Cerebral hemodynamics is altered in patients with sleep apnea/hypopnea syndrome

According to recent epidemiologic studies, patients with sleep apnea/hypopnea syndrome (SAHS) are at increased risk of cardiovascular diseases, including stroke. However, the mechanisms are not well defined. Nocturnal apneas can trigger acute cerebral ischemia in predisposed patients and impaired vasodilatation is present in SAHS, but few studies have explored vascular cerebral dysfunction and often gave inconclusive results. The aims of our study were to assess whether patients with SAHS have impairment of cerebral hemodynamics with respect to controls, and to investigate a possible relationship with clinical data. We studied two groups, one of 76 SAHS patients and another one of 76 non-SAHS subjects matched for age, sex and main cardiovascular risk factors. All participants underwent a daytime transcranial Doppler study of right middle cerebral artery to record cerebral blood flow velocity and cerebrovascular reactivity by means of breath-holding test (BHT). SAHS patients have a reduction in mean cerebral blood flow velocity (MFV) (52 ± 9 vs 60 ± 12 cms/s, p < 0.001) and BHT (31 ± 12 vs 36 ± 11 %, p = 0.005) when compared to non-SAHS controls. Moreover, MFV correlated negatively with the presence of coronary disease, and BHT with female sex and arterial pressure. On the other hand, in the SAHS group, MFV correlated negatively with oxygen desaturation severity. Patients with SAHS have impaired MFV and cerebrovascular reactivity when compared to controls. Interestingly, poorly controlled or unknown hypertension and severe nocturnal hypoxemia caused additional cerebral hemodynamic disturbances to these patients.