Non-dipping pattern of nocturnal blood pressure in obstructive sleep apnea syndrome: Possible role of oxidative stress and endothelin-1 precursor

Abstract Background There is growing evidence suggesting that obstructive sleep apnea OSA is linked to the occurrence of cardiovascular disorders. Lack of normal nocturnal dipping of blood pressure has also been considered a risk factor for the occurrence of cardiovascular disorders. Non-dipping has been described in patients with OSA and is attributed to autonomic dysfunction. However, the search for a causal link between OSA and cardiovascular disease is still underway. Objective To evaluate the occurrence of non-dipping pattern of nocturnal blood pressure, and the possible role of oxidative stress and ET-1 precursor in patients with OSA. Subjects and methods Thirty eight patients with OSA and fourteen normal control subjects were enrolled in this study and were subjected to history taking, clinical examination, early morning blood samplings for the measurement of serum malondialdehyde (MDA) and endothelin 1 precursor (ET-1 precursor). All patients with OSA were subjected to full polysomnographic study and monitoring of nocturnal blood pressure changes. Results Nocturnal blood pressure measurement of all patients revealed that thirty six patients (94.7%) were non-dippers, 15 patients (39.5%) suffered from ischemic heart disease. Serum endothelin-1 precursor and serum malondialdehyde levels were significantly higher in patients with OSA than in the control group. The systolic blood pressure measured before sleep was also significantly higher in patients than in the control group. The Epworth sleepiness scale and the clinical apnea score were significantly higher in patients than in the control group. Conclusions The high incidence of non-dipping pattern of nocturnal blood pressure in both normotensive and hypertensive patients with OSA may be considered a warning sign for the occurrence of cardiovascular complications in these patients. Both increased oxidative stress and ET-1 precursor may be among the causative factors responsible for the high prevalence of the non-dipping pattern through increasing sympathetic nervous system activity.