PDF(Pubmed)
Abstract：
Aims: Myocardial ischemia-reperfusion (I/R) injury markedly undermines the protective benefits of revascularization, contributing to ventricular dysfunction and mortality. Due to complex mechanisms, no efficient ways exist to prevent cardiomyocyte reperfusion damage. Vagus nerve stimulation (VNS) appears as a potential therapeutic intervention to alleviate myocardial I/R injury. Hence, this meta-analysis intends to elucidate the potential cellular and molecular mechanisms underpinning the beneficial impact of VNS, along with its prospective clinical implications. Methods and Results: A literature search of MEDLINE, PubMed, Embase, and Cochrane Database yielded 10 articles that satisfied the inclusion criteria. VNS was significantly correlated with a reduced infarct size following myocardial I/R injury [Weighed mean difference (WMD): 25.24, 95% confidence interval (CI): 32.24 to 18.23, p < 0.001] when compared to the control group. Despite high heterogeneity (I2 = 95.3%, p < 0.001), sensitivity and subgroup analyses corroborated the robust efficacy of VNS in limiting infarct expansion. Moreover, meta-regression failed to identify significant influences of pre-specified covariates (i.e., stimulation type or site, VNS duration, condition, and species) on the primary estimates. Notably, VNS considerably impeded ventricular remodeling and cardiac dysfunction, as evidenced by improved left ventricular ejection fraction (LVEF) (WMD: 10.12, 95% CI: 4.28; 15.97, p = 0.001) and end-diastolic pressure (EDP) (WMD: 5.79, 95% CI: 9.84; -1.74, p = 0.005) during the reperfusion phase. Conclusion: VNS offers a protective role against myocardial I/R injury and emerges as a promising therapeutic strategy for future clinical application.
摘要：
目的：心肌缺血再灌注（I/R）损伤明显损害了血运重建的保护作用，导致心室功能障碍和死亡率。由于复杂的机制，没有有效的方法来防止心肌细胞再灌注损伤。迷走神经刺激（VNS）似乎是减轻心肌I/R损伤的潜在治疗干预措施。因此，这项荟萃分析旨在阐明支持VNS有益影响的潜在细胞和分子机制，以及其预期的临床意义。方法和结果:MEDLINE文献检索,PubMed,Embase,Cochrane数据库产生了10篇满足纳入标准的文章。与对照组相比，VNS与心肌I/R损伤后梗死面积减少显着相关[加权平均差（WMD）：25.24，95％置信区间（CI）：32.24至18.23，p<0.001]。尽管异质性很高(I2=95.3%，p<0.001)，敏感性和亚组分析证实了VNS在限制梗死扩展方面的稳健功效.此外，元回归未能识别预先指定的协变量的显著影响(即，刺激类型或部位，VNS持续时间,条件,和物种)在初步估计上。值得注意的是,VNS显著阻碍心室重构和心功能不全，再灌注期左心室射血分数(LVEF)(WMD:10.12,95%CI:4.28;15.97,p=0.001)和舒张末期压(EDP)(WMD:5.79,95%CI:9.84;-1.74,p=0.005)得到改善。结论：VNS对心肌I/R损伤具有保护作用，并成为未来临床应用的有希望的治疗策略。
