Outcomes of Popliteal Stent-Graft Placement at the Artery Hinge Point for Popliteal Artery Aneurysm.

BACKGROUND: To assess whether stent-grafts crossing the hinge point (HP) in the popliteal artery are associated with increased complications and decreased patency rates, after endovascular treatment of the popliteal artery aneurysm. METHODS: This was a single-center, case-control study. Patients were allocated to either the HP group (subjects with stent-grafts crossing the HP) or the control group (subjects with stent-grafts above and/or below the HP) based on stent-graft location in the femoropopliteal artery. HP was defined as the main curve in the popliteal artery in the most acute angle toward the femur that appeared during knee flexion, which was identified by reviewing postoperative angiograms. Independent, blinded reviews were performed for all imaging data. Graft evaluation by CTA or duplex ultrasound was performed at 1, 3, 6, and 12 months and annually thereafter. Outcomes measured included: stent-graft patency, stent-graft fracture, other stent-related complications, and major adverse events, including reintervention, death, amputation, stroke, and myocardial infarction. RESULTS: A total of 44 limbs treated with placement of heparin-bonded Viabahn endoprostheses were included in this study. Twenty and twenty-four patients were allocated to the HP group and the control group, respectively. Primary patency rates of the HP group at 1, 2, 3, and 5 years were 84.1 ± 8.4%, 84.1 ± 8.4%, 84.1 ± 8.4%, and 72.1 ± 13.3%, respectively. The primary patency rates of the control group were 87.0 ± 7.0%, 82.4 ± 8.0%, 82.4 ± 8.0%, and 82.4 ± 8.0%, respectively. There was no significant difference between the 2 groups (P = 0.81). No reintervention was performed in the control group. In the HP group, 5 limbs (25.0%) developed endoleak, 3 (15.0%) developed thrombosis, and 1 (5.0%) developed a stent fracture followed by thrombosis. Thrombosis occurred in 2 limbs (8.3%) of the control group, and stent-graft migration was observed in another 2 cases (8.3%). Neither group demonstrated stent-graft infection or acute popliteal artery embolism. Overall, incidence of stent-related complications were significantly higher in the HP group (P= 0.04). Event-free survival rates of the HP group at 1, 2, 3, and 5 years were 75.0 ± 9.7%, 69.6 ± 10.4%, 61.9 ± 11.8%, and 29.0 ± 12.8%, respectively. Corresponding rates in the control group were 79.2 ± 8.3%, 79.2 ± 8.3%, 79.2 ± 8.3%, and 79.2 ± 8.3%, respectively. The difference was not statistically significant between the 2 groups (P = 0.20) CONCLUSIONS: crossing the HP with femoropopliteal artery stent-grafts increased the risk of stent-related complications and reinterventions but did not decrease stent patency or event-free survival.

Deletion of newly described pro-survival molecule Pellino-1 increases oxidative stress, downregulates cIAP2/NF-κB cell survival pathway, reduces angiogenic response, and thereby aggravates tissue function in mouse ischemic models.

INTRODUCTION: In the present study, we aimed to explore the functional role of Pellino-1 (Peli1) in inducing neovascularization after myocardial infarction (MI) and hindlimb ischemia (HLI) using Peli1 global knockout mice (Peli1-/-). Recently we have shown that Peli1, an E3 ubiquitin ligase, induce angiogenesis and improve survivability, with decreased necrosis of ischemic skin flaps. METHODS: Peli1fl/fl and Peli1-/- mice were subjected to either permanent ligation of the left anterior descending coronary artery (LAD) or sham surgery (S). Tissues from the left ventricular risk area were collected at different time points post-MI. In addition, Peli1fl/fl and Peli1-/- mice were also subjected to permanent ligation of the right femoral artery followed by motor function scores, Doppler analysis for blood perfusion and immunohistochemical analysis. RESULTS: Global Peli1 knockout exacerbated myocardial dysfunction, 30 and 60 days after MI compared to wild type (WT) mice as measured by echocardiogram. In addition, Peli1-/- mice also showed decreased motor function scores and perfusion ratios compared with Peli1fl/fl mice 28 days after the induction of HLI. The use of Peli1 in adenoviral gene therapy following HLI in CD1 mice improved the perfusion ratio at 28 days compared to Ad.LacZ-injected mice. CONCLUSION: These results suggest new insights into the protective role of Peli1 on ischemic tissues and its influence on survival signaling.

Cystic adventitial disease of the popliteal artery presenting with features of entrapment syndrome.

Cystic adventitial disease is an uncommon cause of lower extremity claudication resulting from accumulation of mucinous fluid in an arterial subadventitial layer, typically of the popliteal artery. A popliteal bruit and/or reduced distal pulses with knee flexion may be seen on examination. Alternatively, popliteal artery entrapment syndrome triggers claudication via an aberrant arterial pathway or muscular hypertrophy. Decreased distal pressures with plantar or dorsiflexion is a key finding. This report details the case of a middle-aged male with cystic adventitial disease whose diagnosis was complicated by concurrent features of popliteal artery entrapment syndrome. Treatment consisted of venous interposition grafting, which yielded excellent results.

