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Leg swelling is a common cause for vascular surgical evaluation, and iliocaval obstruction due to May-Thurner syndrome (MTS) can be difficult to diagnose. Physical examination and planar radiographic imaging give anatomic information but may miss the fundamental pathophysiology of MTS. Similarly, duplex ultrasonographic examination of the legs gives little information about central impedance of venous return above the inguinal ligament. We have modified the technique of duplex ultrasonography to evaluate the flow characteristics of the leg after tourniquet-induced venous engorgement, with the objective of revealing iliocaval obstruction characteristic of MTS. Twelve patients with signs and symptoms of MTS were compared with healthy control subjects for duplex-derived maximal venous outflow velocity (MVOV) after tourniquet-induced venous engorgement of the leg. The data for healthy control subjects were obtained from a previous study of asymptomatic volunteers using the same MVOV maneuvers. The tourniquet-induced venous engorgement mimics that caused during vigorous exercise. A right-to-left ratio of MVOV was generated for patient comparisons. Patients with clinical evidence of MTS had a mean right-to-left MVOV ratio of 2.0, asymptomatic control subjects had a mean ratio of 1.3, and MTS patients who had undergone endovascular treatment had a poststent mean ratio of 1.2 (P = 0.011). Interestingly, computed tomography and magnetic resonance imaging results, when available, were interpreted as positive in only 53% of the patients with MTS according to both our MVOV criteria and confirmatory venography. After intervention, the right-to-left MVOV ratio in the MTS patients was found to be reduced similar to asymptomatic control subjects, indicating a relief of central venous obstruction by stenting the compressive MTS anatomy. Duplex-derived MVOV measurements are helpful for detection of iliocaval venous obstruction, such as MTS. Right-to-left MVOV ratios and postengorgement spectral analysis are helpful adjuncts to duplex imaging for leg swelling. The MVOV maneuvers are well tolerated by patients and yields physiological data regarding central venous obstruction that computed tomography and magnetic resonance imaging fail to detect.

Background A primary component in the development of intimal hyperplasia (IH) in response to vascular injury is basement membrane remodeling. Matrix metalloproteinases (MMPs) play a major role in this process by degradation of basement membrane proteins, mainly collagen type IV. Vascular injury initiates an inflammatory cascade with the release of tumor necrosis factor-alpha (TNF α ), interleukin-1beta (IL-1 β ), and C-reactive protein (CRP). We hypothesize serum levels of these elements may serve as biomarkers of the development of IH. Methods and Results At baseline, 2, 7, 10, and 14 days post-balloon angioplasty of the carotid artery, rat tissue samples were stained with Masson trichrome elastin to examine IH. Intima:media ratios (I:M) increased significantly over time postinjury. Serum samples were collected at the time of tissue sampling, and levels of MMP-2, MMP-9, collagen type IV, TNF α , IL-1 β , and CRP were assayed using sandwich enzyme-linked immunosorbent assay (ELISA). MMP-2 serum levels at 7, 10, and 14 days postinjury were significantly elevated compared with baseline. Other elements were not significantly elevated. Conclusion Early and persistent elevation in the serum levels of MMP-2 may be a useful biomarker of basement membrane remodeling and the presence of IH.

Los objetivos del presente estudio fueron desarrollar y evaluar el cuestionario REAL_VS (1) (Rapid Estimate of Adult Literacy in Vascular Surgery) para los investigadores que estudian la influencia del nivel cultural en lo que respecta al conocimiento y desarrollo de la cirugia vascular, y una version breve, el REAL_VSs (2), que permita a los medicos evaluar la familiaridad de los pacientes con los terminos relacionados con la cirugia vascular. Se uso un proceso de tres fases para identificar los terminos potenciales a incluir en el REAL_VS, incluida una revision del contenido del material educativo para pacientes existente en internet y la audicion de una muestra aleatoria de 50 grabaciones archivadas de encuentros cirujano vascular-paciente. El REAL_VS estuvo formado por 75 terminos (p. ej., stent, gangrena, cruento, aneurisma) de dificultad variable. Para participar en el presente estudio se incluyeron a 152 pacientes que hablaban ingles (≥ 18 anos de edad) que asistian a una clinica de cirugia vascular universitaria (media de edad = 61,4 ± 14,6 anos). Durante las entrevistas personales, se obtuvo la informacion sociodemografica de los pacientes, y se les administro la Rapid Estimate of Adult Literacy in Medicine (REALM), una encuesta de amplia utilizacion, al igual que el REAL_VS. Las puntuaciones medias obtenidas en la primera (56,9 ± 14,0) y en la segunda (63,3 ± 15,6) se correlacionaron de manera significativa (correlacion de rango de Spearman [ρ] = 0,91; p

Les buts de cette etude etaient de developper et valider (1) une Evaluation Rapide des Connaissances de la population generale Adulte en Chirurgie Vasculaire (ERCA_CV) pour les chercheurs etudiant l'impact des connaissances des patients sur les resultats en chirurgie vasculaire et (2) une version courte du ERCA_CV (ERCA_CVc) pour permettre a des cliniciens d'evaluer les connaissances de leurs patients en ce qui concerne les termes techniques specifiques a la chirurgie vasculaire. Un processus en trois phases a ete utilise pour identifier les mots potentiels incluables dans l' ERCA_CV, avec une etude du contenu des sites internets de vulgarisation a la disposition des patients ainsi que d'extraits d'enregistrements d'entretiens chirurgien-patient en consultation. L' ERCA_CV se composait ainsi de 75 mots-cles (par exemple stent, gangrene, invasif, anevrysme) de difficulte variable de prononciation. Cent cinquante-deux patients anglophones (âge ≥ 18 ans) ayant consulte dans un service de chirurgie vasculaire universitaire ont ete inclus dans cette etude (âge moyen = 61.4 ± 14.6 ans). Au cours d'entretiens personnalises, les informations sociodemographiques ont ete collectees, et on a demande aux patients de remplir le tres utilise questionnaire d'evaluation rapide des connaissances en medecine (ERCM) ainsi que l'ERCA_CV. La correlation entre les scores moyens de l'ERCM (56.9 ± 14.0) et de l'ERCA_CV (63.3 ± 15.6) etait tres forte (indice de correlation de Spearman [ρ] = 0.91 ; p p p

