Vascular responses to hypoxia are not impaired in obstructive sleep apnoea patients free of overt cardiovascular disease

New Findings

What is the central question of this study?

Does treatment of obstructive sleep apnoea (OSA) with nocturnal oxygen or continuous positive airway pressure (CPAP) improve hypoxic vascular responses, which are reportedly impaired in OSA?

What is the main finding and its importance?

Cerebrovascular and cardiovascular hypoxic responses were not impaired in OSA patients free of overt cardiovascular disease and known risk factors, and were not altered by nocturnal oxygen or CPAP treatment. We conclude that this OSA patient phenotype has normal vascular responses to hypoxia and are unlikely to obtain long term cardiovascular benefits from nocturnal oxygen or CPAP therapy.

Abstract

Cerebral blood flow (CBF) and cardiovascular responses to hypoxia are reportedly impaired in obstructive sleep apnoea (OSA) patients and corrected by continuous positive airway pressure (CPAP); beneficial effects that are ascribed to correction of OSA‐related intermittent hypoxia (IH). However, CPAP corrects both IH and ancillary OSA features (i.e., intermittent hypercapnia, sympathetic activation, blood pressure surges, negative intrathoracic pressure swings and sleep fragmentation). Whether correction of these ancillary OSA features contribute to CPAP's beneficial effects on vascular hypoxic responses is unknown. Nocturnal oxygen corrects OSA‐induced IH, but apnoeas and ancillary features persist. Thus, we examined the effects of nocturnal oxygen and CPAP on cerebrovascular and cardiovascular hypoxic responses in untreated OSA patients. Responses were assessed in 52 OSA patients free of overt cardiovascular disease and known risk factors at baseline, after 2‐weeks of nocturnal oxygen (n = 26) or no treatment (n = 26), and after ∼4‐weeks of CPAP treatment (n = 40). Twenty‐two age‐matched controls were assessed at baseline and follow‐up visits. Resting, isocapnic‐euoxia mean blood pressure was decreased following nocturnal oxygen (‐3.6 ± 6.0 mmHg; p = 0.006) and CPAP (‐4.5 ± 7.5 mmHg; p < 0.001) while cerebrovascular conductance was increased with CPAP (p = 0.001). However, these changes were not different from controls. Unexpectedly, OSA patients and controls had similar hypoxic vascular responses at baseline that were not changed by either nocturnal oxygen or CPAP. We conclude that, OSA patients free of overt cardiovascular disease and known risk factors did not have impaired cerebrovascular or cardiovascular responses to hypoxia and are unlikely to obtain long term cardiovascular benefits from nocturnal oxygen or CPAP therapy.

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