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Frontiers in Anesthesiology ·

Volume 5 - 2026 | https://doi.org/10.3389/fanes.2026.1898474

A narrative review of stellate ganglion block in management of post-operative atrial fibrillation with focus on immunomodulatory mechanisms

  • Dandan Zhu1,2
  • Misty A. Radosevich1
  • Aneta Szofer-Sendrowska3
  • Maciej M. Kowalik4
  • Wen Li2
  • Erica Wittwer1
  • Daniel Diedrich1
  • Krzysztof Laudanski1*corresponding author
  1. 1Department of Anesthesiology and Perioperative Care, Mayo Clinic, Rochester, MN, United States
  2. 2Department of Critical Care Medicine, the Second Hospital of Dalian Medical University, Dalian, China
  3. 3Department of Anesthesiology and Intensive Care, Clinical University Centre, Gdańsk, Poland
  4. 4Department of Anesthesiology and Intensive Care, Medical University of Gdańsk, Gdańsk, Poland
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Abstract

Stellate ganglion blockade (SGB) is an uncommon but increasingly relevant therapy used to modulate the autonomic nervous system and reduce the risk of atrial fibrillation (AF). This narrative review focuses specifically on the potential therapeutic role of SGB in new-onset perioperative atrial fibrillation (POAF), a complication associated with adverse long-term outcomes that may diminish the overall benefits of surgery. SGB may reduce AF through several inflammation-mediated mechanisms, including attenuation of direct sympathetic activation and modulation of perioperative inflammatory responses. Because the clinical effects of SGB may persist beyond the expected duration of local anesthetic nerve blockade, we emphasize immunomodulation as a potential mechanism sustaining its beneficial effects and influencing longer-term outcomes. In this review, we examine the immunological effects of SGB in the context of postoperative AF, with particular emphasis on human studies most relevant to clinical practice. Available evidence suggests that, beyond nonspecific inflammation, several less commonly studied cellular components, including mast cells and T cells, may contribute to the initiation and persistence of POAF. These findings support the hypothesis that SGB may reduce POAF by limiting stellate ganglionitis driven by perioperative localized leukocyte activation. Future studies should define the extent, timing, and frequency of this inflammatory process and determine whether specific inflammatory or autonomic phenotypes can identify patients most likely to benefit from SGB.

Keywords

Introduction

Postoperative atrial fibrillation (POAF) is one of the most common perioperative arrhythmias and a significant source of postoperative morbidity (1). Although traditionally regarded as a transient complication, POAF may delay recovery, prolong hospitalization, and diminish the overall benefits of surgery (2). Its pathogenesis is multifactorial and reflects the interaction between a pre-existing vulnerable atrial substrate and acute perioperative triggers. Structural remodeling, including atrial dilation, fibrosis, altered geometry, and increased wall stress, may predispose the atrium to conduction heterogeneity and re-entry. Electrophysiological remodeling, characterized by changes in atrial refractoriness, conduction velocity, calcium handling, and ion-channel function, further promotes the initiation and maintenance of atrial fibrillation.

These abnormalities may be intensified by perioperative factors such as sympathetic activation, autonomic imbalance, anesthesia and anesthetic exposure, surgical trauma, procedure duration, cardiopulmonary bypass, fluid shifts, myocardial ischemia, oxidative stress, and postoperative tissue injury (3). Patient-related factors, including advanced age, hypertension, obesity, heart failure, atrial enlargement, and other cardiovascular comorbidities, may further increase susceptibility to POAF. Among these mechanisms, inflammation is increasingly recognized as a central contributor. Surgical stress induces cytokine release, leukocyte activation, endothelial dysfunction, and oxidative injury, which may alter atrial conduction and promote electrical and structural remodeling (4–6). Together, these changes create a transient but highly arrhythmogenic postoperative environment.

Stellate ganglion block (SGB) is a relatively uncommon therapeutic approach for reducing the incidence of atrial fibrillation. Its immediate effects are primarily mediated through attenuation of sympathetic cardiac activity. However, emerging evidence suggests that SGB may also modulate inflammatory responses and restore autonomic and immune homeostasis (7–9). These neuroimmune effects may help explain why the clinical benefits of SGB can persist beyond the expected duration of local anesthetic blockade (10). We therefore conducted a focused narrative review of SGB in POAF, emphasizing the inflammatory and neuroimmune mechanisms through which SGB may modify the development and persistence of postoperative atrial fibrillation (8, 11).

Electrophysiology of AF

Atrial fibrillation (AF) develops when ectopic electrical triggers interact with a vulnerable atrial substrate. Key electrophysiological abnormalities include shortened atrial refractoriness, increased automaticity, slowed conduction, and prolonged interatrial conduction (12). Common trigger sites include the pulmonary veins, vein of Marshall, superior vena cava, and coronary sinus (12). In the perioperative setting, autonomic dysregulation, inflammation, and structural and electrical atrial remodeling act synergistically to promote AF (Figure 1) (1, 9, 12–16).

Emergence of atrial fibrillation results from the interplay between triggers (red) and alleviating (green) mechanisms. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.
Figure 1. Emergence of atrial fibrillation results from the interplay between triggers (red) and alleviating (green) mechanisms. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.

Importantly, these mechanisms are strongly influenced by the characteristics of the surgical procedure. General anesthesia and specific anesthetic agents may alter autonomic tone, myocardial electrophysiology, vascular resistance, and inflammatory response (Figures 1, 2) (1, 9, 12–16). Surgical trauma promotes catecholamine release, tissue injury, oxidative stress, and cytokine activation, while prolonged procedures increase exposure to these arrhythmogenic stimuli (17–21). Cardiopulmonary bypass, myocardial manipulation, ischemia-reperfusion injury, fluid shifts, hypoxia, acid-base disturbances, and electrolyte abnormalities may further increase atrial excitability and conduction heterogeneity (1, 13, 14).

Surgery results in emergence of additional factors (inflammation, microcirculation impairment) indirectly supporting emergence of POAF. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.
Figure 2. Surgery results in emergence of additional factors (inflammation, microcirculation impairment) indirectly supporting emergence of POAF. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.

