JACC:终末期心衰患者的心肌血管紧张素代谢

2021-04-13 Nebula MedSci原创

衰竭心脏中含有相当多的经典RAS的代谢物,导致HF持续发展

心力衰竭(HF)仍然是工业化国家死亡和残疾的主要原因。肾素-血管紧张素系统(RAS)的激活是射血分数降低的HF(HFrEF)的特征,可导致HF持续发展。

在这类患者中,心肌表现出一种适应性的组织特异性RAS系统,局部失衡可能绕过药物抑制RAS的预期效果,抑制RAS是治疗HFrEF的主要手段。

本研究旨在探讨衰竭心脏心肌组织中RAS系统的调节作用

共招募了52位接受心脏移植的终末期HFrEF患者(9位未接受RAS抑制剂治疗,28位接受血管紧张素转换酶抑制剂[ACEI],8位接受血管紧张素受体阻滞剂[ARB],7位接受血管紧张素受体[ARNi])。用质谱法测定左心室组织中与血管紧张素1-8(AngII)和Ang1-7代谢有关的心肌血管紧张素代谢产物和酶活性。

HF患者心肌组织中的血管紧张素代谢产物

总体上,在HF患者心肌组织中,AngⅡ和Ang2-8占主导地位,其他代谢产物,尤其是Ang1-7均低于检测下限。接受ARB成分(即ARB或ARNi)治疗的患者的AngⅡ和AngⅢ明显更高(AngII:242[IQR 145.7-409.9]fmol/g vs 63.0[19.9-124.1]fmol/g;p<0.001;AngIII:87.4[46.5-59.3]fmol/g vs 23.0[<5.0 -59.3]fmol/g;p=0.002)。

心肌AngII浓度与循环AngII水平密切相关。心肌RAS酶的调节与使用的RAS抑制剂的种类无关,特别是在有无接受ARNi治疗的患者中观察到了相似的心肌脑啡肽酶活性。组织糜酶(而不是ACE)是心脏血管生成的主要调节酶,而AngⅡ被脯氨酰羧肽酶代谢成了Ang1-7,但不被ACE2代谢。未观察到ACE2的活性迹象。

总结示意图

综上所述,衰竭心脏中含有相当多的经典RAS的代谢物,而AngIII可能是心血管结构有害影响的尚未被充分认识的介质。这些结果强调了减少AngⅡ作用的药物干预的重要性,同时也为开发心脏组织特异性的RAS药物提供了思路。

原始出处:

Pavo Noemi,Prausmüller Suriya,Spinka Georg et al. Myocardial Angiotensin Metabolism in End-Stage Heart Failure. J Am Coll Cardiol, 2021, 77: 1731-1743. https://doi.org/10.1016/j.jacc.2021.01.052

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    2021-04-14 ms4000001975205411

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    2021-04-14 梅干儿

    三人行,必有我师。 #梅斯医学科研互助群# 欢迎您的加入,添加【梅斯医学科研助手WeChat:medsci_2021】邀您进群! 【社群简介】👉 梅斯医学目前已建立覆盖肿瘤、心血管、神经、消化、内分泌、呼吸等30个科室的学习交流社群。 【入群福利】👉 群内可实时交流病例,提问同行,跨群讨论,每天更新前沿医学资讯和指南共识,每周推出至少1场专业直播,不时共享科研干货,入群即可获得100份SCI写作攻略!

    0

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