The study population consisted of 46 hypertensive subjects with high clinical evidence of OSAS and 53 hypertensive subjects without clinical evidence of OSAS who were referred to the outpatient hypertensive unit of the institution in the last 30 months.
Symptoms of OSAS include excessive daytime sleepiness, choking or gasping during sleep or recurrent awakening from a sleep, daytime fatigue and impaired concentration.
The presence of OSAS was confirmed or excluded by an in-hospital polysomnography study. From a morning blood sample, the following was assessed: serum glucose, lipid profile assays and sub-clinical inflammation markers C reactive protein, adhesion molecules (ICAM-1, VCAM, and p-selectine) and interleukins (IL-6, 11-18).
The results demonstrated that hypertensives with OSAS had 40-percent more C reactive protein; 20-40-percent more adhesion molecule levels, and as much as 45-percent higher interleukins levels than non-OSAS hypertensives.
Glucose and lipid profile estimates were similar between the two groups. Interestingly, the more apnea episodes, the greater the ICAM-1 and IL-6 levels.
Nowadays, OSAS is recognized as an emerging cardiovascular risk factor. After the adjustment for confounders such as age, sex, body weight, and metabolic status, epidemiological studies indicate a close relationship between OSAS and cardiovascular disorders.
In the setting of arterial hypertension, OSAS is considered as an identifiable cause of hypertension and is a misdiagnosed cause of resistant hypertension. The link between OSAS and cardiovascular disease it not yet well determined.
Repetitive episodes of apnea and nocturnal hypoxia elicit a wide variety of autonomic, haemodynamic, and humoral responses. Common denominator to all OSAS effects is sympathetic activation, increasing the risk of diurnal hypertension and promoting sub-clinical cardiovascular damage.
Substantially, chronic intermittent hypoxia causes a specific disturbance in the vascular wall regulation with inflammatory, vasoconstrictive and coagulative components, a condition identified as endothelial dysfunction.
According to some studies, treatment of hypertensive subjects with OSAS with nasal continuous positive airway pressure (n-CPAP) not only improves OSAS symptoms and 24h BP levels but also attenuates endothelial dysfunction.
This accumulating evidence from cross sectional observational studies in the setting of hypertension relating OSAS and sub-clinical inflammation need to be further enforced by longitudinal prospective studies and clarified by more refined studies targeting the functional status of human inflammation cells and finally the gene status in appropriate animal models.
Sub-clinical inflammation in hypertensives with OSAS might constitute an early step of an accelerated atherosclerotic process accompanied by adverse cardiovascular prognosis. Early and probably aggressive management of OSAS may attenuate its effects on vascular function, reducing cardiovascular risk in an early phase.
It could be suggested that multifaceted treatment including weight loss, n-CPAP devices and anti-inflammatory agents (i.e. statins) would act beneficially in hypertensive subjects with OSAS. If the efficacy of anti-inflammatory agents is ascertained by appropriate studies, they might constitute an alternative treatment for those subjects who refuse or discontinue n-CPAP therapy.