Sympathetic activation through the stellate ganglion or circulating catecholamines alters Ca2⁺ handling and potassium currents, whereas excessive parasympathetic activity may shorten atrial refractoriness and increase electrical heterogeneity (17). Inflammation further promotes AF through cytokine signaling, oxidative stress, leukocyte activation, and pyroptosis (1, 9, 15, 19, 22–25). Specific anti-inflammatory therapies, such as colchicine, have shown potential in reducing postoperative atrial fibrillation recurrence. However, their routine use is not yet recommended in general AF management due to the high incidence of adverse side effects and inconsistent clinical benefit (26). Structural changes, including atrial dilation, wall stress, fibrosis, and scarring, slow conduction and facilitate re-entry (13, 14, 27, 28).

The magnitude of these effects also depends on patient-related factors. Advanced age, hypertension, obesity, diabetes, heart failure, valvular disease, atrial enlargement, renal dysfunction, and pre-existing structural heart disease may reduce atrial resilience and amplify the electrophysiological, autonomic, and inflammatory effects of surgery. Thus, POAF reflects an interaction between procedural stressors and a pre-existing susceptible atrial substrate.

Postoperative atrial fibrillation: incidence, clinical outcomes, and current management

Postoperative atrial fibrillation (POAF) occurs after approximately 20%–40% of cardiac surgeries and is associated with prolonged hospitalization, recurrent AF, thromboembolic events, and increased long-term morbidity and mortality (29–31). Management includes correction of reversible triggers, rate or rhythm control, and individualized stroke prevention (29, 32, 33). Hemodynamically unstable patients require immediate synchronized cardioversion. In stable patients, β-blockers are generally preferred for rate control, while amiodarone is commonly used for rhythm control, particularly when AF is symptomatic, hemodynamically harmfull or persistent (30, 33–37). Anticoagulation should be considered according to AF duration, thromboembolic risk, and postoperative bleeding risk, with reassessment after recovery (33–35). Catheter ablation is not routinely indicated for an isolated episode of POAF but may be considered if the patient subsequently develops symptomatic recurrent or persistent AF warranting a long-term rhythm-control strategy (30, 36–38).

Anti-inflammatory therapies have been investigated as a strategy to reduce the risk of postoperative atrial fibrillation by attenuating the inflammatory response triggered by surgical trauma, cardiopulmonary bypass, ischemia-reperfusion injury, and oxidative stress. Agents such as colchicine, corticosteroids, statins, and selected cytokine-modulating therapies may limit leukocyte activation, cytokine release, and inflammation-mediated atrial electrical remodeling (39–44). Although several studies have demonstrated reductions in POAF incidence, the results remain inconsistent, and potential adverse effects—including infection, impaired wound healing, gastrointestinal intolerance, and metabolic complications—limit routine use. Therefore, anti-inflammatory therapy may be most beneficial in carefully selected high-risk patients, but further studies are needed to identify the optimal agent, dose, timing, and duration of treatment (45).

Stellate ganglion blockade to achieve functional cardiac sympathectomy and reduce cardiac arrhythmias

The stellate ganglion is typically located at the C7–T1 level, anterior to the transverse process of C7 and the neck of the first rib, superior to the cervical pleura, and posterior to the subclavian artery. It lies beneath the prevertebral fascia, with the carotid and subclavian vessels positioned anteriorly. Anatomical variation is common, including differences in size, shape, and the presence of a separate vertebral ganglion near the origin of the vertebral artery. Functional asymmetry also exists between the two sides: the right stellate ganglion exerts a greater influence on heart rate and atrioventricular conduction, whereas the left more strongly affects ventricular electrophysiology and refractoriness. Despite these differences, blockade of either stellate ganglion may reduce susceptibility to atrial fibrillation through attenuation of cardiac sympathetic activity.

Stellate ganglion block (SGB) is most safely performed using ultrasound or fluoroscopic guidance to deposit a small volume of local anesthetic near the stellate ganglion (46–48). During an ultrasound-guided approach, the cricoid cartilage is identified and the transducer is moved laterally to visualize the carotid artery and longus colli muscle. The anesthetic is then injected beneath the prevertebral fascia, anterior to the longus colli muscle and posterior to the carotid artery, with careful aspiration and real-time visualization to avoid intravascular injection and injury to adjacent structures (47).

Common complications include Horner's syndrome and phrenic nerve blockade. Uncommon complications are accidental intra-arterial injection, hematoma development adjacent to the airway, and dysphagia (49). A systematic review of 67 studies reported 260 events, of which 178 (68.4%) were drug-related or systemic, and 82 (31.5%) were procedure-related or local injection, though the total number of procedures was not reported (49).

For practical use around cardiac surgery, SGB is most performed under ultrasound guidance at the C6–C7 level with 5–10 mL of long-acting local anesthetic. Left-sided blockade preferentially attenuates cardiac sympathetic tone, whereas bilateral blockade is generally reserved for intubated patients due to the risk of recurrent laryngeal nerve paresis (50). If right-sided stellate ganglion blockade does not reduce atrial fibrillation after cardiac surgery, left-sided stellate ganglion blockade should be investigated. Additionally, the timing of the block and the optimal local anesthetic agent should be determined. In the study described above by Zhu and colleagues, patients were injected with 7 mL 0.5% ropivacaine near the stellate ganglion under ultrasound guidance before anesthesia (46, 51). Connors et al. reported perioperative ultrasound-guided stellate ganglion block in cardiac surgery patients, using a long-acting local anesthetic (ropivacaine, 0.25%, 4 mL, combined with lidocaine) (52). In the ongoing research by Wittwer and colleagues, a right-sided SGB is performed preoperatively with bupivacaine (47). Liposomal bupivacaine may be ideal for preventing atrial fibrillation due to its longer duration of action.

In the context of preventing or treating postoperative atrial fibrillation, stellate ganglion block appears to have a generally favorable safety profile when performed by experienced clinicians under ultrasound or fluoroscopic guidance. Most adverse effects, including transient Horner syndrome, hoarseness, dysphagia, or phrenic nerve blockade, are rare (1.7 per 1,000 SGB procedures) and self-limited. Serious complications, such as inadvertent intravascular injection, seizure, pneumothorax, or airway-compromising hematoma, are uncommon but potentially severe. Therefore, the potential antiarrhythmic benefit of SGB should be balanced against procedural risk, particularly in anticoagulated patients or those with limited respiratory reserves. Careful patient selection, image guidance, low-volume injection, and post-procedural monitoring are essential to maximize safety in the perioperative setting (49, 52, 53). Maximizing procedural safety through careful patient selection, image guidance, low-volume injection, and appropriate monitoring may substantially improve the benefit–risk ratio of stellate ganglion block. This is particularly important because POAF is associated with prolonged hospitalization, thromboembolic complications, recurrent arrhythmia, increased healthcare utilization, and worse long-term outcomes (2, 6, 13, 15, 29, 31, 54).

