The management of a number of medical conditions is controversial. It is, therefore, often difficult for individual practitioners to judge objectively which one of several treatments is best for their patients. Because of this, guidelines have evolved as a way to facilitate optimal patient outcomes by summarizing current knowledge when it is complex, evolving, and difficult for interested parties to assess on their own. Unfortunately, the process of defining guidelines is flawed, and the potential for this is highlighted in a recently published systematic review of 34 current international guidelines dealing with the treatment of carotid disease in patients with moderate or severe asymptomatic (ACS) or symptomatic carotid stenosis (SCS).1Abbott A.L. Paraskevas K.I. Kakkos S.K. Golledge J. Eckstein H.H. Diaz-Sandoval L.J. et al.Systematic review of guidelines for the management of asymptomatic and symptomatic carotid stenosis.Stroke. 2015; 46: 3288-3301Crossref PubMed Scopus (173) Google Scholar In a comprehensive analysis of guideline treatment recommendations from 23 countries, published in six languages from 32 different writing groups, Abbott and colleagues1Abbott A.L. Paraskevas K.I. Kakkos S.K. Golledge J. Eckstein H.H. Diaz-Sandoval L.J. et al.Systematic review of guidelines for the management of asymptomatic and symptomatic carotid stenosis.Stroke. 2015; 46: 3288-3301Crossref PubMed Scopus (173) Google Scholar have documented guideline weaknesses leading to a variability in treatment recommendations. For instance, 100% of applicable guidelines endorsed carotid endarterectomy (CEA) for average-CEA-risk SCS, and 96% endorsed CEA for average-CEA-risk ACS. However, there was a more notable variation in carotid artery stenting (CAS) recommendations. CAS was endorsed (recommended that it should or may be provided) for average-CEA-risk ACS by 63% of applicable guidelines, while 30% explicitly opposed it. CAS was endorsed for average-CEA-risk SCS by approximately 50% of applicable guidelines, while approximately 25% explicitly opposed it. Endorsements of CAS for ACS and SCS were common, despite the lack of randomized trial data showing that CAS is at least as good as CEA or medical treatment alone for stroke prevention. Randomized trial and registry evidence of the dangers of CAS for average-CEA-risk patients2Abbott A.L. Adelman M.A. Alexandrov A.V. Barber P.A. Barnett H.J. Beard J. et al.Why calls for more routine carotid stenting are currently inappropriate: an international, multispecialty, expert review and position statement.Stroke. 2013; 44: 1186-1190Crossref PubMed Scopus (49) Google Scholar, 3Paraskevas K.I. Kalmykov E.L. Naylor A.R. Stroke/death rates following carotid artery stenting and carotid endarterectomy in contemporary administrative dataset registries: a systematic review.Eur J Vasc Endovasc Surg. 2016; 51: 3-12Abstract Full Text Full Text PDF PubMed Scopus (106) Google Scholar was under represented in many of these guidelines. CAS was also variably endorsed for patients considered at high-risk-for-CEA because of vascular anatomy, medical comorbidities, or undefined reasons. Such endorsements were found in 49% of applicable guidelines with respect to ACS and 84% of guidelines with respect to SCS. This is despite the absence of any randomized data showing that any procedure improves outcomes over medical treatment alone, and the limited life-expectancy of many such patients.1Abbott A.L. Paraskevas K.I. Kakkos S.K. Golledge J. Eckstein H.H. Diaz-Sandoval L.J. et al.Systematic review of guidelines for the management of asymptomatic and symptomatic carotid stenosis.Stroke. 2015; 46: 3288-3301Crossref PubMed Scopus (173) Google Scholar There was also a notable variation in the inclusion of medical treatment recommendations. Any recommendations regarding general medical treatment were included in only 68% of guidelines regarding ACS, and in 91% regarding SCS. Specific recommendations regarding peri-CEA or peri-CAS medical treatment were found in only 50% and 32% of applicable guidelines, respectively, for ACS. Only 48% of guidelines contained such recommendations regarding SCS. Furthermore, when medical treatment recommendations were included, they were usually incomplete and often separated from procedural recommendations and omitted from summaries. Perhaps of more importance were the weaknesses in current international guidelines brought to light by what they have in common. In all 34 guidelines identified in the review by Abbott et al., all procedural endorsements were based directly or indirectly on old comparisons of carotid endarterectomy and what is now obsolete medical treatment in patients who were randomized 12–34 years ago.4Veith F.J. How can good randomized controlled trials in leading journals be so misinterpreted?.J Vasc Surg. 2013; 57: 3S-7SAbstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar, 5Abbott A.L. Bias in the use of randomized trials for carotid stenosis management.Gefasschirurgie. 