The Effect of Simulated Obstructive Apnea and Hypopnea on Aortic Diameter and BP

Stöwhas, Anne-Christin; Namdar, Mehdi; Biaggi, Patric; Russi, Erich W.; Bloch, Konrad E.; Stradling, John; Kohler, Malcolm

doi:10.1378/chest.10-2799

Cited by 33 publications

(23 citation statements)

References 23 publications

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“…Three studies have investigated the pathophysiological effects of OSA using breathing manoeuvres that simulate OSA features in healthy volunteers (table 3) [62][63][64]. The Müller manoeuvre (simulated obstructive apnoea) has proven to be an elegant way to partially simulate acute effects of OSA without the confounding factors of profound hypoxaemia, arousals from sleep and comorbidities often present in patients with OSA [65].…”

Section: Physiological Studies In Healthy Volunteersmentioning

confidence: 99%

“…The Müller manoeuvre (simulated obstructive apnoea) has proven to be an elegant way to partially simulate acute effects of OSA without the confounding factors of profound hypoxaemia, arousals from sleep and comorbidities often present in patients with OSA [65]. In humans, the Müller manoeuvre and simulated obstructive hypopnoea (inspiration through threshold load) induced considerable changes in blood pressure and simulated obstructive hypopnoea has been shown to be associated with an increase in proximal aortic diameter and aortic area [62,64]. The underlying forces of this increase were quantified in a second study, which concluded that simulated obstructive apnoea/hypopnoea increased aortic wall dilatory pressures [63].…”

Section: Physiological Studies In Healthy Volunteersmentioning

confidence: 99%

“…Studies investigating the impact of OSA on aortic disease have discussed several pathomechanisms (for thoracic aorta, see figure 2), including intrathoracic pressure changes leading to shear stress on artery walls [41,43,49,51,54,55,62,63], intermittent hypoxia leading to oxidative stress and sympathetic stimulation [49, 50,55], and arousal-induced sympathetic activation with subsequent repetitive blood pressure surges [45,47,50,54,55,59,61]. These mechanisms are discussed in the following section.…”

Section: Current Limitations Of Published Studiesmentioning

confidence: 99%

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The impact of obstructive sleep apnoea on the aorta

2015

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Obstructive sleep apnoea (OSA) has been shown to be a causal factor in the pathogenesis of vascular dysfunction and hypertension, conditions which can promote dilation and subsequent aortic dissection and rupture. The objective of this review is to summarise the current literature on the possible association between OSA and aortic disease and delineate the underlying mechanisms.Relevant studies were found by searching for terms including "obstructive sleep apnoea" in combination with "aortic aneurysm, dissection, and dilation" in the MEDLINE and EMBASE databases.Observational studies consistently reported that OSA is highly prevalent among patients with aortic aneurysms and aortic dissections. Patients with co-occurring OSA and Marfan's syndrome as well as patients at the more severe end of the spectrum of OSA seem to be especially vulnerable to aortic disease.Several mechanisms are discussed concerning the link between OSA and aortic disease: nocturnal negative intrathoracic pressure surges leading to mechanical stretching of the aorta and ultimately aortic distension; arousal-induced reflex sympathetic activation with subsequent hypertension; and intermittent hypoxia associated with autonomic nervous system activation and consequently increased oxidative stress. Further well controlled studies are needed in order to define the exact role of OSA as a risk factor for aortic disease. @ERSpublications Several studies have shown an association between obstructive sleep apnoea and aortic aneurysms/dissections http://ow.ly/Nh9jc

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Section: Physiological Studies In Healthy Volunteersmentioning

confidence: 99%

Section: Physiological Studies In Healthy Volunteersmentioning

confidence: 99%

Section: Current Limitations Of Published Studiesmentioning

confidence: 99%

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The impact of obstructive sleep apnoea on the aorta

2015

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“…During the Mueller manoeuvre, the negative intrathoracic pressure transmitted to the pericardial cavity leads to an increase in the left ventricular afterload, in the pressure developed during the left ventricular isovolumetric phase, and in left ventricular volume [52,53]. In healthy subjects, simulated obstructive apnoea or hypopnoeas were associated with an acute increase in proximal aortic diameter and in left ventricular volume, as assessed by echocardiography, while left atrial volume and left ventricular ejection fraction were reduced [53][54][55]. These findings suggest that repeated intrathoracic pressure changes in OSA might play a role in the onset of cardiac arrhythmias by promoting both mechanical and electrical remodelling of the heart, as evidenced by recent findings [48].…”

