Objective: Resistin has been associated with increased risk for cardiovascular complications. However, the underlying mechanisms are not yet fully elucidated. This study aimed to investigate whether resistin modulated plasma cytokines, chemokines, and growth factors in patients undergoing carotid revascularization procedures. Methods: Patients undergoing carotid artery stenting (CAS) and carotid endarterectomy (CEA) at a single institution were recruited to participate. Blood plasma collection was performed within 48 hours following intervention using an established protocol, and demographics were recorded. Samples were stored at -80 °C and analyzed with a Luminex magnetic beads-based assay. Patients were divided into tertiles based on plasma resistin concentration (mean pg/mL): low (2237.6, n=30), medium (4252.3, n=31), and high (7467.5, n=30). Levels of cytokines were compared using ANOVA. Results: 91 male patients with a mean age of 69 years were included (50 CAS, 41 CEA). Most patients had a history of smoking (84%). Medical comorbidities included hypertension (93%), diabetes (45%), CAD (49%), and obesity (44%). The distribution of comorbidities was similar within each tertile. The levels of resistin were not significantly different in CAS vs CEA patients. There was also no significant difference in various growth factors (VEGF-A, M-CSF, and GM-CSF), neurotrophic factors (BDNF and β-NGF), or adhesion molecules (ICAM-1 and VCAM-1). However, significantly higher levels of the pro-inflammatory cytokines/chemokines were observed in the high resistin tertile compared to the low tertile: TNF-α (p < 0.001), IL-6 (p < 0.05), IL-12p40 (p < 0.01), IL-12p70 (p < 0.05), MIP-1α (p < 0.05), MIP-1β (p < 0.05), and MCP-3 (p < 0.01). Similarly, significantly higher levels of the aforementioned pro-inflammatory cytokines (except MCP-3) were observed in the high compared to the medium tertile. Conclusions: Patients with higher resistin levels exhibit higher levels of inflammatory profiles post-intervention independent of procedure type or comorbidities, implicating that resistin-induced inflammation may be a mechanism for resistin-related vascular complications.