高血压可能是由阻塞性睡眠呼吸暂停(OSA)引起的,现在在国际指南中得到认可[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 [5–8]。OSA是高血压的公认原因,应在任何具有高血压的患者中考虑,特别是在具有抗性高血压的患者中[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.]。
连接睡眠呼吸暂停和高血压的机制已被广泛审查[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.]。在后一种型号模型中,值得注意的是,在夜间间歇性缺氧不会产生血压立即增加,可能是由于血液抑制因响应间歇性缺氧而抵消交感神经激活的影响[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 still tending to persist after 5 days of intermittent hypoxia exposure withdrawal [15.]。Blood pressure lowering response to continuous positive airway pressure (CPAP) treatment appears to be dependent on sleep apnoea severity [16.–18.]。困倦在预测血压下的CPAP相关降低方面是否重要是迄今为止的争论[18.–20],但可能不太可能[21]。In any case, the reduction in blood pressure obtained when treating OSA seems relatively limited [18.,21,22]并且远远少于先前在早期的研究中报道的[17.], even when including only hypertensive patients [21,22]。More recently, however, it has been clearly demonstrated that a reduction in blood pressure, as well as a reduced incidence of hypertension, cannot be achieved unless a minimum of 4–6 h of CPAP usage is achieved [8,23]。
In this issue of the欧洲呼吸杂志,P.arati.et al. [24]报告由参加OSA的欧洲联盟成本(科技研究)行动B26的欧盟成本(在科技研究)行动B26的专家小组执行的工作,以欧洲呼吸协会(ERS)和欧洲高血压学会(ESH)的认可。188bet官网地址这组专家在2005年至2010年期间,在睡眠呼吸暂停和心血管疾病领域的一些建议[3,25],OSA管理[26], and driving [27,28]。由于OSA现在是一个公认的高血压原因,包括呼吸师,睡眠专家和心脏病学家,认为需要审查目前的知识并提出对临床医生和研究人员的建议。重要的是,这个立场文件不仅是由两个有关科学社团的认可,i.e.ESH和ESE,但也是联合发表的[24,25]。
该文件旨在解决流行病学,病理生理学,诊断程序和治疗方案中的现有技术,以获得心血管患者OSA的最佳管理,以及在OSA患者中管理动脉高血压。该建议具有提醒心血管专家的目标,以考虑高血压患者睡眠相关的呼吸障碍,以及睡眠和呼吸医生,以考虑睡眠相关呼吸障碍患者的高血压发生。我们认为,这项合作工作提供了一个非常有价值的知识体系,这强调需要不断更新当前的国家和国际对这些高度普遍障碍之间的关系的指导方针。
Footnotes
Statement of Interest
None declared.
- ©ers 2013.