Omega-3与房颤风险:迷走神经介导的双刃剑。

Evan L O'Keefe, James H O'Keefe, Hussam Abuissa, Mark Metzinger, Ellen Murray, Grant Franco, Carl J Lavie, William S Harris
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引用次数: 0

摘要

目的:关于ω -3脂肪酸,特别是二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)对房颤(AF)风险影响的研究报告结果不一致。本综述的目的是阐明海洋摄入omega-3对房颤风险的影响。患者和方法:PubMed检索使用术语:心房颤动,omega-3, EPA, DHA,迷走神经张力。我们总结了随机临床试验(rct)、流行病学研究和评估DHA + EPA对房颤风险的影响/关联的荟萃分析的结果。此外,迷走神经张力作为omega-3与房颤风险之间的中介进行了探讨。8项随机对照试验和17项前瞻性队列研究的荟萃分析,分别包括83,112和54,799人,调查了ω -3摄入量与AF事件之间的联系。随机对照试验报告称,DHA和/或EPA治疗与AF相对风险增加24% %相关(绝对风险4.0 % vs 3.3 %;相对危险度[RR] 1.24, 95 %置信区间[CI] 1.11-1.38, p = 0.0002)。这是剂量依赖性的;DHA + EPA剂量为~1000 mg/d使房颤风险增加~12 %,而1800 ~ 4000 mg/d使房颤风险增加~50 %。相反,关注DHA + EPA血液水平或饮食摄入的观察性研究普遍报道,较高的omega-3水平/摄入与较低的房颤风险相关。最大限度降低房颤风险。(12 %)发生在~650 mg/d的膳食DHA + EPA。其他研究表明,omega-3脂肪酸可以剂量依赖性地增加迷走神经张力,这可以解释DHA + EPA与房颤风险之间的双相关系。实验研究表明,低水平的迷走神经刺激可降低AF的风险,而高水平的迷走神经刺激可增加AF的风险。结论:饮食中摄入更多的omega-3与降低AF的风险有关。相反,药物剂量的omega-3增加心房颤动以剂量依赖的方式,这可能是由迷走神经张力介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Omega-3 and Risk of atrial fibrillation: Vagally-mediated double-edged sword.

Objective: Studies regarding effects of omega-3 fatty acids, specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), on risk of atrial fibrillation (AF) have reported discordant results. The aim of this review is to clarify effects of marine omega-3 intake on risk of AF.

Patients and methods: A PubMed search was performed using terms: atrial fibrillation, omega-3, EPA, DHA, vagal tone. We summarized findings from randomized clinical trials (RCTs), epidemiology studies, and meta-analyses evaluating effects/associations of DHA + EPA on risk of AF. Also, vagal tone was explored as a mediator between omega-3 and risk of AF.

Results: Meta-analyses of 8 RCTs and 17 prospective cohort studies comprised of 83,112 and 54,799 individuals, respectively, investigated the link between omega-3 intake and incident AF. The RCTs reported that treatment with DHA and/or EPA was associated with a 24 % increased relative risk of AF (absolute risk 4.0 % vs 3.3 %; relative risk [RR] 1.24, 95 % confidence interval [CI] 1.11-1.38, p = 0.0002). This was dose-dependent; DHA + EPA doses of ∼1000 mg/d increased AF risk ∼12 %, whereas 1800 to 4000 mg/d increased AF risk by ∼50 %. In contrast, observational studies focused on DHA + EPA blood levels or dietary intake have generally reported that higher omega-3 levels/consumption are associated with lower AF risk. Maximal AF risk reduction. (12 %) occurred at ∼650 mg/d of dietary DHA + EPA. Other studies have indicated that omega-3 fatty acids can dose-dependently increase vagal tone, which could explain the biphasic relationship between DHA + EPA and AF risk. Experimental studies show that low-level vagal stimulation decreases risk of AF, whereas high-level vagal stimulation increases risk of AF.

Conclusion: Higher consumption of dietary omega-3 is associated with decreased AF risk. In contrast, pharmaceutical dosing of omega-3 increases AF in a dose-dependent manner, which may be mediated by vagal tone.

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