Decreased cerebral vasomotor reactivity in patients with obstructive sleep apnea syndrome (original) (raw)
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Impaired Vascular Regulation in Patients with Obstructive Sleep Apnea
American Journal of Respiratory and Critical Care Medicine, 2009
Impaired endothelium-dependent vasodilation has been documented in patients with sleep apnea. This impairment may result in blood flow dysregulation during apnea-induced fluctuations in arterial blood gases. Objectives: To test the hypothesis that hypoxic and hypercapnic vasodilation in the forearm and cerebral circulation are impaired in patients with sleep apnea. Methods: We exposed 20 patients with moderate to severe sleep apnea and 20 control subjects, to isocapnic hypoxia and hyperoxic hypercapnia. A subset of 14 patients was restudied after treatment with continuous positive airway pressure. Measurements and Main Results: Cerebral flow velocity (transcranial Doppler), forearm blood flow (venous occlusion plethysmography), arterial pressure (automated sphygmomanometry), oxygen saturation (pulse oximetry), ventilation (pneumotachograph), and endtidal oxygen and carbon dioxide tensions (expired gas analysis) were measured during three levels of hypoxia and two levels of hypercapnia. Cerebral vasodilator responses to hypoxia (20.65 6 0.44 vs.-1.02 6 0.72 [mean 6 SD] units/% saturation; P 5 0.03) and hypercapnia (2.01 6 0.88 vs. 2.57 6 0.89 units/mm Hg; P 5 0.03) were smaller in patients versus control subjects. Hypoxic vasodilation in the forearm was also attenuated (20.05 6 0.09 vs. 20.10 6 0.09 unit/% saturation; P 5 0.04). Hypercapnia did not elicit forearm vasodilation in either group. Twelve weeks of continuous positive airway pressure treatment enhanced hypoxic vasodilation in the cerebral circulation (20.83 6 0.32 vs. 20.46 6 0.29 units/% saturation; P 5 0.01) and forearm (20.19 6 0.15 vs. 20.02 6 0.08 units/% saturation; P 5 0.003), and hypercapnic vasodilation in the brain showed a trend toward improvement (2.24 6 0.78 vs. 1.76 6 0.64 units/mm Hg; P 5 0.06). Conclusions: Vasodilator responses to chemical stimuli in the cerebral circulation and the forearm are impaired in many patients with obstructive sleep apnea. Some of these impairments can be improved with continuous positive airway pressure.
Sleep Medicine, 2009
Background: OSAS has been associated with surrogate markers of atherosclerosis and is a known risk factor for stroke. However, there is limited data on the effects of recurring apneas in severe OSAS on cerebral circulation and their consequences on cerebrovascular reactivity and compliance. Objective: To evaluate cerebral blood flow velocity (CBFV) changes and vascular compliance in patients with severe obstructive sleep apnea syndrome (OSAS) using transcranial Doppler sonography (TCD) and cerebral pulse transit time (PTT). Methods: Seven patients (1 woman, 6 men, mean age 57.4 years) with severe OSAS underwent polysomnography at the sleep laboratory of the Neurology Department of Innsbruck Medical University. TCD was performed continuously during the whole night using a pulsed wave probe and was coregistered with routine polysomnography. Cerebrovascular reactivity was assessed by calculation of apnea and hypopnea-related CBFV changes. Arterial compliance was characterized by PTT derived from phase difference analysis between ECG and TCD signals. Sleep time was dichotomized into periods with high density of consecutive respiratory events (CRE) vs. periods with low density of consecutive respiratory events (non-CRE).
Cerebral hemodynamics is altered in patients with sleep apnea/hypopnea syndrome
SpringerPlus, 2016
Background Stroke is a serious and common disorder and a major cause of death worldwide. The pathogenesis of stroke is multifactorial and not fully understood. Although several triggering factors have been already identified, they do no account for all the cases of stroke and new risk factors have been proposed (Díaz and Sempere 2004). Among them, sleep apnea/hypopnea syndrome (SAHS) is now recognized as an important and independent risk factor for cardiovascular disease and stroke, as demonstrated in cross-sectional (Yaggi et al. 2005) and longitudinal (Arzt et al. 2005) studies. Intermittent hypoxia,
How does obstructive sleep apnea alter cerebral hemodynamics?
SLEEP
Study Objectives We aimed to characterize the cerebral hemodynamic response to obstructive sleep apnea/hypopnea events, and evaluate their association to polysomnographic parameters. The characterization of the cerebral hemodynamics in obstructive sleep apnea (OSA) may add complementary information to further the understanding of the severity of the syndrome beyond the conventional polysomnography. Methods Severe OSA patients were studied during night sleep while monitored by polysomnography. Transcranial, bed-side diffuse correlation spectroscopy (DCS) and frequency-domain near-infrared diffuse correlation spectroscopy (NIRS-DOS) were used to follow microvascular cerebral hemodynamics in the frontal lobes of the cerebral cortex. Changes in cerebral blood flow (CBF), total hemoglobin concentration (THC), and cerebral blood oxygen saturation (StO2) were analyzed. Results We considered 3283 obstructive apnea/hypopnea events from sixteen OSA patients (Age (median, interquartile range) ...
