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Objective: We retrospectively investigated the association between the imaging features of spontaneous isolated superior mesenteric artery dissection (SISMAD) accompanied by total true lumen occlusion and the clinical symptoms to identify the patients at high risk and establish personalized therapeutic options. Methods: Among 261 patients with SISMAD, we selected 37 with Yun's type III dissection; 35 patients underwent successful conservative management and 2 patients underwent exploratory laparotomy. After discharge, all patients were periodically followed up on an outpatient basis. We recorded patients' general condition, symptoms, time until symptom relief, imaging findings and follow-up results. Results: All patients experienced acute abdominal pain prior to admission, with an onset time of 29.95 ± 24.66 hours. The mean time until relief of abdominal pain in patients who received conservative treatment was 42.17 ± 38.09 hours. Correlation analysis revealed no correlation between the length of dissection or of the occluded segment and abdominal pain intensity. Pain scores were lower and time until pain relief was shorter in patients with a definite arc of Riolan (AOR) on admission than in those without an AOR. No collateral circulation was observed in the two patients who underwent exploratory laparotomy, and distal intestinal perfusion was poor in these cases. Complete and partial remodeling of the superior mesenteric artery (SMA) was observed in 6 and 16 patients, respectively at the 12-month follow-up. Although the SMA remained occluded in 12 patients, abundant collateral circulation was detected. Three patients were lost to follow-up. Conclusion: This study highlights that conservative treatment should be attempted as first-line therapy in most patients with Yun's type III SISMAD. Complete AOR can contribute to remission of clinical symptoms during the acute stage. Poor distal blood flow of occluded vessels may serve as an important indicator for identification of patients at high risk of ischemic intestinal necrosis. [ABSTRACT FROM AUTHOR]

Recently, the architectural remodeling of venous vessel wall ranks as the basis of varicose veins development based on the phenotypic state of vascular smooth muscle cells (VSMCs). In this study, we firstly demonstrated an obvious up-regulation of IQ-domain GTPase-activating protein 1 (IQGAP1) in patients with varicose veins. Importantly, following stimulation with PDGF-BB for 4 h, a common inducer of phenotypic switch in VSMCs, a dramatically time-dependent increase in IQGAP1 expression was observed in human venous smooth muscle cells (HUVSMCs), concomitant with the down-regulation of SMC markers [including α-smooth muscle actin (SMA), smooth muscle calponin (CNN), SM22α (SM22)], suggesting a critical function of IQGAP1 during the switch of synthetic VSMC phenotype. Further analysis ascertained that IQGAP1 overexpression significantly inhibited the expression of SMA, SM and CNN, while its silencing dramatically promoted their expression levels. Moreover, the elevated IQGAP1 enhanced cell proliferation, migration and rearrangement. Mechanism assay confirmed that IQGAP1 overexpression notably blocked myocardin levels. Importantly, after transfection with myocardin siRNA, IQGAP1 down-regulation-induced decrease in cell proliferation, migration and cell rearrangement was remarkably attenuated. Together, these results demonstrated that IQGAP1 may regulate the phenotypic switch of VSMCs by myocardin pathway, which is critical for the pathological progression of varicose vein. Therefore, this study supports a prominent insight into how IQGAP1 possesses its benefit function in varicose veins development by regulating vascular remodeling.