ObjectivePostmenopausal women receiving hormone replacement therapy (HRT) have been reported to have more adverse outcomes after vascular reconstructions, including increased intimal hyperplasia development and bypass graft failure. HRT may be affecting the pathway contributing to intimal hyperplasia. An important component of this pathway involves matrix metalloproteinases (MMPs), implicated in vascular remodeling due to their ability to degrade components of the extracellular matrix. We hypothesize that estrogen (Est) and progesterone (Prog) upregulate the MMP pathway in vascular smooth muscle cells (VSMCs) thereby increasing MMP activity and function.Methods and ResultsVSMCs were incubated with Est (5 ng/mL), Prog (50 ng/mL), Est + Prog combination (Est/Prog), and/or doxycycline (40 μg/mL; Doxy). Using reverse transcriptase polymerase chain reaction (RT-PCR) analysis we have previously shown membrane type 1-MMP (MT1-MMP) messenger ribonucleic acid (mRNA) levels are significantly increased by Est. Here, Western blot analyses indicated MT1-MMP and MMP-2 protein levels, not tissue inhibitor of MMP-2 (TIMP-2), were increased in response to Est and Est/Prog (P < .05 vs control). In-gel zymography revealed that Est and Est/Prog resulted in increased MMP-2 activity (hormone groups, P < .05 vs control) with no significant difference among the hormone groups. VSMC migration was increased by 45 ± 14% in response to Est (P < .05 vs control), as measured using a modified Boyden chamber assay. Doxycycline significantly inhibited basal and Est/Prog-stimulated increases in MMP-2 activity (P < .05 vs control; P < .05 vs hormone groups), and partially blocked basal and hormonally stimulated migration (P < .05 vs control and Est).ConclusionEstrogen and progesterone affects the MMP pathway by increasing MMP-2 enzymatic activity, possibly via the upregulation of MT1-MMP expression without a corresponding increase in TIMP expression. This increased collagenase activity increases VSMC motility and their ability to migrate through a collagen type IV lattice. Est/Prog upregulation of MT1-MMP may contribute to the adverse effect of HRT on vascular interventions.Clinical RelevancePostmenopausal women receiving HRT have more adverse outcomes after vascular reconstructions, including intimal hyperplasia, restenosis, and decreased graft patency. MMPs play a major role in vascular remodeling due to their degradation of components of the basement membrane separating vascular cell layers. Specifically, MMP-2 has a strong affinity for collagen type IV degradation, and MT1-MMP is a transmembrane protein known to activate MMP-2 by proteolytic cleavage. Here we provide strong evidence for MT1-MMP's role in increased MMP-2 activity and increased cellular migration in VSMCs exposed to estrogen and progesterone. Manipulations of the MMP pathway specifically targeting MT1-MMP expression at the time of vascular interventions may improve outcomes in females receiving HRT.

Surgery of the thoracic aorta continues to have a significant risk of neurologic complication. Several strategies to minimize this risk are emerging. Pharmacologic protection from these complications continues to be researched, but at this point few medications are being used clinically. This article reviews the pathophysiology of ischemic spinal cord injury and summarizes the investigational pharmacology that may prevent these serious complications.

Introduction Injury to the subclavian and axillary arteries is uncommon. Exposure of these vessels is associated with significant morbidity, and mortality ranges from 5% to 30%. Endovascular methods may offer an alternative approach to these technically challenging injuries. Methods We retrospectively studied patients with blunt or penetrating (including iatrogenic) injuries to the subclavian or axillary artery between January 1, 1996 and July 30, 2002. Demographic data, mechanism of injury, concomitant injuries, angiographic findings, and treatment method and outcome were recorded. Results Twenty-seven patients with injury to the subclavian or axillary artery were seen at our institution during the study. Twenty-three patients underwent interventions. Eleven patients required open repair; 12 patients had lesions amenable to endovascular repair. Depending on the preference of the surgeon, 5 patients with injuries amenable to endovascular repair underwent open repair, and 7 underwent endovascular repair. A Wallgraft endoprosthesis was used in all patients; two grafts were required in 1 patient. Endovascular repair was associated with shorter operative time ( P = .04) and less blood loss ( P = .01). One-year patency was similar between the two groups. Conclusion Covered stents are a feasible alternative to open repair in properly selected patients with subclavian or axillary artery injury, resulting in shorter procedure time and less blood loss.

Purpose To study in an experimental aneurysm model the differential distribution of strain/pressure (S/P) on the aneurysm wall before and after endograft exclusion and in the presence of individual type I and type II endoleaks. Methods Two tapered elliptical Gore-Tex patches were sutured to an anterior and posterior longitudinal arteriotomy of an 8-mm Gore-Tex tube graft, thus creating a fusiform aneurysm. Two S/P transducers were placed at the proximal sac adjacent to the proximal neck, 2 at the site of the widest sac diameter, and 2 at the sac adjacent to the distal neck. The aneurysm, which was connected to a pulsatile pump system, was excluded using a 10-mm endograft. Type I and type II endoleaks were created and tested individually. S/P measurements were obtained at systemic systolic pressures (BP) of 80, 110, and 150 mmHg. Thrombosis of the sac contents was induced by injection of thrombin and calcium in the sac. Angiography was used to verify presence or absence of flow in the sac. Results Aneurysm exclusion resulted in significant S/P reductions at all 3 BP levels versus prior to exclusion (p 0.05 for all 3 BP levels). In the presence of a proximal type I endoleak, S/P distribution was not uniform, and S/P at the proximal neck was close to S/P prior to exclusion (p>0.05 no graft versus type I endoleak for all 3 BP levels). This was also true in the presence of thrombus. With a type II endoleak, S/P was more evenly distributed and was not significantly elevated compared to the pressure without an endoleak (p>0.05, graft versus type II endoleak for all 3 BP levels). Thrombus had no effect on intrasac S/P with a type II endoleak. Intrasac S/P was significantly higher in the presence of a type I endoleak compared to a type II endoleak when BP=150 mmHg (p=0.008). Conclusions Endovascular exclusion of an aneurysm results in uniform S/P reduction in the aneurysm sac. Type I endoleak, but not type II endoleak, results in significantly higher S/P in an area of the sac adjacent to the proximal neck. Thrombus does not result in significantly different S/P distribution in the aneurysm sac.

Background . The adenosine A 2A agonist ATL-146e ameliorates reperfusion inflammation, reducing subsequent paralysis and neuronal apoptosis after spinal cord ischemia. We hypothesized that neuroprotection with ATL-146e involves inducible neuronal adenosine A 2A receptors (A 2A -R) that are upregulated after ischemia. Methods . Eighteen rabbits underwent laparotomy, and 14 sustained spinal cord ischemia from cross-clamping the infrarenal aorta for 45 minutes. One group (ischemia-reperfusion [I/R] + ATL) received ATL-146e intravenously for 3 hours during spinal cord reperfusion. A second group (I/R) received equivolume intravenous saline solution for 3 hours and served as an ischemic control, and a third group (Sham) underwent sham laparotomy. At 48 hours, all subjects were assessed for motor impairment using the Tarlov scoring system (0 to 5). Lumbar spinal cord sections were immunolabeled for A 2A -R and graded in a blinded fashion using light microscopy. Results . There was a significant improvement in Tarlov scores in I/R + ATL animals compared with the I/R group. Sham-operated animals demonstrated no A 2A -R immunoreactivity. There was a dramatic increase in A 2A -R immunoreactivity in neurons of lumbar spinal cord sections from I/R compared with I/R + ATL and sham-operated animals. Conclusions . Reduction in paralysis in animals receiving ATL-146e correlates with the new finding of A 2A -R expression on lumbar spinal cord motor neurons after ischemia. Adenosine A 2A agonists may exert neuroprotective effects by binding to inducible neuronal A 2A -R that are upregulated during spinal cord reperfusion, and reduced in response to administration of an A 2A -R-specific agonist.

