Sleep apnea has complex role in cardiovascular disease
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CHARLOTTE, N.C. — The link between sleep apnea and cardiovascular disease involves multiple pathways and outcomes, Susan Redline, MD, MPH, Peter C. Farrell Professor of Sleep Medicine at Harvard Medical School, said at SLEEP 2022.
“There are multiple pathways that will lead from the cycle of apnea and recovery to multiple cardiovascular disease [CVD] outcomes, including arrhythmias, stroke, increased IOP, increased heart rate, organ dysfunction, etc.,” she said during the plenary session. “However, that complexity doesn’t even begin to address the variation in disease states that individual patients labeled with sleep apnea have. There are marked differences in microdoses of hypoxia of sleep fragmentation, very different genetics and other background factors that modulate tissue and systemic responses to hypoxia.”
Redline said patients with sleep apnea should not be described in “such an inflexible way,” and that clinicians must identify tools to tailor interventions for meeting these physiologic abnormalities.
“As just one example, we understand hypoxia as a key driver of CVD, but other studies have shown that the effects of hypoxia may be quite different according to the dose,” Redline said. “Mild levels can cause angiogenic response that may reduce the size of heart attack or stroke.
“On the other extreme, with more severe hypoxia, we know there’s endothelial function and cerebral autoregulation,” she continued. “And many of our patients lie in the middle.”
Heterogeneity also exists in clinical presentation, Redline said. Sleep apnea is seen commonly in older adults but also in children and during pregnancy; it occurs in people who are obese, as well as those who are not.
“Clinical variety is further re-emphasized across the spectrum of sleep symptoms,” she said. “One patient may complain of debilitating brain fog, where the same patient at the same AHI [apnea-hypopnea index] will have nothing. It’s not just a multifactorial disease, but multiple diseases.
“When we use the AHI we are in no way beginning to address multiple potential mechanisms, like loop gain, arousal threshold, muscle responsiveness and airway anatomy,” Redline said. “Also, there’s duration and distribution of events. The AHI does not inform about physiological consequences such as sleep fragmentation, hypoxic burden, pressure swings and autonomic cardiovascular responses, all of which may be the pathways leading to CVD.”
Redline said one of her passions is to understand gender disparities, because it appears that the underlying mechanisms of sleep apnea may vary fundamentally between men and women.
“The implications include that women may indeed have CVD markers that differ from men,” she said. “Maybe less hypoxia but more arousal. Women may likely report insomnia and may not be as tolerant to continuous positive airway pressure therapy, because they’re likely to wake up.”
Redline’s research also has uncovered differences based on ancestry.
“We shouldn’t be looking at sleep apnea in isolation but in the context of lifestyle factors that not only influence CVS but also sleep apnea,” Redline said.