Update on Hypertension Management: Obstructive sleep apnea and hypertension

Jp, Baguet; Narkiewicz, Krzysztof; Jm, Mallion

doi:10.1097/01.hjh.0000198039.39504.63

Cited by 53 publications

(39 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hypertension can be caused by OSA, as is now recognised in international guidelines [119,120]. Although not fully understood, the role of hypoxia in promoting an increase in BP seems prominent, as evidenced both in animal models [121] and more recently in a model that was developed in normal volunteers [30,31].…”

Section: Osa Diagnosismentioning

confidence: 99%

Sleep apnoea syndrome in 2011: current concepts and future directions

Lévy¹,

Tamisier²,

Minville³

et al. 2011

Eur Respir Rev

View full text Add to dashboard Cite

Section: Osa Diagnosismentioning

confidence: 99%

Sleep apnoea syndrome in 2011: current concepts and future directions

Lévy¹,

Tamisier²,

Minville³

et al. 2011

Eur Respir Rev

View full text Add to dashboard Cite

“…It is now well established and recognised in international guidelines that hypertension can be caused by OSA [88,89]. However, nonapnoeic respiratory events generating no or very little oxygen desaturation, such as upper airway resistance syndrome, although generating increased nocturnal sympathetic activity, may not be associated with daytime hypertension.…”

Section: Blood Pressurementioning

confidence: 99%

Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives

Lévy¹,

Pépin²,

Arnaud³

et al. 2008

Eur Respir J

173

111

View full text Add to dashboard Cite

There are three major types of sleep-disordered breathing (SDB) with respect to prevalence and health consequences, i.e. obstructive sleep apnoea syndrome (OSAS), CheyneStokes respiration and central sleep apnoea (CSR-CSA) in chronic heart failure, and obesity hypoventilation syndrome (OHS). In all three conditions, hypoxia appears to affect body functioning in different ways. Most of the molecular and cellular mechanisms that occur in response to SDB-related hypoxia remain unknown.In OSAS, an inflammatory cascade mainly dependent upon intermittent hypoxia has been described. There is a strong interaction between haemodynamic and inflammatory changes in promoting vascular remodelling. Moreover, during OSAS, most organ, tissue or functional impairment is related to the severity of nocturnal hypoxia. CSR-CSA occurring during heart failure is primarily a consequence of cardiac impairment. CSR-CSA has deleterious consequences for cardiac prognosis and mortality since it favours sympathetic activation, ventricular ectopy and atrial fibrillation. Although correction of CSR-CSA seems to be critical, there is a need to establish therapy guidelines in large randomised controlled trials.Finally, OHS is a growing health concern, owing to the worldwide obesity epidemic and OHS morbidities. The pathophysiology of OHS remains largely unknown. However, resistance to leptin, obesity and severe nocturnal hypoxia lead to insulin resistance and endothelial dysfunction. In addition, several adipokines may be triggered by hypoxia and explain, at least in part, OHS morbidity and mortality.Overall, chronic intermittent hypoxia appears to have specific genomic effects that differ notably from continuous hypoxia. Further research is required to fully elucidate the molecular and cellular mechanisms.

show abstract

“…Free radicals have also been linked to endothelial dysfunction and increased sympathetic tone (2,16), whereas intravenous infusion of antioxidants reduces free radical levels and attenuates sympathetic activity in animal models of HF (32). It has been suggested that hydrogen gas produced in the large intestine by intestinal bacteria might scavenge hydroxyl radicals (6), and it was recently reported that hydrogen gas selectively scavenges hydroxyl radicals and exerts an antioxidant effect (23).…”

mentioning

confidence: 99%

Hydrogen gas attenuates embryonic gene expression and prevents left ventricular remodeling induced by intermittent hypoxia in cardiomyopathic hamsters

Kato

Nomura

Sakamoto

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

T. Hydrogen gas attenuates embryonic gene expression and prevents left ventricular remodeling induced by intermittent hypoxia in cardiomyopathic hamsters. Am J Physiol Heart Circ Physiol 307: H1626 -H1633, 2014. First published October 3, 2014; doi:10.1152/ajpheart.00228.2014.-The prevalence of sleep apnea is very high in patients with heart failure (HF). The aims of this study were to investigate the influence of intermittent hypoxia (IH) on the failing heart and to evaluate the antioxidant effect of hydrogen gas. Normal male Syrian hamsters (n ϭ 22) and cardiomyopathic (CM) hamsters (n ϭ 33) were exposed to IH (repeated cycles of 1.5 min of 5% oxygen and 5 min of 21% oxygen for 8 h during the daytime) or normoxia for 14 days. Hydrogen gas (3.05 vol/100 vol) was inhaled by some CM hamsters during hypoxia. IH increased the ratio of early diastolic mitral inflow velocity to mitral annulus velocity (E/e=, 21.8 vs. 16.9) but did not affect the LV ejection fraction (EF) in normal Syrian hamsters. However, IH increased E/e= (29.4 vs. 21.5) and significantly decreased the EF (37.2 vs. 47.2%) in CM hamsters. IH also increased the cardiomyocyte cross-sectional area (672 vs. 443 m 2 ) and interstitial fibrosis (29.9 vs. 9.6%), along with elevation of oxidative stress and superoxide production in the left ventricular (LV) myocardium. Furthermore, IH significantly increased the expression of brain natriuretic peptide, ␤-myosin heavy chain, c-fos, and c-jun mRNA in CM hamsters. Hydrogen gas inhalation significantly decreased both oxidative stress and embryonic gene expression, thus preserving cardiac function in CM hamsters. In conclusion, IH accelerated LV remodeling in CM hamsters, at least partly by increasing oxidative stress in the failing heart. These findings might explain the poor prognosis of patients with HF and sleep apnea. heart failure; intermittent hypoxia; oxidative stress; cardiomyopathic hamster; hydrogen gas SLEEP APNEA SYNDROME (SAS) is a breathing disorder characterized by recurrent episodes of apnea and/or hypopnea that increases the risk of cardiovascular morbidity and mortality (10,19,26). In persons with SAS, recurrent hypopnea/apnea leads to intermittent hypoxia (IH). The prevalence of SAS is much higher in patients with established cardiovascular disease, and central sleep apnea is associated with the more severe forms of heart failure (17), although the mechanisms underlying periodic breathing in patients with heart failure (HF) are complex and multifactorial.Oxidative stress arises because of an imbalance between free radical production and endogenous antioxidant defenses and is increased in patients with HF (4). Free radicals have also been linked to endothelial dysfunction and increased sympathetic tone (2, 16), whereas intravenous infusion of antioxidants reduces free radical levels and attenuates sympathetic activity in animal models of HF (32). It has been suggested that hydrogen gas produced in the large intestine by intestinal bacteria might scavenge hydroxyl radicals (6), and it was recen...

show abstract

Update on Hypertension Management: Obstructive sleep apnea and hypertension

Cited by 53 publications

References 56 publications

Sleep apnoea syndrome in 2011: current concepts and future directions

Sleep apnoea syndrome in 2011: current concepts and future directions

Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives

Hydrogen gas attenuates embryonic gene expression and prevents left ventricular remodeling induced by intermittent hypoxia in cardiomyopathic hamsters

Contact Info

Product

Resources

About