Introduction Some investigators have suggested that high pulmonary artery flow rates increase the risk of severe reperfusion injury after lung transplantation. We hypothesized that controlling the initial flow rate and pulmonary artery pressure would decrease the severity of lung dysfunction in the setting of high-flow reperfusion. Methods Using our isolated, ventilated, blood-perfused rabbit lung model, all groups underwent lung harvest, 4-hour storage (4°C), and blood reperfusion. We measured pulmonary artery pressure, peak inspiratory pressure, arterial oxygenation, and wet-to-dry weight ratio. Group 1 (control, n = 8) underwent reperfusion at 60 ml/min for 30 minutes. Group 2 (high flow, n = 8) underwent reperfusion at 120 ml/min for 30 minutes. Group 3 (controlled flow, n = 8) underwent initial reperfusion at 60 ml/min for 5 minutes, followed by reperfusion at 120 ml/min for 25 minutes. Results Group 1 had significantly improved pulmonary artery pressure, peak inspiratory pressure, arterial oxygenation, and wet-to-dry weight ratio measurements compared with groups 2 and 3 after 30 minutes of reperfusion. However, Group 3 had improved pulmonary artery pressure, peak inspiratory pressure, arterial oxygenation, and wet-to-dry weight ratio measurements compared with Group 2. Conclusions High-flow reperfusion results in severe reperfusion injury after lung transplantation. Controlled reperfusion using a low initial flow rate decreases the severity of reperfusion injury associated with high-flow rates.

Reperfusion injury is the most common cause of early mortality following lung transplantation. Although cold graft ischemic time has been reported to influence this injury, some lung grafts with short ischemic times develop significant reperfusion injury, whereas other grafts with more prolonged ischemic times do not develop injury. Our hypothesis was that ischemic time did not significantly influence reperfusion injury or other outcomes following lung transplantation.Data on 136 patients who had lung transplantation over a 10 year period was used for analysis.Cold graft ischemic timeor = 6 hours did not increase the risk of reperfusion injury, acute rejection, cytomegalovirus infection, bacterial or fungal pneumonia, bronchiolitis obliterans syndrome, 1-month mortality, 1-year mortality, or 5-year mortality compared with ischemic times of either4 hours or 4 to 6 hours. The incidence of reperfusion injury was at least 20% for each time group.At least 20% of all patients will develop reperfusion injury regardless of cold graft ischemic time. Prolonged ischemic times up to 8 hours do not result in a significant increase in adverse short-term, intermediate, or long-term outcomes. Cautious extension of ischemic time beyond the current target of 4 to 6 hours may be warranted for geographic expansion of the donor lung pool.

Recent literature advocates carotid endarterectomy on duplex alone. The authors hypothesized that carotid angiography adds information that alters clinical management in a substantial number of patients compared to the use of carotid duplex examination alone. The records of 182 consecutive patients who underwent carotid artery duplex and subsequent carotid/cerebral angiography for suspected carotid artery stenosis between January 1998 and April 1999 were reviewed retrospectively. Carotid artery duplex examinations were stratified based on stenosis

Background . Tracheobronchial injuries are encountered with increasing frequency because of improvements in prehospital care and early initiation of the Advanced Trauma Life Support protocol. We review our experience with these injuries with the hypothesis that the leading determinant of patient outcome is the time interval to diagnosis. Methods . Patients with tracheobronchial injury were identified from the registry of our level 1 trauma center during a 10-year period ending December 1997. Clinical presentation, diagnostic evaluation, surgical management, and outcome were reviewed. Results . Twenty patients with ten cervical tracheal injuries and ten intrathoracic tracheobronchial injuries were treated. The mechanism of injury involved blunt trauma in 11 and penetrating trauma in 9. All patients underwent surgical debridement and primary repair. Patients with isolated airway injuries were discharged home after a mean hospital stay of 6 days and had no early complications. Three patients had delayed diagnosis (> 24 hours), and all sustained complications including death (1 patient) and multiorgan system failure (2 patients). The overall mortality rate was 15%. Conclusions . Operative management of tracheobronchial injuries can be achieved with acceptable mortality. Independent of mechanism or anatomic location of injury, delay in diagnosis is the single most important factor influencing outcome. Early recognition of tracheobronchial injury and expedient institution of appropriate surgical intervention are essential in these potentially lethal injuries.

Background It is generally accepted that a significant portion of our population harbors asymptomatic compression of the left iliac vein by the right iliac artery. This was demonstrated originally in autopsy studies by McMurrich in 1908 (33% of 107 cadavers) and more recently by the analysis of Contrast CT scans 1 (66% of 50 patients). Authors have found that Venography may lack the sensitivity to be considered a true “gold standard” (66% sensitive) while IVUS is over 90% sensitive 2. No studies have addressed the physiologic difference in flow hemodynamics between the left and right lower extremities in normal individuals. We use Doppler ultrasound to demonstrate asymmetric flow in the lower extremities of normal individuals. Methods Maximum venous outflow velocity (MVOV) in the Common femoral veins were recorded using Doppler ultrasound on 30 volunteers. Inclusion criteria included age 18–30, BMI Results The average age was 20.9 years (range 19–28 years) and the average BMI was 21.9 (range, 18–25). MVOV was slower on the left side in 22, slower on the right in 7 and equal in one volunteer. The mean right MVOV was 117.23 cm/sec, SD 46.95 and the mean left MVOV was 95.44 cm/sec, SD 32.94 ( P = 0.0095). There was no correlation between left and right MVOV with respect to age, BMI or height. Conclusions Significant differences in lower extremity venous flow are present in normal individuals at rest. This finding correlates with anatomic studies demonstrating a predilection towards narrowing of the left iliac vein in normal subjects. This simple, non-invasive method of quantifying venous hemodynamics may aid in selecting patients for further diagnostic testing or intervention.

Congestive heart failure and septic embolism complicate the clinical course of patients with infective endocarditis (IE). This study reviews the clinical records of patients with systemic disease secondary to IE and stratifies their disease severity according to individual risk factors and medical, and surgical interventions. The hospital records of all patients presenting to our institution from 1992 through 1997 with heart valve destruction secondary to IE were reviewed. Ten patients with hemodynamically significant valve lesions were included in this study: seven with aortic valve disease and two with mitral valve disease, and one with combined aortic and mitral valve lesions. All were diagnosed by echocardiogram. All ten patients experienced systemic septic arterial emboli: four intracranial lesions, four visceral lesions, and three extremity arterial occlusive events. Two patients required peripheral arterial repair. Cultures revealed infection secondary to Staphylococcus aureus in five, Streptococcus species in three, Coxiella species in one, and an unidentified organism in one patient. Seven patients underwent valve replacement. Three patients died from their disease processes. Statistical significance was established by Wilcoxon rank analysis with a two-tailed P < 0.05. Patients with IE secondary to staphylococcal infections suffered a more acute and virulent disease process (P = 0.04), with a 40 per cent mortality rate in the first 48 hours. There was no increased incidence of embolization associated with longer duration of symptoms (P = 0.32). Surgical repair conferred improved clinical outcome as compared with no surgical intervention (P = 0.03). Improved patient outcome was associated with nonstaphylococcal infection (P = 0.02), and a successful initial antibiotic regimen (P = 0.03). Peripheral arterial repair was successful in both cases.

