Blood Pressure Changes After Automatic and Fixed CPAP in Obstructive Sleep Apnea: Relationship with Nocturnal Sympathetic Activity
Institute of Biomedicine and Molecular Immunology, National Research Council, Palermo, Italy. Clinical and Experimental Hypertension
(Impact Factor: 1.23).
05/2011; 33(6):373-80. DOI: 10.3109/10641963.2010.531853
Treatment of obstructive sleep apnea (OSA) by continuous positive airway pressure (CPAP) usually causes a reduction in blood pressure (BP), but several factors may interfere with its effects. In addition, although a high sympathetic activity is considered a major contributor to increased BP in OSA, a relationship between changes in BP and in sympathetic nervous system activity after OSA treatment is uncertain. This study was undertaken to assess if, in OSA subjects under no pharmacologic treatment, treatment by CPAP applied at variable levels by an automatic device (APAP) may be followed by a BP reduction, and if that treatment is associated with parallel changes in BP and catecholamine excretion during the sleep hours. Nine subjects underwent 24-h ambulatory BP monitoring and nocturnal urinary catecholamine determinations before OSA treatment and 2 months following OSA treatment by APAP (Somnosmart2, Weinmann, Hamburg, Germany). Eight control subjects were treated by CPAP at a fixed level. After APAP treatment, systolic blood pressure (SBP) decreased during sleep (p < 0.05), while diastolic blood pressure (DBP) decreased both during wakefulness (p < 0.05) and sleep (p < 0.02). Similar changes were observed in subjects receiving fixed CPAP. Nocturnal DBP changes were correlated with norepinephrine (in the whole sample: r = .61, p < 0.02) and normetanephrine (r = .71, p < 0.01) changes. In OSA subjects under no pharmacologic treatment, APAP reduces BP during wakefulness and sleep, similarly to CPAP. A reduction in nocturnal sympathetic activity could contribute to the reduction in DBP during sleep following OSA treatment.
Available from: Anne-Laure Borel
- "Loss of the BP dipping pattern is mainly attributable to an increase in nocturnal sympathetic activity, which in turn leads to a diurnally permanent increase in sympathetic tone. Indeed, OSA is associated with increased levels of urinary catecholamines   and increased muscle sympathetic nerve activity that are both lowered by CPAP treatment . Sleep deprivation has also been shown to increase sympathetic tone [43e45,88] and PLMs induce a surge in BP due to an acute rise in sympathetic activity . "
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ABSTRACT: Cardiovascular autonomic control changes across sleep stages. Thus, blood pressure (BP), heart rate and peripheral vascular resistances progressively decrease in non rapid eye movement sleep. Any deterioration in sleep quality or quantity may be associated with an increase in nocturnal BP which could participate in the development or poor control of hypertension. In the present report, sleep problems/disorders, which impact either the sleep quality or quantity, are reviewed for their interaction with BP regulation and their potential association with prevalent or incident hypertension. Obstructive sleep apnea syndrome, sleep duration/deprivation, insomnia, restless legs syndrome and narcolepsy are successively reviewed. Obstructive sleep apnea is clearly associated with the development of hypertension that is only slightly reduced by continuous positive airway pressure treatment. Shorter and longer sleep durations are associated with prevalent or incident hypertension but age, gender, environmental exposures and ethnic disparities are clear confounders. Insomnia with objective short sleep duration, restless legs syndrome and narcolepsy may impact BP control, needing additional studies to establish their impact in the development of permanent hypertension. Addressing sleep disorders or sleep habits seems a relevant issue when considering the risk of developing hypertension or the control of pre-existent hypertension. Combined sleep problems may have potential synergistic deleterious effects.
Available from: David Gozal
- "These differences in the response to therapy can be attributed to a large number of confounders such as ethnicity, gender, age, presence of underlying diseases, as well as genetic polymorphisms. It is possible that the more favorable reduction in diastolic blood pressure reflects its dependency on arteriolar tone, which is highly influenced by sympathetic activity, the latter being high in patients with OSA both during wakefulness and during sleep (Marrone et al., 2011). Because of the unique roles that catecholamines play in the transduction of sympathetic activity, multiple studies have assessed their concentrations, and shown the presence of elevated levels of catecholamines in both urine and plasma among patients with OSA. "
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ABSTRACT: Sleep is involved in the regulation of major organ functions in the human body, and disruption of sleep potentially can elicit organ dysfunction. Obstructive sleep apnea (OSA) is the most prevalent sleep disorder of breathing in adults and children, and its manifestations reflect the interactions between intermittent hypoxia, intermittent hypercapnia, increased intra-thoracic pressure swings, and sleep fragmentation, as elicited by the episodic changes in upper airway resistance during sleep. The sympathetic nervous system is an important modulator of the cardiovascular, immune, endocrine and metabolic systems, and alterations in autonomic activity may lead to metabolic imbalance and organ dysfunction. Here we review how OSA and its constitutive components can lead to perturbation of the autonomic nervous system in general, and to altered regulation of catecholamines, both of which then playing an important role in some of the mechanisms underlying OSA-induced morbidities.
Available from: erj.ersjournals.com
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ABSTRACT: Obstructive sleep apnoea (OSA) is linked to increased cardiovascular risk. This risk can be reduced by nasal continuous positive airway pressure (nCPAP) treatment. As OSA is associated with an increase of several vasoconstrictive factors, we investigated whether nCPAP influences the digital volume pulse wave. We performed digital photoplethysmography during sleep at night in 94 consecutive patients who underwent polysomnography and 29 patients treated with nCPAP. Digital volume pulse waves were obtained independently of an investigator and were quantified using an algorithm for continuous automated analysis. In patients with OSA and an apnoea/hypopnoea index (AHI) of >10 events · h(-1), a significant vasoconstriction was observed during the night (p<0.0001 by Friedman's test). A significant positive correlation existed between vasoconstriction and AHI (Spearman correlation, r = 0.27; p<0.01; n = 94) and the arousal index (Spearman correlation, r = 0.21; p < 0.05; n = 94). After 6 months of nCPAP treatment, the AHI was significantly reduced from 27 ± 3 events · h(-1) to 4 ± 2 events · h(-1) (each n = 29; p<0.001) and vasoconstriction during the night was significantly reduced from 10 ± 3% to 3 ± 1% (p<0.01). We show changes in the reflective index during the night consistent with vasoconstriction in patients with OSA, which are significantly reduced after 6 months of nCPAP treatment.
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