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. 2012 Aug;1(4):e000091.
doi: 10.1161/JAHA.111.000091. Epub 2012 Aug 24.

Cerebrovascular consequences of obstructive sleep apnea

David J Durgan  1 , Robert M Bryan Jr
Affiliations

Cerebrovascular consequences of obstructive sleep apnea

David J Durgan et al. J Am Heart Assoc. 2012 Aug.
No abstract available

Keywords: cerebrovascular circulation; cerebrovascular disease; dementia; ischemic attack, transient; sleep apnea syndromes; sleep apnea, obstructive; stroke.

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Figures

Figure 1.
Figure 1.
The effects of OSA lead to a pathological cascade that is responsible for cerebrovascular and other cardiovascular diseases. Adapted from Somers et al.
Figure 2.
Figure 2.
Incidence of vascular events over an 18-month period after stroke in CPAP users (n=15) and those who discontinued the use of CPAP (n=36). All patients in the study had an AHI ≥20. *P=0.03. Created with data from Martinez-Garcia et al.
Figure 3.
Figure 3.
Changes in blood flow velocity in the middle cerebral artery (CBFV; top) and mean arterial blood pressure (MABP; bottom) during an episode of apnea (shaded in light blue). Created with data from Klingelhofer et al.
Figure 4.
Figure 4.
Resistances to blood flow through the middle cerebral artery in control subjects (n=26) and patients with OSA (n=78) after an orthostatic hypotension challenge, obtained by having individuals stand from a squatting position. The patients with OSA had a mean AHI of 78. The resistance was calculated by dividing mean arterial blood pressure (MABP) by blood flow velocity in the middle cerebral artery (CBFV). The increased resistance in the patients with OSA during orthostatic hypotension indicates that autoregulatory mechanisms responsible for dilating cerebral arteries were impaired relative to the control subjects. The response of the cerebral circulation to the hypotensive challenge was less dynamic in patients with OSA during the initial phase of the hypotensive challenge. That is, the rate of change in resistance in patients with OSA was only 62% of that in control subjects (100×[−0.13/−0.21]). Created with data from Urbano et al.
Figure 5.
Figure 5.
Proposed pathway for activation of NADPH oxidase, generation of superoxide, and upregulation of the endothelin system in the peripheral circulation after OSA and chronic intermittent hypoxia (black lines). An alternative pathway that could be responsible for generation of superoxide in the cerebral circulation (red lines). Dashed red lines (and “?”), which lack any experimental evidence, represent hypothetical pathways. HIF indicates hypoxia inducible factor.
Figure 6.
Figure 6.
A, The effects of 35 days of chronic intermittent hypoxia (CIH) on increases in laser Doppler perfusion (CBF) in the sensory cortex accompanying whisker stimulation. Sham mice were not exposed to CIH. A, In wild-type mice (WT) and mice lacking NADPH oxidase-2 (NOX2−/−). B, After administration of vehicle (Veh), a peptide inhibitor of NADPH oxidase (PI), or a scrambled control peptide (SC). *P<0.05. Created with data from Capone et al.
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References

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