Symptomatic peripheral septic embolism is a rare systemic complication of infective endocarditis. This case report describes abdominal pain secondary to a septic pseudoaneurysm in the distal superior mesenteric artery. Presentation, imaging, surgical intervention, and histologic evaluation are described, and a review of recent literature relating to this phenomenon is outlined.

Surgery for venous thoracic outlet syndrome (TOS) may be required for symptoms ranging from severe recalcitrant arm swelling to acute axillo-subclavian vein thrombosis. The etiology appears to be multi-factorial, involving not only mechanical compression of the subclavian vein between the anterior scalene muscle, first rib, clavicle, subclavius muscle and costoclavicular ligament, but also hematological factors such as acquired and hereditary thrombophilia. Although the visible incisions appear rather small, a sizeable operation is often required to effectively decompress the subclavian vein after clot dissolution. Such surgery and the associated need for postoperative anticoagulation carry a number of risks and considerations. Attention to the many details of successfully helping a patient recover through first rib resection and postoperative care is required for an ultimately successful outcome. This chapter is intended to describe the general approach used in our institution for venous TOS and includes historical considerations and data supporting some of the surgical and medical decision-making.

For the pediatric patient with end-stage lung disease in need of transplantation, two potential donor options currently exist: size-matched immature whole lungs or reduced-size mature lobes. To determine which of these options provides superior long-term function, we studied airway mechanics in a chronic porcine model of pediatric lung transplantation. Three groups of animals were studied: the first group underwent left upper lobectomy at 9 +/- 1 weeks of age (innervated left lower lobes). These animals served as controls. A second group of 9-week-old animals received an immature whole left lung allograft from age-matched donors. The third group received a reduced-size mature left lower lobe from 6-month-old donors. Measurements of dynamic airway resistance, pulmonary compliance, and functional residual capacity of the isolated lobes or lungs, and of the nonoperated right lungs, were recorded 12 +/- 1 weeks later, and mean values were calculated for each group. Results showed that transplantation of an immature whole lung resulted in abnormal dynamic airway resistance to airflow, which was not seen in the mature lobar transplants. In addition, compliance was impaired most significantly in the immature whole lung transplants. We conclude that in this experimental model of pediatric lung transplantation, transplantation of a mature lobar segment results in superior long-term airway function when compared with immature whole lung transplants.

The use of mature pulmonary lobes for pediatric lung transplantation has recently been described. Successful application of this technique could help alleviate the pediatric donor lung shortage. Whether an already mature lobe can grow by forming new alveolar units after transplantation into a developing recipient is not known. We therefore measured functional residual capacity, fixed lung volume and weight, alveolar size and air space volume percent, and total number of alveoli in mature left lower lobe porcine lung transplants 12 weeks after transplantation into growing piglets. Comparisons were made with nontransplanted mature left lower lobes to determine if functional or morphologic growth had occurred after transplantation. The transplanted and control lobes were all taken from 6-month-old animals (mean body weight 105 ± 4 kg). Recipients of the transplanted lobes were 9 weeks old and weighed 22 ± 2 kg. By the end of the 12-week holding period, the recipient animals increased their body weight approximately fourfold (85 ± 4 kg). No significant differences were seen in functional residual capacity or morphologic analysis of total alveolar number and alveolar size between the transplanted and nontransplanted lobes (p = not significant). Although the reduced-size mature porcine lobar transplants did not display a significant increase in either functional residual capacity or total alveolar number, there was significant growth of the transplanted mature lobes as determined by fixed volume and total lobar weight (p ≤ 0.05 versus control animals). (J T horac C ardiovasc S urg 1992; 104:1329-32)

Recent studies have indicated postmenopausal women receiving hormone replacement therapy (HRT) have more adverse outcomes of peripheral arterial disease after vascular reconstruction, including increased intimal hyperplasia (IH) and restenosis. The major cellular processes contributing to IH pathogenesis are extracellular matrix (ECM) degradation and vascular smooth muscle cell (VSMC) proliferation, migration, and invasion of the ECM. We have previously shown hormone exposure results in unbalanced matrix metalloproteinase (MMP) regulation in VSMCs, a family of ECM degradative enzymes known to play a role in vascular remodeling. Here we examine the role of hormonally-stimulated MMP activity in the regulation of the cellular processes contributing to IH development. Data from the type of analyses presented here could be used to develop a computational model of vascular restenosis focusing on the importance of hormone-modulated VSMC function.

Background The need for surgeons to exhibit adequate communication skills is paramount to providing exemplary patient care. The manner in which patients are greeted by their surgeon sets the stage for the remainder of the clinical encounter. This study examined patients' expectations for greetings upon meeting a surgeon for the first time. Materials and Methods A convenience sample of 152 English-speaking patients (≥21 y of age) attending a university-based vascular surgery clinic were recruited to participate in this study. Eligible patients were interviewed prior to their consultation using valid and reliable questionnaires to obtain data about sociodemographic characteristics and expectations for greetings upon meeting a surgeon for the first time. Results Patients' mean age was 61.4 ± 14.6 approximately half ( n = 81;54.3%) were male, and most were Caucasian ( n = 148; 97.4%). Most ( n = 132; 86.8%) patients wanted the surgeon to shake their hand, 113 (74.3%) wanted their first name to be used when a surgeon greets them, and 86 (56.6%) wanted a surgeon to introduce him/herself using his/her last name. Patients also desired for surgeons to be attentive/calm and make patient feel like a priority, adjust vocabulary and/or explain better, and be friendly, personable, polite, respectful, and/or courteous. Conclusions Surgeons should shake hands, use patients' first names, and introduce themselves using their last names when greeting patients for the first time. They should also be pleasant, personable, and make the patient feel like a priority. Additionally, surgeons should be cognizant of the way in which they present information to patients and verify understanding.