Stellate sympathetic blockade can also be achieved by thoracic epidural anesthesia. By blocking upper thoracic sympathetic fibers, TEA may attenuate the perioperative catecholamine response, improve myocardial oxygen balance, enhance coronary perfusion, and reduce autonomic fluctuations that promote atrial electrical instability. A meta-analysis of randomized controlled trials suggested that TEA may reduce the incidence of postoperative atrial fibrillation compared with general anesthesia and systemic analgesia alone (55). However, the included trials were generally small and differed in epidural technique, anesthetic regimens, perioperative β-blocker use, AF monitoring, and outcome definitions. Consequently, the certainty and generalizability of the observed benefit remain limited. Subsequently, we focused on direct stellate ganglion blockade (55).

Modulatory effects of SGB

Stellate ganglion block may reduce perioperative atrial fibrillation through several complementary mechanisms, reducing the incidence of POAF (Figures 3, 4). Its primary effect is attenuation of cardiac sympathetic activity, which limits catecholamine-driven increases in atrial excitability, abnormal calcium handling, and conduction heterogeneity (7, 16, 56). SGB may also block some parasympathetic nerve fibers, thereby limiting its effectiveness (33). In contrast, spinal cord stimulation and modulation of parasympathetic activity involve distinct mechanisms and pathways, producing immunomodulatory outcomes that are not directly equivalent to those achieved by SGB (57, 58). Cardiac sympathectomy can also be achieved by thoracic epidural as discussed above.

Stellate ganglion anatomical location **(A)** and interneural connection defining potential functions **(B)**. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.
Figure 3. Stellate ganglion anatomical location (A) and interneural connection defining potential functions (B). Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.
SGB restores the balance between pro-arrhythmogenic and anti-arrhythmogenic factors, which is disbalanced as the illness triggering surgery progresses from healthy **(A)** to preclinical illness **(B)**. Surgery exacerbates the pr-AF condition **(C)**, while SGB at least partially restores the balance **(D)**. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.
Figure 4. SGB restores the balance between pro-arrhythmogenic and anti-arrhythmogenic factors, which is disbalanced as the illness triggering surgery progresses from healthy (A) to preclinical illness (B). Surgery exacerbates the pr-AF condition (C), while SGB at least partially restores the balance (D). Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.

In addition, emerging evidence suggests that sympathetic blockade may suppress neuroimmune activation, cytokine release, oxidative stress, and inflammation-mediated atrial remodeling. The immunomodulatory effect of SGB underlies its therapeutic benefit Raynaud's disease, hyperhidrosis, asthma, atopic dermatitis, eosinophilic dermatitis, polyangiitis, ulcerative colitis, complex regional pain syndrome, PTSD, mechanical trauma, headaches, pain, and anxiety (59, 60).

Stellate ganglion block may also reduce perioperative atrial fibrillation by improving hemodynamic stability. Attenuation of excessive sympathetic activity can limit perioperative tachycardia, vasoconstriction, and abrupt fluctuations in blood pressure and cardiac filling pressures. These effects may reduce atrial stretch, myocardial oxygen demand, and reflex sympathetic surges triggered by pain, blood loss, fluid shifts, or vasoactive therapy. By stabilizing loading conditions and autonomic responses, SGB may decrease atrial electrical heterogeneity and lower susceptibility to AF.

Perioperative condition and rationale for SGB as the modulator of surgical inflammation

During the perioperative phase, the balance between autonomic drivers and suppressors of AF is tilted heavily towards sympathetic influence (Figure 4). This sympathetic overdrive emerges due to perioperative stress (trauma to the tissues, electrolyte abnormalities, utilization of cardiopulmonary bypass), iatrogenic influences (utilization of medications, operative approach), and preoperative conditions (heart failure, diabetes, obesity). Sympathetic activation increases catecholamine release, disrupts calcium handling, and promotes atrial electrophysiological heterogeneity (54, 61). Tissue trauma, pro-inflammatory cytokines, oxidative stress, endothelial dysfunction, and microcirculatory impairment may destabilize atrial electrophysiology and increase susceptibility to POAF (62–64). Specifically, during cardiac surgery, atrial manipulation and ischemia-reperfusion injury may directly alter atrial conduction properties. An anti-arrhythmic procedure may also be added to address POAF risk directly (15, 65–67). Postoperatively, inflammation, hemodynamic alterations, autonomic imbalance, and structural remodeling perpetuate POAF even after the initial surgical insult has resolved (Figure 5).

Perioperative conditions create a complicated network if drivers and suppressors of POAF. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.
Figure 5. Perioperative conditions create a complicated network if drivers and suppressors of POAF. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.

Stellate ganglion block (SGB) may attenuate perioperative proarrhythmic effects via three complementary mechanisms: reduction of sympathetic outflow and of perioperative cardiovascular hemodynamics. and immunomodulation. The latter one includes suppression of pro-inflammatory cytokine release and attenuation of systemic inflammatory responses and is the focus of this review (68, 69). Both mechanisms provide a mechanistic rationale for its use, though SGB is not the only approach to modulating them (Figure 4) (70, 71).

SGB application to treat arrhythmias, including POAF

In treating cardiac arrhythmias, SGB was successfully used to manage ventricular and supraventricular tachyarrhythmias, as well as long QT syndrome (50, 56, 72). Most directly, this effect is achieved by prolongation of the atrial effective refractory period (48), SGB was shown to be effective in alleviating supraventricular arrhythmias (48, 73, 74). In a study enrolling 117 patients with ventricular arrhythmias secondary to acute coronary syndromes, SGB resulted in a significant reduction of defibrillation within the first 24 h (50). In some surgical settings, no reduction of POAF was observed, but early patient discharge suggests that SGB may be beneficial in ways beyond reducing arrhythmia burden (75). 2012 meta-analysis by demonstrated that the incidence of side effects did not differ significantly, even in patients receiving ongoing anticoagulation, demonstrating procedural safety (76).

