类固醇药物治疗改善了心力衰竭患者的运动肌肉微血管反应性,这些患者有保存的喷射分数
Jarred J Iacovelli1, Jeremy K Alpenglow2,3, Stephen M Ratchford3
1Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah, United States.
概括
低剂量阿托瓦斯塔丁可以通过减少氧化应激来改善心力衰竭下肢微血管反应能力,这些患者有保存的喷射分数 (HFpEF). 这项研究提供了新的证据,证明他类药物在提高HFpEF中微血管功能的有效性.
科学领域:
- 心血管医学 心血管医学
- 翻译研究是翻译研究.
- 药理学 药理学是指药理学的学科.
背景情况:
- 周围微血管功能障碍是心力衰竭的标志性特征,具有保存的射出分数 (HFpEF),与炎症和氧化应激有关.
- 解决HFpEF中微血管功能障碍的有效策略仍然有限.
- 了解氧化应激在HFpEF病理生理学中的作用,对于开发向疗法至关重要.
研究的目的:
- 评估30天阿托瓦斯塔丁在HFpEF患者下肢微血管活性上的有效性.
- 评估阿托瓦斯塔丁在HFpEF中对功能能力和炎症和氧化应激生物标志物的影响.
- 探索潜在的机制,包括减少氧化应激,是他类药物对微血管功能的潜在影响.
主要方法:
- 一项并行,双盲,安慰剂控制的研究,涉及16名HFpEF患者 (8名他类药物,8名安慰剂).
- 干预措施:在30天内服用阿托瓦斯塔丁 (每天10毫克) 或安慰剂.
- 评估包括被动四肢运动 (PLM) 诱导的高血压 (曲线下腿部血流区域 - LBFAUC),6分钟步行测试 (6MWT) 和循环生物标志物 (例如,马隆迪化物 - MDA).
主要成果:
- 阿托瓦斯塔丁显著增加了对PLM的总高血压反应 (LBFAUC) (前:60±68毫升;后:164±90毫升;P <0.01),与安慰剂 (P = 0.99) 不同.
- 脂质过氧化的标志物马隆迪化 (MDA) 在阿托瓦斯塔丁干预后显著减少 (前:0.68±0.10;后:0.51±0.11;P <0.01).
- 没有观察到6MWT距离或其他测量的循环生物标志物的显著变化.
结论:
- 低剂量阿托瓦斯塔丁在患有HFpEF的患者中有效改善运动肌肉的微血管反应性.
- 观察到的微血管功能的改善可能部分归因于氧化应激的减少,这是MDA水平降低所表明的.
- 这些发现提供了支持他类药物治疗增强HFpEF微血管功能的新证据.
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