The purposes of this study were to develop and validate the (1) Rapid Estimate of Adult Literacy in Vascular Surgery (REAL_VS) for researchers studying the impact of literacy skills as related to vascular surgery-related knowledge and outcomes and (2) short version of the REAL_VS (REAL_VSs) to allow clinicians to gauge their patients' familiarity with vascular surgery-related terms. A three-phase process was used to identify potential words for inclusion in the REAL_VS, including reviewing Internet-based patient education material content and listening to a random sample of 50 archived audiorecordings of vascular surgeon-patient encounters. The REAL_VS was composed of 75 terms (e.g., stent, gangrene, invasive, aneurysm) of varying pronunciation difficulty. One hundred fifty-two English-speaking patients (>or=18 years of age) attending a university-based vascular surgery clinic were recruited to participate in this study (mean age = 61.4 +/- 14.6 years). During face-to-face interviews, patients' sociodemographic information was collected, and patients were administered the widely used Rapid Estimate of Adult Literacy in Medicine (REALM) and REAL_VS. Mean scores on the REALM (56.9 +/- 14.0) and REAL_VS (63.3 +/- 15.6) were highly correlated (Spearmans rank correlation [rho] = 0.91; p < 0.00). Internal consistency of the REAL_VS (Cronbachs alpha = 0.98) was excellent. Mean scores on the REAL_VSs (4.1 +/- 2.7) were highly correlated with both the REALM (rho = 0.82; p < 0.00) and REAL_VS (rho = 0.94; p < 0.00). Internal consistency, measured using Cronbachs alpha, of the REAL_VSs was 0.86. This study demonstrates that both the REAL_VS and REAL_VSs are both promising tools for use in vascular surgery research and clinical practice, respectively.

Background Postmenopausal women receiving hormone replacement therapy have more adverse outcomes after vascular reconstructions. Estrogen-binding receptors have been identified on vascular smooth muscle cells (VSMCs), indicating that vascular function may be under direct hormonal control. A key group of enzymes involved in vascular remodeling are matrix metalloproteinases (MMPs). Here we studied the effect of estrogen (Est) and progesterone (Prog) on MMP gene expression in human VSMCs. Methods and results VSMCs were incubated with Est (5 ng/mL), Prog (50 ng/mL), Est+Prog combination (Est/Prog), and interleukin-1β (100 U/mL; IL-1β). Gene array analysis indicated Est+IL-1β increased the expression of MMP-3. Reverse transcriptase-polymer chain reaction (RT-PCR) analyses revealed MMP-3 mRNA levels were significantly increased by Est/Prog+IL-1β treatment. However, Western blot and further RT-PCR analyses indicated no change in MMP-3 in response to hormones alone. RT-PCR analyses revealed membrane type 1 (MT1)-MMP mRNA levels, not MMP-2 or tissue inhibitor of MMP (TIMP), were significantly increased by Est/Prog+IL-1β, and Western blot analyses confirmed a significant increase in MT1-MMP protein in response to Est alone. Conclusion Estrogen and progesterone affect the MMP pathway of VSMCs via isoform specific mechanisms and may lead to unbalanced MMP regulation. Estrogen up-regulates MT1-MMP without a corresponding increase in TIMP-2, known activator and inhibitor of MMP-2, respectively. Additionally, estrogen up-regulates MMP-3 only in the presence of IL-1β. This differential regulation, combined with case-specific variations in degree of inflammatory response, may explain why some women receiving exogenous hormone therapy at the time of vascular interventions are more susceptible to complications.

Background Health literacy skills (HLS) have been shown to have a major impact on patient outcomes. To identify patients with limited or marginal HLS, the accuracy of three established screening items were examined. Materials and methods We studied English-speaking adults (≥21 years) attending a university-based vascular surgery clinic. Structured interviews were conducted to assess sociodemographic characteristics, screening items, and HLS. Area under the receiver operating characteristic (AUROC) curves were plotted to assess the discriminatory capacity of each screening item in detecting patients with limited/marginal HLS. Results One hundred patients agreed to enter the study and met inclusion criteria. The mean age was 62.0 ± 12.9; 65 were female; 96 were Caucasian; and 32 had not completed high school. The three screening items were effective in detecting patients with limited ( n = 18) or marginal ( n = 21) HLS. “How often do you have someone (like a family member, friend, or hospital worker) help you read hospital materials?” (AUROC of 0.83; 95% confidence interval [CI] = 0.73, 0.92), “How often do you have problems learning about your medical condition because of difficulty understanding written information?” (AUROC of 0.77; 95% CI = 0.67, 0.86), and “How confident are you filling out medical forms by yourself?” (AUROC of 0.76; 95% CI = 0.66, 0.86) were effective in detecting those with limited/marginal HLS skills. Conclusions Our findings provide further evidence of the clinical usefulness of these screening items for detecting inadequate HLS in this patient population. Surgeons should consider administering these easy screening items to identify patients at greatest risk of limited or marginal HLS.

ialysis access steal syndrome (DASS) occurs in 2% to 8% of atients after hemodialysis access surgery and affects thouands of people in the United States each year. Dialysis ccess steal syndrome occurs when blood that normally suplies a distal arterial bed reverses flow and is redirected hrough the AV fistula. Factors such as high fistula flow rates, ative vessel stenosis or occlusions, and poor collateral flow ct synergistically to cause DASS. Diabetics are particularly rone to developing a steal because of their diffuse calcific icrovascular disease. Fistulas that originate from the brachial rtery are the most at risk for DASS because they lack the ollateral flow found in radial-based fistulas. Autogenous vein rafts dilate slowly and typically result in DASS symptoms that evelop gradually over time while exogenous (PTFE) grafts evelop early ( 24 h) symptoms because of their immediate igh flow rate. Studies of tapered PTFE grafts designed to ncrease resistance, and hypothetically to reduce DASS, have hown little benefit. The symptoms of DASS range from mild, intermittent ain or numbness to tissue loss, motor dysfunction, and ontracture. Frequently, a patient’s symptoms are worse on emodialysis because dialysis lowers the mean arterial presure exacerbating the steal. It is difficult to determine which atients will benefit from early revascularization because ild symptoms often resolve over time and there are no eliable predictors of progression. Valintine et al prospecively performed preoperative finger pressures on 72 patients n an effort to classify patients at risk for DASS. They found n increased incidence of DASS in patients with lower preperative finger pressures but no absolute pressure below hich a steal was inevitable. Digital photoplethysmography, ressure indices, and nerve conduction studies are good ethods to quantitatively follow patients with DASS in the

