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Chronic contained rupture of an abdominal aortic aneurysm with vertebral body erosion most commonly presents with symptoms of low back pain. Although not well known, vertebral body erosion or destruction may be seen in up to 25% of patients with sealed or contained rupture of an abdominal aortic aneurysm. This appearance on cross-sectional imaging may mimic a malignant or infectious process. Although these cases can present a diagnostic challenge, published cases of chronic contained rupture of an abdominal aortic aneurysm with vertebral body erosion demonstrate clinical and imaging similarities that, when recognized, can assist in diagnosis.

Objective: Peripheral arterial disease (PAD) is a significant age-related medical condition with limited pharmacologic options. Severe PAD, termed critical limb ischemia, can lead to amputation. Skeletal muscle is the end organ most affected by PAD, leading to ischemic myopathy and debility of the patient. Currently, there are not any therapeutics to treat ischemic myopathy, and proposed biologic agents have not been optimized owing to a lack of preclinical models of PAD. Because a large animal model of ischemic myopathy may be useful in defining the optimal dosing and delivery regimens, the objective was to create and to characterize a swine model of ischemic myopathy that mimics patients with severe PAD., Methods: Yorkshire swine (N = 8) underwent acute right hindlimb ischemia by endovascular occlusion of the external iliac artery. The effect of ischemia on limb function, perfusion, and degree of ischemic myopathy was quantified by weekly gait analysis, arteriography, hindlimb blood pressures, femoral artery duplex ultrasound scans, and histologic examination. Animals were terminated at 5 (n = 5) and 6 (n = 3) weeks postoperatively. Ossabaw swine (N = 8) fed a high-fat diet were used as a model of metabolic syndrome for comparison of arteriogenic recovery and validation of ischemic myopathy., Results: There was persistent ischemia in the right hindlimb, and occlusion pressures were significantly depressed compared with the untreated left hindlimb out to 6 weeks (systolic blood pressure, 31 ± 21 vs 83 ± 15 mm Hg, respectively; P = .0007). The blood pressure reduction resulted in a significant increase of ischemic myopathy in the gastrocnemius muscle in the treated limb. Gait analysis revealed a functional deficit of the right hindlimb immediately after occlusion that improved rapidly during the first 2 weeks. Peak systolic velocity values in the right common femoral artery were severely diminished throughout the entire study (P < .001), and the hemodynamic environment after occlusion was characterized by low and oscillatory wall shear stress. Finally, the internal iliac artery on the side of the ischemic limb underwent significant arteriogenic remodeling (1.8× baseline) in the Yorkshire but not in the Ossabaw swine model., Conclusions: This model uses endovascular technology to produce the first durable large animal model of ischemic myopathy. Acutely (first 2 weeks), this model is associated with impaired gait but no tissue loss. Chronically (2-6 weeks), this model delivers persistent ischemia, resulting in ischemic myopathy similar to that seen in PAD patients. This model may be of use for testing novel therapeutics including biologic therapies for promoting neovascularization and arteriogenesis., (Published by Elsevier Inc.)

The biomechanics of large- and medium-sized arteries influence the pathophysiology of arterial disease and the response to therapeutic interventions. However, a comprehensive comparative analysis of human arterial biaxial mechanical properties has not yet been reported. Planar biaxial extension was used to establish the passive mechanical properties of human thoracic (TA, [Formula: see text]) and abdominal (AA, [Formula: see text]) aorta, common carotid (CCA, [Formula: see text]), subclavian (SA, [Formula: see text]), renal (RA, [Formula: see text]) and common iliac (CIA, [Formula: see text]) arteries from 11 deceased subjects ([Formula: see text] years old). Histological evaluation determined the structure of each specimen. Experimental data were used to determine constitutive parameters for a structurally motivated nonlinear anisotropic constitutive model. All arteries demonstrated appreciable anisotropy and large nonlinear deformations. Most CCA, SA, TA, AA and CIA specimens were stiffer longitudinally, while most RAs were stiffer circumferentially. A switch in anisotropy was occasionally demonstrated for all arteries. The CCA was the most compliant, least anisotropic and least frequently diseased of all arteries, while the CIA and AA were the stiffest and the most diseased. The severity of atherosclerosis correlated with age, but was not affected by laterality. Elastin fibers in the aorta, SA and CCA were uniformly and mostly circumferentially distributed throughout the media, while in the RA and CIA, elastin was primarily axially aligned and concentrated in the external elastic lamina. Constitutive modeling provided good fits to the experimental data for most arteries. Biomechanical and architectural features of major arteries differ depending on location and functional environment. A better understanding of localized arterial mechanical properties may support the development of site-specific treatment modalities for arterial disease.

Background: Peripheral artery disease (PAD), a manifestation of systemic atherosclerosis that produces blockages in the arteries supplying the legs, affects approximately 5% of Americans. We have previously, demonstrated that a myopathy characterized by myofiber oxidative damage and degeneration is central to PAD pathophysiology., Objectives: In this study, we hypothesized that increased oxidative damage in the myofibers of the gastrocnemius of PAD patients is myofiber-type selective and correlates with reduced myofiber size., Methods: Needle biopsies were taken from the gastrocnemius of 53 PAD patients (28 with early PAD and 25 with advanced PAD) and 25 controls. Carbonyl groups (marker of oxidative damage), were quantified in myofibers of slide-mounted tissue, by quantitative fluorescence microscopy. Myofiber cross-sectional area was determined from sarcolemma labeled with wheat germ agglutinin. The tissues were also labeled for myosin I and II, permitting quantification of oxidative damage to and relative frequency of the different myofiber Types (Type I, Type II and mixed Type I/II myofibers). We compared PAD patients in early (N=28) vs. advanced (N=25) disease stage for selective, myofiber oxidative damage and altered morphometrics., Results: The carbonyl content of gastrocnemius myofibers was higher in PAD patients compared to control subjects, for all three myofiber types (p<0.05). In PAD patients carbonyl content was higher (p<0.05) in Type II and I/II fibers compared to Type I fibers. Furthermore, the relative frequency and cross-sectional area of Type II fibers were lower, while the relative frequencies and cross-sectional area of Type I and Type I/II fibers were higher, in PAD compared to control gastrocnemius (p<0.05). Lastly, the type II-selective oxidative damage increased and myofiber size decreased as the disease progressed from the early to advanced stage., Conclusions: Our data confirm increased myofiber oxidative damage and reduced myofiber size in PAD gastrocnemius and demonstrate that the damage is selective for type II myofibers and is worse in the most advanced stage of PAD.

Peripheral artery disease (PAD) is characterized by chronic muscle ischemia. Compensatory angiogenesis is minimal within ischemic muscle despite an increase in angiogenic factors. This may occur due to the prevalence of angiostatic factors. Regulatory mechanisms that could evoke an angiostatic environment during ischemia are largely unknown. Forkhead box O (FoxO) transcription factors, known to repress endothelial cell proliferation in vitro, are potential candidates. Our goal was to determine whether FoxO proteins promote an angiostatic phenotype within ischemic muscle. FoxO1 and the angiostatic matrix protein thrombospondin 1 (THBS1) were elevated in ischemic muscle from PAD patients, or from mice post-femoral artery ligation. Mice with conditional endothelial cell-directed deletion of FoxO proteins (Mx1Cre (+), FoxO1,3,4 (L/L) , referred to as FoxOΔ) were used to assess the role of endothelial FoxO proteins within ischemic tissue. FoxO deletion abrogated the elevation of FoxO1 and THBS1 proteins, enhanced hindlimb blood flow recovery and improved neovascularization in murine ischemic muscle. Endothelial cell outgrowth from 3D explant cultures was more robust in muscles derived from FoxOΔ mice. FoxO1 overexpression induced THBS1 production, and a direct interaction of endogenous FoxO1 with the THBS1 promoter was detectable in primary endothelial cells. We provide evidence that FoxO1 directly regulates THBS1 within ischemic muscle. Altogether, these findings bring novel insight into the regulatory mechanisms underlying the repression of angiogenesis within peripheral ischemic tissues.

