抑制交感神经过度激活在高血压管理中的重要作用

2020-09-13 门诊杂志 门诊新视野

交感神经系统过度激活会导致心血管系统多重损害,造成高血压的病理变化和靶器官损害的严重后果。心率增快导致高血压患者心血管事件及死亡率增加,如何控制高血压患者心率,使得血压心率双达标是临床医生关注的重点。

交感神经系统过度激活会导致血管系统多重损害,造成高血压的病理变化和靶器官损害的严重后果。心率增快导致高血压患者心血管事件及死亡率增加,如何控制高血压患者心率,使得血压、心率双达标是临床医生关注的重点问题。

高血压患者交感神经过度激活的机制与危害

交感神经可通过心、肾、血管多途径激活,最终导致心血管系统的多重损害(图1)。神经、免疫系统及心血管疾病之间的关系可以看成一个三角关系。当交感神经占上风时,炎症反应过度激活成为“死亡三角”。多项研究结果表明,交感神经过度激活在高血压前期就已存在,并且与高血压发病和进展显着相关,血压水平越高交感激活越严重,从正常血压、高血压前期、临界高血压、中等至严重高血压,直至难治性高血压患者的肌肉交感神经活动(MSNA)平均值显着增高。此外,交感神经激活在不同类型患者中表现有所差异,在中青年高血压患者中更为突出,并且高血压伴发的心血管危险因素/疾病越多,交感激活越严重。

图1. 交感神经可通过多途径激活导致心血管系统损害

控制心率在临床管理中的作用

心率增快作为交感神经过度激活的标志,有效控制心率在临床管理中至关重要。高血压患者心率管理中国专家共识指出,心率增快导致高血压患者心血管事件及死亡率增加。我国唐山市开展的一项观察性、前瞻性和基于人群的队列研究表明,静息心率升高是中国高血压患者全因死亡的长期危险因素,心率>82 bmp的高血压患者死亡风险增加33%。因此,合理控制心率和血压达标同样重要。2018年欧洲高血压指南已将静息心率>80 bmp列为高血压患者心血管事件的危险因素之一。中国大样本高血压干预研究纳入205,900例高血压患者,研究发现:高血压患者的平均收缩压和舒张压水平随心率增快而增高(P<0.001),心率每增加10 bmp,收缩压/舒张压增加1.7/1.1 mmHg;心率60~79 bmp的患者平均血压水平最低且血压达标率最高。

高血压患者血压心率双重管理目标和原则

临床常用降压药物包括CCB、ACEI、ARB、利尿剂和β受体阻滞剂五类药物,以及由上述药物组成的固定配比的复方制剂。中国高血压防治指南(2018年修订版)推荐β受体阻滞剂用于高血压初始及维持治疗。《ESH高血压合并心率增快患者管理共识》强调,对于交感神经兴奋的患者,应考虑使用减慢心率的药物(多数为选择性β1受体阻滞剂)。高血压患者心率管理中国专家共识(2017)推荐高血压患者使用β受体阻滞剂进行心率管理,并对高血压合并心衰、高血压伴房颤以及高血压伴冠心病患者的心率提出不同要求,具体标准如下:对于慢性HFrEF患者,建议将静息窦性心率控制在<70 bmp。对于高血压伴房颤患者,建议将快速房颤的心室率控制在<110 bmp。对于急性冠脉综合征患者,建议将静息心率维持在50~60次bmp;对于慢性冠脉综合征患者,建议将静息心率控制在55~60 bmp。

比索洛尔在血压心率双重控制中的作用

β受体阻滞剂降压作用的机制包括:减慢心率、减低心排量;抑制中枢神经系统和肾素释放;减少静脉回流和血浆容量;降低外周血管阻力和血管舒张张力;改善血管顺应性;重置压力感受器水平;阻断突触前β受体从而减少交感神经末梢释放去甲肾上腺素;减弱运动和应激时儿茶酚胺释放引起的升压反应。β受体阻滞剂可以全面抑制中枢、外周和心脏交感神经活动以实现多重心血管保护作用。β受体阻滞剂还可实现心血管事件链中的多点干预(图2)。

图2. β受体阻滞剂可实现心血管事件链中的多点干预

《β受体阻滞剂在高血压应用中的专家共识2019》指出,对于有β受体阻滞剂治疗适应证的患者,推荐优先使用选择性β1受体阻滞剂。比索洛尔是高选择性β1受体阻滞剂,半衰期为10~12小时,血压控制谷峰比为78%,每日给药一次可实现24小时平稳降压。比索洛尔治疗后显着升高压力反射敏感性(BRS),有效控制交感神经活性。GENRES研究表明,比索洛尔用于高血压治疗,可有效、显着控制诊室血压及24小时动态血压。CREATIVE研究显示,比索洛尔降低动态血压作用与美托洛尔缓释片相当(P =0.5495)

总 结

心率增快是交感神经过度激活的标志,心率增快导致高血压患者心血管事件及死亡率增加,控制心率在减少风险的同时还有助于血压达标。指南推荐高血压患者进行血压和心率的双重管理,推荐伴交感神经活性增高、伴高动力状态、快速性心律失常、冠心病或慢性心力衰竭的高血压患者使用β受体阻滞剂。

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    2020-09-15 咻凡

    高血压患者到底该怎么预后呢

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    2020-09-14 ms1000000223698072

    理论强大

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