Leukocyte and platelet adhesion to endothelial cells, an early step in the pathogenesis of atherosclerosis, is mediated through adhesion molecules. It has been shown that statins decrease adhesion molecule expression. We examined the hypothesis that fluvastatin decreased intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expression through a nitric oxide-mediated pathway. Human iliac artery endothelial cells were exposed to fluvastatin in the presence or absence of 2 mM N-monomethyl-L-arginine (L-NMMA). Flow cytometry analysis was used to measure ICAM-1 and PECAM-1 expression. In a separate experiment, confluent cell cultures were exposed in a serum-free medium to fluvastatin 20 microM, and the supernatant was collected for nitrate/nitrite determination after 6 and 48 hr of incubation. Protein was isolated and processed for immunoblotting with monoclonal antibodies specific for endothelial nitric oxide synthase (eNOS), Ser(1177)-phosphorylated eNOS, and AMP kinase. Relative band intensity was assessed with densitometry. Results are presented as the mean +/- standard deviation (SD), and p0.05 was considered significant. ICAM-1 and PECAM-1 were expressed constitutively. Human iliac artery endothelial cells (HIAECS) treated with 5 microM fluvastatin did not exhibit reduced expression of PECAM-1 or ICAM-1. Incubation with 10 microM fluvastatin reduced basal expression of both ICAM-1 and PECAM-1. Fluorescence intensity (FI) for these substance was as follows: 3638 +/- 1671, p = 0.01 and PECAM-1 vs. control FI 276 +/- 52 vs. 522 +/- 78, p = 0.02. In the presence of 2 mM L-NMMA, fluvastatin failed to decrease the expression of ICAM-1 (fluvastatin 10 microM + L-NMMA: FI was 3042 +/- 1378 vs. 3638 +/- 1671 for the control p = 0.01) or PECAM-1 (fluvastatin 10 microM + L-NMMA: FI was 415 +/- 188 vs. 522 +/- 78 for the control, p = 0.1). Incubation with 20 microM fluvastatin similarly reduced ICAM-1 expression (FI was 2014 +/- 1595 vs. 3638 +/- 1671 for the control, p = 0.02) and PECAM-1 expression (FI was 196 +/- 109 vs. 522 +/- 78 for the control, p = 0.02). This reduction was prevented in the presence of 2 mM L-NMMA. L-NMMA in a concentration of 2 mM had no significant effect on adhesion molecule expression (p0.05 for all comparisons of the control FI versus 2 mM L-NMMA mean FI). After a 48 hr incubation with 20 microM fluvastatin there was a 219 +/- 35% increase in the cell eNOS protein content (p = 0.01) and a 170 +/- 26% increase in the cell AMPK protein content (p = 0.02). Ser(1177)-phosphorylated eNOS protein levels were increased by 41 +/- 8% (p = 0.03). The nitric oxide concentration in the medium of the HIAEC treated with 20 microM fluvastatin for 48 hr was significantly higher than that in the control (p = 0.0004), pointing to increased production during the incubation period. Fluvastatin thus decreases basal expression of ICAM-1 and PECAM-1. Competitive inhibition of eNOS with L-NMMA abolishes the effect of fluvastatin on ICAM-1 and PECAM-1 expression. The statin up-regulates eNOS and AMP kinase, one of the enzymes that activates eNOS via phosphorylation at Ser(1177). We have shown that after a 48-hr exposure to fluvastatin there is an increased amount of the phosphorylated enzyme in the endothelial cells.

Objective: To analyze and compare open (OR) versus endovascular (EVAR) abdominal aortic aneurysm repair at our institution. Methods: EVAR was attempted in 256 patients at the University of Tennessee Medical Center, Knoxville, between December 1999 and November 2002. One hundred forty patients underwent attempted EVAR, and 116 underwent OR. All patients were included on an intent-to-treat basis, and results were reviewed retrospectively. Statistical methods included the Student t test and chi-square analysis. Results: Patients were age matched between the 2 groups (70.2 years versus 69.0 years; P = .936). Patients in the OR group had significantly higher American Society of Anesthesiologists classes than the EVAR group (2.96 versus 3.07; P = .006). However, there was no difference between the groups, OR versus EVAR, with respect to the presence of chronic obstructive pulmonary disease (55% versus 46%; P = .129), coronary artery disease (69% versus 66%; P = .638), diabetes mellitus (12% versus 18%; P = .167), mean left ventricular ejection fraction (51.8% versus 53.9%; P = .28), or mean preoperative creatinine level (1.2 mg/dL versus 1.1 mg/dL; P = .167). Tobacco use was more prevalent in the OR group (78.4% versus 64.2%; P = .013), and known carotid artery disease was more prevalent in the EVAR group (20.0% versus 6.9%; P = .003). The EVAR group had significantly shorter lengths of stay ( 4.2 versus 9.0 days; P = .000), intensive care unit days (0 versus 3.2; P = .000), time in the operating room (119.6 minutes versus 225.7 minutes; P = .000), and estimated blood loss (189.1 mL versus 897.9 mL; P = .000). Mean aneurysm size was larger in the OR group (5.6 cm versus 4.9 cm; P = .000). Perioperative complications occurred in 31 patients in the OR group and 5 in the EVAR group (P = .000). Two perioperative deaths occurred in the OR group and none in the EVAR group. As of this writing there has been no significant difference in all-cause mortality in the 2 groups (OR 9.6% versus EVAR 8.0%; P = .651). Seven patients in the EVAR group needed secondary interventions. Six were managed with endovascular techniques, and 1 underwent femoral-femoral bypass. Conclusions: Patients who undergo EVAR have significantly less morbidity and mortality in the perioperative period than do equally matched patients undergoing open repair. In midterm follow-up (2-5 years), mortality is no different. Morbidity conferred by the need for secondary intervention in the endovascular group is minimal.

Open abdominal aortic aneurysm repair has been reported to be associated with impairment of sexual function in men, most likely because of autonomic nerve injury and pelvic blood flow changes. Endovascular aneurysm repair does not involve dissection in the area of the iliac bifurcation and therefore may be associated with lower incidence of sexual dysfunction as compared to open repair. We conducted a retrospective study of males after open and endovascular abdominal aortic aneurysm repair to determine if there is a significant difference in the incidence of sexual dysfunction between the two procedures. A modified International Index of Erectile Function Questionnaire was used to access sexual function before and after aneurysm repair. The questionnaire was mailed to all male patients who underwent abdominal aortic aneurysm repair from January 1, 1999 to July 15, 2002. The questionnaire asked patients questions regarding their sexual function before and 3 months after the repair. Questionnaire scores for domains of sexual function (erectile function, orgasmic function, intercourse satisfaction, and overall satisfaction) as well as the total questionnaire score were analyzed. The chi-square and Wilcoxon's signed ranks test were used for statistical comparisons, with p0.05 considered significant. Logistic regression was used to examine association. Two hundred ninety-three questionnaires were mailed and 90 were returned completed. There was no difference for the total questionnaire score or the erectile function score before the procedure. Based on the questionnaire score, erectile function worsened after open AAA repair ( p = 0.002). Orgasmic function also deteriorated after open AAA repair ( p = 0.001). Endovascular repair was not accompanied by decreased erectile or orgasmic function ( p = 0.057 and p = 0.068, respectively). Impairment of erectile function was not associated with age, diabetes, or the number of patent hypogastric arteries after aneurysm repair, but there was a significant association between impaired erectile function and open aneurysm repair ( p = 0.036). Endovascular repair of abdominal aortic aneurysms is associated with significantly less impairment of erectile and orgasmic function than that with open repair. Preservation of sexual function after endovascular as compared to open repair should be among the factors considered when weighing treatment options for an abdominal aortic aneurysm in a sexually active male.