SGB reduces the duration and frequency of AF episodes during emergence from anesthesia in the postoperative period, with effects observed across multiple clinical settings (Tables 1, 2). Evidence from non-cardiac settings supports the potential antiarrhythmic and hemodynamic effects of stellate ganglion block (Table 1). In patients with paroxysmal atrial fibrillation undergoing pulmonary vein isolation, unilateral left- or right-sided lidocaine SGB reduced AF inducibility by approximately 50%, with no significant difference between sides (45). In a randomized trial of 200 patients undergoing lung lobectomy, right-sided SGB with ropivacaine reduced postoperative AF from 10% to 3% and decreased other atrial arrhythmias from 38% to 20%; postoperative leukocytosis was also lower, suggesting a possible anti-inflammatory effect (37). In patients undergoing laparoscopic radical gastrectomy, SGB attenuated peri-intubation and intraoperative increases in heart rate and mean arterial pressure while preserving perioperative T-cell profiles, without delaying recovery or increasing adverse events (78). By contrast, in patients with inappropriate sinus tachycardia, SGB produced only a modest and transient reduction in resting heart rate. In context of cardiac surgery, a randomized controlled trial of 62 off-pump CABG patients found that those who received post-operative right SGB had lower rates of POAF (9.7% vs. 32.3%, p = 0.029) and reduced high-sensitivity troponin levels (Table 2) (51). An ongoing clinical trial is evaluating pre-surgery SGB in patients undergoing mitral or aortic valve procedures, with or without CABG (ClinicalTrials.gov ID NCT05357690). Low-level vagal nerve stimulation (LL-VNS) and epicardial injections significantly reduced POAF incidence and burden (79, 86). In contrast, the incidence of ventricular arrhythmias was not significant when SGB was applied (99). In off-pump CABG, pre-emptive left SGB with ropivacaine increased radial artery graft flow and was associated with a lower incidence of postoperative atrial fibrillation, reduced inotrope requirement, and fewer ischemic ECG changes, suggesting both anti-spasm and anti-arrhythmic benefits (88). SGB increased the diameter of internal mammary and radial arteries and altered norepinephrine-mediated contractile responses (100). Garneau et al. demonstrated that preoperative ultrasound-guided left stellate ganglion block improved intraoperative oxygenation and modestly altered right ventricular loading conditions. However, it did not attenuate pulmonary artery pressures during cardiopulmonary bypass separation. Small reductions in right ventricular functional indices and higher CK-MB levels were observed, but without increased perioperative complications (77). Zhou et al. showed that preemptive left SGB reduced the incidence and severity of cardiac surgery–associated acute kidney injury (78). This effect was mediated by improved intraoperative renal perfusion and concomitant decline in postoperative IL-6, CRP, and norepinephrine, indicating concurrent hemodynamic and anti-inflammatory benefits (78).

Table 1. Review of literature facusing on the effect of SGB and AF with emphasis on post-surgical AF.

SettingPMIDInterventionPopulationDesignOutcome
Non-cardiac surgical settings(45)Unilateral injection of lidocaine left or right (1:1)Patient with PAF scheduled for pulmonary vein isolation2:1 randomizedIn the SGB group, AF inducibility was decreased to half of the patients after SGB. No significant differences were observed between right and left SGB
(77)1:1 mixture of 1% lidocaine and 0.5% bupivacaine12 symptomatic and refractory to other treatment patients with inappropriate sinus tachycardiaObservationSGB blockade slightly lowers resting HR without affecting exercise HR for the first two hours and recovers to baseline at the 5th hour
(37)0.2% ropivacaine injected at the R stellate ganglion block200 patients undergoing lung lobectomyRandomizedAtrial fibrillation occurred in 3% of the SGB group and 10% of the C group (p = 0.045); other atrial arrhythmias in 20% vs. 38% (p = 0.005); and ventricular arrhythmias in 28% vs. 39% (p = 0.09). Leukocytosis in the SGB group was significantly lower than the control group.
(78)Stellate ganglion block (SGB) with 7 mL of 0.5% ropivacaine added to total intravenous anesthesia112 patients undergoing elective laparoscopic radical gastrectomy for gastric cancer; randomized into SGB group (n = 56) and control group (n = 56)Prospective randomized controlled observational studyHemodynamics: HR and MAP were significantly lower in the SGB group after intubation and during surgery (p < 0.05). No significant difference in NRS pain scores between groups at 2, 12, 24, and 48 h post-op (p > 0.05). Immune function: CD3⁺, CD4⁺, and CD4⁺/CD8⁺ levels were significantly better preserved in the SGB group; CD8⁺ levels were lower (p < 0.001) Safety: No significant differences in propofol dosage, awakening time, extubation time, or adverse reactions
(62)Preoperative ultrasound-guided right-sided stellate ganglion block (SGB) with 7 mL of 0.5% ropivacainePatients undergoing thoraco-laparoscopic McKeown esophagectomy for esophageal cancer (n = 100)Double-blind, randomized, placebo-controlled trial (1:1 allocation)No difference in POAF incidence (10% in both groups), but it was associated with improved postoperative recovery
Cardiac surgery(52)Postoperative right stellate ganglion block (RSGB) using 4 mL of 1% lidocaine and 0.25% ropivacaine62 adult patients undergoing OPCABG; randomized into RSGB group (n = 31) and control group (n = 31)Double-blind, randomized controlled trialPrimary: hs-cTnT levels significantly lower in RSGB group at 12 h, 24 h, and 7 days post-op (e.g., 132.7 vs. 202.6 ng/L at 24 h, p < 0.001) Secondary: Lower incidence of postoperative atrial fibrillation (9.7% vs. 32.3%, p = 0.029). Lower mean and max NRS pain scores within 24 h (p < 0.001). Lower rate-pressure product (RPP) values post-op (p < 0.05). No significant differences in opioid consumption, ICU stay, extubation time, or 30-day mortality
(58)Pre-emptive stellate ganglion block (SGB) using 10 mL of 0.5% ropivacaine administered before anesthesia induction100 patients undergoing elective off-pump CABG; randomized into SGB group (n = 50) and control group (n = 50)Prospective randomized controlled trialRadial artery blood flow significantly increased in SGB group (pre-op: 46.4 vs. 45.2 mL/min; post-anastomosis: 60.0 vs. 47.3 mL/min; p < 0.05). Lower incidence of atrial fibrillation in SGB group (3 vs. 9 patients; p = 0.048). Lower need for inotropic agents and ST-segment elevation in SGB group. Angiographic evidence of reduced radial artery spasm in SGB group (1 vs. 7 cases; p = 0.023).
(61)Preemptive Lesft Stellate Ganglion Block (L-SGB) with 5 mL 0.375% ropivacaine administered after general anesthesia (GA) induction138 patients in intention-to-treat (ITT), (69 SGB, 69 control) and 119 patients in per-protocol analysis (PPA) (59 SGB, 60 control). Mixed cardiac surgical procedures (CABG 64%, valve 26%, mixed 10%); ASA III-IV.Prospective randomized control trialIncidence and severity of CSA-AKI was significantly lower in the SGB group. The intraoperative resistive index and pulsatility index (PI) of left renal artery in TEE were significantly lower in the SGB group. Postoperatively, the SGB group demonstrated significant reductions in IL-6, CRP, and norepinephrine.
(59)L-SGB before induction of GA under USG guidance20 patients with L-SGB and 20 controls—90/80% CABG, others valve surgeryProspective cohort study with matched controlsL-SGB did not reduce PAP at separation from CPB, increased CVP, mildly reduced RV function by TEE and higher CK-MB, but higher PaO2/FiO2 ratios.
(60)L-SGB before induction of GA through paratracheal approach with 15 mL 0.25% bupivacaine18 patients undergoing CABG, 19 patients matchedProspective RCTDilation of left radial and mamarian internal arteries, increased reactivity to noradrenaline.

