From Resistant Airway to Resistant Hypertension.

From Resistant Airway to Resistant Hypertension.
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从抵抗气道到抵抗性高血压。

DOI:
10.1161/circulationaha.118.038591
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发表时间:
2019
期刊:
影响因子:
37.8
通讯作者:
Somers,VirendK
Somers,VirendK
中科院分区:
医学1区
文献类型:
--
作者:
Covassin,Naima;Somers,VirendK

文献摘要

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高血压是黑人心血管风险增加的重要因素,在黑人中比白人更常见,也更严重。尽管进行了更强化的治疗,但只有48%的治疗黑人达到了血压(BP)目标。1黑人表现出更多的顽固性高血压,伴随着异常的昼夜血压模式和更多的压力相关并发症和靶器官损伤。顽固性高血压的一个重要决定因素是阻塞性睡眠呼吸暂停(OSA)。阻塞性睡眠呼吸暂停的特征是睡眠中反复发作的部分或完全上呼吸道塌陷,随之而来的是自主神经、呼吸和血流动力学紊乱,连同间歇性低氧血症和睡眠片段化,导致短暂的血压飙升,最终导致持续性高血压。在药物治疗的高血压患者中,OSA会损害压力控制,特别是在夜间,尽管有多种药物。2可见OSA在顽固性高血压中非常普遍(70%-90%),与昼夜血压异常及预后密切相关。2,3重要的是,尽管相对于白人,OSA的患病率和严重程度增加,但在黑人中OSA经常未被诊断,因此未得到治疗。这种高血压和OSA的易感性,以及这些疾病之间的病理生理学关系,有力地证明了OSA在黑人难以控制的高血压中的主要作用。然而,针对这一假设的研究却少得惊人。在最新一期的《循环》杂志中,约翰逊和他的同事们提出了有助于弥合这一差距的重要见解。这些研究者将杰克逊心脏睡眠研究(JHSS)作为一个平台,该研究是杰克逊心脏研究(一个以社区为基础的黑人队列研究)的辅助研究。睡眠呼吸暂停不依赖于患者报告的诊断或问卷评分,而是通过动态多导睡眠描记术客观量化,这是一种有效且具有成本效益的金标准实验室多导睡眠描记术的替代方法,被接受为具有至少中度睡眠呼吸暂停高预测概率的无并发症患者的替代诊断工具。5高血压患者分为控制性高血压、不控制性高血压和顽固性高血压。后一组占样本的14.5%,而48.2%的血压不受控制。大约四分之一的受试者至少患有中度OSA,定义为呼吸事件指数(REI)≥ 15起事件/h。由于使用了监测时间的推荐定义(即,总记录时间减去可能的觉醒和伪影)6,因此推导出的REI更接近基于多导睡眠图的呼吸暂停低通气指数。在多变量分析中,中度或重度OSA患者患顽固性高血压的几率高2倍,累积夜间低氧血症(定义为血氧饱和度< 90%的睡眠时间百分比)具有相似的预测性。根据OSA严重程度分层显示,
Hypertension contributes importantly to heightened cardiovascular risk in blacks, in whom it is more common and more severe than in whites. Despite more intensive therapy, only 48% of treated blacks meet blood pressure (BP) goals. 1 Blacks manifest more resistant hypertension, accompanied by aberrant diurnal BP patterns and more pressure-related complications and target-organ injury. A potent determinant of resistant hypertension is obstructive sleep apnea (OSA). OSA is characterized by repetitive episodes of partial or complete upper airway collapse in sleep, with consequent autonomic, ventilatory, and hemodynamic disruptions that, together with intermittent hypoxemia and sleep fragmentation, lead to transient BP surges and eventually to sustained hypertension. In medicated hypertensive people, OSA compromises pressure control, especially at nighttime and in spite of polypharmacy. 2 It follows that OSA is extremely prevalent (70%–90%) in resistant hypertension, is associated with abnormal day/night BP profiles, and worsens prognosis. 2, 3 Importantly, OSA often remains undiagnosed and therefore untreated among blacks, despite increased prevalence and greater severity of OSA, relative to whites.This predisposition to both hypertension and OSA, as well as the pathophysiological relationship between these conditions, argues strongly for a major role of OSA in difficult-to-control hypertension in blacks. Yet there is a striking paucity of research addressing this hypothesis. In the current issue of Circulation, Johnson and colleagues4 present important insights that help bridge this gap. These investigators used as a platform the Jackson Heart Sleep Study (JHSS), an ancillary of the parent Jackson Heart Study, a community-based cohort of blacks. Instead of relying on patient-reported diagnosis or questionnaire scores, sleep apnea was objectively quantified through ambulatory polygraphy, a valid and cost-effective alternative to the gold standard in-laboratory polysomnography that is accepted as a substitute diagnostic tool in uncomplicated patients with a high pretest probability of at least moderate sleep apnea. 5 Those with hypertension were classified as having controlled, uncontrolled, or resistant hypertension. The latter group constituted 14.5% of the sample, whereas 48.2% had uncontrolled BP. Approximately one-fourth of the subjects had at least moderate OSA, defined as a respiratory event index (REI) of≥ 15 events/h. Because the recommended definition of monitoring time (ie, total recording time minus probable wakefulness and artifacts) 6 was used, the derived REI more closely approximates the polysomnographically based apnea-hypopnea index. In multivariable analysis, odds of resistant hypertension were 2-fold higher in moderate or severe OSA, and cumulative nocturnal hypoxemia (defined as percentage of sleep time with oxygen saturation< 90%) was similarly predictive. Stratification by OSA severity revealed that severe