Venous thoracic outlet syndrome progressing to the point of axilosubclavian vein thrombosis, variously referred to as Paget-Schroetter syndrome or effort thrombosis, is a classic example of an entity which if treated correctly has minimal long-term sequelae but if ignored is associated with significant long-term morbidity. The subclavian vein is highly vulnerable to injury as it passes by the junction of the first rib and clavicle in the anterior-most part of the thoracic outlet. In addition to extrinsic compression, repetitive forces in this area frequently lead to fixed intrinsic damage and extrinsic scar tissue formation. Once primary thrombosis is recognized, catheter-directed thrombolytic therapy is usually successful if initiated within ten to 14 days of clot formation, but often unmasks an underlying lesion. The vast majority of investigators believe that decompression of the venous thoracic outlet, usually by means of first rib excision, partial anterior scalenectomy, resection of the costoclavicular ligament, and thorough external venolysis, is necessary, although opinion is less uniform as to the need for and method of treatment of the venous lesion itself. Using this algorithm, long-term success rates of 95 to 100% have been reported by many investigators. This review, in addition to discussing the overall treatment algorithm in more detail, attempts to point out controversies that still exist and research directions, both clinical and basic, that need to be pursued. Prospective randomized trials addressing this entity are surprisingly lacking, and although there is consensus based on experience, it may be necessary to step back and rigorously explore several aspects of this entity.

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These data support the use of CTA as an accurate method of calculating carotid artery stenosis based on agreement with Strandness criteria applied to CDUS velocities. When additional imaging beyond CDUS is necessary, we report no significant difference between diameter and CSA measurements obtained from CTA for preoperative evaluation of carotid disease.

Objective The molecular mechanisms leading to the development of abdominal aortic aneurysms (AAAs) remain poorly understood. The aim of this study was to determine the expression of Sonic Hedgehog (SHh), transforming growth factor β (TGF-β), and Notch signaling components in human aneurysmal and nonaneurysmal aorta in vivo. Methods Paired tissue samples were obtained from aneurysmal and nonaneurysmal (control) segments of the aortic wall of eight patients with suitable anatomy undergoing open repair of infrarenal AAAs. Protein and messenger RNA (mRNA) expression levels were determined by Western blot and quantitative real-time polymerase chain reaction analysis. Results Aneurysm development resulted in a significant reduction in vascular smooth muscle (vSMC) differentiation genes α-actin and SMC22α at both mRNA and protein levels. In parallel experiments, an 80.0% ± 15% reduction in SHh protein expression was observed in aneurysmal tissue compared with control. SHh and Ptc-1 mRNA levels were also significantly decreased, by 82.0% ± 10% and 75.0% ± 5%, respectively, in aneurysmal tissue compared with nonaneurysmal control tissue. Similarly, there was a 50.0% ± 9% and 60.0% ± 4% reduction in Notch receptor 1 intracellular domain and Hrt-2 protein expression, respectively, in addition to significant reductions in Notch 1, Notch ligand Delta like 4, and Hrt-2 mRNA expression in aneurysmal tissue compared with nonaneurysmal tissue. There was no change in Hrt-1 expression observed in aneurysmal tissue compared with control. In parallel experiments, we found a 2.2 ± 0.2-fold and a 5.6 ± 2.2-fold increase in TGF-β mRNA and protein expression, respectively, in aneurysmal tissue compared with nonaneurysmal tissue. In vitro, Hedgehog signaling inhibition with cyclopamine in human aortic SMCs resulted in decreased Hedgehog/Notch signaling component and vSMC differentiation gene expression. Moreover, cyclopamine significantly increased TGF-β1 mRNA expression by 2.6 ± 0.9-fold. Conclusions These results suggest that SHh/Notch and TGF-β signaling are differentially regulated in aneurysmal tissue compared with nonaneurysmal tissue. Changes in these signaling pathways and the resulting changes in vSMC content may play a causative role in the development of AAAs.