Important new recommendations are provided for the care of patients with an AAA, including suggestions to improve mutual decision-making between the treating physician and the patients and their families as well as a number of new strategies to enhance perioperative outcomes for patients undergoing elective and emergent repair. Areas of uncertainty are highlighted that would benefit from further investigation in addition to existing limitations in diagnostic tests, pharmacologic agents, intraoperative tools, and devices.

Management of carotid bifurcation stenosis is a cornerstone of stroke prevention and has been the subject of extensive clinical investigation, including multiple controlled randomized trials. The appropriate treatment of patients with carotid bifurcation disease is of major interest to the community of vascular surgeons. In 2008, the Society for Vascular Surgery published guidelines for treatment of carotid artery disease. At the time, only one randomized trial, comparing carotid endarterectomy (CEA) and carotid stenting (CAS), had been published. Since that publication, four major randomized trials comparing CEA and CAS have been published, and the role of medical management has been re-emphasized. The current publication updates and expands the 2008 guidelines with specific emphasis on six areas: imaging in identification and characterization of carotid stenosis, medical therapy (as stand-alone management and also in conjunction with intervention in patients with carotid bifurcation stenosis), risk stratification to select patients for appropriate interventional management (CEA or CAS), technical standards for performing CEA and CAS, the relative roles of CEA and CAS, and management of unusual conditions associated with extracranial carotid pathology. Recommendations are made using the GRADE (Grades of Recommendation Assessment, Development and Evaluation) system, as has been done with other Society for Vascular Surgery guideline documents.[corrected] The perioperative risk of stroke and death in asymptomatic patients must be<3% to ensure benefit for the patient. CAS should be reserved for symptomatic patients with stenosis of 50% to 99% at high risk for CEA for anatomic or medical reasons. CAS is not recommended for asymptomatic patients at this time. Asymptomatic patients at high risk for intervention or with <3 years life expectancy should be considered for medical management as the first-line therapy.

Hemodynamically significant left common iliac vein compression is a frequent anatomic variant in asymptomatic individuals. Therefore compression of the left iliac vein may represent a normal anatomic pattern that has thus far been thought of as a pathologic condition.

Subclavian revascularization procedures can be performed with relatively low risk. Complications are rare, and patient recovery is rapid. Although this is not necessary in all cases, we advocate subclavian to carotid transposition when the aortic lesion is within 15 mm of the left subclavian orifice to prevent type II endoleak or perfusion of a dissected false lumen when the ipsilateral vertebral artery is patent and dominant or when coronary revascularization using an ipsilateral internal mammary artery is anticipated and in cases that necessitate extensive coverage of intercostals that contribute to spinal cord perfusion. Carotid to subclavian artery bypass should be reserved for patients with a patent internal mammary artery conduit perfusing a coronary vessel and should be combined with proximal subclavian ligation.

Aortic endograft infection can be eradicated by excision and in situ or extra-anatomic replacement but is often associated with early postoperative morbidity and mortality and occasionally with a need for late removal for reinfection. Prosthetic graft replacement after explanation is associated with higher reinfection and graft-related complications and decreased survival compared with autogenous reconstruction.

To our knowledge, no large multicenter prospective randomized trial comparing endoTTAT and openTTAT has been published in the literature. This meta-analysis of pooled data serves as a surrogate, demonstrating a significant reduction in mortality, paraplegia, and stroke rates in patients who undergo endoTTAT; however, the long-term durability of endoTTAT remains in question.

Cellular mechanisms of sepsis-induced ileus remain an enigma. The study aim was to determine the role of nitric oxide (NO) in mediating the suppression of rat jejunal circular smooth muscle activity during endotoxemia. Isolated muscularis inducible NO synthase (iNOS) mRNA was measured by RT-PCR, immunohistochemistry was employed to localize iNOS protein, and contractile activity was measured in an organ bath. The low basal expression of muscularis iNOS mRNA expression was increased in a time-dependent fashion after lipopolysaccharide (LPS), resulting in a 20-fold increase over controls 3 h after injection. Immunohistochemistry of muscularis whole mounts and dissociated muscularis cells for iNOS revealed staining only in the muscularis macrophages 12 h after LPS. LPS caused a 68% reduction in spontaneous muscle activity 12 h after injection, which improved by 53% after the in vitro application of the selective iNOS inhibitorl- N 6-(1-iminoethyl)lysine. Similar results were obtained in C57BL/6 mice but not in iNOS knockout mice. These data demonstrate that macrophage iNOS plays an important role in mediating LPS-induced intestinal circular muscle suppression.

Bacterial lipopolysaccharide (LPS) is a causative agent of sepsis-induced ileus. Although it is known that LPS activates macrophages and initiates inflammation, the consequences of LPS on the macrophage network and a potential inflammatory response within the intestinal muscularis have not been investigated. This study was designed to identify cellular and functional changes in rat intestinal muscularis after intraperitoneal LPS. Histo- and immunohistochemistry were used to phenotype leukocytes. Functional alterations were determined using an organ bath. Compared with controls, LPS caused a 21-fold increase in staining for the lymphocyte activation marker-1 (LFA-1) localized to the ED2+ macrophage network 1 h after injection. This was followed by a significant infiltration of neutrophils, mast cells, and monocytes into the muscularis. LPS also caused a 62% reduction in spontaneous circular muscle activity and a 91% suppression of bethanechol-stimulated contractions 12 h after injection. These results demonstrate that endotoxemia 1) acutely activates the muscularis macrophage network, 2) causes the extravasation of leukocytes, and 3) results in circular muscle impairment.