Key result
Vagus nerve stimulation significantly reduced infarct size following myocardial ischemia/reperfusion injury compared to control (WMD -25.24) in preclinical animal models.
Why the study?
No efficient ways exist to prevent myocardial ischemia-reperfusion injury, but vagus nerve stimulation has emerged as a potential therapeutic intervention.
Does vagus nerve stimulation reduce infarct size and improve cardiac function in animal models of myocardial ischemia/reperfusion injury?
Meta-Analysis (n=238)
Does vagus nerve stimulation reduce infarct size and improve cardiac function in animal models of myocardial ischemia/reperfusion injury?
Mean Difference: -25.24 (95% CI -32.24–-18.23)
p-value: p=<0.001
In preclinical models, vagus nerve stimulation significantly reduces infarct size and improves left ventricular function following myocardial ischemia/reperfusion injury, suggesting a potential adjunctive therapeutic strategy for revascularization.
VNS may protect against myocardial I/R injury; extends preclinical evidence but leaves clinical translation open.
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 (I 2 = 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.
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Xu et al. (2023) conducted a meta-analysis in Myocardial ischemia/reperfusion (I/R) injury (n=238). Vagus nerve stimulation vs. Control therapy (no treatment or sham) was evaluated on Infarct size (percentage of infarct area over the area at risk) (WMD -25.24, 95% CI -32.24 to -18.23, p=<0.001). Vagus nerve stimulation significantly reduced infarct size following myocardial ischemia/reperfusion injury compared to control (WMD -25.24) in preclinical animal models.
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