Case control study of magnetic resonance image defined subclinical cerebrovascular damage in patients with obstructive sleep apnoea and normal control subjects
Davies CWH., Crosby JH., Mullins RL., Traill ZC., Anslow P., Davies RJO., Stradling JR.
A number of studies have demonstrated a relationship between the clinical syndrome of obstructive sleep apnoea (OSA) and hypertension. There is also an excess of cardiovascular morbidity and mortality in subjects with OSA, but studies examining important clinical endpoints of cardiovascular disease, e.g. left ventricular hypertrophy (LVH) in OSA subjects have produced conflicting results. Cerebral magnetic resonance imaging (MRI) detects clinically silent abnormalities relating to hypertensive cerebrovascular disease, which are seen as small areas of high signal foci in deep white matter (DWM) and lacunae. These lesions are permanent and known to be associated with stroke, age, hypertension, LVH and carotid atherosclerosis. We performed a case control study of cerebral MRI in patients with OSA and closely matched controls. 37 sleep clinic patients with moderate to severe OSA and excessive daytime sleepiness were matched to 37 controls without evidence of OSA on a sleep study. Matched variables included age, body mass index (BMI), alcohol and cigarette consumption, treated hypertension and history of ischaemic heart disease. 24-hour ABP recordings were performed in all subjects, and before treatment in the patients with OSA. All subjects underwent standard sagittal T1 and axial T2 MRI imaging, which were analysed for high signal abnormalities. Lacunae/high signal foci in DWM were present in 15 (40%) OSA subjects and 19 (51%) controls, despite significant increases in mean daytime diastolic blood pressure (5.0mmHg,p<0.05) and nighttime diastolic (7.8mmHg,p<0.001) and systolic blood pressures (11.7mmHg,p<0.05). Subclinical cerebrovascular disease is common in the populations studied - both OSA and matched controls. Despite increased ABP, there is no increase in MRI evident subclinical cerebrovascular disease in OSA.