Sleeping Beauty or the Beast? – The Metabolic Syndrome from an Obstructive Sleep Apnoea Perspective

Abstract

Obstructive sleep apnoea (OSA) is a significant health issue. Patients with cardiovascular disease as well as patients with diabetes have a high prevalence of OSA, and the prevalence of coronary heart disease, heart failure, stroke and diabetes is increased in patients with obstructive sleep apnoea. Physiological responses to OSA include sympathetic activation, neurohumoral changes and inflammation, all of which are precursors for cardiovascular disease and diabetes. International guidelines are starting to recognise the importance of OSA for patients with cardiovascular conditions such as heart failure and hypertension. Diagnosis is important, and home-based sleep testing devices can facilitate this process. Treating OSA with continuous positive airway pressure (CPAP) has been shown to reduce blood pressure (BP) in patients with hypertension, but more research is needed to determine which components of the metabolic syndrome respond best to the addition of CPAP therapy.

MRI evaluation of cerebral metabolic rate of oxygen (CMRO2) in obstructive sleep apnea

“…4 Some studies have demonstrated an association of intermittent nocturnal hypoxemia and hypercapnia with a greater propensity of hypertension, stroke, cardiovascular disease and type-2 diabetes. 5–7 Among neurologic findings in OSA patients is neuronal loss in the hippocampus and frontal cortex. These structural changes have been associated with a decline of memory and executive function, findings that have been attributed to intermittent hypoxia.…”

MRI evaluation of cerebrovascular reactivity in obstructive sleep apnea

“…3,4 The intermittent nocturnal hypoxemia and hypercapnia, and the resulting periodic episodes of oxygen desaturation and reoxygenation, have been causally associated with a greater propensity of stroke, hypertension, cardiovascular diseases and type-2 diabetes. [4][5][6][7] Cerebral blood flow (CBF) is tightly regulated (cerebral autoregulation) to maintain constancy of cerebral perfusion in response to variations in systemic blood pressure (mechanoregulation) and carbon dioxide (CO 2 ) concentration (chemoregulation). 8 In healthy subjects performing voluntary breath holding, the normal mechanism in response to hypercapnia is dilation of the brain's blood vessels, resulting in increased CBF.…”

“…8 In healthy subjects performing voluntary breath holding, the normal mechanism in response to hypercapnia is dilation of the brain's blood vessels, resulting in increased CBF. 9,10 In patients with OSA, chronic cyclical hypoxia is thought to result in impaired vascular reactivity due to oxidative stress 6,11,12 causing depletion of vasodilatory nitric oxide. 13 Cerebrovascular reactivity (CVR), the temporal change in CBF in response to a vasoactive stimulus, is an index of the capacity of cerebral vessels to respond to a vasoactive stimulus.…”