Insufficient blood flow is one possible mechanism contributing to altered gait patterns in lower extremity peripheral arterial disease (PAD). Previously, our laboratory found that induced occlusion alters gait variability patterns in healthy young individuals. However the effect of age was not explored. The purpose of this study was to account for age by investigating gait variability following induced vascular occlusion in healthy older individuals and to identify amount of change from baseline to post vascular occlusion between younger and older individuals. Thirty healthy younger individuals and 30 healthy older individuals walked on a treadmill during baseline and post vascular occlusion conditions while lower extremity joint kinematics were captured. Vascular occlusion was induced by thigh cuffs inflated bilaterally on the upper thighs. Amount and temporal structure of gait variability was assessed. Older individuals exhibited significantly increased values of temporal structure of variability post vascular occlusion. Post vascular occlusion values were similar between younger and older individuals after adjusting for baseline measurements. Results show blood flow contributes to altered gait variability. However alterations were less severe than previously documented in symptomatic PAD patients, suggesting that neuromuscular problems in the lower extremities of PAD patients also contribute to gait alterations in these patients.

Patch angioplasty is the most common technique used for the performance of carotid endarterectomy. A large number of materials are available, but little is known to aid the surgeon in choosing a patch while caring for a patient with carotid disease. The objective of this study was to investigate biomechanics of the carotid artery (CA) repaired with patch angioplasty, study the influence of patch width and location of closure on hemodynamics, and to select the optimal patch material from those commonly used. For this purpose, a mathematical model was built that accounts for fluid-structure interaction, three-dimensional arterial geometry, non-linear anisotropic mechanical properties, non-Newtonian flow and in vivo boundary conditions. This model was used to study disease-related mechanical factors in the arterial wall and blood flow for different types of patch angioplasty. Analysis indicated that patch closures performed with autologous vein and bovine pericardium were hemodynamically superior to carotid endarterectomy with synthetic patch angioplasty (polytetrafluoroethylene, Dacron) in terms of restenosis potential. Width of the patch and location of arteriotomy were found to be of paramount importance, with narrow patches being superior to wide patches, and anterior arteriotomy being superior to the lateral arteriotomy. These data can aid vascular surgeons in their selection of patch angioplasty technique and material for the care of patients undergoing open CA repair.

Objective: Carotid angioplasty and stenting (CAS) has challenged carotid endarterectomy (CEA) as the therapy of choice for carotid disease. This meta-analysis aims at summarizing the most current body of evidence., Methods: All prospective, controlled clinical trials comparing CEA versus CAS were included. The outcome measures of interest were relative risk (RR) of 30-day stroke, 30-day stroke/death, long-term risk of stroke, and risk of restenosis., Results: The RR of 30-day stroke for CAS was 1.6 times that of CEA (RR 1.6; 95%CI 1.2-2.0, P = .001). The 30-day RR of stroke/death was 1.5 times higher for CAS (RR 1.5; 95%CI 1.1-2.1, P = .008). There was a higher risk of long-term stroke (RR 1.2; 95%CI 1.0-1.5, P = .043). The risk of restenosis was twice for CAS (RR 1.8; 95%CI 1.1-3.1, P = .04)., Conclusion: The 30-day RR of stroke, stroke/death, long-term risk of stroke, and risk of restenosis are consistently higher for carotid artery stenting (CAS).

Background: Recent research demonstrated that intermittent claudication patients have increased gait variability prior to the onset of claudication. However, it is unknown if these patients experience additional gait adaptations after the onset of claudication. Thus, we sought to determine how gait variability is affected by claudication in an effort to contribute to improved clinical management., Methods: Twenty-six intermittent claudication patients and 20 controls walked on a treadmill at self-selected speed; intermittent claudication patients were tested before (pain free) and after (pain) the onset of claudication. Variability of the ankle, knee, and hip joint angles was assessed using the largest Lyapunov exponent, standard deviation and coefficient of variation. Dependent t-tests were used to compare the pain free and pain conditions. Independent t-tests were used to compare intermittent claudication patients and controls., Findings: Pain free and pain conditions were not significantly different for any of the parameters evaluated except the ankle. Compared to controls, patients had significantly greater values for the largest Lyapunov exponent in both conditions for all joints., Interpretation: Gait variability was essentially the same before and after the onset of claudication at the knee and the hip, and was increased in both conditions compared to controls. This indicates altered cooperation between components of the locomotor system of intermittent claudication patients, likely due to the associated myopathy since differences were present even before the onset of claudication. This research helps provide essential biomechanical knowledge of intermittent claudication that contributes to improved clinical management., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Background: Perioperative myocardial infarction or cardiac arrest is associated with significant morbidity and mortality. The Revised Cardiac Risk Index is currently the most commonly used cardiac risk stratification tool; however, it has several limitations, one of which is its relatively low discriminative ability. The objective of the present study was to develop and validate a predictive cardiac risk calculator., Methods and Results: Patients who underwent surgery were identified from the American College of Surgeons' 2007 National Surgical Quality Improvement Program database, a multicenter (>250 hospitals) prospective database. Of the 211 410 patients, 1371 (0.65%) developed perioperative myocardial infarction or cardiac arrest. On multivariate logistic regression analysis, 5 predictors of perioperative myocardial infarction or cardiac arrest were identified: type of surgery, dependent functional status, abnormal creatinine, American Society of Anesthesiologists' class, and increasing age. The risk model based on the 2007 data set was subsequently validated on the 2008 data set (n=257 385). The model performance was very similar between the 2007 and 2008 data sets, with C statistics (also known as area under the receiver operating characteristic curve) of 0.884 and 0.874, respectively. Application of the Revised Cardiac Risk Index to the 2008 National Surgical Quality Improvement Program data set yielded a relatively lower C statistic (0.747). The risk model was used to develop an interactive risk calculator., Conclusions: The cardiac risk calculator provides a risk estimate of perioperative myocardial infarction or cardiac arrest and is anticipated to simplify the informed consent process. Its predictive performance surpasses that of the Revised Cardiac Risk Index.

Background: The benefit of carotid endarterectomy (CEA) is heavily influenced by the risk of perioperative stroke. Our objective was to use the American College of Surgeons' 2007 and 2008 National Surgical Quality Improvement Program (NSQIP) database to assess the postoperative stroke and death rate after CEA among the more than 180 NSQIP participating hospitals, and to identify the preoperative risk factors., Materials and Methods: Univariate analysis included 56 preoperative variables. Outcomes were studied for 30 d. Multivariate logistic regression was used for assessment of risk factors., Results: Of 13,316 patients, 7503 (56.5%) were asymptomatic, while 5770 (43.5%) were symptomatic. Combined stroke or death was seen in 262 patients (2.0%). Postoperative stroke occurred in 186 patients (1.4%). One hundred patients (0.8%) died within 30 d. In asymptomatic and symptomatic patients, stroke or death was seen in 1.3% and 2.9% of patients; stroke in 0.9% and 2% of patients; and death in 0.5% and 1.1% of patients, respectively (all P < 0.001). On multivariate analysis for symptomatic patients, dialysis dependence, chronic open wound, impaired sensorium, and dependent functional status were risk factors for stroke or death (all P < 0.05). Among asymptomatic patients, acute renal failure, corticosteroid use, COPD, paraplegia, and dependent functional status were risk factors for stroke or death (all P < 0.05)., Conclusions: This prospective database confirms that CEA is currently performed with low peri-procedural stroke rate in participating ACS NSQIP hospitals and provides a contemporary framework for comparison of other treatment modalities to CEA. Identification of the above risk factors may help with risk stratification and patient counseling for CEA., (Published by Elsevier Inc.)

