Assessment of continuous positive airway pressure treatment in obstructive sleep apnea syndrome using 24-hour urinary catecholamines

Abstract

SummaryBackground: Obstructive sleep apnea syndrome (OSAS) is related to diurnal sympathetic hyperactivity and increased blood pressure, both factors that are likely to lead to the development of cardiovascular disease.Hypothesis: The study investigated whether 24-h urinary catecholamines would reflect the effect of obstructive sleep apnea on autonomic activity.Methods: Standard polysomnography was performed in 17 patients with OSAS (age 53.7 ± 13.5 years, mean ± standard deviation). The number of apnea/hypopnea episodes per hour of sleep (apnea/hypopnea index [AHI]); number of oxygen desaturation episodes per hour (desaturation index [DSI]); arousals per hour (arousal index); lowest oxygen saturation (lowest SpO2); and percentages of stages 1, 2, 3/4, and rapid eye movement sleep (% stage 1, Ϫ2, and Ϫ3/4, and % REM, respectively) were measured. Overnight continuous positive airway pressure (CPAP) titration was performed the night after the baseline sleep measurements had been taken. Twenty-four-hour urinary adrenaline and noradrenaline were also examined.Results: During the CPAP treatment, both 24-h urinary adrenaline and noradrenaline were significantly lower com-

Contribution of Autonomic Nervous System to the Hypertension Induced by Obstructive Sleep Apnea

“…Prospective studies also showed a strong association between AHI and THE increased arterial blood pressure [85]. It is relevant to note that the OSA-hypertension link is independent from other comorbidities like obesity [33,45,51,79,100]. Other study performed in OSA patients without hypertension, which were follow-up during five years for the risk of hypertension, concluded that there is a trend of association between AHI > 30 and the occurrence of the hypertension [75].…”

“…Indeed, OSA patients show a positive relationship between AHI and the hypertension, which is independent of other risks [23,60,61,85,96,100,111,112]. Moreover, results obtained from the Wisconsin Sleep Cohort (an ongoing 21-years longitudinal study performed on 1500 Wisconsin state employees) have shown that untreated OSA patients have a high mortality risk associated with AHI [74,112].…”

“…However, according to a report of the American Heart Association in collaboration with the National Center on Sleep Disorders Research, "85% of patients with clinically significant and treatable OSA have never been diagnosed, and referral populations of OSA patients represent only the tip of the iceberg of OSA prevalence". Therefore, the estimated adult population that present an AHI of 5 is ~20% [100]. The OSA syndrome is associated with clinical neurobehavioral dysfunction, such as daytime sleepiness, fatigue, depressed mood, attention and executive deficits, and verbal and visualspatial memory impairments [5,67].…”

“…The most accepted explanation proposes that chronic intermittent hypoxia produces oxidative stress, inflammation, and sympathetic hyperactivity, which led to endothelial dysfunction and hypertension [19,25,28,41,43,52,53,65,99,100], but it is likely that intrathoracic pressure changes causing excessive mechanical stress on large artery walls and the heart, and arousal-induced sympathetic hyperactivity may also contribute to the endothelial dysfunction [47]. OSA is characterized by repeated episodes of total or partial airflow detention during sleep produced by the pharyngeal collapse, eliciting intermittent hypoxia and hypercapnia, negative intrathoraxic pressure, sleep fragmentation and arousal.…”

“…During the airflow occlusion, the resulting hypoxia and hypercapnia stimulates the carotid body chemoreceptors producing reflex ventilatory, sympathetic and hypertensive responses. Among these disturbances, the chronic intermittent hypoxia is considered the main factor for the development of the hypertension [1,19,33,41,43,51,55,56,82,83,88,93,100]. However, conclusions from studies performed in OSA patients are partial and somehow controversial, because invasive procedures are precluded because of ethical reasons in humans, and OSA patients often present concomitant morbidities (i.e.…”