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Cerebrovascular reactivity and neurovascular coupling in patients with obstructive sleep apnea.
International Journal of Neuroscience 2017 January
AIM: Obstructive sleep apnea syndrome (OSAS) has been implicated as an independent risk factor for stroke. There are data suggesting the presence of lower cerebrovascular reactivity (CVR) as determined by transcranial Doppler (TCD) in patients with OSAS. We concurrently investigated neurovascular coupling (NVC) with visual stimulation, and CVR using breath-holding (BH) test on TCD in patients with OSAS.
MATERIALS AND METHODS: Data were collected in 49 patients with moderate to severe OSAS, and compared to 15 healthy subjects matched for age and risk factors. The CVR to hypercapnia was measured by BH test, and the NVC was performed with visual stimulation.
RESULTS: There were no significant differences in baseline characteristics of patients and controls, except for BMI, which was significantly higher in patients with OSAS (p = 0.036). OSAS patients showed significantly lower reactivity during BH in comparison to controls (36.9% ± 14.0% vs. 46.6% ± 20.1%; p = 0.019). The reactivity time was also significantly shorter in the OSAS group (8.0 ± 4.2 s) when compared to controls (10.1 ± 4.3 s; p = 0.015). The visual stimulation produced similar reactivity in patients (27.7% ± 9.4%) and controls (29.1 ± 13.9; p > 0.05).
CONCLUSIONS: Our data demonstrate a diminished vasodilator response capacity only to a strong stimulator such as hypercapnia in OSAS patients. However, the NVC, as shown by the TCD, is quite normal, suggesting that a weak or mild stimulation produces a proper reactivity among OSAS patients.
MATERIALS AND METHODS: Data were collected in 49 patients with moderate to severe OSAS, and compared to 15 healthy subjects matched for age and risk factors. The CVR to hypercapnia was measured by BH test, and the NVC was performed with visual stimulation.
RESULTS: There were no significant differences in baseline characteristics of patients and controls, except for BMI, which was significantly higher in patients with OSAS (p = 0.036). OSAS patients showed significantly lower reactivity during BH in comparison to controls (36.9% ± 14.0% vs. 46.6% ± 20.1%; p = 0.019). The reactivity time was also significantly shorter in the OSAS group (8.0 ± 4.2 s) when compared to controls (10.1 ± 4.3 s; p = 0.015). The visual stimulation produced similar reactivity in patients (27.7% ± 9.4%) and controls (29.1 ± 13.9; p > 0.05).
CONCLUSIONS: Our data demonstrate a diminished vasodilator response capacity only to a strong stimulator such as hypercapnia in OSAS patients. However, the NVC, as shown by the TCD, is quite normal, suggesting that a weak or mild stimulation produces a proper reactivity among OSAS patients.
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