Non-invasive vagus nerve stimulation (VNS) represents a transformative approach for managing a broad spectrum of inflammatory and autoimmune conditions, including rheumatoid arthritis and inflammatory bowel disease. This comprehensive review delineates the mechanisms underlying VNS, emphasizing the cholinergic anti-inflammatory pathway, and explores interactions within the neuro-immune and vagus-gut axes based on both clinical outcomes and pre-clinical models. Clinical applications have confirmed the efficacy of VNS in managing specific autoimmune diseases, such as rheumatoid arthritis, and chronic inflammatory conditions like inflammatory bowel disease, showcasing the variability in stimulation parameters and patient responses. Concurrently, pre-clinical studies have provided insights into the potential of VNS in modulating cardiovascular and broader inflammatory responses, paving the way for its translational application in clinical settings. Innovations in non-invasive VNS technology and precision neuromodulation are enhancing its therapeutic potential, making it a viable option for patients who are unresponsive to conventional treatments. Nonetheless, the widespread adoption of this promising therapy is impeded by regulatory challenges, patient compliance issues, and the need for extensive studies on long-term efficacy and safety. Future research directions will focus on refining VNS technology, optimizing treatment parameters, and exploring synergistic effects with other therapeutic modalities, which could revolutionize the management of chronic inflammatory and autoimmune disorders. 

Non-invasive vagus nerve stimulation in anti-inflammatory therapy: mechanistic insights and future perspectives

Abstract Cardiovascular disease (CVD) remains a leading cause of death worldwide, and identification of its risk factors is pivotal in ensuring a lower socioeconomic burden on society. Psychological stress shows a strong causal link with CVD through the interaction of physiological and behavioral risk factors. Importantly, there is an association between the duration and level of stress and propensity for CVD. Chronic stress exerts its physiological effects through the release of glucocorticoids (GCs) such as cortisol, which subsequently promote proinflammatory effects, exacerbating atherosclerotic plaque development. Stress also exacerbates the secretion of cardiokines such as tumor necrosis factor-alpha (TNF-α). Elevated TNF-α is associated with endothelial dysfunction and angiogenesis-mediated atherosclerotic plaque progression, with increased secretion as the duration of stress is extended. Stress-induced GC secretion also inhibits glucose uptake leading to hyperglycemia and consequent hyperinsulinemia. This increases an individual’s susceptibility to another CVD risk factor, type 2 diabetes mellitus (T2DM). These risk factors are further exacerbated by the impact of chronic stress on behavior such as eating habits. Increased consumption of comfort foods, typically containing high fat and sugar contents, is directly associated with increased body mass index and increased low-density lipoprotein (LDL) cholesterol, both of which are well-known drivers of atherosclerosis. Moreover, chronic stress often results in reductions in physical activity, particularly in individuals at low baseline levels of activity. This further increases an individual’s susceptibility to obesity, T2DM, and increased LDL-cholesterol levels, all of which promote the development of CVD. This review outlines key research findings relating to the role chronic psychological stress plays in altering physiological and behavioral risk factors for CVD. 

Impact of Chronic Psychological Stress on Cardiovascular Disease Risk: A Narrative Review

Vagus nerve stimulation (VNS) is emerging as potential treatment for several chronic diseases. However, limited control of fiber activation, e.g., to promote desired effects over side effects, restricts clinical translation. Towards that goal, we describe a VNS method consisting of intermittent, interferential sinusoidal current stimulation (i2CS) through multi-contact epineural cuffs. In experiments in anesthetized swine, i2CS elicits nerve potentials and organ responses, from lungs and laryngeal muscles, that are distinct from equivalent non-interferential sinusoidal stimulation. Resection and micro-CT imaging of a previously stimulated nerve, to resolve anatomical trajectories of nerve fascicles, demonstrate that i2CS responses are explained by activation of organ-specific fascicles rather than the entire nerve. Physiological responses in swine and activity of single fibers in anatomically realistic, physiologically validated biophysical vagus nerve models indicate that i2CS reduces fiber activation at the interference focus. Experimental and modeling results demonstrate that current steering and beat and repetition frequencies predictably shape the spatiotemporal pattern of fiber activation, allowing tunable and precise control of nerve and organ responses. When compared to equivalent sinusoidal stimulation in the same animals, i2CS produces reduced levels of a side-effect by larger laryngeal fibers, while attaining similar levels of a desired effect by smaller bronchopulmonary fibers. Vagus nerve stimulation (VNS) is emerging as a potential treatment for several chronic diseases. Here, the authors describe a VNS method using intermittent interferential current stimulation (i2CS) that allows precise control of organ-specific fiber activation in swine.

