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Left Main & Coronary Bifurcation Summit (CBS) was founded in 2006 as a think tank dedicated to the treatment of left main and coronary bifurcation lesions. CBS aims to improve cardiological care by refreshing fundamental researches, clinical trials, yearly published guidelines, emerged ideas and case-based discussion.

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Original Research

JOURNAL：CBSMD Article Link

HFpEF最新科学探索之抑制一氧化氮合酶

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心力衰竭是仅有的几种发病率持续增加的心血管疾病之一, 两种疾病亚型正在世界范围内蔓延开来：一种为射血分数降低心力衰竭（heart failure with reduced ejection fraction, HFrEF），治疗方法包括药物、装置和移植；另一种射血分数保留的心力衰竭（heart failure with preserved ejection fraction, HFpEF），目前因缺乏充分代表HFpEF复杂疾病进展的相关实验模型，现今的治疗选择主要针对症状、心血管基础疾病和合并症、心血管疾病危险因素，采取综合性治疗手段，仍旧处于摸石头过河的阶段, 而诊疗方向的最新探索或为HFpEF的治疗带来了新的曙光。

2018年4月“Permanent pacemaker use among patients with heart failure and preserved ejection fraction: Findings from the Acute Decompensated Heart Failure National Registry (ADHERE) National Registry”注册研究数据指出，HFpEF患者接受永久性心脏起搏置入治疗的发生率及患者群特征。

传统的右心室心脏起搏器或可导致左心室机电不同步，并加重左心室收缩功能障碍和心衰，“Prior Pacemaker Implantation and Clinical Outcomes in Patients With Heart Failure and Preserved Ejection Fraction”使用CHARM-Preserved, I-PRESERVE和TOPCAT研究数据，对其中置入心脏起搏器的患者进行了预后随访，揭示了该类型心脏起搏器对HFpEF患者不良临床预后的影响。

2019年4月“Novel percutaneous interventional therapies in heart failure with preserved ejection fraction: an integrative review”阐述了HFpEF的病理生理机制并集中介绍了经皮介入治疗HFpEFd的最新疗法。

既往HFpEF心力衰竭模型侧重于提高一氧化氮合酶（nitric oxide synthase, NO）酶的水平, 而疾病临床表现常与该假设相反，NO酶水平在HFpEF患者中常表达过高。2019年4月10日美国德克萨斯大学西南医学中心研究Hill JA研究团队发表的“Nitrosative stress drives heart failure with preserved ejection fraction”在细胞水平上研究了利用新病理生理模型获得的结果，并将其与人类细胞进行比较，研究结果提示抑制一氧化氮合酶有望治疗HFpEF型心力衰竭，提示受iNOS影响的IRE1α-XBP1通路的失调或是HFpEF心肌细胞功能障碍的一个重要机制。

Abstract

Recommended Article

HFpEF最新科学探索之抑制一氧化氮合酶

Pre-reading