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Bifurcation Stenting

Abstract

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Original Research

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HFpEF最新科学探索之抑制一氧化氮合酶

CBSMD

Pre-reading

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。