OSAHS impairs coronary microvascular function in patients with hypertension

10 giờ trước
Stephen Padilla
Stephen PadillaSenior Editor; MIMS
Stephen Padilla
Stephen Padilla Senior Editor; MIMS
OSAHS impairs coronary microvascular function in patients with hypertension

Patients with hypertension and co-existing moderate-to-severe obstructive sleep apnoea‒hypopnoea syndrome (OSAHS) are susceptible to more severe coronary microvascular dysfunction and elevated levels of inflammatory markers, suggests a study.

“[T]he detrimental effect of OSAHS on coronary microcirculatory function in hypertensive patients is markedly severity–dependent,” the investigators said. “Moderate-to-severe OSAHS significantly impairs coronary microvascular function, whereas the deleterious effect of mild OSAHS is comparatively limited.”

Eighty-seven patients underwent cardiac stress echocardiography, and 376 submitted themselves to angiography-derived microvascular resistance (AMR) assessment based on quantitative flow ratio (QFR) technology. All participants completed portable sleep monitoring.

Using the monitoring results and hypertension history, the investigators categorized patients into the following groups: control, hypertension alone, OSAHS alone, hypertension with mild OSAHS, and hypertension with moderate-to-severe OSAHS. They also compared parameters including sleep monitoring data, coronary flow velocity reserve (CFVR), AMR, high-sensitivity C-reactive protein (hs-CRP), and interleukin-6 (IL-6) across groups.

Finally, the impact of these groupings on coronary microvascular dysfunction was explored through multivariable logistic regression analysis.

Patients with hypertension and moderate-to-severe OSAHS had significantly reduced CFVR (p<0.05) and substantially increased left anterior descending artery (LAD) AMR, hs-CRP, and IL-6 levels compared with the other groups (p<0.05). [J Hypertens 2026;44:1547-1555]

In multivariable analysis, hypertension with moderate-to-severe OSAHS independently correlated with both lower CFVR (odds ratio [OR], 6.06, 95 percent confidence interval [CI], 2.87‒12.78) and higher LAD-AMR (OR, 5.60, 95 percent CI, 4.10‒7.10).

Chronic inflammation

“The underlying mechanism may be attributed to the chronic intermittent hypoxia and nocturnal arousals induced by moderate-to-severe OSAHS, which activate oxidative stress and systemic inflammation, leading to the release of abundant reactive oxygen species and inflammatory factors,” according to the investigators.

“These processes directly damage the vascular endothelium, reduce nitric oxide bioavailability, and ultimately impair vasodilatory function,” they added. [Clin Otolaryngol 2019;44:412-415]

At the same time, both hypoxia and hypercapnia stimulate the sympathetic nervous system. This results in nocturnal hypertension, sustained vasoconstriction, and vascular modelling, worsening microcirculatory impairment. [J Brasil Pneumol 2023;49:e20220314]

Results from the 2021 study by Yoshitaka and colleagues in patients with acute myocardial infarction are consistent with the findings of the current study. [Eur Heart J Acute Cardiovasc Care 2021;10:645-652]

“Furthermore, our study found no statistically significant differences in CFVR or AMR values between the hypertension with mild OSAHS group and either the hypertension-only or OSAHS-only groups,” the investigators said.

“This indicates that the detrimental effect of OSAHS on the coronary microcirculation in hypertensive patients is not an ‘all-or-nothing’ phenomenon but rather follows a dose-response relationship with disease severity,” they added.

Mild OSAHS also involves intermittent hypoxia and sleep fragmentation, but its frequency and depth of desaturation may not reach the threshold required to induce detectable changes in coronary microvascular function, according to the investigators, noting the gradual progression of microvascular endothelial dysfunction and structural remodelling. [J Clin Med 2021;10:277]

“The pathological stimulus intensity provided by mild OSAHS might be insufficient to produce an additional synergistic worsening effect atop the pre-existing microvascular injury associated with hypertension,” the investigators said.

“Future prospective cohort studies are warranted to validate the causal relationship between OSAHS and coronary microvascular dysfunction in hypertensive patients and to investigate its long-term effects on the coronary microcirculation,” they added.