Purpose: To study in an experimental aneurysm model the differential distribution of strain/pressure (S/P) on the aneurysm wall before and after endograft exclusion and in the presence of individual type I and type II endoleaks. Methods: Two tapered elliptical Gore-Tex patches were sutured to an anterior and posterior longitudinal arteriotomy of an 8-mm Gore-Tex tube graft, thus creating a fusiform aneurysm. Two S/P transducers were placed at the proximal sac adjacent to the proximal neck, 2 at the site of the widest sac diameter, and 2 at the sac adjacent to the distal neck. The aneurysm, which was connected to a pulsatile pump system, was excluded using a 10-mm endograft. Type I and type II endoleaks were created and tested individually. S/P measurements were obtained at systemic systolic pressures (BP) of 80, 110, and 150 mmHg. Thrombosis of the sac contents was induced by injection of thrombin and calcium in the sac. Angiography was used to verify presence or absence of flow in the sac. Results: Aneurysm exclusion resulted in significant S/P reductions at all 3 BP levels versus prior to exclusion (p0.05 for all 3 BP levels). In the presence of a proximal type I endoleak, S/P distribution was not uniform, and S/P at the proximal neck was close to S/P prior to exclusion (p>0.05 no graft versus type I endoleak for all 3 BP levels). This was also true in the presence of thrombus. With a type II endoleak, S/P was more evenly distributed and was not significantly elevated compared to the pressure without an endoleak (p>0.05, graft versus type II endoleak for all 3 BP levels). Thrombus had no effect on intrasac S/P with a type II endoleak. Intrasac S/P was significantly higher in the presence of a type I endoleak compared to a type II endoleak when BP=150 mmHg (p=0.008). Conclusions: Endovascular exclusion of an aneurysm results in uniform S/P reduction in the aneurysm sac. Type I endoleak, but not type II endoleak, results in significantly higher S/P in an area of the sac adjacent to the proximal neck. Thrombus does not result in significantly different S/P distribution in the aneurysm sac.

Introduction: High pulmonary artery flow rates can result in severe reperfusion injury after lung transplantation. Our hypothesis was that selective activation of the adenosine A 2A receptor with a highly specific analog (ATL-146e) would inhibit leukocyte activation and decrease reperfusion injury after high-flow reperfusion. Methods: Using our isolated, ventilated, blood-perfused rabbit lung model, all groups (n = 8 per group) underwent lung harvest, 4 hours of cold storage, and blood reperfusion for 30 minutes. Measurements of pulmonary artery pressure (in millimeters of mercury), arterial oxygenation (in millimeters of mercury), myeloperoxidase, peak inspiratory pressure, and wet/dry weight ratio were obtained. Groups 1 (high flow) and 2 (high flow ATL-146e) underwent reperfusion at 120 mL/min for 30 minutes. Groups 3 (controlled high flow) and 4 (controlled high flow ATL-146e) underwent controlled reperfusion with an initial reperfusion of 60 mL/min for the first 5 minutes, followed by a rate of 120 mL/min for 25 minutes. During reperfusion, groups 2 and 4 received ATL-146e at 4 μg · kg −1 · min −1 . Results: ATL-146e significantly improved lung physiologic measurements under both high-flow (group 1 vs group 2) and controlled high-flow (group 3 vs group 4) conditions after 30 minutes. Conclusions: The adenosine A 2A receptor analogue ATL-146e significantly decreases the severity of reperfusion injury in the setting of both high-flow and controlled high-flow reperfusion. J Thorac Cardiovasc Surg 2002;124:973-8

The adenosine A2A agonist ATL-146e ameliorates reperfusion inflammation, reducing subsequent paralysis and neuronal apoptosis after spinal cord ischemia. We hypothesized that neuroprotection with ATL-146e involves inducible neuronal adenosine A2A receptors (A2A-R) that are upregulated after ischemia.Eighteen rabbits underwent laparotomy, and 14 sustained spinal cord ischemia from cross-clamping the infrarenal aorta for 45 minutes. One group (ischemia-reperfusion [I/R] + ATL) received ATL-146e intravenously for 3 hours during spinal cord reperfusion. A second group (I/R) received equivolume intravenous saline solution for 3 hours and served as an ischemic control, and a third group (Sham) underwent sham laparotomy. At 48 hours, all subjects were assessed for motor impairment using the Tarlov scoring system (0 to 5). Lumbar spinal cord sections were immunolabeled for A2A-R and graded in a blinded fashion using light microscopy.There was a significant improvement in Tarlov scores in I/R + ATL animals compared with the I/R group. Sham-operated animals demonstrated no A2A-R immunoreactivity. There was a dramatic increase in A2A-R immunoreactivity in neurons of lumbar spinal cord sections from I/R compared with I/R + ATL and sham-operated animals.Reduction in paralysis in animals receiving ATL-146e correlates with the new finding of A2A-R expression on lumbar spinal cord motor neurons after ischemia. Adenosine A2A agonists may exert neuroprotective effects by binding to inducible neuronal A2A-R that are upregulated during spinal cord reperfusion, and reduced in response to administration of an A2A-R-specific agonist.

Background: ATL-146e, an adenosine A 2A agonist, reduces paralysis after spinal cord ischemia-reperfusion. We hypothesized that systemic ATL-146e could improve neurologic outcome after blunt spinal cord trauma. Methods: Twenty rabbits survived a thoracic spinal cord impact of 30 g-cm. One group received 0.06 μg/kg/min ATL-146e for the first 3 hours after impact (A2A group), whereas a second group received saline carrier (T/C group). Neurologic outcome was measured using the Tarlov scale (0-5). Histologic sections from the A2A and TIC groups were compared for neuronal viability. Results: There was significant improvement in Tarlov scores of A2A animals compared with T/C animals at 12 hours (p = 0.007), with a trend toward improvement at 36 (p = 0.08) and 48 (p = 0.09) hours after injury. There was decreased neuronal attrition in A2A animals (p = 0.06). Conclusion: Systemic ATL-146e given after spinal cord trauma results in improved neurologic outcome. Adenosine A 2A agonists may hold promise as a rapidly acting alternative to steroids in the early treatment of the spinal cord injured patient.

Objective: Inflammation is likely a major contributor to spinal cord reperfusion injury after aortic reconstruction. Systemic 4-{3-[6-amino-9-(5-ethylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl}-cyclohexanecarboxylic acid methyl ester (ATL-146e), a selective adenosine A2A agonist, has been shown to reduce paralysis after spinal cord ischemia. We hypothesized that ATL-146e reduces cytokine production during spinal cord reperfusion, curtailing inflammation and decreasing spinal cord capillary platelet-endothelial cell adhesion molecule-1 (PECAM-1) expression. Study design: New Zealand White rabbits sustained spinal cord ischemia with 45-minute cross-clamping of the infrarenal aorta. One group of animals received intravenous ATL-146e at 0.06 μg/kg/min for 3 hours during reperfusion, beginning after 30 minutes of ischemia. A second group received saline solution vehicle alone for 3 hours, serving as an ischemic control. A third group served as sham-operated animals, undergoing laparotomy with anesthesia. Serum was assayed with enzyme-linked immunosorbent assay for tumor necrosing factor-α (TNF-α). Animals were allowed to recover for 48 hours and were evaluated for hind-limb motor function with the Tarlov (0 to 5) scoring system. At necropsy, animals from each group yielded spinal cords for immunohistochemical staining for PECAM-1. Data are expressed as mean ± standard error of the mean, with statistical analysis with Student t test and Kruskal-Wallis nonparametric test. Results: Markedly improved Tarlov scores were seen in rabbits with ATL-146e (P

Blunt injury to the aortic arch vessels is rare and can be life-threatening. Historically urgent repair of these injuries is emphasized. We describe the initial nonoperative management of a blunt injury to the brachiocephalic trunk in the setting of bovine arch anomaly, followed by delayed surgical management.

