Is sleep apnea-hypopnea index relevant for impaired brain perfusion and desaturation in patients with severe obstructive sleep apnea syndromes?

Background Obstructive sleep apnea syndrome (OSAS) is a common sleep disorder with the prevalence of 9-38% in the general population. Severe OSAS defined as apnea-hypopnea index (AHI) ≥ 30/h is a major risk factor for developing cerebro-cardiovascular diseases like stroke. Treatments such as continuous positive airway pressure (CPAP) therapy are recommended for those patients because untreated OSA can cause tremendous medical expenses and economic burden. Understanding the mechanisms of how repetitive sleep apneas/hypopneas induce changes in cerebral hemodynamics in severe OSAS is crucial for the understanding of disease severity, disease progression in brain damage and the treatment efficacy. However, these mechanisms and the association between AHI and the induced changes in cerebral hemodynamics in severe OSAS are essentially unknown. Using a stepwise incremental CPAP titration protocol we aim to identify the most relevant physiological factors including AHI and their quantitative contributions to cerebral hemodynamic changes before and during CPAP treatment in severe OSAS patients. Methods and findings 29 newly diagnosed severe OSAS patients underwent incremental CPAP titration during polysomnography recordings: 1-h sleep without CPAP served as self-controlled baseline followed by stepwise increments of 1-cmH2O pressure per-hour starting from 5-8 cmH2O individually. Frequency-domain near-infrared spectroscopy measured the changes in blood volume (BV) and oxygen saturation (StO2) in the left forehead. The coefficients of variation of BV (CV-BV) and the decreases of StO2 (de-StO2) during more than 2000 respiratory events were predicted by various predictors including AHI using linear mixed-effect models, respectively. The best predictors were automatically selected by stepwise regression. Surprisingly, AHI was excluded from the final selected models. Longer events and apneas rather than hypopneas induce larger changes in CV-BV and stronger cerebral desaturation. Respiratory events occurring during higher baseline StO2 before their onsets, during rapid-eye-movement sleep and those associated with higher heart rate (HR) during the events trigger smaller changes in CV-BV and de-StO2. CPAP pressures attenuate the changes in CV-BV and de-StO2. Conclusions In severe OSAS the length and the type of respiratory event rather than widely used AHI may be better parameters to indicate the severity of cerebral vascular damage. Thus both, length and type of respiratory events should be considered as predictors of cerebro-cardiovascular events in future epidemiological studies and in clinical practice. OSAS patients with profound long apnea events need to pay special attention and quickly treated with CPAP therapy as it can restore the induced cerebral hemodynamic changes.