Although arterial limb tourniquet is one of the first-line treatments to prevent exsanguinating hemorrhage in both civilian pre-hospital and battlefield casualty care, prolonged application of a limb tourniquet can lead to serious ischemia-reperfusion injury. However, the underlying pathomechanisms of tourniquet-induced ischemia-reperfusion injury are still poorly understood. Using a murine model of acute limb ischemia-reperfusion, we investigated if acute limb ischemia-reperfusion injury is mediated by superoxide overproduction and mitochondrial dysfunction. Hind limbs of C57/BL6 mice were subjected to 3h ischemia and 4h reperfusion via placement and release of a rubber tourniquet at the greater trochanter. Approximately 40% of the gastrocnemius muscle suffered infarction in this model. Activities of mitochondrial electron transport chain complexes including complex I, II, III, and IV in the gastrocnemius muscle were decreased in the ischemia-reperfusion group compared to sham. Superoxide production was increased while activity of manganese superoxide dismutase (MnSOD, the mitochondria-targeted SOD isoform) was decreased in the ischemia-reperfusion group compared to the sham group. Pretreatment with tempol (a SOD mimetic, 50mg/kg) or co-enzyme Q(10) (50mg/kg) not only decreased the superoxide production, but also reduced the infarct size and normalized mitochondrial dysfunction in the gastrocnemius muscle. Our results suggest that tourniquet-induced skeletal muscle ischemia-reperfusion injuries including infarct size and mitochondrial dysfunction may be mediated via superoxide overproduction and reduced antioxidant activity. In the future, this murine ischemia-reperfusion model can be adapted to mechanistically evaluate anti-ischemic molecules in tourniquet-induced skeletal muscle injury., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Background: The role of ischemia reperfusion contributing to functional impairment in lower extremity peripheral arterial disease (PAD) patients has not previously been elucidated. The evaluation of gait variability patterns has proven useful in many pathologic populations. Therefore, the purpose of this study is to isolate and determine the specific effect of the acute reperfusion phase of ischemia-reperfusion on gait variability in young individuals with no vascular disease., Materials and Methods: Thirty healthy young individuals walked on a treadmill during baseline and the acute reperfusion phase of ischemia-reperfusion conditions while lower extremity joint kinematics were captured. Stride to stride variability was assessed using the largest Lyapunov exponent, approximate entropy, standard deviation, and coefficient of variation. Differences in gait variability between conditions were assessed using dependent t-tests., Results: The largest Lyapunov exponent values and approximate entropy values were significantly higher in the acute reperfusion phase of ischemia-reperfusion condition for the ankle, knee, and the hip. Coefficient of variation was significantly higher at the hip and standard deviation was higher at the knee and the hip during the acute reperfusion phase of ischemia-reperfusion condition., Conclusions: The acute reperfusion phase of the ischemia-reperfusion cycle alters gait variability patterns at the ankle, knee, and the hip in healthy young individuals. Our findings indicate increased noise and irregularity of gait variability patterns post-ischemia. In young healthy individuals who do not have neuromuscular impairments, significant gait alterations are present during walking after a period of interruption of blood flow., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Unlabelled: To review 20 years of literature on chronic mesenteric ischemia (CMI), examining its complex clinical presentation and comparing open and endovascular treatment options., Methods: The PubMed and EBSCOHost electronic databases were queried to identify English-language articles published over the last 20 years. Scrutiny of the retrieved articles identified 1939 patients (mean age 65 years). Of these, 1163 patients underwent open surgery: 714 between 2000 and 2009 and 449 between 1990 and 1999. Of the 776 patients undergoing endovascular repairs, the majority (684) were performed between 2000 and 2009; 92 patients were treated between 1990 and 1999. Data were entered in an electronic database and were pooled for categorical analysis., Results: No major differences were seen among open surgeries or among endovascular surgeries performed when comparing the 2 time periods. On comparing open and endovascular surgeries performed between 2000 and 2009, symptom improvement was 2.4 times more likely after open compared to endovascular surgery (95% CI 1.5 to 3.6, p<0.001). Five-year primary patency and 5-year assisted primary patency were 3.8 (95% CI 2.4 to 5.8, p<0.001) and 6.4 (95% CI 1.3 to 30.1, p = 0.02) times greater in the open group. Freedom from symptoms at 5 years was 4.4 times greater for open versus endovascular (95% CI 2.8 to 7.0, p<0.001). The complication rate for open versus endovascular surgery was 3.2 times greater (95% CI 2.5 to 4.2, p<0.001). The difference in mortality was not statistically significant (p = 0.75)., Conclusion: Our data demonstrate that open revascularization surpasses endovascular procedures in long-term vessel patency and control of symptoms. Patients undergoing open procedures do, however, develop increased complications perioperatively. The preferred revascularization approach used in treating this condition should be tailored to the anatomy and physiology of each patient.

Objective: Claudication is the most common manifestation of peripheral arterial disease, producing significant ambulatory compromise. Our study evaluated patients with bilateral lower limb claudication and characterized their gait abnormality based on advanced biomechanical analysis using joint torques and powers., Methods: Twenty patients with bilateral claudication (10 with isolated aortoiliac disease and 10 with combined aortoiliac and femoropopliteal disease) and 16 matched controls ambulated on a walkway while 3-dimensional biomechanical data were collected. Patients walked before and after onset of claudication pain. Joint torques and powers at early, mid, and late stance for the hip, knee, and ankle joints were calculated for claudicating patients before and after the onset of claudication pain and were compared to controls., Results: Claudicating patients exhibited significantly reduced hip and knee power at early stance (weight-acceptance phase) due to decreased torques produced by the hip and knee extensors. In mid stance (single-limb support phase), patients had significantly reduced knee and hip power due to the decreased torques produced by the knee extensors and the hip flexors. In late stance (propulsion phase), reduced propulsion was noted with significant reduction in ankle plantar flexor torques and power. These differences were present before and after the onset of pain, with certain parameters worsening in association with pain., Conclusions: The gait of claudication is characterized by failure of specific and identifiable muscle groups needed to perform normal walking (weight acceptance, single-limb support, and propulsion). Parameters of gait are abnormal with the first steps taken, in the absence of pain, and certain of these parameters worsen after the onset of claudication pain., (Copyright (c) 2010 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.)

Pharmacological treatment has been used to alleviate the claudication symptoms and improve walking performance in peripheral arterial disease (PAD) patients. However, the effects of claudication treatments on gait mechanics have not been objectively identified with biomechanical techniques. For this study, 20 PAD patients were assigned to take either pentoxifylline (n=11) or cilostazol (n=9), the two FDA-approved pharmacological therapies used to treat intermittent claudication symptoms. All patients completed a gait evaluation protocol that involved the acquisition of kinematic and kinetic gait data before use of the medication and after 12 weeks of treatment. Results showed that treatment with either pentoxifylline or cilostazol resulted in limited overall improvement in gait parameters including joint angles and joint moments. Walking speed was unchanged, in either treatment group, as a result of the medication. These results suggest that to improve biomechanical walking parameters of PAD patients, clinicians cannot rely on drug therapies alone.

Background: Pharmacological treatment has been advocated as a first line therapy for Peripheral Arterial Disease (PAD) patients suffering from intermittent claudication. Previous studies document the ability of pharmacological treatment to increase walking distances. However, the effect of pharmacological treatment on gait biomechanics in PAD patients has not been objectively evaluated as is common with other gait abnormalities., Methods: Sixteen patients were prescribed an FDA approved drug (Pentoxifylline or Cilostazol) for the treatment of symptomatic PAD. Patients underwent baseline gait testing prior to medication use which consisted of acquisition of ground reaction forces and kinematics while walking in a pain free state. After three months of treatment, patients underwent repeat gait testing., Results: Patients with symptomatic PAD had significant gait abnormalities at baseline during pain free walking as compared to healthy controls. However, pharmacological treatment did not produce any identifiable alterations on the biomechanics of gait of the PAD patients as revealed by the statistical comparisons performed between pre and post-treatment and between post-treatment and the healthy controls., Conclusions: Pharmacological treatment did not result in statistically significant improvements in the gait biomechanics of patients with symptomatic PAD. Future studies will need to further explore different cohorts of patients that have shown to improve significantly their claudication distances and/or their muscle fiber morphology with the use of pharmacological treatment and determine if this is associated with an improvement in gait biomechanics. Using these methods we may distinguish the patients who benefit from pharmacotherapy and those who do not.

Intraluminal thrombus adjunct to internal carotid artery plaque is a rare finding on traditional diagnostic imaging. Prompt diagnosis is important as it carries a high risk of recurrent stroke. We describe 2 symptomatic patients with severe stenosis on duplex scanning and internal carotid artery thrombus (ICAT) identified on subsequent computed tomographic angiography. Histology of the surgical specimen confirmed the composition predicted by computed tomography. Computed tomographic angiography can provide accurate diagnosis and characterization of internal carotid thrombus and lead to prompt therapeutic intervention.

