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Could CPAP prevent aortic aneurysm rupture?

Reuters Health • The Doctor's Channel Daily Newscast

NEW YORK (Reuters Health) – Perturbed sleep and high blood pressure aren’t the only consequences of obstructive sleep apnea (OSA).

New data suggest that OSA is common in people with abdominal aortic aneurysm (AAA), and that severe OSA may be a risk factor for AAA rupture. Researchers therefore speculate that its treatment with continuous positive airway pressure could lower that risk.

“Animal studies and work conducted … in patients with Marfan’s syndrome suggest that OSA may be a risk factor for development and progression of thoracic aortic aneurysms,” Dr. Rebecca H. Mason from Churchill Hospital, Oxford, U.K., told Reuters Health in email. Her research team wondered if OSA affects AAAs the same way.

They used the ApneaLinK (ResMed, MAP Medicine Technology), which records nasal respiratory pressure, snoring sounds, and finger oximetry, to evaluate sleep in 127 subjects (ages 43 to 75, mean 68) in an AAA surveillance program.

According to their article in the American Journal of Respiratory and Critical care Medicine, published online July 9th, more than 40% of subjects had an apnea-hypoxia index (AHI) and an oxygen desaturation index (ODI) > 10. [

Based on published research, “It appears that the prevalence of OSA in patients with AAA is higher than in a comparable normal population,” Dr. Mason said. In people of similar age and body mass index, the prevalence of an ODI >/= 10 was 8%, while that for an AHI >/=15 was 19%, versus 29% in this study.

However, the patients were asymptomatic, as “the vast majority” had a normal Epworth Sleepiness Score, which did not correlate with either AHI or ODI.

The authors used ultrasound to measure AAA diameter change over a median interval of 18 months. Median AAA expansion was 2.9 mm/y for an ODI > 30, significantly greater than the 1.0 to 1.3 mm/year expansion associated with lower ODIs.

In multivariate analyses controlled for cardiovascular risk factors and medications, both an ODI and an AHI > 30/h were significantly associated with higher AAA expansion rates compared with less affected subjects.

According to Dr. Mason, OSA appears to exert a threshold effect. “It may be that only the more pronounced and frequent intrathoracic pressure swings and sympathetic bursts (with resultant rises in blood pressure) lead to irreversible changes in aortic diameter.” Another mechanism may involve the recurrent intermittent hypoxia that “increases oxidative stress, endothelial dysfunction and vascular inflammation.”

The researchers suggest a controlled interventional trial to see if continuous positive airway pressure could attenuate AAA expansion in patients with severe OSA.

However, Dr. Frank A. Lederle, director of the Minneapolis VA Center for Epidemiological and Clinical Research, is skeptical of their conclusions.

“It is often problematic to define a ‘disease’ as a test value in an asymptomatic person,” he told Reuters Health in email. “In this study there was no control group, so… their statement that 40% ‘seems’ high is about all you can say.”

He found the data far from convincing for the association between severe OSA and AAA expansion. “The multivariate model with 13 predictors is probably overfit, i.e., too many predictors for the size of the study. You would need to see these results validated in another population before concluding it was more than a quirk.”

He noted that before any organization would approve a grant for an interventional trial, they would require larger studies as well as some evidence that OSA treatment could slow AAA expansion.

“Some third factor could be causing both phenomena, so fixing one might not fix the other,” Dr. Lederle said. He was not involved in the research.

Reference:

Obstructive Sleep Apnea in Patients with Abdominal Aortic Aneurysms: Highly Prevalent and Associated with Aneurysm Expansion

Am J Respir Crit Care Med 2010.