Section: Increased Negative Intrathoracic Pressurementioning

confidence: 99%

Effects of obstructive sleep apnoea on heart rhythm

2012

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Symptomatic obstructive sleep apnoea (OSA) has been proven to be a risk factor for hypertension and vascular dysfunction, and has been proposed to be causally related with cardiac arrhythmias and sudden cardiac death.Searches of bibliographical databases revealed that several mechanisms seem to underpin the association between OSA and cardiac arrhythmias: intermittent hypoxia associated with autonomic nervous system activation and increased oxidative stress, which may lead to cardiac cellular damage and alteration in myocardial excitability; recurrent arousals, resulting in sympathetic activation and coronary vasoconstriction; and increased negative intrathoracic pressure which may mechanically stretch the myocardial walls and, thus, promote acute changes in myocardial excitability as well as structural remodelling of the myocardium.Findings from cross-sectional studies suggest a high prevalence of cardiac arrhythmias in patients with OSA and a high prevalence of OSA in those with cardiac arrhythmias. Preliminary evidence from uncontrolled interventional studies suggests that treatment of OSA may prevent cardiac arrhythmias.In conclusion, there is preliminary evidence that OSA is associated with the development of cardiac arrhythmias. Data from randomised controlled studies are needed to definitively clarify the role of OSA in arrhythmogenesis.

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“…Possible underlying pathophysiological mechanisms are post-apnea reflex sympathetic activation and consequent marked increases in blood pressure [13]. In addition, large negative intrathoracic pressure swings, which are produced during obstructive apneas, increase transaortic pressure and may therefore accelerate aortic dilatation [14,15]. However, there are currently no data investigating the impact of OSA on the risk of needing aortic root replacement surgery or of death in Marfan's syndrome.…”

Section: Introductionmentioning

confidence: 99%

The Impact of Obstructive Sleep Apnea on Aortic Disease in Marfan's Syndrome

Kohler¹,

Pitcher

Blair³

et al. 2012

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Background: Aortic dissection is a life-threatening manifestation of Marfan's syndrome. Preliminary evidence suggests that obstructive sleep apnea (OSA) is associated with aortic disease in Marfan's syndrome. Objectives: To study the effect of OSA on aortic events in Marfan's syndrome. Methods: In patients with Marfan's syndrome, a sleep study was performed at baseline and OSA was defined as >5 events of apnea/hypopnea (A+H) per hour in bed. Operation because of progressive aortic dilatation and death because of aortic rupture were defined as ‘aortic events'. Kaplan-Meier survival analyses were used to compare event-free survival in patients with and without OSA. Cox regression models were used to explore the effects of covariates on event-free survival. Results: Data from 44 patients (mean age 37.4 years, 30 females) were available for analysis; 15 patients (34.1%) had OSA. The median follow-up time was 29 (interquartile range 24-36) months. Five patients had an aortic event within the follow-up time. Median event-free survival was 51.6 months. Event-free survival was significantly shorter in patients with OSA compared to patients without OSA (p = 0.012). In univariate analysis, A+H was associated with aortic events [hazard ratio (HR) 1.09, 95% confidence interval (CI) 1.01-1.18, p = 0.023]. Taking the interaction between BMI and A+H into account increased the HR for A+H (HR 1.75, 95% CI 1.003-3.048, p = 0.049). This association was no longer significant when other covariates were forced into the multivariate analysis. Conclusions: These data suggest that aortic event-free survival may be shorter in patients with Marfan's syndrome and OSA compared to patients without OSA, but more data from well-designed studies are needed to prove this association.

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The Effect of Simulated Obstructive Apnea and Hypopnea on Aortic Diameter and BP

Cited by 33 publications

References 23 publications

The impact of obstructive sleep apnoea on the aorta

The impact of obstructive sleep apnoea on the aorta

Effects of obstructive sleep apnoea on heart rhythm

The Impact of Obstructive Sleep Apnea on Aortic Disease in Marfan's Syndrome

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