Obstructive sleep apnea as a potential risk factor for aortic disease

Abstract

Obstructive sleep apnea (OSA) is not only a cause of hypertension; it also possibly affects the pathogenesis and progression of aortic disease because an inspiratory effort-induced increase in negative intrathoracic pressure generates mechanical stress on the aortic wall. The objective of the present study was to examine the incidence by location of OSA as a complication in patients with aortic aneurysm and patients with aortic dissection (AD). An overnight sleep study was conducted in the following study groups: the aortic disease group (n = 95) consisting of patients with thoracic aortic aneurysm (TAA, n = 32), patients with abdominal aortic aneurysm (AAA, n = 36), and patients with AD (n = 27); and a control group (n = 32), consisting of patients with coronary risk factors who were matched with the aortic disease group for age, gender, and body mass index (BMI). The 3% oxygen desaturation index (ODI) was significantly higher in all the TAA, AAA, and AD groups (P = 0.045, P = 0.003, and P = 0.005, respectively) than in the control group. The incidence of moderate to severe OSA [apnea hypopnea index (AHI) ≥15 events/h] was significantly higher in the first three groups (P = 0.026, P = 0.001, P = 0.003, respectively) than in the control group, while no significant difference was found between the TAA group and the AAA group with respect to these variables. Furthermore, no significant differences were found between the thoracic AD subgroup and the abdominal AD subgroup with respect to AHI and 3% ODI, as well as with respect to the incidences of moderate to severe OSA. Patients with TAA, patients with AAA, and patients with AD showed high incidences of moderate to severe OSA. Although this result suggests that OSA may be one of risks for aortic disease, unelucidated mechanism(s) other than negative intrathoracic pressure may be involved in the pathogenesis of aortic disease.

The impact of obstructive sleep apnoea on the aorta

“…Other studies using indirect measures of OSA (Berlin Questionnaire) reported that about 60% of AAA patients are likely to have OSA [60]. Finally, SARUHARA et al [61] conducted a case-control study where TAA, AAA and AD patients were found to have a higher incidence of moderate to severe OSA (AHI >15 events·h −1 ) than controls. Table 2 summarises studies on the prevalence of OSA among aortic disease patients.…”

“…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.…”

“…Negative intrathoracic pressure changes are also thought to contribute to aortic dilation in patients with Marfan's syndrome [41,43]. Due to the fact that OSA subgroups are evenly distributed among AD, TAA and AAA patients, mechanisms other than solely thoracic ones must play a role in the pathogenesis of aortic disease in general [61].…”

“…Although some studies included in this review have considered inflammation as a potential mechanism, none specifically investigated its impact [44,53,55,56,59,61].…”

“…However, it is important to keep in mind that there are very few observations and high inter-individual variability of both parameters; hence, only a limited group of OSA patients might actually be affected via these mechanisms. Although some clinical studies suggest a common adverse effect of OSA on TAA, AAA and AD [61], one must consider the possibility that the pathophysiology of each disease may differ. This view is encouraged by the fact that TAA, AAA and AD do not share the same risk factors [94].…”