EP, electrophysiology.

Table 2. Animal research demonstrating immunological effects of the SGB.

ReferencesSurgery typePlexus block interventionImmunological outcomes of the blocksOutcomes of the blockRemarks
Stavrakis et al. (79)Middle cerebral artery occlusion (MCAO) model in diabetic ratsStellate Ganglion Block (SGB) using 1% lidocaine via percutaneous posterior approach, administered 15 min before reperfusion and again at 20 and 44 h post-reperfusion
Liu et al. (80)Lipopolysaccharide (LPS)-induced Acute Lung Injury (ALI) via intratracheal instillation in ratsStellate ganglion block (SGB) performed via lateral percutaneous approach using 0.3 mL of 0.5% ropivacaine, administered 30 min after LPS instillation
Yokoyama et al. (81)Sleep deprivation model using modified multiple platform water environment methodRight Stellate Ganglion Block (SGB), posterior approach, 0.2 mL of 0.2% bupivacaine, once daily for 6 days before and during sleep deprivationRight SGB alleviates cognitive dysfunction induced by sleep deprivation via anti-inflammatory and anti-apoptotic effects in the hippocampus; potential preventive strategy for sleep-related memory impairment
Wu et al. (82)Hemorrhagic shock model in rats with mesenteric lymph drainage and resuscitationStellate Ganglion Block (SGB) using 0.2 mL of 2.5% ropivacaine via right-sided injection; confirmed by Horner's syndrome
Zhu et al. (51)Canine model: open-chest LAD ligation (MI induction)Microinjection of cromolyn sodium (mast cell stabilizer) into left stellate ganglion (LSG)Local dose: 25 mg cromolyn sodium; also oral ketotifen (2 mg every 5–6 days) used for systemic comparison
Zhang et al. (83)Stellate ganglionectomy and/or thoracic vagotomy in rats; chemical treatments with capsaicin or 6-OHDA to the stellate ganglionSurgical stellate ganglionectomy or local capsaicin injection into the stellate ganglionStellate ganglion contributes to neurogenic inflammation via nonvagal spinal sensory fibers. SGB or capsaicin application reduces inflammation and SP-IR axon density, suggesting a regulatory role in airway neuroimmune responses.
Rizzo et al. (84)Canine myocardial infarction (MI) model created ∼1 month after left stellate ganglion (LSG) manipulationAdeno-associated virus (AAV)–mediated IL-6 overexpression injected into the LSG (vs. empty AAV vector)
Moss et al. (85)Non-surgical; experimental asthma model in mice using ovalbumin sensitization and challengeStellate Ganglion Irradiation (SGI) using infrared polarized light (1,000 mW/cm2, 15 min/session, 6 sessions)
Fatahian et al. (86)Partial liver resection in aged rat model (POCD induction)Preoperative stellate ganglion block (SGB) with 0.25% bupivacaine (0.2 mL)Improved spatial memory (shorter probe time, more platform crossings, better quadrant performance in Morris water maze)SGB prevents POCD via inhibiting TLR4/NF-κB-mediated neuroinflammation; effect reversed by TLR4 agonist LPS
Tse et al. (87)Experimental spinal cord injury (SCI) model in rats (laminectomy + compression at T10)Stellate Ganglion Block (SGB), performed 10 min post-SCI via dissection and disruption of the right stellate ganglionSGB effectively mitigates neuropathic pain and secondary injury post-SCI by modulating inflammation, apoptosis, and autophagy. It may serve as a promising non-pharmacological intervention for SCI-related pain and recovery.
Yildirim et al. (88)Non-surgical; ovalbumin (OVA)-induced airway hyperresponsiveness (AHR) mouse modelStellate Ganglion Block (SGB), performed using 0.15% ropivacaine (0.1 mL), with varying frequencies (2–8 times); 6 interventions (OVA + SGB6 group) showed optimal effect
Duffy et al. (89)Left anterior descending coronary artery occlusion (LADO) in beagle dogs to induce myocardial ischemiaLocal microinjection of Endothelin-1 (ET-1) into the left stellate ganglion (LSG); not a traditional anesthetic block but a targeted activationET-1 activation of the LSG aggravates ischemia-induced ventricular arrhythmias via ETA-R signaling and inflammation. Findings suggest a novel mechanism and therapeutic target for malignant arrhythmias involving sympathetic neural remodeling.
Sugimoto et al. (90)Moderate to severe traumatic brain injury (TBI) patients in ICUUltrasound-guided stellate ganglion block (SGB) at C6 with 8 mL 0.5% levobupivacaine
Wang et al. (91)Experimental rat model of severe acute pancreatitis (SAP) induced by retrograde injection of sodium taurocholateStellate Ganglion Block (SGB) via surgical dissection and ligation of the right cervical sympathetic nerve trunkSGB attenuated SAP-induced acute lung injury through anti-inflammatory mechanisms.
Wang et al. (92)Experimental canine model of acute myocardial infarction (AMI) via coronary occlusionGene therapy: microinjection of adeno-associated virus (AAV) vector encoding IL-10 into the left stellate ganglion (LSG)Chronic IL-10 overexpression via AAV in the LSG modulates cardiac sympathetic remodeling and suppresses ischemia-induced ventricular arrhythmias. This neuromodulation strategy shows promise as a gene therapy-based neuroimmunotherapy for cardiovascular diseases involving sympathetic overactivation.
Chouairi et al. (50)Rat model of chronic heart failure (CHF) induced by left anterior descending (LAD) coronary artery ligationBilateral Renal Denervation (RDN): surgical cutting of renal nerves + 70% ethanol application around renal vesselsRDN reduces ventricular arrhythmogenesis in CHF by attenuating GM-CSF–induced macrophage activation and neuroinflammation in stellate ganglia. Targeting the GM-CSF signaling axis may offer a novel therapeutic strategy for antiarrhythmic effects in CHF.
Zeisberger et al. (93)Obesity-induced cardiac sympathetic neuropathy model in rats (via high-fat diet)Pharmacological intervention: Imperatorin (IMP) administration and P2X4 shRNA injection targeting stellate sympathetic ganglion (SG)Imperatorin alleviates obesity-induced cardiac sympathetic neuropathy by inhibiting P2X4 receptor expression and activity in satellite glial cells of the SG. Its protective effects are linked to anti-inflammatory action, suppression of pyroptosis, and ERK pathway inhibition. IMP shows promise as a therapeutic agent for obesity-related autonomic dysfunction.
Li et al. (94)Cecum ligation and puncture (CLP) to induce sepsis and acute lung injury (ALI) in ratsStellate Ganglion Block (SGB) via transection of the cervical sympathetic trunk (TCST)SGB significantly attenuates sepsis-induced acute lung injury in rats by modulating systemic inflammation. It reduces proinflammatory cytokines, neutrophil infiltration, and NF-κB signaling, while enhancing anti-inflammatory IL-10. SGB may offer a novel therapeutic approach for sepsis-related lung injury.
Yu et al. (95)CSTT is considered a form of Stellate Ganglion Block (SGB) targeting the sympathetic nervous system
Leftheriotis et al. (73)LAD ligation to induce myocardial infarction and chronic heart failure (CHF) in ratsMicroinjection of clodronate liposomes into bilateral stellate ganglia (SGs)
Sanghai et al. (76)Left thoracotomy in canine model with LAD occlusion (acute ischemia)Local microinjection into LSG: Leptin (18 μg) ± mast cell stabilizer DSCG (25 mg)
Shen et al. (96)Left thoracotomy in canine model (normal structural heart)Local microinjection into LSG: IL-17A (2.5 μg) ± anti-IL-17A mAb (2.5 mg/mL)
Scher (74)None (Study used a rat model of acute lung injury via bleomycin instillation; no surgical intervention)Pharmacological inhibition of stellate ganglion (SG) inflammation using oral minocycline (20 mg/kg/day), not a physical block or resection
Duan et al. (97)Large animal model with induced inappropriate sinus tachycardia (IST) via right stellate ganglion stimulationImplantable closed-loop piezoelectric theranostic platform (TP-IST) enabling on-demand vagus nerve stimulation (VNS)
Li et al. (98)Open-heart surgery model [canine sterile pericarditis mimicking postoperative atrial fibrillation (POAF)]Stellate Ganglion Nerve Stimulation (SNS) ± Vagus Nerve Stimulation (VNS) to induce autonomic dysfunction

