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Given the very ill nature of patients with critical limb ischemia (CLI), the use of percutaneous vascular interventions (PVIs) for limb salvage may or may not be efficacious; in particular, for those with polyvascular arterial disease. Herein, we reviewed large, multi-institutional outcomes of PVI in polyvascular and peripheral arterial disease (PAD) patients with CLI. An 18-hospital consortium collected prospective data on patients undergoing endovascular interventions for PAD with 6-month follow-up from January 2008 to December 2011. The patient cohort included 4459 patients with CLI; of those, 3141 patients had polyvascular (coronary artery disease, cerebrovascular disease and PAD) disease, whereas 1318 patients suffered from only PAD. All patients were elderly and with significant comorbidities. The mean ankle–brachial index (ABI) was 0.44 and was not different between those with and without polyvascular disease. Polyvascular patients had more femoropopliteal and infra-inguinal interventions and less aortoiliac interventions than PAD patients. Pre- and post-procedural cardioprotective medication use was less in the PAD patients as compared with polyvascular patients. Vascular complications requiring surgery were higher in PAD patients whereas other access complications were similar between groups. At 6-month follow-up, death was more common in the polyvascular group (6.7% vs 4.1%, p

Abdominal aortic aneurysms (AAAs) comprise the tenth leading cause of death in Caucasian males 65 to 74 years of age and accounted for nearly 16,000 deaths overall in 2000. Therefore, understanding the pathophysiology of AAAs is an important undertaking. Clinically, multiple risk factors are associated with the development of AAAs, including increasing age, positive smoking history, and hypertension. Male gender is also a well-established risk factor for the development of an AAA, with a 4:1 male to female ratio. The reason for this gender disparity is unknown. The pathogenesis of AAAs formation is complex and multifactorial. Histologically, AAAs are characterized by early chemokine-driven leukocyte infiltration into the aortic wall. Subsequent destruction of elastin and collagen in the media and adventitia ensues owing to excessive local production of matrix-degrading enzymes and is accompanied by smooth muscle cell loss and thinning of the aortic wall. At present, no medical therapies are available to treat patients with aortic aneurysms, using only the crude measurement of aortic diameter as a threshold for which patients must undergo life-threatening and costly surgery. Defining the early mechanisms underlying gender-related differences in AAA formation is critical as understanding differences in disease patterns based on gender may allow us to develop new translational approaches to the prevention and treatment of patients with aortic aneurysms.

The objective of this report is to provide a contemporary in-theater account on the systematic management of wartime vascular injury. Included are strategies at each echelon of care that affect the treatment of these injuries. In addition, the aim of this report is to present a modern wartime vascular registry describing rates and distribution of injury in what is now a mature military conflict. A 15-month review (September 1, 2004 through December 1, 2005) from the central level III echelon facility in Iraq (332nd EMDG/Air Force Theater Hospital) presented by the in-theater Consultants for Vascular Surgery. During this period 13 460 casualties were treated at or evacuated through our location, 3096 (23%) with battle-related injuries. Vascular injuries comprised 6.6% (N = 209) of battle-related trauma in the following distribution: extremity 79% (n = 166), neck 13% (n = 27), thoracoabdominal 8% (n = 16). Three levels (formerly echelons) of care are active in theater each with strategies that affect vascular injury management: Level 1: use of commercial tourniquets; level 2: use of temporary vascular shunts as damage control adjuncts; and level 3: definitive repair of arterial and venous injuries in theater using autologous vein. Evacuation patterns and the position of the Air Force Theater Hospital have allowed the formation of a contemporary wartime vascular registry. The rate of vascular injury appears increased compared to that of Vietnam with extremity injuries most prevalent. Effective strategies are in place at each of 3 levels of care that affect the management of vascular injury.

