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

Abstract

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 is 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.

Nocturnal oxygen therapy in obstructive sleep apnoea: a systematic review and meta-analysis

“…Both office and home blood pressure measurements were reported in one study [ 16 ], another study reported ambulatory blood pressure and 24-h mean blood pressure measurement [ 13 ], and the remaining studies reported office blood pressure only. Change in blood pressure following intervention was reported in two studies [ 15 , 16 ] and calculated for four more studies [ 11 – 13 , 17 ] from mean differences and pooled sd s.…”

“…1295 papers were identified with the primary literature search (figure 1). After abstract and full-text review, nine studies with a total of 502 participants were included in the analysis [11][12][13][14][15][16][17][18][19]. No study was excluded based on the risk of bias assessment (table 1).…”

“…The effect of NOT on blood pressure Eight studies reported post-intervention blood pressure (figure 4) [11][12][13][15][16][17][18][19]. Both office and home blood pressure measurements were reported in one study [16], another study reported ambulatory blood pressure and 24-h mean blood pressure measurement [13], and the remaining studies reported office blood pressure only.…”

Hypoxia signaling in human health and diseases: implications and prospects for therapeutics

“…342 The occurrence and development of cardiovascular diseases can be induced by sympathetic excitation disorder, oxidative stress, inflammatory response, endothelial injury, abnormal glucose, and lipid metabolism caused by hypoxia. [343][344][345][346] HIF-1α is the primary controller of physiological and pathological hypoxia and is widely expressed in cardiovascular diseases. 141,216,347 Almost all genes related to hypoxia, including glucose transporter (GLUT), VEGF, glycolytic enzymes, cell survival factors, and cell surface receptors, are directly or indirectly regulated by HIF-1.…”

Relationships between obstructive sleep apnea syndrome and cardiovascular risk factors

“…Действительно, как показали A.E. Beaudin [55] и соавт., у больных с СОАС без диагностированных ССЗ и факторов риска со средним индексом массы тела 27-31 кг/м 2 не наблюдается долгосрочного положительного эффекта при СИПАП-терапии, но этих пациентов отличает нормальная сосудистая реакция на гипоксию. У коморбидных пациентов последствия СОАС без специфической терапии могут быть тяжелыми.…”