Impaired cerebrovascular reactivity in obstructive sleep apnea: a case-control study

Obstructive sleep apnea (OSA) is an independent risk factor for stroke. Little is known about the cerebrovascular hemodynamic changes during apnea. Hypercapnia occurs in apneas and hypopneas, and a reduced cerebral vasodilatory response to CO₂ could compromise the cerebral blood flow (CBF). Therefore, we aimed to evaluate whether the apnea-hypopnea index (AHI) affected the cerebrovascular response to CO₂.

A total of 11 patients with OSA were compared to 16 controls. We assessed the cerebrovascular responses with arterial spin labeling (ASL) and blood oxygen level-dependent (BOLD) magnetic resonance imaging during hypercapnia or breath-holding tasks.

The CBF response to CO₂ was impaired with increasing AHI (average CBF: p = 0.018; gray matter: p = 0.038; white matter: p = 0.045), that is, increased OSA severity. When comparing the OSA patients to the control subjects, the OSA patients had a significantly reduced CO₂ response of the white matter CBF (p = 0.04). However, the BOLD response to CO₂ and the breath-holding task did not show any significant differences between OSA patients and control subjects.

The cerebrovascular CO₂ reactivity, measured by the CBF, was impaired with increasing AHI, that is, OSA severity. These findings may add to the understanding of the increased stroke risk found in OSA patients.