Citations

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.

Variability in novel inflammatory markers (HBP and SAA) post-surgery could indicate ongoing perioperative inflammation. This pilot cohort study collected blood from 99 patients undergoing elective cardiac surgery at baseline, 24 hours, 7 days, and 3 months post-surgery. Inflammatory markers (HBP, SAA, PCT, CRP, IL-6) were measured with a point-of-care device. Demographic and clinical data were extracted from health records. Serum SAA increased significantly in the acute postoperative phase (M e [IQR];SAA baseline =81.1[87] vs SAA 24hr= 232.65[88.02];U[72]=2343,p<0.0001), remained elevated at 7 days (Me 7d =252.6[88.56];U[57]=1484,p<0.0001) and were still more pronounced than baseline at t 3m (Me 3m =118.44[101.52];U[38]=448,p=0.0008). HBP showed a significant rise at seven days (HBP baseline =45[26;89] vs HBP 7d =121[69.75;224.5]; U[56]=805,p<0.0001) then returned to near baseline by t 3m (Me 3m =32.5[15.75;98.5]). Traditional inflammatory markers PCT, CRP, and IL-6 demonstrated a rapid increase at t 24h and plateaued at t 7d . None of the biomarkers showed variability at baseline or postoperatively with preoperative status or postoperative complications. Cluster analysis of the inflammatory markers at 24 hours (t 24h ) identified distinct subgroups. Cluster #1-patients with a modest increase in all markers; Cluster#2 characterized with a robust increase in IL-6; Cluster #3 showed increase in CRP and decline in HBP; Cluster #4 showed a modest increase in IL-6 and decline in HBP; Cluster #5 represented a decline in both CRP and SAA. Patients in these clusters differ with respect to age, pre-existing peripheral artery disease, and borderline differences in perioperative acetaminophen use. SAA and HBP remain elevated longer than IL-6, CRP, and PCT after surgery, suggesting that inflammation may persist beyond 3 months.