Impact of Sleep Apnea on Retinal Microvasculature

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Obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) are both associated with high blood pressure, which con­tributes to small vessel narrowing and microvascular retinopathy. However, the effects of OSA alone on the retinal microvasculature remain unclear because approximately one in three people with OSA also have COPD.

Researchers from the University of Melbourne in Australia investigated the alterations in retinal microvasculature in patients with OSA or COPD alone, excluding those who had both condi­tions.¹ They found that OSA affected the blood vessels throughout the body, causing blood vessel narrowing. Addi­tionally, patients with OSA had higher blood pressure than did those with COPD, despite being younger in age.

“Although OSA and COPD often coexist, OSA causes hypertension on its own,” said coauthor Judy Savige, MBA, PhD, at the University of Melbourne. “OSA often occurs in young adults, increasing the risk of heart disease, stroke, and diabetic retinopathy. Our findings highlight the importance of treating the underlying hypertension by managing OSA through weight control and con­tinuous positive airway pressure.”

RETINOPATHY. Retinal images showing (1) mild and (2) moderate microvascular retinopathy in patients with obstructive sleep apnea. Arteriovenous or microvascular nicking (black arrows) and hemorrhage (white arrow) are evident.

Study design. To evaluate the effects of OSA on the retinal microvasculature, the team reviewed the medical history and retinal photographs of patients with OSA alone (n = 79), COPD alone (n = 132), or a control group of hospi­talized patients with neither condition (n = 143). “Our hypothesis was that people with OSA and COPD would have hypertension. However, we did not know if OSA alone would cause hypertension or if changes in the mi­crovasculature would be worse in OSA than in COPD,” said Dr. Savige.

Results. When compared with con­trols, people with OSA had significantly higher mean arterial pressure (93.2 ± 12.2 mm Hg vs. 89.2 ± 8.9 mm Hg; p = .02), narrower retinal arterioles (134.2 ± 15.9 μm vs. 148.0 ± 16.2 μm; p < .01), and higher prevalence of retinopa­thy (97% vs. 50%; p < .001).

When compared with individuals with COPD, people with OSA still had higher mean arterial pressure (93.2 ± 12.2 mm Hg vs. 89.7 ± 12.8 mm Hg; p = .07), narrower arterioles (134.2 ± 15.9 μm vs. 152.3 ± 16.8 μm; p < .01), and a higher prevalence of microvas­cular retinopathy (97% vs. 80%; p = .001).

The nocturnal challenge. The findings indicate a disparity between diagnosed hypertension, blood pressure readings taken in the clinic, and the occurrence of retinal microvascular changes. This may be because OSA-associated hypertension is primarily nocturnal and thus difficult to assess, Dr. Savige noted.

Looking ahead. “Our next steps are to assess the effects of OSA treatment methods and weight loss on micro­vascular retinopathy by measuring the changes in vessel caliber and blood pressure,” Dr. Savige said.

Reflecting on the implications of their findings, Dr. Savige said that physicians need to change the way they measure hypertension in the clinic. As microvascular retinopathy reflects poor blood pressure control over several months, it actually provides a more accurate picture of hypertension than even 24-hour blood pressure monitor­ing, she said.

—Christos Evangelou, PhD

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1 Chew S et al. Sci Rep. 2022:12(1):13350.

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Relevant financial disclosures: Dr. Savige—None.

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