A Tumultuous Course of Exogenous Testosterone by a Bodybuilder Causing a Catastrophic Hypercoagulable State in the Surgical Intensive Care Unit.

Present literature demonstrates an equivocal relationship between testosterone and thrombogenicity. Herein, we describe a case in which a patient used an unspecified amount and duration of exogenous testosterone injections, subsequently developing thrombotic events in his: right radial artery, right iliac artery, superficial femoral artery, splenic artery and a bilateral lower lobe pulmonary embolism. As a result, clinicians should consider exogenous testosterone use as a potential risk factor when the etiology of a patient's thrombotic events are not clear. We also completed a literature review of the molecular mechanisms in which testosterone can increase the clot burden through an increases human platelet thromboxane A2 receptor density and an increase in erythropoiesis.

Isolated Great Saphenous Vein Thrombus Is Associated with High Rates of Complications regardless of Management.

BACKGROUND: Isolated great saphenous vein thrombus (GSVT) is generally regarded as benign, and treatment is heterogeneous. Complications include thrombus propagation, new saphenous vein thrombosis, deep vein thrombosis (DVT), pulmonary embolism (PE), and symptom persistence. Our objective was to review our institution's experience with isolated GSVT to understand its natural history, the frequency of complications, real-world treatment, and the impact of proximity to the saphenofemoral junction (SFJ), on the rate of complications. METHODS: Records of patients who had lower extremity venous duplex (LEVD) demonstrating GSVT without concomitant DVT between July 2008 and June 2014 were reviewed. Demographic, medical, management, outcomes, and follow-up LEVD data were collected. RESULTS: Of 605 patients with acute GSVT, 67 limbs in 61 patients with isolated GSVT were the study group; 14.8% of patients had a hypercoagulable state, 31.1% had prior GSVT or DVT, and 23.0% of patients had malignancy; 28.4% of GSVT were observed, 13.4% were treated with aspirin/NSAIDs, and 58.2% were anticoagulated; 38.8% of limbs remained symptomatic following treatment at a mean follow-up period of 761 days; 37 limbs had GSVT <5 cm of the SFJ (group 1), and 30 had GSVT >5 cm from the SFJ (group 2). Seven patients developed PE, all in group 1 (P = 0.02). Twenty-nine limbs (43.3%) had follow-up LEVD at a mean of 23 days. In this subset, 13 patients at the initial scan (44.8%) had thrombus <5 cm of the SFJ (group 1) and 16 (55.2%) had thrombus >5 cm from the SFJ (group 2). Five limbs (17.2%) had GSVT propagation/new superficial vein thrombosis (SVT), and 6 (20.7%) developed new DVT. There was no GSVT propagation/new SVT in group 1, whereas 5 limbs (31.2%) had GSVT propagation/new SVT in group 2 (P = 0.048). DVT occurred in 2 limbs (15.3%) in group 1 and 4 limbs (25%) in group 2. CONCLUSIONS: Isolated GSVT tends to affect patients with hypercoagulable states, prior venous thromboembolism, malignancy, or recent surgery. Management is heterogeneous, and type of treatment does not seem to affect outcomes. Patients with GSVT have significant risk of persistent symptoms, recurrence, DVT, and PE. GSVT within 5 cm of the SFJ seemed to be associated with an increased rate of PE. GSVT more than 5 cm from the SFJ seemed to be associated with propagation/new SVT. Proximity to the SFJ did not impact occurrence of DVT.

The Role of Endovascular In Situ Revascularization in the Treatment of Arterial and Graft Infections.

Mycotic aneurysms and prosthetic graft infections are traditionally treated with excision of the infected tissue or graft, often requiring anatomical or extraanatomical bypass, carrying significant morbidity and mortality. Currently, the role of endovascular repair without excision in this setting has yet to be defined. We present 2 case scenarios, whereby mycotic pseudoaneurysms were successfully treated with endovascular stent-graft coverage and to present an in-depth review of endovascular in situ revascularization in the treatment of arterial and graft infections. There are data to support the use of stent grafting in mycotic aortic and iliac aneurysms, lower and upper extremity native arterial infections, lower extremity prosthetic bypass infections, and infections of carotid artery aneurysms. It is our belief that this technique may be utilized as primary therapy if there is no significant contamination and certainly serves an essential role in acute rupture or hemorrhage. In situations where there is significant tissue infection, stent grafting should be considered as a bridge if traditional excision is warranted.

Comparison of time utilization in an academic inpatient versus an outpatient vascular laboratory.

