiocerebral vascular morbidity. Subjects and methods. Consecutive adult subjects referred to the sleep centre because of suspicion of OSA were considered. The diagnosis of OSA was made on the basis of standard clinical and polygraphic nocturnal findings (MESAM IV). The following conditions were ruled out before the subjects entered the study: past or recent history of cardio and/or cerebrovascular accidents, hypothyroidism, renal failure, alcoholism, or tabagism. So far 22 OSA patients entered the study (mean age 51 years ± 9.5; body mass index 30.6 ± 4.6; mean nocturnal oxygen desaturation index 42.7 ± 23.6; mean nocturnal HbSaO2 nadir 83.7% ± 5; 9 out of the 22 subjects were affected by mild to moderate hypertension). Ten subjects, in whom OSA diagnosis was negative and who were comparable in age and body mass index served as controls. Fasting HC plasma levels as well as conventional cardiovascular risk factors and vitamin B12, and folate levels were also measured. Results. Mean plasma level of HC did not differ significantly between OSA patients and controls (11.1 mmol/1 vs. 10) even though in 4 OSA patients (i.e. 19% of the cases), mild hyperhomocystheinemia was found (16 mmol/l to 24) in spite of normal levels of vitamin B12 and folate. Conclusion. The recruitment of further patients and the long-term follow-up will better clarify the preliminary findings of a mild increase of HC in OSA.
|Issue number||4 SUPPL.|
|Publication status||Published - 2000|
ASJC Scopus subject areas
- Clinical Neurology