Objectives: Symptomatic peripheral arterial disease (PAD) results in significant gait impairment. In an attempt to fully delineate and quantify these gait alterations, we analyzed joint kinematics, torques (rotational forces), and powers (rotational forces times angular velocity) in patients with PAD with unilateral claudication for both the affected and nonaffected legs., Methods: Twelve patients with unilateral PAD (age, 61.69 +/- 10.53 years, ankle-brachial index [ABI]: affected limb 0.59 +/- 0.25; nonaffected limb 0.93 +/- 0.12) and 10 healthy controls (age, 67.23 +/- 12.67 years, ABI >1.0 all subjects) walked over a force platform to acquire gait kinetics, while joint kinematics were recorded simultaneously. Data were collected for the affected and nonaffected limbs during pain free (PAD-PF) and pain induced (PAD-P) trials. Kinetics and kinematics were combined to quantify torque and powers during the stance period from the hip, knee, and ankle joints., Results: The affected limb demonstrated significantly (P <.05) reduced ankle plantar flexion torque compared to controls during late stance in both PAD-PF and PAD-P trials. There were significant reductions in ankle plantar flexion power generation during late stance for both the affected (P <.05) and nonaffected limbs (P <.05) compared to control during PAD-PF and PAD-P trials. No significant differences were noted in torque comparing the nonaffected limbs in PAD-PF and PAD-P conditions to control for knee and hip joints throughout the stance phase. Significant reductions were found in knee power absorption in early stance and knee power generation during mid stance for both limbs of the patients with PAD as compared to control (P <.05)., Conclusion: Patients with PAD with unilateral claudication demonstrate significant gait impairments in both limbs that are present even before they experience any claudication symptoms. Overall, our data demonstrate significantly reduced ankle plantar flexion torque and power during late stance with reduced knee power during early and mid stance for the affected limb. Further studies are needed to determine if these findings are dependent on the location and the severity of lower extremity ischemia and whether the changes in the nonaffected limb are the result of underlying PAD or compensatory changes from the affected limb dysfunction., (Copyright 2010 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.)

Atherothrombosis, characterized by atherosclerotic plaque rupture and subsequent occlusive or subocclusive thrombus formation is the primary cause of acute ischemic syndromes involving all vascular beds and accounts for more than one-third of all deaths in the developed world. Platelet activation and aggregation constitute the most critical component in the pathophysiology of atherothrombotic disease. Aspirin is currently the most commonly used antiplatelet agent and one of the most frequently prescribed drugs, with as many as 30 million Americans on chronic aspirin regimens. Multiple well-designed prospective randomized clinical trials have demonstrated aspirin's efficacy in both primary and secondary prevention of a wide variety of entities that the atherothrombotic disease spectrum encompasses, such as cerebrovascular, coronary artery, and peripheral vascular disease. Despite its proven benefit, however, a growing body of evidence suggests that up to 70% of aspirin-takers may still be at risk for atherothrombotic complications due to resistance. Patients with laboratory-confirmed aspirin resistance seem to have an almost fourfold increase in their risk for acute thrombotic episodes, which underlines the magnitude of the problem for the vascular specialist. In this article, we review the physiology of platelet activation and the role of aspirin as an antiplatelet agent; the various laboratory assays used in assessing aspirin effectiveness; and current data on aspirin resistance and its clinical implications in patients with cardiovascular disease. We also review the studies that explore this phenomenon in patients with peripheral arterial disease and discuss the optimal management options in aspirin-resistant individuals. Suggestions are advanced for the direction of future trials evaluating aspirin resistance in patients with vascular disease.

Introduction: The hemodynamic effects of carotid artery patching are not well known. Our objective was to develop a fluid-solid finite element model of the endarterectomized and patched carotid artery., Methods: Hyperelastic materials parameters were determined from studies of 8 cadaveric carotids. Blood flow characteristics were based on intraoperative data from a patient undergoing endarterectomy. Wall shear stress, cyclic strain and effective stress were computed as hemodynamic parameters with known association with endothelial injury, neointimal hyperplasia and atherogenesis., Results: Low wall shear stress, high cyclic strain and high effective stress were identified diffusely in the carotid bulb, at the margins around the patch and in the flow divider., Conclusion: Endarterectomy and polytetrafluoroethylene patching produce considerable abnormalities in the hemodynamics of the repaired carotid. Advanced mechanical modeling can be used to evaluate different carotid revascularization approaches to obtain optimized biomechanical and hemodynamic results for the care of patients with carotid bifurcation disease.

Purpose: To compare through a systematic review of published literature the stroke outcomes in protected and unprotected carotid artery stenting (CAS)., Methods: PubMed and Cochrane electronic databases were queried to identify peer-reviewed publications from 1995 to 2007 meeting our pre-defined criteria for inclusion (English language, human only, at least 20 patients reported) and exclusion (procedures performed for the treatment of total occlusion, dissection, or aneurysmal disease; urgently performed procedures; use of covered stents; access other than transfemoral). Information was collected on a standardized data abstraction form for pooled analysis of total strokes within 30 days of procedure in all patients and in symptomatic and asymptomatic subgroups. A random effects meta-analysis of studies with concurrently reported data on protected and unprotected CAS was performed., Results: Initial database query resulted in 2485 articles, of which 134 were included in the final analyses (12,263 protected CAS patients and 11,198 unprotected CAS patients). Twenty-four studies included data on both protected and unprotected CAS. Using pooled analysis of all 134 reports, the relative risk (RR) for stroke was 0.62 (95% CI 0.54 to 0.72) in favor of protected CAS. Subgroup analysis revealed a significant benefit for protected CAS in both symptomatic (RR 0.67; 95% CI 0.52 to 0.56) and asymptomatic (RR 0.61; 95% CI 0.41 to 0.90) patients (p<0.05). Meta-analysis of the 24 studies reporting data on both protected and unprotected stenting demonstrated a relative risk of 0.59 (95% CI 0.47 to 0.73) for stroke, again favoring protected CAS (p<0.001)., Conclusion: Our systematic review indicated that the use of cerebral protection devices decreased the risk of perioperative stroke with CAS. A well designed randomized trial can further confirm our findings and possibly indicate the device with the best outcomes.

Background: Concern is growing about missed test results, but data assessing their effect on patient safety are limited., Objective: To examine the frequency with which computed tomography (CT)-documented dilations of the abdominal aorta are accompanied by evidence in the electronic medical record (EMR) that a clinician recognized the abnormality., Design: Retrospective cohort study., Setting: 2 hospitals in the Veterans Affairs Health Care System., Patients: Patients with new dilations of the abdominal aorta detected on CT performed in 2003., Measurements: Radiology report and EMR evidence that the radiologist notified the clinical service, aneurysm size, and interval between CT and EMR recognition., Results: Computed tomography scans of 4112 patients were reviewed and 440 (11%) aortic dilations were identified, of which 91 were new findings. Radiologists directly notified clinical teams about 5 (5%) new dilations. Clinical teams did not record in the EMR recognition of 53 of 91 (58%) dilations within 3 months of the CT, and 9% of these dilations were 5.5 cm or larger. The median time to recognition of aneurysm in the EMR was 237 days, and no EMR documentation existed for 16 abnormalities (29% of surviving patients) during a mean follow-up of 3.2 years. No evidence indicated that any of the aneurysms ruptured or that patient deaths resulted from the delayed follow-up., Limitation: Clinicians may have recognized some aneurysms but did not document them in the EMR., Conclusion: Clinicians neglect to note a substantial proportion of new aortic dilations in the EMR. The findings highlight the need for better strategies to ensure documentation of follow-up of tests.