The adenosine A2A agonist ATL-146e (4-[3-[6-Amino-9-(5-ethylcarbamoyl-3,4-dihydroxytetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl]-cyclohexanecarboxylic acid methyl ester) has been shown to prevent reperfusion injury in multiple organ systems through inhibition of activated leukocyte-endothelial interaction. We hypothesized that systemic ATL-146e could reduce spinal cord reperfusion injury after aortic clamping.Twenty-six rabbits underwent cross-clamping of the infrarenal aorta for 45 minutes. One group received intravenous ATL-146e for 3 hours during reperfusion. A second cohort received only vehicle and served as controls. Animals were assessed at 24 and 48 hours using the Tarlov (0 to 5) scoring system for hind limb function. To evaluate neuronal attrition, immunostaining of lumbar spinal cord sections was performed using anti-SMI 33 antibody against neurofilament.Systemic ATL-146e was tolerated without hemodynamic lability. Animals that received ATL-146e had significantly improved neurologic outcomes 24 and 48 hours after spinal cord ischemia (p0.001). There was preservation of neuronal architecture in the ventral horn of spinal cord sections from animals receiving ATL-146e compared with control animals.Intravenous ATL-146e given during reperfusion is tolerated without hemodynamic lability, and results in substantially improved spinal cord function after ischemia by preservation of ventral horn neurons.

The proximal suture line is a vulnerable area after abdominal aortic aneurysm repairs. This area has been implicated in various postoperative complications, such as pseudoaneurysm formation, graft-enteric fistula, and suture line disruption. We present a technique that provides safe and adequate coverage of this suture line by using the aneurysm sac. This technique is derived from the z-plasty technique used for scar revision. The technique is illustrated with detailed line drawings. None of the patients in whom we used this technique have had any complications related to the proximal suture line. (J Vasc Surg 2001;34:367-8.)

We hypothesized that inflammation during spinal cord reperfusion worsens ischemic injury. ATL-146e, an adenosine A(2A) agonist with known anti-inflammatory properties, was used to test this hypothesis at varied intervals to determine the time course of reperfusion injury.Forty rabbits underwent cross-clamping of the infrarenal aorta for 45 minutes. One group (n = 14 animals) received 0.06 microg/kg/min systemic ATL-146e over 3 hours, beginning after 30 minutes of ischemic time. A second group (n = 6 animals) received ATL-146e over 1.5 hours. A third group (n = 3 animals) received ATL-146e over 1 hour, and a fourth group (n = 17 animals) received saline solution. All animals were assessed at 48 hours for hind limb motor function (Tarlov scale, 0-5).Animals that received ATL-146e for 3 hours (Tarlov score, 4.3 +/- 0.22; P.001) or 1.5 hours (Tarlov score, 2.7 +/- 0.6; P.05) had improved neurologic outcomes compared with rabbits that received saline solution (Tarlov score, 0.6 +/- 0.29). Animals that received ATL-146e for 1 hour (Tarlov score, 0.7 +/- 0.8) were not significantly different from those animals that received saline solution.Systemic ATL-146e, given during reperfusion, results in time-dependent improvement in spinal cord function after ischemia. This implies that the mechanism of spinal reperfusion injury includes leukocyte-mediated inflammation at a critical post-ischemic time interval.

A 28-year-old woman with end-stage renal disease secondary to diabetes mellitus and hypertension underwent cadaver renal transplant in April 1992. After surgery, she developed bilateral breast enlargement while she was taking cyclosporine for immunosuppression therapy and felodipine, a calcium channel blocker, for blood pressure control. She underwent bilateral reduction mammoplasty in June 1995 to treat progressive breast enlargement which interfered with her normal life activities. Through mechanisms only partially understood, calcium channel blockers and cyclosporine are reported to increase the serum prolactin level, producing gynecomastia in men. There is no report in current literature to support a similar phenomenon in women.

Background: We hypothesized that systemic ATL-146e, an adenosine A2A agonist, would decrease spinal cord reperfusion inflammatory stress and inhibit apoptosis and that these effects would correlate with improved neurologic functional outcome. Methods: Thirty rabbits underwent cross-clamping of the infrarenal aorta for 45 minutes. One group of animals (n = 14) received 0.06 μg/kg per minute of ATL-146e infused intravenously for 3 hours, beginning 15 minutes before reperfusion. A second group of animals (n = 16) underwent spinal cord ischemia with saline vehicle alone and served as ischemic controls. Animals (n = 9, 11) from each group survived for 48 hours and assessed for neurologic impairment with the Tarlov (0-5) scoring system. Four animals from each group were humanely killed at the end of the 3-hour treatment period, and the remainder killed after 48 hours' survival. In all animals, lumbar spinal cord tissue specimens were frozen for subsequent Western blot analysis of heat shock protein 70 (HSP 70), and for the p85 fragment of poly (ADP-ribose) polymerase (PARP). Neuronal viability indices were determined at 48 hours with hematoxylin and eosin staining. Results: There was improvement in neurologic function in rabbits receiving ATL-146e (P

Purpose: We investigated the mechanical characteristics of lyophilized human saphenous vein valves to determine their suitability for use as allogeneic transplants to treat chronic venous insufficiency. Methods: Fresh cadaveric veins were lyophilized in vacuum bottles within 24 hours of harvest and were stored at room temperature. The veins were reconstituted in saline solution and then were placed in an in vitro flow circuit for evaluation. At varied flow rates, pressures proximal and distal to valves during prograde and retrograde flow were measured. Valve closure times were determined with Doppler examination and spectral analysis. The valves were also stressed to 350 mm Hg on a separate apparatus. Results: All pressures proximal and distal to the valves remained less than 10 mm Hg during prograde flow. A pressure gradient developed immediately on the reversal of flow. Pressure as high as 200 mm Hg applied against the closed valves was not transmitted beyond the valve. Valve closure times had a mean of 0.31 ± 0.03 seconds and 0.21 ± 0.01 seconds for the Doppler examination and spectral analysis, respectively. All valves withstood stress pressures to 350 mm Hg. Conclusions: The in vitro mechanical characteristics of the valves of lyophilized veins are similar to known values for normal in vivo valves. (J Vasc Surg 1997;26:823-8.)

Percutaneous mechanical thrombectomy can be an effective procedure performed with low morbidity. We have observed clinically significant pancreatitis after successful clot extraction by percutaneous thrombectomy. Pancreatitis developed postoperatively in four patients who underwent thrombectomy at our hospital. Each patient experienced abdominal symptoms with serologic and radiographic evidence of pancreatitisor=24 hours after thrombectomy. The presence of renal failure and extensive clot degradation seemed to be related. Two of the patients underwent surgery that potentially could have been avoided had the etiology of pancreatitis been known preoperatively.