Purpose: To demonstrate a direct operative approach to vascular lesions of the internal carotid artery (1CA) at the level of the skull base. Methods: Between January 1993 and October 1999, five patients underwent lateral skull base resection with cervical-to-petrous carotid artery saphenous vein bypass for repair of distal 1CA lesions. This report describes operative methods, morbidity, graft patency, and long-term outcome with this experience. Results: Of the five patients with skull base ICA lesions, all had aneurysmal disease. Three were atherosclerotic and two were dysplastic. Preoperative neurologic symptoms including transient ischemic attacks (2) and Horner's syndrome with vascular headaches (1) were completely resolved after operation. Preoperative dysphagia (2) was resolved in one patient and clinically improved in the other. Postoperative complications included transient paresis in the cranial nerve (CN) VII distribution, as well as permanent loss of the eustachian tube and chorda tympani nerve in all five patients. One patient had lasting paresis in the CN XI distribution as well as a mild stroke resulting in arm weakness. No residual arm weakness was detected at one year. There were no graft occlusions by duplex ultrasound at 45.8 months mean objective follow-up, and no ipsilateral stroke or mortality at 51.2 months mean clinical follow-up. Conclusions: Saphenous vein bypass from the cervical-to-petrous ICA is technically feasible and provides a valuable reconstruction option for patients with skull base ICA lesions.

Abdominal aortic coarctation (AAC) is an uncommon vascular lesion with serious sequelae related to uncontrolled hypertension. Balloon-expandable stents have recently been utilized in the treatment of AAC as an alternative to surgical intervention. A 17-year-old female presented with hypertension uncontrolled by beta blockade. She underwent angiography, which revealed an isolated supraceliac aortic coarctation without visceral or renal artery involvement. Balloon angioplasty with stent placement was performed. At 2-year follow-up, a restenosis was identified and was treated with repeat balloon-expandable stent placement. Implantation of balloon-expandable stents is a safe and technically feasible treatment modality for abdominal aortic coarctation not involving the renal and mesenteric arteries. However, it is currently unknown whether the long-term durability of this approach may limit its effectiveness when compared to traditional surgical interventions.

Introduction Calf muscle atrophy is commonly noted after lower-extremity immobilization. Air plethysmography (APG) provides an easily reproducible, noninvasive diagnostic test that is useful in measuring calf ejection fraction. Quantitative measurements can be preformed before and after physical therapy as a tool to evaluate effectiveness of treatment. Method We report the case of a 26-year-old woman who presented to the vascular surgery clinic with right lower extremity cyanosis, paresthesias, and swelling after hip dislocation. The patient had been immobile for a month. An arteriogram was performed to rule out arterial injury and a lower-extremity ultrasound was performed to rule out deep venous thrombosis and venous reflux. APG revealed a profoundly abnormal ejection fraction of 36%. Physical therapy was recommended, with special attention towards calf muscle strengthening. Results After 3 months of physical therapy, the APG ejection fraction increased to a normal value of 74%. In addition to normalization of the APG, all symptoms of cyanosis, paresthesias, and swelling were resolved. Conclusion APG may be a useful tool in measuring the restoration of calf muscle function in patients with injuries requiring extended immobilization.

In a previous study in apolipoprotein E-deficient mice treated with angiotensin II (Ang II), the authors demonstrated that urokinasetype plasminogen activator (uPA) is highly expressed in the aneurysmal segment of the abdominal aorta. The authors conducted the present study to determine if uPA is essential for the formation of abdominal aortic aneurysm (AAA) in this same mouse model. Male mice were implanted for 1 month with a subcutaneous osmotic minipump that delivered 1.44 mg/kg per day of Ang II. AAA was induced in 90% of apoE deficient mice, but only 22% of the mice deficient in both apoE and uPA developed AAA. In 18 strainmatched wild type control mice, Ang 11 induced AAA in 39%. The author's concluded that a uPA deficiency has a protective effect against Ang II-induced AAA development, that uPA is not required for normal vascular development and maintenance, and that preexisting hyperlipidemia and atherosclerosis are not essential for Ang II-induced AAA formation.