Objective: Claudication is the most common presentation of peripheral arterial disease (PAD), producing significant ambulatory compromise. Claudicating patients, most of whom are elderly, have reduced mobility and poor health outcomes, including an increased risk of falls. The gait of elderly fallers is characterized by increased variability. Increase in the variability of the locomotor system makes the gait more noisy and unstable. The purpose of this study is to investigate gait variability in patients with PAD., Methods: Nineteen symptomatic PAD patients (age, 63.6 +/- 9.8 years; body mass, 82.1 +/- 18.5 kg; height, 1.71 +/- 0.06 m) walked on a treadmill in the absence of pain or claudication symptoms while joint flexion and extension kinematics were captured. Results were compared with results obtained from 17 matched healthy controls (age, 65.2 +/- 12.5 years; body mass, 82.0 +/- 25.9.5 kg; height, 1.73 +/- 0.08 m). Relative joint angles were calculated for the ankle, knee, and hip flexion/extension, and the stride-to-stride variability of joint flexion and extension was calculated from at least 30 consecutive footfalls. Variability was expressed using the largest Lyapunov exponent, standard deviation, and coefficient of variation. Independent t tests were used to compare gait variability between groups., Results: Symptomatic PAD patients had significantly higher largest Lyapunov exponent values and coefficient of variation values for all joints, and higher standard deviation values at the ankle and the hip (P < .05)., Conclusion: Symptomatic PAD patients have increased gait variability at the ankle, knee, and hip joints at baseline ambulation in the absence of claudication pain. Our findings indicate significant baseline deterioration in the locomotor system of symptomatic PAD patients. This deterioration results in increased noise and instability of gait and is a potential contributing factor to the falls and mobility problems experienced by symptomatic PAD patients.

Objective: Claudication is the most common manifestation of peripheral arterial disease (PAD) producing significant ambulatory compromise. The purpose of this study was to use advanced biomechanical analysis to characterize the kinematic ambulatory pattern of claudicating patients. We hypothesized that compared with control subjects, claudicating patients have altered kinematic gait patterns that can be fully characterized utilizing advanced biomechanical analysis., Methods: The study examined fourteen PAD patients (age: 58 +/- 3.4 years; weight: 80.99 +/- 15.64 kg) with clinically diagnosed femoro-popliteal occlusive disease (Ankle Brachial Index (ABI): 0.56 +/- 0.03, range 0.45 to 0.65) and five healthy controls (age: 53 +/- 3.4 years; weight: 87.38 +/- 12.75 kg; ABI >or= 1). Kinematic parameters (hip, knee, and ankle joint angles in the sagittal plane) were evaluated during gait in patients before and after the onset of claudication pain and compared with healthy controls. Joint angles were calculated during stance time. Dependent variables were assessed (maximum and minimum flexion and extension angles and ranges of motion) and mean ensemble curves were generated. Time to occurrence of the discrete variables was also identified., Results: Significantly greater ankle plantar flexion in early stance and ankle range of motion during stance was observed in PAD patients (P < .05). Time to maximum ankle plantar flexion was shorter and time to maximum ankle dorsiflexion was longer in PAD patients (P < .05). These differences were noted when comparing PAD patients prior to and after the onset of claudication with healthy controls. The analysis of the kinematic parameters of the knee and the hip joints revealed no significant differences between PAD patients and controls., Conclusion: PAD patients with claudication demonstrate significant gait alterations in the ankle joint that are present prior to the onset of claudication pain. In contrast, the joint motion of the hip and knee did not differ in PAD patients when compared with controls. Further research is needed to verify our findings and assess the impact of more proximal disease in PAD patients as well as the effect of revascularization on joint kinematics.

Internal carotid artery (ICA) flow reversal is an effective means of cerebral protection during carotid stenting. Its main limitation is that in the absence of adequate collateral flow it may not be tolerated by the patient. The purpose of this study was to determine if preoperative identification of intracranial collaterals with computerized tomographic (CTA) or magnetic resonance (MRA) angiography can predict adequate collateral flow and neurological tolerance of ICA flow reversal for embolic protection. This was a study of patients undergoing transcervical carotid angioplasty and stenting. Neuroprotection was established by ICA flow reversal. All patients underwent preoperative cervical and cerebral noninvasive angiography with CTA or MRA and had at least one patent intracranial collateral. Mean carotid artery back pressure was measured. Neurological changes during carotid clamping and flow reversal were continuously monitored with electroencephalography (EEG). Thirty-seven patients with at least one patent intracranial collateral on brain imaging with CTA or MRA were included. Mean carotid artery back pressure was 58 mm Hg. All procedures were technically successful. No EEG changes were present with common carotid artery occlusion and ICA flow reversal. One patent intracranial collateral provides sufficient cerebral perfusion to perform carotid occlusion and flow reversal with absence of EEG changes. Continued progress in noninvasive imaging modalities is becoming increasingly helpful in our understanding of cerebral physiology and selection of patients for invasive carotid procedures.

With the increasing complexity of endovascular procedures, concern has grown regarding patient radiation exposure. Abdominal aortic aneurysm (AAA) repair represents the most common complex endovascular procedure currently performed by vascular specialists. Our study evaluates the patient radiation dose received during endovascular AAA repair. Over a 3-month period we prospectively monitored the radiation dose in a series of consecutive patients undergoing endovascular AAA repair. All patients underwent standard endovascular AAA repair with one of two commercially available grafts using the GE OEC 9800 unit. Direct measurement of maximum radiation dose at skin level (peak skin dose, PSD) was recorded using GAFCHROMIC radiographic dosimetry film. Indirect measurements of radiation dose (fluoroscopy time and dose-area-product [DAP]) were recorded with the C-arm dosimeter. A total of 12 consecutive patients undergoing standard endovascular AAA repair were evaluated. Mean PSD was 0.75 Gy (range 0.27-1.25). Mean total fluoroscopy time was 20.6 min (range 12.6-34.2) with an average of 92% spent in standard fluoroscopy and 8% spent in cinefluoroscopy. Regarding total fluoroscopy time, 49% was spent in normal field of view and 51% in magnified view. Mean DAP was 15,166 cGy x cm(2) (range 5,207-24,536). PSD correlated with DAP (r = 0.9, p < 0.05) but not total fluoroscopy time (r = 0.18, p > 0.05). PSD also correlated with body mass index (BMI; r = 0.82, p < 0.05). Obese patients had a mean PSD of 1.1 Gy compared to 0.5 Gy in nonobese patients. PSD of all patients was well below the accepted 2.0 Gy threshold for skin injury. PSD correlated with DAP but not total fluoroscopy time. PSD also correlated with BMI, and the mean PSD was significantly increased in obese compared to nonobese patients. Despite the complexity and duration of endovascular AAA repair, the procedure can be performed safely without excessive radiation exposure.

A myopathy characterized by mitochondrial pathology and oxidative stress is present in patients with peripheral arterial disease (PAD). Patients with PAD differ in disease severity, mode of presentation, and presence of comorbid conditions. In this study, we used a mouse model of hindlimb ischemia to isolate and directly investigate the effects of chronic inflow arterial occlusion on skeletal muscle microanatomy, mitochondrial function and expression, and oxidative stress. Hindlimb ischemia was induced by staged ligation/division of the common femoral and iliac arteries in C57BL/6 mice, and muscles were harvested 12 wk later. Muscle microanatomy was examined by bright-field microscopy, and mitochondrial content was determined as citrate synthase activity in muscle homogenates and ATP synthase expression by fluorescence microscopy. Electron transport chain (ETC) complexes I through IV were analyzed individually by respirometry. Oxidative stress was assessed as total protein carbonyls and 4-hydroxy-2-nonenal (HNE) adducts and altered expression and activity of manganese superoxide dismutase (MnSOD). Ischemic muscle exhibited histological features of myopathy and increased mitochondrial content compared with control muscle. Complex-dependent respiration was significantly reduced for ETC complexes I, III, and IV in ischemic muscle. Protein carbonyls, HNE adducts, and MnSOD expression were significantly increased in ischemic muscle. MnSOD activity was not significantly changed, suggesting MnSOD inactivation. Using a mouse model, we have demonstrated for the first time that inflow arterial occlusion alone, i.e., in the absence of other comorbid conditions, causes myopathy with mitochondrial dysfunction and increased oxidative stress, recapitulating the muscle pathology of PAD patients.

In recent years, an increasing number of studies have demonstrated that a myopathy is present, contributes, and, to a certain extent, determines the pathogenesis of peripheral arterial occlusive disease. These works provide evidence that a state of repetitive cycles of exercise-induced ischemia followed by reperfusion at rest operates in patients with peripheral arterial occlusive disease and mediates a large number of structural and metabolic changes in the muscle, resulting in reduced strength and function. The key players in this process appear to be defective mitochondria that, through multilevel failure in their roles as energy, oxygen radical species, and apoptosis regulators, produce and sustain a progressive decline in muscle performance. In this 2-part review, the currently available evidence that characterizes the nature and mechanisms responsible for this myopathy is highlighted. In part 1, the functional and histomorphological characteristics of the myopathy were reviewed, and the main focus was on the biochemistry and bioenergetics of its mitochondriopathy. In part 2, accumulating evidence that oxidative stress related to ischemia reperfusion is probably the major operating mechanism of peripheral arterial occlusive disease myopathy is reviewed. Important new findings of a possible neuropathy and a shift in muscle fiber type are also reviewed. Learning more about these mechanisms will enhance our understanding of the degree to which they are preventable and treatable.