Control of spatiotemporal activation of organ-specific fibers in the swine vagus nerve by intermittent interferential current stimulation

Protective Role of Acetylcholine and the Cholinergic System in the Injured Heart

The pathophysiology of atrial fibrillation and ventricular tachycardia that result in cardiac arrhythmias is related to the sustained complicated mechanisms of the autonomic nervous system. Atrial fibrillation is when the heart beats irregularly, and ventricular arrhythmias are rapid and inconsistent heart rhythms, which involves many factors including the autonomic nervous system. It's a complex topic that requires careful exploration. Cultivation of speculative knowledge on atrial fibrillation; the irregular rhythm of the heart and ventricular arrhythmias; rapid oscillating waves resulting from mistakenly inconsistent P waves, and the inclusion of an autonomic nervous system is an inconceivable approach toward clinical intricacies. Autonomic modulation, therefore, acquires new expansions and conceptions of appealing therapeutic intelligence to prevent cardiac arrhythmia. Notably, autonomic modulation uses the neural tissue's flexibility to cause remodeling and, hence, provide therapeutic effects. In addition, autonomic modulation techniques included stimulation of the vagus nerve and tragus, renal denervation, cardiac sympathetic denervation, and baroreceptor activation treatment. Strong preclinical evidence and early human studies support the annihilation of cardiac arrhythmias by sympathetic and parasympathetic systems to transmigrate the cardiac myocytes and myocardium as efficient determinants at the cellular and physiological levels. However, the goal of this study is to draw attention to these promising early pre-clinical and clinical arrhythmia treatment options that use autonomic modulation as a therapeutic modality to conquer the troublesome process of irregular heart movements. Additionally, we provide a summary of the numerous techniques for measuring autonomic tone such as heart rate oscillations and its association with cutaneous sympathetic nerve activity appear to be substitute indicators and predictors of the outcome of treatment. 

Autonomic Neuronal Modulations in Cardiac Arrhythmias: Current Concepts and Emerging Therapies

Autonomic dysfunction and chronic inflammation contribute to the pathogenesis and progression of several cardiovascular diseases (CVD), such as heart failure with preserved ejection fraction, atherosclerotic CVD, pulmonary arterial hypertension, and atrial fibrillation. The vagus nerve provides parasympathetic innervation to the heart, vessels, and lungs, and is also implicated in the neural control of inflammation through a neural pathway involving the spleen. Stimulation of the vagus nerve (VNS) can in principle restore autonomic balance and suppress inflammation, with potential therapeutic benefits in these diseases. Although VNS ameliorated CVD in several animal models, early human studies have demonstrated variable efficacy. The purpose of this review is to discuss the rationale behind the use of VNS in the treatment of CVD, to critically review animal and human studies of VNS in CVD and their limitations, and to propose possible means to overcome the challenges in the clinical translation of VNS in CVD. 

Vagus Nerve Stimulation for Cardiovascular Diseases: Is There Light at the End of the Tunnel?


 
 
 Autonomic neuromodulation and particularly stellate ganglion blockade (SGB) has been tested in ventricular arrhythmia (VA) storm, but there is so far no robust evidence to inform clinical practice and its use remains limited.
 
 
 
 We aimed to summarize the efficacy and safety of SGB in patients with VA storm.
 
 
 
 We searched PubMed, the Cochrane Library and Scopus from inception to 15th March 2022, for studies performing either pharmacological or electrical SGB in the context of drug-refractory VA storm. Case series with less than 10 patients were excluded. We performed a single-arm random effects meta-analysis of studies to calculate the pooled proportion estimate of freedom from VA recurrence after SBG and the overall mean change of VA burden from baseline.
 
 
 
 Of 409 articles identified and screened, we considered eligible six studies comprising a total of 106 patients. The mean age was 61.6±13.9 years, 79.2% were male, the mean left ventricular ejection fraction was 28.8±12.7%, and 47.1% had underlying ischemic cardiomyopathy. In five trials the patients received pharmacological SGB with bupivacaine, ropivacaine, or/and lidocaine (left-sided or bilateral), while in one study transcutaneous magnetic stimulation of the left stellate ganglion was used. The pooled proportion of patients free of VA recurrences was 65% (95% CI 51–78%, I2=46%) at the first 24 hours post-SGB (Figure 1A), and 54% (95% CI 43–64%, I2=0%) at 72 hours (Figure 1B). The number of VA episodes was significantly reduced from a mean baseline of 7.01±8.34 episodes/24h before SGB to 0.93±1.64 episodes/24h after SGB. The mean absolute reduction of VA episodes was 5.44 (95% CI 2.83–8.05, I2=88%) (Figure 1C) while the mean absolute reduction of external or internal defibrillation events was 3.36 (95% CI 0.62–6.09, I2=84%) (Figure 1D). No serious procedure-related complications were reported. The overall in-hospital mortality was 28.4%.
 
 
 
 SGB appears an effective and safe treatment in patients with VA storm with approximately 1 in 2 patients exhibiting complete suppression of VA for 72 hours and an approximately 80% mean relative reduction in VA burden.
 
 
 
 Type of funding sources: None.


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Stellate ganglion blockade for treatment of ventricular arrhythmia storm: a meta-analysis

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Vagus Nerve Stimulation for Cardiovascular Diseases: Is There Light at the End of the Tunnel?

Stellate ganglion blockade for treatment of ventricular arrhythmia storm: a meta-analysis