Background and Objectives: This study aimed to investigate the association between circulating monocyte subset profiles and carotid artery stenosis (CAS) severity and to examine their relationships with inflammatory and atherosclerosis-related parameters. Materials and Methods: This cross-sectional study included 73 adult patients who underwent carotid Doppler ultrasonography. Participants were classified according to internal CAS severity as <50% (n = 44) or ≥50% (n = 29). Monocyte subsets were analyzed using flow cytometry and categorized as classical (CD14++CD16−), intermediate (CD14++CD16+), and non-classical (CD14+CD16++) monocytes. Serum MCP-1 concentrations were measured using an enzyme-linked immunosorbent assay. Clinical characteristics, biochemical parameters, inflammatory indices, and carotid intima–media thickness (cIMT) were compared between the groups. Multivariate logistic regression analyses were performed to identify independent associations with significant stenosis. Results: Patients with CAS ≥50% exhibited significantly higher classical monocyte percentages and lower non-classical monocyte percentages than those with CAS < 50% (p = 0.044 and p = 0.027, respectively). Intermediate monocyte percentages did not differ significantly between the groups. Significant stenosis was also associated with a higher white blood cell count, neutrophil count, systemic inflammatory response index, fibrinogen, and HbA1c levels. Non-classical monocyte percentages showed a significant inverse correlation with cIMT (r = −0.320, p = 0.006). In a multivariable model adjusted for age, sex, and systolic blood pressure, lower non-classical monocyte percentage was associated with significant CAS (OR 0.872, 95% CI 0.765–0.994; p = 0.040). However, this association was no longer statistically significant after further adjustment for fibrinogen, neutrophil count, and HbA1c, whereas fibrinogen remained independently associated with significant CAS. Conclusions: Lower circulating non-classical monocyte percentages were associated with significant CAS and inversely correlated with cIMT and inflammatory markers. However, the attenuation of this association after adjusting for inflammatory parameters suggests that monocyte subset distribution should be interpreted within the broader inflammatory context that accompanies advanced carotid atherosclerosis.

Objective: The aim of this study was to evaluate the technical success, procedural safety, and short-term clinical outcomes of the retrograde pedal approach in patients with chronic limb-threatening ischemia following unsuccessful antegrade revascularization. Methods: This retrospective study included 68 consecutive patients (mean age, 68.5±8.2 years; 70.6% male) presenting with severe chronic limb-threatening ischemia (Rutherford categories 4–6). All underwent an attempted retrograde pedal or anterior tibial artery (ATA) access after initial antegrade or contralateral crossover approaches proved unfeasible. Ultrasound-guided access was performed via the posterior tibial artery (66.2%) or ATA (33.8%) following failure of conventional routes. Primary endpoints were access success, technical success, clinical success (freedom from major amputation for at least 6 months), and complication rates. Results: Successful retrograde puncture and target vessel access were achieved in 64 patients (94.1%). Among these, lesion crossing and luminal patency were accomplished in all cases, yielding a 94.1% technical success rate. Interventions included balloon angioplasty (82.3%) and stenting (11.7%), notably including five cases of proximal iliac stenting through distal access. No major access-site complications occurred; minor complications (16.2%) were managed conservatively. Clinical success and symptom improvement were achieved in 88.2% (60/68) of the entire patient cohort. During follow-up, the major amputation rate was 10.3% (7/68), and the mortality rate was 2.9% (2/68). Conclusion: The retrograde pedal approach represents a safe, versatile, and highly effective bailout strategy for complex lower extremity chronic total occlusions. It provides excellent technical and limb salvage rates with minimal access-site complications when conventional antegrade revascularization strategies prove unsuccessful.

Objective: The primary goal in the treatment of abdominal aortic aneurysms (AAA) is to reduce long-term morbidity and mortality by preventing aneurysm rupture. This study aimed to evaluate the effect of aneurysm morphology before endovascular aneurysm repair (EVAR) in AAA on prognosis, compare the changes in aneurysm morphology after mid- and long-term follow-up after EVAR with extensive randomized studies, and evaluate the treatment efficacy. Methods: A total of 75 patients who were evaluated with pre-operative computed tomography angiography (CTA) with a preliminary diagnosis of AAA in our institution and had a perioperative digital subtraction angiography examination and at least one post-operative follow-up CTA examination >12 months were included in the study. Additional interventions were recorded during the procedure, complications, endoleak types, demographic data, and changes in aneurysm morphology. The results were compared with the data in the literature. Results: The mean follow-up period was calculated as 37 months. A mean decrease of 4.5 mm was detected in AAA diameter. A mean reduction of 4 mm in thickness was observed in accompanying common iliac artery (CIA) aneurysms (p=0.016). Complications were observed in 32% of the patients. The most common complication was Type 2 endoleak, which was observed in 25% of the patients. We did not observe a significant difference in pre-operative and post-operative mean thrombus thickness (p=0.588). Endoleak rate was increased in patients with bilateral CIA aneurysms accompanying AAA (p=0.044). While there was no significant effect of changing the AAA diameter in those with increasing thrombus diameter, it was observed that the aortic diameter decreased in those with decreasing thrombus diameter (p=0.012). Conclusion: Our 10-year experience with EVAR shows that many complications may occur after stent grafting. Caution should be exercised regarding Type 2 endoleaks. Lifelong follow-up is necessary to prevent aneurysm rupture after EVAR.