Sleep apnoea and hypertension: time for recommendations

Abstract

H ypertension can be caused by obstructive sleep apnoea (OSA), as now recognised in international guidelines [1,2]. The relationship between OSA and hypertension is well established, which has important consequences for the cardiovascular system [3,4]. Many studies have shown an increase in the incidence and prevalence of hypertension in patients with OSA, independent of confounding factors, such as anthropometric parameters, alcohol consumption and smoking [5][6][7][8]. OSA is a recognised cause of hypertension that should be considered in any patient with high blood pressure, particularly in those with resistant hypertension [1,2]. More than 50% of patients with OSA are hypertensive [7,9] and more than 80% of patients with resistant hypertension also have OSA [10]. Hypertension related to OSA is predominantly nocturnal with a frequent non-dipper profile (which corresponds to a limited fall in nocturnal blood pressure) and an increase in diastolic blood pressure in the majority of patients [9,11].The mechanisms linking sleep apnoea and hypertension have been extensively reviewed [3,4,12]. There is increased sympathetic activity, which has been demonstrated in patients with OSA using sympathetic micro-neurography of the nerves supplying muscles, and also using plasma and urinary catecholamine assays. Potential mechanisms contributing to OSA-related hypertension include endothelial dysfunction leading to inhibition of nitric oxide production, decreased vasodilatation, and increased vasoconstriction; systemic inflammation, which favours endothelial dysfunction; oxidative stress, which results in the production of reactive oxygen species and causes vasoconstriction as a result of nitric oxide synthase blockade, increased generation of endothelin-1, and activation of angiotensin II; activation of the renin-angiotensin-aldosterone system, which increases plasma aldosterone levels; and metabolic anomalies leading to hyperinsulinism and resistance to the metabolic effects of leptin, the adipocyte-derived hormone. Activation of the endothelin system results in vasoconstriction and depressed baroreflexes. A genetic contribution to the association between OSA and hypertension might also exist, but there is currently only a limited amount of data available to support this possibility. Although not fully understood, the role of hypoxia in promoting an increase in blood pressure appears prominent, as evidenced both in animal models [13] and more recently in a model developed in normal volunteers [14,15]. In this latter model, it is notable that intermittent hypoxia during the night did not produce an immediate increase in blood pressure, presumably due to vasodilation occurring in response to intermittent hypoxia counteracting the effects of sympathetic activation [15]. However, there was a sustained increase in sympathetic activity that seems to be responsible for the daytime increase in blood pressure observed in these subjects after only one night of intermittent hypoxia, which is more pronounced after 13 nights, and stil...

Obstructive sleep apnea: transition from pathophysiology to an integrative disease model

“…Continuous PAP therapy reduces BP, especially in younger subjects and those with uncontrolled hypertension or severe oxygen desaturation (Pengo et al, 2020), and in more CPAP-compliant patients (Levy & McNicholas, 2013). CPAP may also restore the nocturnal dipping pattern in normotensive patients with OSA (Crinion et al, 2021;Sapina-Beltran et al, 2019).…”

The quality and characteristics of sleep of hypertensive patients

“…Another disease with high morbidity in the population is the Obstructive Sleep Apnea Syndrome (OSAS), and it is estimated that approximately 40% of hypertensive patients and 80% of those with resistant hypertension have OSAS (8)(9) and about 55% individuals with OSAS have hypertension (10) .…”

Bidirectional relationships of comorbidity with obstructive sleep apnoea

“…While many studies indicate a reduction in BP with CPAP therapy, the effect is small at 2 mmHg in 24 h mean BP [45], although greater in younger subjects and those with uncontrolled hypertension or severe oxygen desaturation [46], and in more CPAP-compliant patients [47].…”