Mi-Er Jiang

Background: Peripheral artery disease accounts for more than 400 000 hospitalizations in the USA and results in symptoms ranging from claudication to gangrene. Recent advances in endovascular techniques have led to a more aggressive approach for treating peripheral artery disease. The aim of this retrospective study was to evaluate the outcomes of endovascular interventions on TransAtlantic InterSociety Consensus (TASC) II C and D femoropopliteal occlusive disease. Methods: Data for all patients undergoing endovascular interventions for femoropopliteal occlusive disease from December 2007 through December 2010 were reviewed. Demographic data, risk factor data, preprocedural and postprocedural ankle-brachial indices, technical success rates, and complication rates were obtained. Primary, assisted primary, and secondary patency were determined by Kaplan-Meier survival analysis. Univariate and multivariate analyses were performed to identify factors adversely affecting primary patency. Results: The study group included 52 TASC II C and 106 TASC II D limbs in 126 patients (mean age, (68.0±18.0) years). The technical success rate was 91.1%. Complications occurred in 19 limbs (12.0%), including 8 (5.1%) major complications. The mean follow-up period was (17.6±5.1) months (range, 12.0-48.0 months). Primary patency rates at 1, 2, 3, and 4 years were 95%, 78%, 74%, and 74% in TASC II C lesions and 89%, 62%, 52%, and 52% in TASC II D lesions, respectively. Secondary patency rates at 1, 2, 3, and 4 years were 97%, 94%, 94%, and 94% in TASC II C lesions and 97%, 95%, 83%, and 83% in TASC II D lesions, respectively. It is significantly different between primary patency rates (P 0.05). Predictors of restenosis/occlusion included hyperlipidemia, lesion length, and popliteal artery involvement. Conclusions: Endovascular treatment of TASC II C and D femoropopliteal artery occlusion has a high technical success rate with favorable mid-term secondary patency rate. Hyperlipidemia, lesion length, and popliteal artery involvement were independent risk factors for in-stent restenosis.

To analyze the experience with diagnosis and surgical treatment of visceral artery aneurysms (VAAs). From June 2003 to December 2008, 8 patients (2 male and 6 female) with 9 VAAs underwent surgical treatment. Mean age was 49 years (ranged from 30 to 72 years). The site of aneurysmal disease was splenic artery in 4 cases, superior mesenteric artery in 2 cases, renal artery in 2 cases (3 aneurysms). In 1 patient of splenic artery aneurysm, portal vein hypertension coexisted. All the VAAs of preoperative diagnostic workup consisted of a ultrasound, computed tomography (CT) scan, and digital subtraction angiography. Six patients were operated on and two patients was treated with endovascular procedures. Only one small VAAs was treated with follow-up. No deaths or major complications occurred in the perioperative period. All the patients remained symptom free during a follow-up of 26.5 months (ranged from 2 to 60 months). Follow-up consisted of clinical and ultrasound scan examinations or CT scan at 1 and 6 months, and yearly thereafter. Aggressive approach to the treatment of VAAs is essential. Elective open surgical treatment and an endovascular procedure of visceral artery aneurysms are both safe and effective, and offers satisfactory early and long term results. There is some evidence that small (< 2 cm) and asymptomatic VAAs may be safely observed.

Background: Peripheral arterial disease (PAD), a major manifestation of atherosclerosis, is associated with significant cardiovascular morbidity, limb loss and death. However, mechanisms underlying the genesis and progression of the disease are far from clear. Genome-wide gene expression profiling of clinical samples may represent an effective approach to gain relevant information. Results: After histological classification, a total of 30 femoral artery samples, including 11 intermediate lesions, 14 advanced lesions and 5 normal femoral arteries, were profiled using Affymetrix microarray platform. Following real-time RT-PCR validation, different algorithms of gene selection and clustering were applied to identify differentially expressed genes. Under a stringent cutoff, i.e., a false discovery rate (FDR) <0.5%, we found 366 genes were differentially regulated in intermediate lesions and 447 in advanced lesions. Of these, 116 genes were overlapped between intermediate and advanced lesions, including 68 up-regulated genes and 48 down-regulated ones. In these differentially regulated genes, immune/inflammatory genes were significantly up-regulated in different stages of PAD, (85/230 in intermediate lesions, 37/172 in advanced lesions). Through literature mining and pathway analysis using different databases such as Gene Ontology (GO), and the Kyoto Encyclopedia of Gene and Genomics (KEGG), genes involved in immune/inflammatory responses were significantly enriched in up-regulated genes at different stages of PAD(p < 0.05), revealing a significant correlation between immune/inflammatory responses and disease progression. Moreover, immune-related pathways such as Toll-like receptor signaling and natural killer cell mediated cytotoxicity were particularly enriched in intermediate and advanced lesions (P < 0.05), highlighting their pathogenic significance during disease progression. Conclusion: Lines of evidence revealed in this study not only support previous hypotheses, primarily based on studies of animal models and other types of arterial disease, that inflammatory responses may influence the development of PAD, but also permit the recognition of a wide spectrum of immune/inflammatory genes that can serve as signatures for disease progression in PAD. Further studies of these signature molecules may eventually allow us to develop more sophisticated protocols for pharmaceutical interventions.