2015; 20: 252-257Crossref Scopus (7) Google Scholar In addition, when included in the guidelines, the 30-day risk of stroke or death said to confer an overall patient benefit from CEA (usually 3% for ACS and 6% for SCS) was derived from the same old, and now obsolete, randomized trials. The stroke prevention efficacy of medical treatment alone (encouraging a healthy lifestyle and appropriate use of medication) has improved by at least 80% since the randomized trials of CEA versus medical treatment began.6Abbott A.L. Medical (nonsurgical) intervention alone is now best for prevention of stroke associated with asymptomatic severe carotid stenosis: results of a systematic review and analysis.Stroke. 2009; 40: e573-e583Crossref PubMed Scopus (553) Google Scholar, 7Naylor A.R. Time to rethink management strategies in asymptomatic carotid artery disease.Nat Rev Cardiol. 2011; 9: 116-124Crossref PubMed Scopus (146) Google Scholar, 8Abbott A.L. Stroke rates associated with asymptomatic carotid stenosis and medical treatment alone continue to fall: results of an updated meta-analysis (late breaking science abstract presented at the AHA international stroke conference, 2013).Stroke. 2013; (American Heart Association website) ([accessed 11.08.15])http://my.americanheart.org/idc/groups/ahamah-public/@wcm/@sop/@scon/documents/downloadable/ucm_448656.pdfPubMed Google Scholar, 9Hadar N. Raman G. Moorthy D. O'Donnell T.F. Thaler D.E. Feldmann E. et al.Asymptomatic carotid artery stenosis treated with medical therapy alone: temporal trends and implications for risk assessment and the design of future studies.Cerebrovasc Dis. 2014; 38: 163-173Crossref PubMed Scopus (51) Google Scholar The observation of better outcomes now in patients with ACS without procedural intervention and its implications for patients with SCS (including the need for better patient selection and tighter peri-procedural stroke and death rate standards) have hardly impacted on guideline recommendations. Abbott et al. highlighted the over-reliance on, and limitations of, randomized trial data in current guidelines.1Abbott A.L. Paraskevas K.I. Kakkos S.K. Golledge J. Eckstein H.H. Diaz-Sandoval L.J. et al.Systematic review of guidelines for the management of asymptomatic and symptomatic carotid stenosis.Stroke. 2015; 46: 3288-3301Crossref PubMed Scopus (173) Google Scholar Although randomized trials can be useful if well designed and interpreted without bias, they are not the Holy Grail of evidence-based medicine. Randomized trials can become obsolete, may be misinterpreted, are not usually the best way to evaluate outcomes in routine practice, and are not appropriate for answering all medical questions.4Veith F.J. How can good randomized controlled trials in leading journals be so misinterpreted?.J Vasc Surg. 2013; 57: 3S-7SAbstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar, 5Abbott A.L. Bias in the use of randomized trials for carotid stenosis management.Gefasschirurgie. 2015; 20: 252-257Crossref Scopus (7) Google Scholar Current guidelines often underutilize and undervalue quality, independently validated, non-randomized observational data. Such data, for example, have shown improved patient outcomes with medical treatment alone6Abbott A.L. Medical (nonsurgical) intervention alone is now best for prevention of stroke associated with asymptomatic severe carotid stenosis: results of a systematic review and analysis.Stroke. 2009; 40: e573-e583Crossref PubMed Scopus (553) Google Scholar, 7Naylor A.R. Time to rethink management strategies in asymptomatic carotid artery disease.Nat Rev Cardiol. 2011; 9: 116-124Crossref PubMed Scopus (146) Google Scholar, 8Abbott A.L. Stroke rates associated with asymptomatic carotid stenosis and medical treatment alone continue to fall: results of an updated meta-analysis (late breaking science abstract presented at the AHA international stroke conference, 2013).Stroke. 