Background: Claudication secondary to peripheral arterial disease leads to reduced mobility, limited physical functioning, and poor health outcomes. Disease severity can be assessed with quantitative clinical methods and qualitative self-perceived measures of quality of life. Limited data exist to document the degree to which quantitative and qualitative measures correlate. The current study provides data on the relationship between quantitative and qualitative measures of symptomatic peripheral arterial disease., Method: This descriptive case series was set in an academic vascular surgery unit and biomechanics laboratory. The subjects were symptomatic patients with peripheral arterial disease patients presenting with claudication. The quantitative evaluation outcome measures included measurement of ankle-brachial index, initial claudication distance, absolute claudication distance, and self-selected treadmill pace. Qualitative measurements included the Walking Impairment Questionnaire (WIQ) and the Medical Outcomes Study Short Form-36 (SF-36) Health Survey. Spearman rank correlations were performed to determine the relationship between each quantitative and qualitative measure and also between the WIQ and SF-36., Results: Included were 48 patients (age, 62 +/- 9.6 years; weight, 83.0 +/- 15.4 kg) with claudication (ABI, 0.50 +/- 0.20). Of the four WIQ subscales, the ankle-brachial index correlated with distance (r = 0.29) and speed (r = 0.32); and initial claudication distance and absolute claudication distance correlated with pain (r = 0.40 and 0.43, respectively), distance (r = 0.35 and 0.41, respectively), and speed (r = 0.39 and 0.39 respectively). Of the eight SF-36 subscales, no correlation was found for the ankle-brachial index, initial claudication distance correlated with Bodily Pain (r = 0.46) and Social Functioning (r = 0.30), and absolute claudication time correlated with Physical Function (r = 0.31) and Energy (r = 0.30). The results of both questionnaires showed reduced functional status in claudicating patients., Conclusions: Initial and absolute claudication distances and WIQ pain, speed, and distance subscales are the measures that correlated the best with the ambulatory limitation of patients with symptomatic peripheral arterial disease. These results suggest the WIQ is the most specific questionnaire for documenting the qualitative deficits of the patient with claudication while providing strong relationships with the quantitative measures of arterial disease. Future studies of claudication patients should include both quantitative and qualitative assessments to adequately assess disease severity and functional status in peripheral arterial disease patients.

In recent years, an increasing number of studies have demonstrated that a myopathy is present, contributes, and, to a certain extent, determines the pathogenesis of peripheral arterial occlusive disease (PAD). These works provide evidence that a state of repetitive cycles of exercise-induced ischemia followed by reperfusion at rest operates in PAD patients and mediates a large number of structural and metabolic changes in the muscle, resulting in reduced strength and function. The key players in this process appear to be defective mitochondria that, through multilevel failure in their roles as energy, oxygen radical species, and apoptosis regulators, produce and sustain a progressive decline in muscle performance. In this 2-part review, we highlight the currently available evidence that characterizes the nature and mechanisms responsible for this myopathy. In part 1, the authors review the functional and histomorphological characteristics of the myopathy and focus on the biochemistry and bioenergetics of its mitochondriopathy. In part 2, they then review accumulating evidence that oxidative stress related to ischemia reperfusion is probably the major operating mechanism of PAD myopathy. Important new findings of a possible neuropathy and a shift in muscle fiber type are also reviewed. Learning more about these mechanisms will enhance our understanding of the degree to which they are preventable and treatable.

The signs and symptoms of peripheral arterial occlusive disease (PAD), including claudication, rest pain, and tissue loss, are consequences of compromised bioenergetics and oxidative tissue injury within the affected lower extremities. Compromised bioenergetics is the result of a combination of low blood flow through diseased arteries and diminished adenosine triphosphate production by dysfunctional mitochondria. The tissue injury appears to be secondary to increased production of reactive oxygen species by dysfunctional mitochondria and by inflammation, in association with ischemia and ischemia/reperfusion. In this review, we present the current histomorphologic, physiologic, and biochemical evidence defining the nature of this mitochondriopathy and discuss its contribution to the pathogenesis and clinical manifestations of PAD.

Objective: Claudication is the most common manifestation of peripheral arterial disease (PAD), producing significant ambulatory compromise. The gait of claudicating patients has been evaluated using primarily temporal and spatial parameters. With the present study, we used advanced biomechanical measures to further delineate the ambulatory impairment of claudicating patients. We hypothesized that the claudicating legs of PAD patients have an altered kinetic gait pattern compared with normal legs from control subjects., Methods: Ambulation kinetics (ground reaction forces) were evaluated in claudicating patients and compared with age-matched healthy controls. Forces were analyzed in the vertical, anterior-posterior, and medial-lateral directions. Time from heel touch-down to toe-off (stance time) and time spent in double-limb support were also evaluated., Results: The study recruited 14 PAD patients (age, 58 +/- 3.4 years; weight, 80.99 +/- 15.64 kg) with femoropopliteal occlusive disease (ankle-brachial index [ABI], 0.56 +/- 0.03) and five controls (age, 53 +/- 3.4 years; weight, 87.38 +/- 12.75 kg; ABI, >or=1.00). Vertical force curve evaluation demonstrated significant flattening in claudicating patients resulting in a lower and less fluctuant center of mass when ambulating. In the anterior-posterior direction, claudicating patients demonstrated significantly decreased propulsion forces. In the medial-lateral direction, they had significantly increased forces consistent with wider steps and an inability to swing their legs straight through. Claudicating patients demonstrated a greater stance time and time in double limb support compared with healthy controls. Most importantly, gait abnormalities were present before the onset of claudication, with gait worsening after the onset of claudication., Conclusion: Claudicating patients demonstrate significant gait impairments that are present even before they experience any limb discomfort. These alterations may make them feel more stable and secure while attempting to minimize use of the affected limb. Advanced biomechanical analysis, using ambulation kinetics, permits objective and quantitative evaluation of the gaits of claudicating patients. Such evaluation may point to new rehabilitation strategies and provide objective measurement of functional outcomes after medical and surgical therapy.

Background: Pulmonary embolism (PE) is a leading cause of mortality after bariatric surgery. We evaluated inferior vena cava (IVC) filter use for PE risk reduction in high-risk super morbidly obese bariatric surgery patients., Methods: IVC filters were inserted according to the patient's risk factors, including immobility, previous deep venous thrombosis (DVT)/PE, venous stasis, and pulmonary compromise. All filters were placed concomitant to bariatric surgery and were placed through a right internal jugular vein access site. We analyzed the prospectively collected data from this cohort and evaluated the incidence of PE and complications., Results: Since April 2003, 41 patients (12 men and 29 women) with a mean age of 47.3 +/- 10.0 years and body mass index of 64.2 +/- 12 kg/m2 (range 47-105) underwent IVC filter placement. These and all other patients underwent standard DVT/PE risk reduction measures. All IVC filter patients had one or more significant risk factors for thromboembolic events. No instances of PE were documented, although 1 patient experienced DVT, and no immediate or late complications related to filter placement occurred. One patient, with a body mass index of 105 kg/m2, died secondary to rhabdomyolysis after an extended procedure. The average filter placement time was 34.3 +/- 9 minutes., Conclusion: IVC filter placement for PE risk reduction is safe and feasible in the super morbidly obese. Our data have shown that the filters can be placed expeditiously and with minimal morbidity concomitant with bariatric surgery. In this limited series, IVC filter placement was associated with no PE. Additional studies are needed to confirm the efficacy of IVC filter placement for PE risk reduction and related mortality in the super morbidly obese.

Introduction: Limb salvage can now be achieved in many cases of lower extremity sarcoma. Obtaining disease-free margins may require resection of adjacent vascular structures. We present our experience with a consecutive series of patients undergoing resection of lower extremity sarcomas en block with the artery and vein, focusing on the mid- and long-term outcomes of their vascular reconstruction., Methods: Records were reviewed retrospectively for patient age, tumor location and type, procedure, and early and late outcomes. Between 1991 and 2004, 10 children (mean age 12 years, range 6-18 years) and 9 adults (mean age 48 years, range 24-73 years) underwent wide resection of lower extremity sarcomas to include the involved arterial and venous segments. All children had bone sarcomas, and because of their skeletal immaturity, they were treated with rotationplasty--a type of intercalary amputation that removes the distal thigh, knee, and proximal tibia while preserving the distal leg and foot. In rotationplasty, the distal residual limb is preserved, rotated 180 degrees, and attached to the thigh, positioning the ankle at the level of the former knee joint. In these cases, the residual vessels were reconstructed by primary anastomosis. All of the adults except one had soft tissue sarcomas; the resected vessels were reconstructed with contralateral saphenous vein. In all cases, the operative approach included shunting of artery and vein during tumor removal and orthopedic reconstruction., Results: The mean follow-up was 5.7 years. Three patients died of metastatic disease, and one died from a postoperative pulmonary embolism. No patient had local recurrence. Two patients ultimately required above-knee amputation: one child for tissue loss secondary to reperfusion injury, and one adult because of graft thrombosis secondary to progression of peripheral arterial disease. Two patients required early re-exploration for perioperative graft thrombosis. Both required replacement of saphenous vein conduits with polytetrafluoroethylene (PTFE) prosthetic graft; one of the PTFE grafts became infected., Conclusions: Limb salvage can be achieved in the majority of patients who have lower extremity sarcomas even when en bloc resection includes the artery and vein. Intraoperative shunting can limit ischemia and is especially useful when immediate vascular repair is delayed by orthopedic reconstruction. The long-term patency rate of the reconstructed vessels is high. Saphenous vein is the preferred conduit when it is of adequate caliber.

Carotid angioplasty and stenting are progressively earning a role as a less invasive alternative in the treatment of carotid occlusive disease. The most common approach for carotid artery stenting involves transfemoral access and use of a filter or balloon device for neuroprotection. This approach has limitations related to both the site of access and the method of neuroprotection. Specifically, an aortoiliac segment with advanced occlusive or aneurysmal disease or an anatomically unfavorable or atheromatous arch and arch branches can significantly limit the safety of the retrograde transfemoral pathway to the carotid bifurcation. Additionally, data provided by the use of transcranial Doppler monitoring and diffusion-weighted magnetic resonance imaging in patients undergoing filter- or balloon-protected carotid artery stenting demonstrate that currently available devices are associated with a considerable incidence of cerebral embolization. To address these limitations, we, along with others, have employed a direct transcervical approach for carotid artery stenting that incorporates the principle of flow reversal for neuroprotection. The technique bypasses all of the anatomic limitations of transfemoral access and simplifies the application of flow reversal, which is one of the safest neuroprotection techniques. The purpose of this review is to describe our method of transcervical carotid artery stenting, review the accumulating outcomes data, and discuss the clinical advantages of and indications for this increasingly popular technique.

Abnormal mitochondrial function is present in patients with peripheral arterial disease and may contribute to its clinical manifestations. However, the specific biochemical mitochondrial defects and their association with increased oxidative stress have not been fully characterized. Gastrocnemius muscle was obtained from peripheral arterial disease patients (n = 25) and age-matched controls (n = 16) and mitochondrial parameters were measured. Complexes I through IV of the electron transport chain were individually evaluated to assess for isolated defects. Muscle was also evaluated for protein and lipid oxidative changes by measuring the levels of protein carbonyls, lipid hydroperoxides, and total 4-hydroxy-2-nonenal binding and for the activities of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase. Mitochondrial electron transport chain complexes I, III, and IV in arterial disease patients demonstrated significant reductions in enzymatic activities and mitochondrial respiration compared to controls. Oxidative stress biomarker analysis demonstrated significantly increased levels of protein carbonyls, lipid hydroperoxides, and 4-hydroxy-2-nonenal compared to control muscle. Antioxidant enzyme activities were altered, with a significant decrease in superoxide dismutase activity and significant increases in catalase and glutathione peroxidase. Peripheral arterial disease is associated with abnormal mitochondrial function and evidence of significant oxidative stress.

Temporal arteritis, particularly in its classic form, is exceedingly rare in individuals <50 years old. We report the youngest case of biopsy-proven giant cell temporal arteritis. A 17-year-old male presented with a progressively expanding and pulsatile but otherwise asymptomatic mass in his forehead. The patient's medical history was significant for uveitis since the age of 3, and severe allergic rhinitis, mild asthma, and juvenile rheumatoid arthritis as a young adolescent. Admission laboratory values included a mildly elevated erythrocyte sedimentation rate and C-reactive protein level. A computed tomography evaluation demonstrated aneurysmal degeneration of the frontal branch of the right superficial temporal artery and confirmed no other cerebrovascular changes. Histologically, the aneurysmal arterial segment demonstrated subacute temporal arteritis. The arterial wall had a primarily lymphoplasmacytic infiltrate with rare giant cells and focally marked medial destruction. Additionally, severely obstructive intimal hyperplasia with chronic adventitial and periadvential dense fibrosis was noted. The diagnosis of classic giant cell temporal arteritis was established from the biopsy result. Postoperatively, the patient was treated with prednisone for 3 months. Three years after surgery, the patient remains well and reports no recurrence of temporal artery disease.

An acrylic cement pulmonary embolus is a rare complication of percutaneous vertebroplasty. Many patients remain completely asymptomatic, but others may present with chest discomfort, dyspnea, and even cardiovascular collapse leading to death. Here we present an asymptomatic patient initially thought to have a central venous catheter pulmonary artery embolus based on the morphology of the foreign body on imaging exams. A more thorough investigation established the diagnosis of an acrylic cement pulmonary embolus resulting from percutaneous vertebroplasty procedures performed many months before the embolus discovery. The diagnostic work-up, treatment strategy, and a review of the literature are presented.

Isolated aneurysms of the iliac arteries are extremely rare, comprising less than 2% of all aneurysmal disease. These aneurysms are typically seen in older men. Their natural history, although fairly indolent, carries a significant risk of rupture when the aneurysms have attained a large size. Their operative mortality is significantly higher when undertaken as an emergent versus elective procedure, underscoring the importance of early diagnosis and appropriate management. This article reviews the literature with regard to the natural history, diagnostic workup, and treatment of iliac artery aneurysms. For patients undergoing elective repair, preoperative imaging with computed tomography or magnetic resonance is advocated. Repair is recommended for good-risk patients with aneurysms larger than 3.5 cm. A working classification based on aneurysmal anatomy is provided along with an outline of the suggested open and endovascular surgical options. Results of open and endovascular strategies are summarized and follow-up recommendations are proposed.

Purpose: To report our initial experience using a transcervical approach for carotid angioplasty/stenting (CAS) that employs internal carotid artery (ICA) flow reversal for neuroprotection., Methods: Seventeen patients (15 men; mean age 65 years, range 49-77) with significant carotid stenosis (mean 88%, 8 symptomatic) were treated with protected transcervical CAS. Eleven patients were considered at high risk for carotid endarterectomy; 8 were also considered high risk for transfemoral access (unfavorable aortic arch anatomy or advanced aortoiliac occlusive disease). Anesthesia was based on patient and anesthesiologist preferences. The approach consisted of a 2-cm cutdown over the common carotid artery and placement of a 9-F sheath. ICA flow was reversed and shunted into the jugular vein during the carotid intervention., Results: Access and carotid stenting were successful in all cases. Thirteen procedures were performed under general and 4 under local anesthesia. Mean flow reversal time was 34+/-4 minutes (25 minutes in the last 7 cases). The patients tolerated the procedure well and had no neurological events. Four (23%) patients had significant oozing from the operative site; 2 developed small neck hematomas that were treated conservatively. All patients were discharged on the first postoperative day. There were no deaths, changes in neurological status, or restenosis over a mean follow-up of 12 months (range 1-24)., Conclusions: Our initial experience demonstrates that a transcervical approach is a viable alternative for CAS. The procedure can be performed safely, with good initial clinical outcomes. The approach allows carotid flow reversal and emboli protection without introducing neuroprotection devices. The method appears best suited for patients at high risk for endarterectomy and transfemoral access.

Objective: Discrete morphologic, enzymatic and functional changes in skeletal muscle mitochondria have been demonstrated in patients with peripheral arterial disease (PAD). We examined mitochondrial respiration in the gastrocnemius muscle of nine patients (10 legs) with advanced PAD and in nine control patients (nine legs) without evidence of PAD., Methods: Mitochondrial respiratory rates were determined with a Clark electrode in an oxygraph cell containing saponin-skinned muscle bundles. Muscle samples were obtained from the anteromedial aspect of the gastrocnemius muscle, at a level 10 cm distal to the tibial tuberosity. Mitochondria respiratory rate, calculated as nanoatoms of oxygen consumed per minute per milligram of noncollagen protein, were measured at baseline (V(0)), after addition of substrates (malate and glutamate; (V(SUB)), after addition of adenosine diphosphate (ADP) (V(ADP)), and finally, after adenine nucleotide translocase inhibition with atractyloside (V(AT)). The acceptor control ratio, a sensitive indicator of overall mitochondrial function, was calculated as the ratio of the respiratory rate after the addition of ADP to the respiratory rate after adenine nucleotide translocase inhibition with atractyloside (V(ADP)/ V(AT))., Results: Respiratory rate in muscle mitochondria from patients with PAD were not significantly different from control values at baseline (0.31 +/- 0.06 vs 0.55 +/- 0.12; P =.09), but V(sub) was significantly lower in patients with PAD compared with control subjects (0.43 +/- 0.07 vs 0.89 +/- 0.20; P <.05), as was V(ADP) (0.69 +/- 0.13 vs 1.24 +/- 0.20; P <.05). Respiratory rates after atractyloside inhibition in patients with PAD were no different from those in control patients (0.47 +/- 0.07 vs 0.45 +/- P =.08). Compared with control values, mitochondria from patients with PAD had a significantly lower acceptor control ratio (1.41 +/- 0.10 vs 2.90 +/- 0.20; P <.001)., Conclusion: Mitochondrial respiratory activity is abnormal in lower extremity skeletal muscle in patients with PAD. When considered in concert with the ultrastructural and enzymatic abnormalities previously documented in mitochondria of chronically ischemic muscle, these data support the concept of defective mitochondrial function as a pathophysiologic component of PAD.

Duplex ultrasound scan (DUS) criteria for grading >50% carotid artery stenosis is typically divided into broad categories such as 50-79% stenosis, 80-99% stenosis, and occlusion. The purpose of this study is to validate DUS criteria for stratifying 50 to 100% carotid stenosis into 10% intervals using digital substraction cerebral angiography (DSCA) as the standard of comparison. Between 1996 and 2001, 163 patients were evaluated with duplex ultrasound and angiography. A total of 326 carotid arteries were studied using DUS in an accredited ICAVL vascular laboratory. Threshold velocity criteria for determining the degree of carotid stenosis was defined according to seven categories: <50%, 50-59%, 60-69%, 70-79%, 80-89%, 90-99%, and occlusion. Treatment decisions were based on the angiographic findings. In cases where the degree of stenosis as defined by duplex velocity criteria did not correlate with angiographically defined stenosis, each record was reviewed to determine whether the angiographic findings altered the surgeon's treatment decision. The sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for DUS-defined degree of stenosis as compared to angiographically defined stenosis were determined. There was a high correlation (R = 0.96) between duplex scan and angiography in 93% (302/326) of the cases. Clinical management was altered in only 3% (10/326) of the cases because of the results of angiography. The DUS velocity criteria to grade the severity of carotid disease in 10% intervals is reliable and accurate. Clinical management of patients with carotid stenosis can be based solely on carotid DUS in 97% of patients considered for treatment of carotid artery disease.

Objective: Previous morphologic studies and phosphorus nuclear magnetic resonance spectroscopy (31P MRS) have suggested a primary mitochondrial defect in claudicating skeletal muscle. We hypothesized that pentoxifylline may alleviate this defect., Methods: The response of calf muscle bioenergetics to pentoxifylline was evaluated in 10 male, nondiabetic claudicants with 31P MRS and standard treadmill testing before and after 12 weeks of pentoxifylline therapy. Phosphocreatine (PCr) and adenosinodiphosphate (ADP) recovery rate constants, two very sensitive measures of oxidative mitochondrial function, were measured., Results: Seven of the 10 subjects had abnormal baseline PCr (<0.015 s(-1)) and ADP (<0.024 s(-1)) recovery rate constants. These 7 had significant improvement in mitochondrial function with pentoxifylline; their PCr recovery rate constants increased from 0.009 +/- 0.002 to 0.013 +/- 0.002 s(-1) (P = 0.013) and their ADP recovery rate constants increased from 0.015 +/- 0.002 to 0.022 +/- 0.002 s(-1) (P = 0.004). The remaining 3 patients had normal baseline constants and demonstrated no improvement after pentoxifylline therapy. Baseline PCr and ADP recovery rate constants inversely correlated with their corresponding percentage of improvement after pentoxifylline (P < 0.05). In addition the percentage of improvement in the PCr and ADP recovery rate constants correlated with the percentage of improvement in initial claudication distance and maximum walking capacity (P < 0.05)., Conclusions: Pentoxifylline improves the mitochondriopathy of claudicating muscle, producing the most improvement in limbs with the worse baseline mitochondrial function. These results point to a potential new mode of action for pentoxifylline in the treatment of claudication and identify a subgroup of patients with the best potential for improvement with treatment., ((c)2001 Elsevier Science.)

Purpose: The causative role of consumptive coagulopathy in the development of bleeding complications after supraceliac (SC) aortic cross-clamping (AXC) has been challenged by recent reports that ascribe this coagulopathy to primary fibrinolysis. This theory is made on the basis of evidence that tissue plasminogen activator (t-PA) antigen (Ag) levels increase after SC AXC. However, t-PA Ag levels reflect both active and inactive (bound to serum t-PA inhibitors) forms of serum t-PA, and elevations confirm the presence of fibrinolysis only in conjunction with an increase in t-PA activity., Methods: To investigate the etiology of this coagulopathy, we submitted eight pigs to SC AXC and six pigs to infrarenal (IR) AXC for 30 minutes. Blood was drawn from the portal vein, the hepatic vein, and the carotid artery before AXC, just before unclamping, and 5, 30, and 60 minutes after unclamping. Prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen (FBG), platelets (PLT), thrombin-antithrombin complexes (TAT), t-PA Ag, t-PA activity, plasminogen activator inhibitor-1 (PAI-1), and alpha2-antiplasmin (AP) activities were measured. Statistical analysis was performed by using repeated measures analysis of variance and t tests, Results: The PT did not differ between the two groups at any point. After unclamping, in the SC group there was a drop in PLT levels (P =.005), a decrease in FBG levels (P <.001), and a trend toward PTT prolongation (P =.06) compared with baseline. In contrast, there were no changes in PTT, PLT levels, or FBG levels in the IR group. TAT, a serum marker of thrombin generation, increased with SC AXC (P =.04), remained elevated 5 minutes after unclamping (P =.08), and returned to normal 30 minutes after unclamping. In contrast, TAT levels did not change in the IR control group. In the SC AXC group, the TAT levels did not differ between the three test sites at any time. SC AXC was associated with an increase in t-PA Ag just before unclamping (P <.001) and 5 minutes after unclamping (P =.002), but IR AXC was not. t-PA activity levels decreased in both experimental groups 30 and 60 minutes after unclamping. Levels of alpha2-AP activity decreased to a similar degree in both groups after unclamping when compared with baseline, Conclusion: Thirty minutes of SC AXC results in intravascular thrombosis that cannot be localized to the ischemic visceral circulation. This intravascular thrombosis is associated with consumption of clotting factors. Thirty minutes of SC AXC causes an activation of fibrinolytic pathways that does not result in a hyperfibrinolytic state. An increase in t-PA Ag without a rise in t-PA activity does not represent true fibrinolysis, but rather an increase in the bound, inactive forms of serum t-PA. Both IR and SC AXC result in decreased fibrinolytic activity ("fibrinolytic shutdown") after release of the aortic clamp.