2013
Rationale: Impaired endothelium-dependent vasodilation has been documented in patients with sleep apnea. This impairment may result in blood flow dysregulation during apnea-induced fluctuations in arterial blood gases. Objectives: To test the hypothesis that hypoxic and hypercapnic vasodilation in the forearm and cerebral circulation are impaired in patients with sleep apnea. Methods: We exposed 20 patients with moderate to severe sleep apnea and 20 control subjects, to isocapnic hypoxia and hyperoxic hypercapnia. A subset of 14 patients was restudied after treatment with continuous positive airway pressure. Measurements and Main Results: Cerebral flow velocity (transcranial Doppler), forearm blood flow (venous occlusion plethysmography), arterial pressure (automated sphygmomanometry), oxygen saturation (pulse oximetry), ventilation (pneumotachograph), and endtidal
Impairment of daytime cerebrovascular reactivity in patients with obstructive sleep apnoea syndrome
Journal of Sleep Research, 1998
Several studies have demonstrated a clear association between snoring, sleep apnoea and increased risk of stroke. However, the possible role of sleep apnoea in the pathophysiogenetic mechanisms of cerebrovascular disease is still unknown. Our aim in this study was to investigate cerebral haemodynamic changes during the waking state in eight patients with sleep apnoea syndrome (OSAS) by means of transcranial Doppler (TCD). In particular, we studied cerebral vascular reactivity (CVR) to hypercapnia calculated by means of the breath holding index (BHI). The investigation was performed in the early morning, soon after awakening, and in the late afternoon. Data were compared with those of eight healthy subjects matched for age and vascular risk factors. OSAS patients showed significantly lower BHI values with respect to controls both in the morning (0.56 vs. 1.36; P< 0.0001) and in the afternoon (1.12 vs. 1.53; P< 0.0001). In patients, BHI values in the afternoon were significantly higher than in the morning (P< 0.0001). These data demonstrate a diminished vasodilator reserve in OSAS patients, particularly evident in the morning. This reduction of the possibility of cerebral vessels to adapt functionally in response to stimulation could be linked to hyposensitivity of cerebrovascular chemoreceptors after the continuous stress caused by nocturnal hypercapnia.
Stroke, 1998
Background and Purpose-Epidemiological data link heavy snoring to an increased risk for stroke, an association often ascribed to hypertension and/or sleep apnea. The aim of this study was to determine whether obstructive hypopneas, central apneas, or obstructive apneas during sleep alter blood flow of the middle cerebral artery (MCA). Methods-Doppler sonography of the MCA was performed in conjunction with nightly polysomnography in 11 men and one woman.
Effects of Sleep-disordered Breathing on Cerebrovascular Regulation
American Journal of Respiratory and Critical Care Medicine, 2010
Rationale: Cerebrovascular regulation is impaired in patients with moderate to severe obstructive sleep apnea; however, it is unknown whether this impairment exists in individuals with less severe sleepdisordered breathing. Objectives: To test the hypothesis that cerebrovascular responses to hypercapnia are attenuated in a nonclinical population-based cohort. Methods: A rebreathing test that raised end-tidal CO 2 tension by 10 mm Hg was performed during wakefulness in 373 participants of the Wisconsin Sleep Cohort. Measurements and Main Results: We measured cerebral flow velocity (transcranial Doppler ultrasound); heart rate (electrocardiogram); blood pressure (photoplethysmograph); ventilation (pneumotachograph); and end-tidal CO 2 (expired gas analysis). Cerebrovascular CO 2 responsiveness was quantified as the slope of the linear relationship between flow velocity and end-tidal CO 2 during rebreathing. Linear regression analysis was performed using cerebrovascular CO 2 responsiveness as the outcome variable. Main independent variables were the apnea-hypopnea index and the mean level of arterial oxygen saturation during sleep. We observed a positive correlation between cerebrovascular CO 2 responsiveness and the mean level of oxygen saturation during sleep that was statistically significant in unadjusted analysis and after adjustment for known confounders and the increase in arterial pressure during rebreathing. Each 5% decrease in Sa O 2 during sleep predicted a decrease in cerebrovascular reactivity of 0.4 6 0.2 cm/second/mm Hg P ET CO 2. In contrast, the negative correlation between cerebrovascular CO 2 responsiveness and apnea-hypopnea index was statistically significant only in the unadjusted analysis. Conclusions: Hypercapnic vasodilation in the cerebral circulation is blunted in individuals with sleep-disordered breathing. This impairment is correlated with hypoxemia during sleep.
Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference, 2012
Obstructive Sleep Apnea (OSA) is a major sleep disorder with a prevalence of about 15 % among US adult population and can lead to cardiovascular diseases and stroke. In this study, we have investigated the OSA-induced concurrent rise in cerebral blood flow velocity and blood pressure in 5 positively diagnosed sleep apnea subjects. The subject population had a mean AHI of 57.94±25.73 and BMI of 33.66±7.27 kg/m(2). The results of this preliminary study yielded a relatively high correlation between rise in blood pressure and rise in cerebral blood flow velocity during apnea episodes (r=0.61±0.16) compared to normal breathing (r=0.28±0.26). These findings suggest that cerebral autoregulation may be less effective during apnea episodes.