2013; (American Heart Association website) ([accessed 11.08.15])http://my.americanheart.org/idc/groups/ahamah-public/@wcm/@sop/@scon/documents/downloadable/ucm_448656.pdfPubMed Google Scholar, 9Hadar N. Raman G. Moorthy D. O'Donnell T.F. Thaler D.E. Feldmann E. et al.Asymptomatic carotid artery stenosis treated with medical therapy alone: temporal trends and implications for risk assessment and the design of future studies.Cerebrovasc Dis. 2014; 38: 163-173Crossref PubMed Scopus (51) Google Scholar and with CEA,10Silver F.L. Mackey A. Clark W.M. Brooks W. Timaran C.H. Chiu D. et al.Safety of stenting and endarterectomy by symptomatic status in the carotid revascularization endarterectomy versus stenting trial (CREST).Stroke. 2011; 42: 675-680Crossref PubMed Scopus (263) Google Scholar, 11Munster A.B. Franchini A.J. Qureshi M.I. Thapar A. Davies A.H. Temporal trends in safety of carotid endarterectomy in asymptomatic patients: systematic review.Neurology. 2015; 85: 365-372Crossref PubMed Scopus (41) Google Scholar, 12Kumamaru H. Jalbert J.J. Nguyen L.L. Gerhard-Herman M.D. Williams L.A. Chen C.Y. et al.Surgeon case volume and 30-day mortality after carotid endarterectomy among contemporary medicare beneficiaries: before and after national coverage determination for carotid artery stenting.Stroke. 2015; 46: 1288-1294Crossref PubMed Scopus (33) Google Scholar and a persistence of significantly higher risks from CAS.2Abbott A.L. Adelman M.A. Alexandrov A.V. Barber P.A. Barnett H.J. Beard J. et al.Why calls for more routine carotid stenting are currently inappropriate: an international, multispecialty, expert review and position statement.Stroke. 2013; 44: 1186-1190Crossref PubMed Scopus (49) Google Scholar, 3Paraskevas K.I. Kalmykov E.L. Naylor A.R. Stroke/death rates following carotid artery stenting and carotid endarterectomy in contemporary administrative dataset registries: a systematic review.Eur J Vasc Endovasc Surg. 2016; 51: 3-12Abstract Full Text Full Text PDF PubMed Scopus (106) Google Scholar Abbott et al. also found fundamental organizational omissions and other problems across guidelines.1Abbott A.L. Paraskevas K.I. Kakkos S.K. Golledge J. Eckstein H.H. Diaz-Sandoval L.J. et al.Systematic review of guidelines for the management of asymptomatic and symptomatic carotid stenosis.Stroke. 2015; 46: 3288-3301Crossref PubMed Scopus (173) Google Scholar For instance, of applicable guidelines for ACS and SCS, only 7% and 12%, respectively, completely defined carotid stenosis according to stenosis degree, the method of determining the stenosis, and the timing and territory of any previous stroke or TIA. Such definitions should follow directly from the relevant randomized trials. The lack of target population definition in guidelines encourages procedural over-utilization by not limiting endorsements to patient subgroups who clearly achieved a statistically significant benefit in those trials. In addition, guidelines were often accessible only via professional affiliations rather than popular search engines, were not self-contained, and included inconsistencies and ambiguities. They also often confused procedural recommendations for ACS and SCS, failed to include a fully defined procedural standard that would imply an overall patient benefit, and failed to explain limitations of guideline recommendations. Furthermore, the terminology used to summarize treatment recommendations and the evidence used in making them were not standardized across guidelines, making interpretation and comparisons difficult. It is, therefore, apparent that current international carotid management guidelines have serious flaws that may lead to suboptimal management of patients in routine practice. Standardization of recommendations would follow from objective and accurate interpretation of the evidence base. The numerous flaws in contemporary guidelines can only be explained by the differing and less than objective viewpoints of the individual physicians and sponsoring groups writing them and/or errors that their authors make.4Veith F.J. How can good randomized controlled trials in leading journals be so misinterpreted?.J Vasc Surg. 2013; 57: 3S-7SAbstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar, 5Abbott A.L. Bias in the use of randomized trials for carotid stenosis management.Gefasschirurgie. 2015; 20: 252-257Crossref Scopus (7) Google Scholar, 13Paraskevas K.I. Veith F.J. Riles T.S. Moore W.S. Is carotid artery stenting a fair alternative to carotid endarterectomy for symptomatic carotid artery stenosis?.Eur J Vasc Endovasc Surg. 2011; 41: 717-719Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar Future guidelines should acknowledge that new evidence, including further trials, may be helpful in improving outcomes for patients with carotid stenosis, and that such trials must include better risk stratification models and modern medical and procedural interventions. However, such trials will take many years to complete and may not address the problems discussed in Abbott et al.'s review.1Abbott A.L. Paraskevas K.I. Kakkos S.K. Golledge J. Eckstein H.H. Diaz-Sandoval L.J. et al.Systematic review of guidelines for the management of asymptomatic and symptomatic carotid stenosis.Stroke. 2015; 46: 3288-3301Crossref PubMed Scopus (173) Google Scholar The question that remains is, can this situation be improved? The treatment of any condition will vary with different countries and areas of the world depending on local habits and resources. Therefore, a “one size fits all” guideline policy is probably not appropriate. However, future guidelines should acknowledge the flaws in the randomized trials that form their basis.4Veith F.J. How can good randomized controlled trials in leading journals be so misinterpreted?.J Vasc Surg. 2013; 57: 3S-7SAbstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar They should also include other evidence such as propensity-matched trials (preferably multi-center), audited registries, and multi-registry analyses.3Paraskevas K.I. Kalmykov E.L. Naylor A.R. Stroke/death rates following carotid artery stenting and carotid endarterectomy in contemporary administrative dataset registries: a systematic review.Eur J Vasc Endovasc Surg. 2016; 51: 3-12Abstract Full Text Full Text PDF PubMed Scopus (106) Google Scholar The criteria on which guidelines should be based could be agreed on internationally and could include guidance of the acceptability of studies. For example, they could include guidance on such issues as: i) are the primary outcome end-points and randomization appropriate to the question asked, ii) is the study sufficiently powered, iii) are the evaluations contemporary; and iv) has the procedure been compared with other available treatments? After such agreements have been reached, it would be important that unbiased national organizations, which are not society based, could be asked to oversee guideline development and writing, and suggest treatment options for that country. Such organizations already exist in some countries. Some might say that this approach would be cumbersome and not ideal, but then neither is the present system. The key lesson learned from Abbott et al.'s review is that future guidelines should be written in a way that eliminates factual error, inconsistency, bias, and doctor self-interest, all of which can decrease guideline value. Only in this way will the interest of patients be better served. After all, facilitating improved patient outcomes in routine practice should be the main purpose of guidelines.

The objective of this review was to identify causes of stroke/death after carotid endarterectomy (CEA) and to develop transferable strategies for preventing stroke/death after CEA, via an overview of a 21-year series of themed research and audit projects. Three preventive strategies were identified: (i) intra-operative transcranial Doppler (TCD) ultrasound and completion angioscopy which virtually abolished intra-operative stroke, primarily through the removal of residual luminal thrombus prior to restoration of flow; (ii) dual antiplatelet therapy with a single 75-mg dose of clopidogrel the night before surgery in addition to regular 75 mg aspirin which virtually abolished post-operative thromboembolic stroke and may also have contributed towards a decline in stroke/death following major cardiac events; and (iii) the provision of written guidance for managing post-CEA hypertension which was associated with virtual abolition of intracranial haemorrhage and stroke as a result of hyperperfusion syndrome. The pathophysiology of peri-operative stroke is multifactorial and no single monitoring or therapeutic strategy will reduce its prevalence. Two of the preventive strategies developed during this 21-year project (peri-operative dual antiplatelet therapy, published guidance for managing post-CEA hypertension) are easily transferable to practices elsewhere.

The technique of subintimal angioplasty has been attempted on 200 consecutive femoropopliteal artery occlusions of median (range) length 11 (2-37) cm. The principle of the technique is to traverse the occlusion in the subintimal plane and recanalise by inflating the angioplasty balloon within the subintimal space. The technical success rate was 159/200 (80%) and was not significantly different for occlusions <10 cm (81%, n = 73), 11-20 cm (83%, n = 63) or >20 cm (68%, n = 23), p = 0.20. There were no deaths nor limb loss resulting from the procedure. The median (range) ankle-brachial pressure index increased from 0.61 (0.21-1.0) preangioplasty to 0.90 (0.26-1.50) postangioplasty. The actuarial haemodynamic patencies of technically successful procedures at 12 and 36 months were 71% and 58% respectively, the symptomatic patencies were 73% and 61%. A multiple regression analysis showed that smoking multiplied the risk of reocclusion by 2.70 (p < 0.001), each additional run-off vessel reduced the risk by 0.54 (p < 0.001) and the risk increased by 1.73 (p = 0.020) for every 10 cm of occlusion length. In conclusion, the technical success rate (80%) of subintimal angioplasty for femoropopliteal occlusions is unrelated to occlusion length and for all procedures, including technical failures, cumulative symptomatic and haemodynamic patencies of 46 and 48% can be achieved at 3 years. The factors influencing long-term patency were smoking, the number of calf run-off vessels and occlusion length.

Background. Because subintimal angioplasty (SA) is a technique that can achieve recanalization of long arterial occlusions, it is considered an alternative to lower limb bypass operations. The aim of this prospective study was to identify the risk factors that affect potency of SA in patients suffering from critical limb ischemia (CLI).Methods and results. 51 consecutive infrainguinal SA were done in 46 patients suffered from CLI. The patients were followed-up with regular duplex scans up to 12 months post-intervention. Sex, atherosclerosis risk factors, and some technical details of the procedure (number of patent ran-off vessels after the procedure, length and re-entry point of angioplasty) were examined as potential risk factors of patency, using survival analysis statistical techniques.The overall patency rate at 12 months post-intervention was 50%. According to Cox-regression analysis, the factors that affect patency were the number of run-off vessels and the length of occlusion. Patients with two or three run-off vessels had a hazard of occlusion of 0.30 (P = .027) compared to those who had one rim-off vessel. The 12-months patency in patients with more than one non-off vessels was 81% vs. 25% in patients with one run-off vessel. Regarding the length of angioplasty, the hazard of reocclusion was 1.02 for every centimeter of occlusion (P = .049).Conclusions. The number of patent run-off crural vessels after the angioplasty and the length of occlusion are significant risk factors for reocclusion of infrainguinal SA in patients with CLI. Trying to recanalize more than one run-off vessels could raise the SA potency.

With the purpose of clarifying the nature and outlining certain constituents of such an undesirable condition designated as "endotension", that emerges after transluminal grafting of the aneurysmally changed aorta, a basic theoretical model was worked out for explanation of "endotension". Also, there was designed and constructed in vitro an original experimental model using which the authors carried out a study into the relationship between the pressure in the aneurysm after its complete exclusion from the blood flow by an endovascular graft and the volume of the aneurysmal contents. Some factors described in the literature as influencing the pressure level in the aneurysm were at the given stage purposefully excluded. The volume of the "aneurysm" reproduced in our model was equal to 675 ml; each of five vascular grafts implanted into the aneurysm measured 110 mm in length. The pulsating liquid flow was reproduced in the system using a serial appliance for extracorporeal circulation. The liquid was aspirated from the aneurysm by means of a syringe with concurrent pressure guidance in the sac. To start pressure lowering, it was necessary to evacuate 0.4-1.6 ml of the liquid. The real clinical situations were considered from the standpoint of our results.

In situ replacement of infected vascular grafts is an accepted alternative to total graft excision and extraanatomic replacement. Its success relies upon the ability of the newly inserted graft to resist recurrent infection. This study compares the efficacy of two methods used to reduce the risk of graft reinfection: rifampicin soaking versus silver bonding of grafts. The grafts’ resistance to infection was tested in vitro in two protocols, each using a panel of seven common bacteria, including methicillin-resistant Staphylococcus aureus (MRSA). The length of time the grafts remained free of organisms was compared between the groups. Both the silver graft and the rifampicin-soaked graft were significantly better than control graft at preventing bacterial growth on the graft surface. The rifampicin inhibited the growth of the gram-positive organisms, including MRSA, significantly better than the silver graft on days 2 and 3 ( p < 0.001). Conversely, the silver graft was significantly more effective against the gram-negative organisms until day 4 ( p < 0.0001). Both types of graft inhibit the in vitro growth of bacteria more effectively than controls, with rifampicin being most effective against gram-positive organisms and silver being best against the gram-negative organisms.

Stem cell transplants into damaged myocardium may have the potential to improve cardiac function. We investigated the safety of transplanting unmanipulated autologous bone marrow into infarcted myocardium of patients undergoing coronary bypass surgery and assessed its efficacy to improve cardiac function. Fourteen patients with one or more areas of transmural myocardial infarction were studied. Autologous bone marrow was obtained by sternal bone aspirate at the time of surgery, diluted in autologous serum at a ratio of 1:2, and then injected 1 cm apart into the mid-depth of the left ventricular scar. There were no deaths, no perioperative myocardial infarctions, and no significant ventricular arrhythmias. Dobutamine stress echocardiography demonstrated overall improvement in the global and regional left ventricular function 6 weeks and 10 months after surgery. Of 34 infarcted left ventricular segments, 11 were injected with bone marrow alone, 13 were revascularized with a bypass graft alone, and 10 received bone marrow transplantation and a bypass graft in combination. Only the left ventricle segmental wall motion score of the areas injected with bone marrow and receiving a bypass graft in combination improved at low dose and at peak dobutamine stress. These findings suggest that transplantation of unmanipulated autologous bone marrow into scar tissue of the human heart is safe and enhances cardiac function only when used in combination with myocardial revascularization. This benefit can be seen after 6 weeks of the bone marrow transplant and is maintained after 10 months of follow-up.

Background—Postoperative thromboembolic stroke affects 2% to 3% of patients undergoing carotid endarterectomy (CEA) and is preceded by 1 to 2 hours of increasing cerebral embolization. Previous work has demonstrated that high rates of postoperative embolization are associated with increased platelet reactivity to adenosine 5′-diphosphate (ADP). Our hypothesis was that preoperative administration of the platelet ADP antagonist clopidogrel could reduce postoperative embolization. Methods and Results—One hundred CEA patients on routine aspirin therapy (150 mg) were randomized to 75 mg clopidogrel (n=46) or placebo (n=54) the night before surgery. Platelet response to ADP was assessed by whole-blood flow cytometry. The number of emboli detected by transcranial Doppler within 3 hours of CEA was independently quantified. Time taken from flow restoration to skin closure was used as an indirect measure of the time to secure hemostasis. In comparison with placebo, clopidogrel produced a small (8.8%) but significant reduction in the platelet response to ADP (P <0.05) while conferring a 10-fold reduction in the relative risk of those patients having >20 emboli in the postoperative period (odds ratio, 10.23; 95% CI, 1.3 to 83.3; P =0.01, Fisher’s exact test). However, in the clopidogrel-treated patients, the time from flow restoration to skin closure (an indirect marker of hemostasis) was significantly increased (P =0.04, Fisher’s exact test), although there was no increase in bleeding complications or blood transfusions. Conclusions—This is the first study to show that a CEA patient’s postoperative thromboembolic potential can be significantly reduced by targeted preoperative antiplatelet therapy without increasing the risk of bleeding complications.

OBJECTIVES:Review of the primary results and secondary analyses from the European Carotid Surgery Trial (ECST) and the North American Symptomatic Carotid Endarterectomy Trial (NASCET).DESIGN:Review of 48 ECST and NASCET papers.RESULTS:The simple assumption that all patients with a symptomatic stenosis >70% benefit from CEA is untenable. Approximately 70-75% will not have a stroke if treated medically. The ECST and NASCET have identified subgroups that should have expedited investigation and surgery (male sex, age >75 years, 90-99% stenosis, irregular plaque, hemispheric symptoms, recurrent events for >6 months, contralateral occlusion, multiple co-morbidity). Accordingly development of local protocols for patient selection/exclusion should involve surgeons and physicians and take account of the local operative risk. The ECST and NASCET have also shown that the ubiquitous "string sign" is not associated with a high risk of stroke, and emergency CEA is unnecessary.CONCLUSIONS:Surgeons must quote their own results and be aware that a high operative risk reduces long-term benefit. Accordingly, in those centres with a higher operative death/stroke rate, some "lower risk" patients should probably be considered for best medical therapy alone. It is hoped that pooling of the ECST and NASCET databases will enable more definitive guidelines to be developed regarding who benefits most from CEA.

We presenta case of ruptured AAA treated successfully byendovascular repair, entirely under local anaesthesia(LA).ReportA 79-year-old gentleman presented to the Accidentand Emergency department with sudden onset of left-sided abdominal pain and collapse. Despite severehypotension, he remained conscious and so a com-puted tomography (CT) scan was performed. Thisshowed a ruptured infrarenal aortic aneurysm, whichappeared to be suitable for endovascular repair (Figs. 1and 2).The patient was immediately transferred to theoperating theatre. Bilateral small groin incisions weremade. An 18 French sheath was inserted into the leftcommon femoral artery (CFA) and a 30 mm balloonpassed through this sheath, to gain control of the neckof the aneurysm, should this be necessary. A similarsheath was inserted into the right CFA and thebifurcated Zenith device (Cook UK Ltd) was insertedand deployed. The whole procedure was performedunder LA (Bupivacaine 0.5%, total volume 25–30 ml)in just under 3 h.A completion angiogram revealed the left renalartery to have been occluded by the graft. Unsuccess-ful attempts were made to withdraw the device, priorto accepting this position. The patient’s creatininepeaked at 175mmol/l on the third postoperative day,but had returned to within normal range bydischarge.A total offour units of blood were given intraopera-tively and the patient did not require further transfu-sion. He was observed on the intensive treatment unitfor 48 h and was fit for discharge on the sixthpostoperative day.

Aim: Endovascular aneurysm repair, though extensively used to treat infra-renal aortic aneurysms, has had a limited role with thoraco-abdominal aneurysm (TAA) repair.We have sought to extend the role of stents in TAA repair by combining open and endovascular repair.Patients and methods: Between October 1997 and Dec 2002, 193 patients were treated for TAA.Seventeen patients underwent endovascular stenting; 10 required a combined open/endovascular approach.Median patient age was 64 years (range 25-83 years).Indications for intervention were: asymptomatic (4/17), symptomatic (9/17), leak (2/17) and false aneurysm (2/17).Eight aneurysms were atherosclerotic, 5 associated with chronic dissection, 3 false aneurysms (2 anastomotic, 1 traumatic) and 1 aorto-bronchial fistula.Three of these aneurysms were mycotic.Average maximum diameter was 6•9 cm (range 5•0-12•0 cm).Results: Thoracic stenting was combined with open infra-renal repair (4 patients) and type IV TAAA repair (1 patient).One patient had a carotid-left subclavian transposition to allow aortic arch stenting.In 3 patients visceral and renal arteries were revascularised prior to thoraco-abdominal stent deployment.The median length of stay was 20 days (range 8-53).Major morbidity was 41% (pneumonia: 2, transient paraparesis: 3, bleeding: 2).One patient died from pneumonia; a second patient with an extensive mycotic aneurysm died from gastrointestinal haemorrhage and small bowel infarction. Conclusion:A combined open and endovascular approach was required in 59% of thoraco-abdominal stent repairs.This approach widens the application of endovascular repair and our encouraging initial results appear to suggest that morbidity and mortality are reduced.

INTRODUCTION the rate of rupture of abdominal aortic aneurysms (AAAs) has been shown to have a seasonal variation with more ruptures occurring during the winter months. One of the main meterological changes between the seasons is a change in atmospheric pressure. The aim of this study was to investigate whether there was any relationship between atmospheric pressure and the incidence of AAA rupture. METHODS all cases of ruptured AAA admitted to a single hospital over a ten year period were identified from hospital records. Daily atmospheric pressure readings from the nearest weather recording station to the hospital were obtained for the same period. Cases were only included if rupture could be confirmed by reviewing the patients case-notes. RESULTS admission rates for ruptured AAA showed a monthly variation with the highest rate in December and the lowest in August. There was a statistically significant correlation between the number of cases admitted in any particular month and the mean atmospheric pressure for the previous month. Neither daily minimum, maximum or mean pressure, weekly mean pressure or daily pressure variability were significantly different between those days when a ruptured AAA was admitted and those when no ruptured AAA was admitted. CONCLUSIONS low atmospheric pressure is associated with increased rate of AAA rupture. The method by which this change in pressure precipitates rupture cannot be determined from this study.

Trichodesmium sp., isolated from the Great Barrier Reef lagoon, was cultured in artificial seawater media containing a range of Fe concentration. Fe additions stimulated growth, N 2 fixation, cellular chlorophyll a content, light-saturated chlorophyll a -specific gross photosynthetic capacity (P m chl a ) and the dark respiration rate (R d chl a ). Cell yields only doubled for 9 nM Fe relative to zero added Fe, whereas N 2 fixation increased 11-fold considerably for 450 nM Fe. The results suggest that N 2 fixation of Trichodesmium is more sensitive to Fe limitation than are the cell yields.

Carotid stump syndrome is a rare but recognized cause of cerebrovascular events.1Barnett H.J. Peerless S.J. Kaufmann J.C. “Stump” on internal carotid artery a source for further cerebral embolic ischemia.Stroke. 1978; 9: 448-456Crossref PubMed Scopus (170) Google Scholar The syndrome is associated with carotid territory symptoms despite demonstration of occlusion of the ipsilateral internal carotid artery (ICA) on duplex ultrasound scans or angiograms. It is hypothesized that a residual stump of patent ICA is the source of emboli, which pass through the ipsilateral external carotid artery (ECA) into the middle cerebral artery circulation by way of reversed flow in the ophthalmic artery. To date all published cases of stump syndrome have been treated with surgical exploration and exclusion of the stump. We present the first case, to our knowledge, in which the stump was excluded with endovascular means with a covered stent. A 61-year-old man underwent an uneventful left carotid endarterectomy at another vascular center in 1991. At presentation 11 years later he had a 4-week history of multiple (n = 17) left hemispheric transient ischemic attacks (TIA), with hemisensory and motor signs, usually in association with expressive dysphasia. Duplex scans showed that the ICA was occluded, but with a residual “stump” at the origin of the ICA. The contralateral ICA was 50% to 60% stenosed. In view of the fact that 3 weeks had elapsed since the most recent neurologic event, it was assumed that the ICA had recently become occluded. Risk factor management was optimized, clopidogrel therapy (75 mg/d) was started, and the patient was given an open appointment should any further problems occur. The patient had no neurologic symptoms for 4 weeks before a second cluster of 9 left carotid territory TIA, with hemisensory or motor signs and dysphasia, within 14 hours. The patient denied any ocular symptoms. Systemic heparinization was instituted. Duplex scans confirmed the earlier findings, but in view of the recurrent symptoms, intra-arterial digital subtraction angiograms (IADSA) were obtained. Arch IADSA showed no evidence of inflow arterial disease in the arch or proximal common carotid artery. Selective IADSA (Fig 1) confirmed occlusion of the ICA and presence of a proximal ICA stump. It also demonstrated retrograde filling of the distal ICA through retrograde filling of the ophthalmic artery via branches of the ECA, confirming that the ECA was a collateral source of blood supply to the left hemisphere. There was no evidence of intracranial vascular disease and no evidence of filling of the left middle cerebral artery via transhemispheric crossover flow from the right carotid artery. Continuous transcranial Doppler ultrasound scanning was carried out for 45 minutes, and no emboli were detected in either middle cerebral artery. Functional imaging of the brain was not performed. The differential diagnosis included embolization from the contralateral stenosed ICA via reversed flow in the left anterior cerebral artery,2Georgiadis D. Grosset D.G. Lees K.R. Transhemispheric passage of microemboli in patients with unilateral internal carotid artery occlusion.Stroke. 1993; 24: 1664-1666Crossref PubMed Scopus (42) