Frequency of plaques was much higher in patients with obstructive sleep apnea.
Obstructive sleep apnea has been linked with cardiovascular disease, but it also may be linked with the deadliest type of coronary artery plaque, a small study suggests.
Of patients with obstructive sleep apnea (OSA), 63 percent had noncalcified or mixed plaques compared with 16 percent of those without OSA, according to Sunil Sharma, MD, of East Carolina University in Greenville, N.C., and colleagues.
“The broad confidence interval was most likely due to small sample size, but we cannot rule out the effect of unobserved confounding factors,” researchers noted.
However, Sharma told MedPage Today that the investigators “felt comfortable” with their unique finding regarding more soft plaque in those with OSA because of similar findings linking hard, calcified plaques with OSA.
“We know that hard plaques don’t cause acute events. So we wanted to see if those with sleep-disordered breathing had a higher prevalence of soft plaque,” Sharma said.
Despite the known connection between sleep apnea and cardiovascular disease, data are limited on whether OSA “causes or accelerates the process of atherosclerosis and plaque formations.”
And data are similarly lacking on exactly what type of plaque is most prevalent in those with OSA.
To categorize plaque type, researchers retrospectively reviewed the cardiac CT images of 81 patients who were part of a larger radiology study at the Medical University of South Carolina in Charleston involving emergency room patients with acute chest pain.
All patients had undergone a gold-standard polysomnography test within the prior 3 years of the CT scan, and 51 had OSA.
Baseline characteristics were similar between patients with and without OSA, except in three categories: age, race, and past smoking.
Besides there being an overall strong association of OSA with noncalcified/mixed plaques, the severity of OSA was linearly associated with soft plaques, but the confidence intervals were wide.
This pattern repeated itself when researchers evaluated patients for multivessel disease and stenosis severity. Again, however, the confidence intervals were very wide.
Significantly more patients with OSA had multiple coronary artery involvement (85.7 percent versus 34.5 percent), which correlated linearly with the severity of apnea.
Also, more patients with OSA had significantly higher severity of stenosis (22.5 percent versus 6 percent), and the severity of artery stenosis correlated with the severity of OSA (7.7 percent with multivessel disease had mild OSA compared with 24 percent with severe OSA).
“These findings tend to suggest that sleep-disordered breathing accelerates the process of atherosclerosis,” Sharma told MedPage Today.
However, the results should be confirmed in larger, randomized studies, he said.
There is speculation that OSA might actually influence the duration of soft plaques, meaning that they stay in a soft stage longer than usual, Sharma said. “But this is mere speculation at this point,” he said.
The next steps include determining what impact the higher prevalence of soft plaques has on outcomes and evaluating whether the use of continuous positive airway pressure (CPAP) therapy could make these vulnerable plaques more stable.
There is evidence from carotid ultrasound studies that CPAP therapy is associated with a reduced level of plaque, Sharma said.
Limitations of the current study include its retrospective nature, small number of patients, potential referral bias, and not having data on compliance with CPAP therapy.
By Chris Kaiser
MAY