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.

A 30-year retrospective review identified 13 patients treated for infected aneurysms of the abdominal aorta or iliac arteries, for an overall incidence of 0.65%. A constellation of clinical findings led to the correct preoperative diagnosis in 11 (85%) of 13 patients. Treatment methods included resection and in situ replacement grafting in seven patients, resection and extra-anatomic bypass in five patients, and resection-ligation in one patient. Four (31%) of 13 patients died within 30 days of operation, three of whom died of rupture. Overall, good results were achieved in five patients (38%), while poor results were noted in the remaining eight patients (62%). The determinants of outcome were aneurysm location or rupture, the presence of established infection, and the virulence of the infecting organism. In 10 (77%) of the 13 aneurysms, Salmonella species, Bacteroides fragilis, Staphylococcus aureus, and Pseudomonas aeruginosa accounted for all deaths, ruptures, and suprarenal aneurysm infections. These data suggest that patients with primary infections of the abdominal aorta or iliac arteries continue to present with advanced infections or aneurysm rupture that result in a high mortality.

Background In the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST), the composite primary endpoint of stroke, myocardial infarction, or death during the periprocedural period or ipsilateral stroke thereafter did not differ between carotid artery stenting and carotid endarterectomy for symptomatic or asymptomatic carotid stenosis. A secondary aim of this randomised trial was to compare the composite endpoint of restenosis or occlusion. Methods Patients with stenosis of the carotid artery who were asymptomatic or had had a transient ischaemic attack, amaurosis fugax, or a minor stroke were eligible for CREST and were enrolled at 117 clinical centres in the USA and Canada between Dec 21, 2000, and July 18, 2008. In this secondary analysis, the main endpoint was a composite of restenosis or occlusion at 2 years. Restenosis and occlusion were assessed by duplex ultrasonography at 1, 6, 12, 24, and 48 months and were defined as a reduction in diameter of the target artery of at least 70%, diagnosed by a peak systolic velocity of at least 3·0 m/s. Studies were done in CREST-certified laboratories and interpreted at the Ultrasound Core Laboratory (University of Washington). The frequency of restenosis was calculated by Kaplan-Meier survival estimates and was compared during a 2-year follow-up period. We used proportional hazards models to assess the association between baseline characteristics and risk of restenosis. Analyses were per protocol. CREST is registered with ClinicalTrials.gov, number NCT00004732. Findings 2191 patients received their assigned treatment within 30 days of randomisation and had eligible ultrasonography (1086 who had carotid artery stenting, 1105 who had carotid endarterectomy). In 2 years, 58 patients who underwent carotid artery stenting (Kaplan-Meier rate 6·0%) and 62 who had carotid endarterectomy (6·3%) had restenosis or occlusion (hazard ratio [HR] 0·90, 95% CI 0·63–1·29; p=0·58). Female sex (1·79, 1·25–2·56), diabetes (2·31, 1·61–3·31), and dyslipidaemia (2·07, 1·01–4·26) were independent predictors of restenosis or occlusion after the two procedures. Smoking predicted an increased rate of restenosis after carotid endarterectomy (2·26, 1·34–3·77) but not after carotid artery stenting (0·77, 0·41–1·42). Interpretation Restenosis and occlusion were infrequent and rates were similar up to 2 years after carotid endarterectomy and carotid artery stenting. Subsets of patients could benefit from early and frequent monitoring after revascularisation. Funding National Institute of Neurological Disorders and Stroke and Abbott Vascular Solutions

Phosphorus 31 MRS provides the first direct evidence of defective energy metabolism in the mitochondria of claudicating calf muscle. This defect appears to be independent of both arterial flow and the severity of occlusive disease in patients with mild to moderate claudication. Coupled with documented ultrastructural and DNA abnormalities in the mitochondria of claudicating skeletal muscle, these data provide evidence for a secondary cause of muscle dysfunction in intermittent claudication.

Although MAR for CMI carries a low mortality rate, AMI remains a lethal and frequently unheralded problem. Long-term patency and symptom-free survival can be expected after successful MAR for AMI and is comparable with those rates achieved after MAR for CMI. The patency of the SMA is important in the prevention of symptomatic recurrences. Elective MAR is indicated in patients with CMI and warrants long-term surveillance.

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The management of pancreatic pseudocyst-associated pseudoaneurysms remains a challenging problem with high morbidity and death rates. Operation and PAE play complementary management roles. PAE is recommended as the initial therapy for hemodynamically stable patients. Surgery should be reserved for actively bleeding, hemodynamically unstable patients; for failed embolization; and for other secondary complications such as infection or extrinsic compression.

The small number of reported cases indicates either the rarity of this complication or unawareness of its existence. The true incidence of this complication is probably under-reported. Orthopedic and vascular surgeons should be aware of this potentially fatal problem. Prevention remains the best treatment. Once encountered, a variety of techniques are available to manage this complication with reasonable outcome.