PURPOSE: Efficient, cost-effective services in vascular laboratories (VLs) will be required in tomorrow's health care environment. Inpatient VLs (IPVL) are burdened with complex patients, excessive workload, and a high percentage of bedside tests. Outpatient VLs (OPVL) are therefore presumed to be more productive and efficient. We compared time utilization in OPVLs and IPVL to test this hypothesis. METHODS: Vascular sonographers at an academic IPVL and OPVL were asked to track their daily activities during five consecutive weekdays. Test type, scan time, delays in patient arrival, preparation for the test, computer entry, and administrative time (patient- and non-patient-related) were logged. RESULTS: Delay in patient arrival and non-patient-related administration activities were both significantly greater in the OPVL (p < 0.01 and 0.03, respectively). Actual scan time occupied only 38.8% of the technologist's day, with the rest spent on patient- and non-patient-related activities. CONCLUSIONS: No appreciable differences were noted between IPVL and OPVL in most of the efficiency parameters measured. General administration time and delay in patient arrival were greater in the OPVL. Thus, OPVL were not more efficient than IPVL. In order to maximize efficiency in the OPVL, non-patient-related activities, which occupy over a quarter of the daily workday, must be shifted from technologists to support staff. © 2016 Wiley Periodicals, Inc. J Clin Ultrasound 44:540-544, 2016.

Targeted gene deletion of prolyl hydroxylase domain protein 3 triggers angiogenesis and preserves cardiac function by stabilizing hypoxia inducible factor 1 alpha following myocardial infarction.

The key oxygen sensing molecules, Prolyl-hydroxylase domain 1-3 enzymes (PHD1-3), regulate hypoxia-inducible factor (HIF) under hypoxia. In the settings of cardiomyopathy and ischemia-reperfusion injury, PHD3 expression is elevated, resulting in decreased HIF activation. The role of PHD3 in myocardial injury is poorly understood. Hence, we aimed to determine the effects of PHD3 deletion in mice on HIF-1α and other related pathways following myocardial infarction (MI). Left coronary artery (LAD) in both wild type and prolyl hydroxylase 3 knock out (PHD3⁻/⁻) mice was ligated to induce myocardial infarction. Electrophoretic mobility shift analysis showed significant increase in DNA-binding activity of HIF-1α in PHD3⁻/⁻ mice as compared to wild type (WT) mice post MI. The PHD3⁻/⁻MI group also showed decreased fibrosis. Seven days after MI, enhanced capillary/arteriolar density was observed compared to WTMI group. PHD3⁻/⁻ mice subjected to MI also showed improved cardiac functions (Ejection fraction and Fractional shortening), as assessed by echocardiogram, compared to WT. Western blot analysis showed increased VEGF, Ang-1 & Bcl-2 expression in PHD3⁻/⁻MI group. In conclusion, ablation of the PHD3 gene resulted in increased angiogenesis and cardiac function after infarction thereby offering a potential target for pharmacological management of ischemic myocardial disease.

Disruption of hypoxia-inducible transcription factor-prolyl hydroxylase domain-1 (PHD-1-/-) attenuates ex vivo myocardial ischemia/reperfusion injury through hypoxia-inducible factor-1α transcription factor and its target genes in mice.

Hypoxia-inducible transcription factor (HIF)-prolyl hydroxylases domain (PHD-1-3) are oxygen sensors that regulate the stability of the HIFs in an oxygen-dependent manner. Suppression of PHD enzymes leads to stabilization of HIFs and offers a potential treatment option for many ischemic disorders, such as peripheral artery occlusive disease, myocardial infarction, and stroke. Here, we show that homozygous disruption of PHD-1 (PHD-1(-/-)) could facilitate HIF-1α-mediated cardioprotection in ischemia/reperfused (I/R) myocardium. Wild-type (WT) and PHD-1(-/-) mice were randomized into WT time-matched control (TMC), PHD-1(-/-) TMC (PHD1TMC), WT I/R, and PHD-1(-/-) I/R (PHD1IR). Isolated hearts from each group were subjected to 30 min of global ischemia followed by 2 h of reperfusion. TMC hearts were perfused for 2 h 30 min without ischemia. Decreased infarct size (35%±0.6% vs. 49%±0.4%) and apoptotic cardiomyocytes (106±13 vs. 233±21 counts/100 high-power field) were observed in PHD1IR compared to wild-type ischemia/reperfusion (WTIR). Protein expression of HIF-1α was significantly increased in PHD1IR compared to WTIR. mRNA expression of ß-catenin (1.9-fold), endothelial nitric oxide synthase (1.9-fold), p65 (1.9-fold), and Bcl-2 (2.7-fold) were upregulated in the PHD1IR compared with WTIR, which was studied by real-time quantitative polymerase chain reaction. Further, gel-shift analysis showed increased DNA binding activity of HIF-1α and nuclear factor-kappaB in PHD1IR compared to WTIR. In addition, nuclear translocation of ß-catenin was increased in PHD1IR compared with WTIR. These findings indicated that silencing of PHD-1 attenuates myocardial I/R injury probably by enhancing HIF-1α/ß-catenin/endothelial nitric oxide synthase/nuclear factor-kappaB and Bcl-2 signaling pathway.