The available studies are heterogeneous in population, surgical setting, laterality of blockade, timing of administration, local anesthetic choice, concentration, and injected volume. Several studies included small samples, used observational designs, or evaluated surrogate outcomes such as heart rate, hemodynamic responses, inflammatory markers, or AF inducibility rather than clinically significant postoperative atrial fibrillation. Differences in arrhythmia monitoring, AF definitions, follow-up duration, perioperative β-blocker or antiarrhythmic use, and underlying patient risk further limit comparisons across studies. In addition, some interventions were performed before anesthesia induction, whereas others were administered intraoperatively or postoperatively, making the optimal timing uncertain. Generalizability is also limited because results from non-cardiac surgery, electrophysiology procedures, or patients with inappropriate sinus tachycardia may not directly apply to cardiac surgical patients, in whom cardiopulmonary bypass, atrial manipulation, ischemia-reperfusion injury, and postoperative inflammation substantially alter arrhythmia risk. Although reported safety outcomes are reassuring, most trials were underpowered to detect uncommon but serious complications, and procedural success is highly dependent on operator experience and imaging guidance.

Modulation of the inflammatory mechanism as the beneficial mechanism of SGB

Considering the immunomodulatory nature of the beneficial effect of SGB on POAF we conducted a search of Pubmed utilizing “stellate ganglion AND (inflammation OR immunity)” retrieving 105 manuscripts, with 36 representing original studies in animal models (Table 2) and clinical practice (Table 3).

Table 3. Modulation of the perioperative human inflammation in the context of SGB.

ReferencesSurgery typePlexus block interventionImmunological outcomes of the blocksClinical outcomes of the blockRemarks
Lv et al. (69)Cardiac surgery with cardiopulmonary bypass (valve replacement/repair)Preoperative ultrasound-guided left stellate ganglion block (SGB) with 0.5% ropivacaine (7 mL)SGB modulates the neuroendocrine-immune axis, stabilizes the inflammatory response, and enhances short-term prognosis without major adverse effects
Zhao et al. (59)Not a surgical model; clinical observation in chronic ulcerative colitis (CUC) patientsStellate Ganglion Block (SGB), used to modulate sympathetic nervous system activitySGB may modulate immune dysfunction in autoimmune diseases like ulcerative colitis; further research is encouraged to explore its immunoregulatory potential
Tsuchiya (101)Not a surgical study; includes case reports involving stellate ganglion block for post-COVID taste/saliva disordersStellate Ganglion Block (SGB), performed with local anesthetics (e.g., bupivacaine); right-sided followed by left-sided blockSGB may alleviate COVID-19-associated taste/smell disorders by modulating dysautonomia. Case reports show rapid and sustained recovery, but high-quality clinical trials are needed to confirm efficacy.
Yang et al. (68)Non-surgical; patients with traumatic brain injury (TBI) not requiring craniotomyStellate Ganglion Block (SGB), unilateral, performed every other day for 1 week using 4 mL 2% lidocaine + 1.5 mL 0.75% bupivacaine + 2.5 mL salineSGB modulates the neuro-endocrine-immune network in TBI patients, reducing inflammation and enhancing CGRP-mediated vasodilation. It may offer a novel strategy for managing secondary brain injury and neuroinflammation.
Zakkar et al. (63)None (Healthy volunteer study; no surgical intervention)Stellate Ganglion Block (SGB) using 7 mL of 1% lidocaine via anterior paratracheal approachNo clinical disease model; physiological changes observed in healthy volunteersSGB induces small but significant immunomodulatory effects by altering lymphocyte subset distribution and reducing NK cell activity. These effects are likely mediated via sympathetic nervous system modulation rather than hypothalamic-pituitary-adrenal axis. Findings suggest potential immune regulatory roles of SGB beyond pain management.
Yuan and Chen (102)Emergency surgery under general anesthesia in elderly patients with septic shockStellate Ganglion Block (SGB), ultrasound-guided right-sided injection of 0.5% ropivacaine (4 mL) + dexamethasone (5 mg) + mecobalamin (0.5 mg), total 6 mLSGB significantly improves respiratory and circulatory function in elderly patients with septic shock by reducing inflammation, enhancing gas exchange, and shortening mechanical ventilation duration. It offers a promising nonpharmacological adjunct in critical care settings.
Ashikawa et al. (103)Stellate Ganglion Laser Irradiation (SGL), non-invasive alternative to SGB, performed using SUPER LIZER HA2200™SGL was effective in treating severe orbital inflammation and oculomotor dysfunction secondary to herpes zoster ophthalmicus. It may enhance cerebral and ocular blood flow, contributing to symptom resolution. SGL is less invasive than SGB and may be a valuable adjunct in multimodal early treatment.
Xue et al. (104)Elective laparoscopic gastrointestinal (GI) surgery in elderly patientsUltrasound-guided Stellate Ganglion Block (SGB) with 4 mL of 0.25% ropivacaine administered preoperativelPreoperative ultrasound-guided SGB significantly reduces early POCD in elderly patients undergoing GI surgery. The protective effect is likely mediated by attenuation of oxidative stress and inflammation. SGB also improves short-term pain control and may reduce the need for potent analgesics like butorphanol.
Sugimoto et al. (90)None (Study involved healthy volunteers; procedure was a right-sided stellate ganglion block)Stellate Ganglion Block (SGB) using 6 mL of 1% lidocaine at the C6 transverse process
Dieleman et al. (41)None (Study involved trauma patients receiving stellate ganglion block; no surgical intervention was performed)Right-sided Stellate Ganglion Block (SGB) using 8 mL of 0.75% ropivacaine, administered 4 times over 48 h
Yang et al. (68)Left Cardiac Sympathetic Denervation (LCSD) via videoscopic transthoracic approachSurgical removal of lower half of left stellate ganglion and thoracic ganglia T2–T4

In animal models of lung injury, SGB decreased vascular permeability, peripheral mononuclear leukocyte (PML) infiltration, and serum IL-6 levels (80). Several inflammatory cytokines (such as MCP-1 and TNFα) and mediators (including NFκB) were reduced in stroke-induced generalized inflammation, as evidenced in canine models (80). The moderating effect of SGB on proinflammatory cytokines (TNFα, IL-1β) was not accompanied by a rise in anti-inflammatory cytokines (IL-10). In mechanical trauma victims SGB reduced macrophage, mast cells and NK cell infiltration (60, 81). Reduced leukocyte infiltration correlated with diminished incidence of POAF. Human studies showed that SGB correlated with inflammatory or immune responses (Table 3). Case reports have demonstrated resolution of inflammation driven by conditions such as seborrheic dermatitis, eosinophilic dermatitis, polyangiitis, gastrointestinal autoimmune disorders, or zoster reactivation, all of which are linked to aberrant immunity (59). SGB reduced serum IL-8 in ulcerative colitis (59). Although direct evidence linking reduced IL-8 to lymphocyte infiltration was not presented, the authors’ suggestion aligns with changes in macrophage and NK cell infiltration reported elsewhere (81). It is also noteworthy that symptoms were not reduced in patients (n = 90) as compared to control individuals (n = 30). In trauma, Liu et al. showed a decrease in inflammatory cytokines (IL-1β, IL-6, and TNF-α) but not in immunosuppressive cytokines (IL-4 and IL-10) if SGB was applied (60). In another study SGB reduced inflammatory mediators (NFκB65) and proinflammatory cytokines (TNFα, IL-6, and IL-1β) (46, 82). In patients with subarachnoid hemorrhage, SGB administered over four days immediately after the insult, was associated with a reduction in proinflammatory cytokines (TNF-α, IL-6, and IL-1β), accompanied by improvements in cerebral blood flow and functional outcomes 7 days after injury (83). Anatomical examination showed ganglionitis with heavy infiltration of macrophages and T cells in patients with long QT syndrome or catecholamine-related polymorphic ventricular tachycardia (84). Chronic inflammatory infiltration leads to electrical instability underlying cardiac arrhythmias and sudden death syndrome (85, 87, 89). In healthy volunteers induction of SGB was associated with a significant decrease in T helper cell activity, and some impact on cytotoxic T cells (90). In healthy volunteers, SGB impacted leukocyte composition (NK and B cells) (81). SGB led to reduced macrophage infiltration. Prior studies demonstrated the effect of SGB on NK cells (81, 91, 92). Both studies showed a reduction in ventricular tachyarrhythmias (80, 93). The immunological effect of SGB was associated with clinically significant outcomes (Table 3). Stroke size was reported to be minimized by attenuating the NFκB pathway and microglial activation (94). Post-operative cognitive decline is less frequent with SGB (94, 95). Reduced hippocampal inflammation translated into improved memory and learning. Both effects can mitigate the adverse impact of surgery on cognition and, via neurocognitive pathways, may indirectly modulate inflammation and cardiac arrhythmias (96, 97).

In summary, the available evidence suggests that modulating stellate ganglion activity in hyperinflammatory states may be associated with clinically meaningful benefits. Whether SGB can dampen the initial inflammatory response and affect long-term outcomes remains an open question (Figure 6). However, these findings should be interpreted cautiously. The evidence includes small trials, observational studies, case reports, heterogeneous patient populations, repeated-block protocols, and interventions combining SGB with additional agents such as dexamethasone. Several studies measured surrogate inflammatory biomarkers rather than clinically important outcomes, and the direction of immune effects was not uniform, with some reports suggesting transient immunosuppression. Findings from post-COVID symptoms, ulcerative colitis, trauma, and healthy volunteers cannot be directly extrapolated to postoperative atrial fibrillation. Nevertheless, they provide mechanistic support for the hypothesis that SGB may reduce POAF by attenuating perioperative sympathetic activation, cytokine release, oxidative stress, and inflammation-mediated atrial remodeling. Larger controlled studies are required to determine whether these immunological effects translate into meaningful reductions in postoperative arrhythmias.

Deployment of SGB will reduce both inflammatory drive and sympathetic overcharge in perioperative period. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.
Figure 6. Deployment of SGB will reduce both inflammatory drive and sympathetic overcharge in perioperative period. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.

Although the direct effects of stellate ganglion block are short-lived, emerging evidence suggests that stellate ganglion activity may remain dysregulated beyond the immediate perioperative period, indicating effects that may extend beyond surgery-induced hyperinflammation (Figure 6) (98). Immunomodulation is likely complementary to other mechanisms. By attenuating sympathetic activity, SGB may improve hemodynamic stability, modulate baroreflex responses, and reduce perioperative tachycardia, vasoconstriction, blood pressure fluctuations, atrial stretch, and variability in filling pressures. It may also limit sympathetic surges caused by surgical stress, pain, fluid shifts, or vasoactive therapy, thereby reducing electrophysiological heterogeneity. These pathways remain incompletely defined and should be considered plausible complementary mechanisms rather than established effects.

Conclusion for practical approach to SGB application in the setting of cardiac surgery

Postoperative atrial fibrillation results from the interaction of a vulnerable atrial substrate with perioperative sympathetic activation, inflammation, hemodynamic instability, and structural and electrophysiological remodeling. Stellate ganglion block may influence several of these pathways by reducing cardiac sympathetic outflow, limiting catecholamine-mediated electrical instability, stabilizing perioperative hemodynamics, and attenuating inflammatory and neuroimmune responses. Preliminary clinical studies suggest that SGB may reduce AF inducibility, postoperative atrial arrhythmias, and selected inflammatory markers, including in cardiac and non-cardiac surgical populations. However, the available evidence remains limited by small sample sizes, heterogeneous patient populations, variable block techniques, inconsistent timing and laterality, and reliance on surrogate outcomes. Accordingly, SGB should not currently be recommended as routine prophylaxis for POAF. Its use is best limited to clinical trials or carefully selected high-risk patients in whom sympathetic overactivity is considered an important arrhythmogenic driver and the procedure can be performed by an experienced clinician under image guidance. Established POAF prevention and treatment strategies, including correction of reversible triggers, β-blockade when appropriate, rhythm or rate control, and individualized anticoagulation, should remain the standard of care. Current evidence suggests that SGB is associated with changes in immune and inflammatory signaling (Figure 7A), potentially shifting the balance between proinflammatory processes and recovery pathways involved in POAF (Figure 7B). These observations provide a basis for future mechanistic studies investigating the role of SGB in modulating postoperative arrhythmias. Future studies could examine the extent and frequency of this specific inflammatory process to identify patients who may benefit most from SGB.

SGB reduces systemic and cellular inflammation **(A)** resulting in partial recovery between drivers and suppressors of POAF **(B)**. Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.
Figure 7. SGB reduces systemic and cellular inflammation (A) resulting in partial recovery between drivers and suppressors of POAF (B). Original illustration owned by the Mayo Foundation for Medical Education and Research. Reproduced with permission. © Mayo Foundation for Medical Education and Research. All rights reserved.

Future multicenter randomized trials should standardize block laterality, timing, local anesthetic, dose, rhythm monitoring, and safety reporting. They should also determine whether the immunomodulatory and hemodynamic effects of SGB translate into sustained reductions in clinically meaningful POAF, thromboembolic complications, length of stay, and long-term cardiovascular outcomes. Until such evidence is available, SGB should be regarded as a promising but investigational adjunct rather than an established perioperative therapy.

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Footnotes

Edited by: Marco Fiore, Università degli Studi della Campania 'Luigi Vanvitelli', Italy

Reviewed by: Alexander E. Berezin, Paracelsus Medical University, Austria

Yang Liu, Qilu Medical University, China

Statements

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Funding

The author(s) declared that financial support was not received for this work and/or its publication.

Author contributions

DZ: Writing – original draft, Writing – review & editing, Conceptualization, Software. MR: Writing – review & editing. AS-S: Data curation, Writing – review & editing. MK: Writing – review & editing, Data curation. WL: Writing – review & editing, Resources, Validation, Formal analysis. EW: Data curation, Writing – review & editing. DD: Writing – review & editing. KL: Resources, Conceptualization, Methodology, Validation, Visualization, Project administration, Formal analysis, Supervision, Writing – original draft, Writing – review & editing, Software, Data curation, Investigation.

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Citation

Zhu, D., et al. (2026). A narrative review of stellate ganglion block in management of post-operative atrial fibrillation with focus on immunomodulatory mechanisms. Frontiers in Anesthesiology, Volume 5. https://doi.org/
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5 - 2026

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© 2026 Zhu, Radosevich, Szofer-Sendrowska, Kowalik, Li, Wittwer, Diedrich and Laudanski.

License: https://creativecommons.org/licenses/by/4.0/

*Correspondence: Krzysztof Laudanski

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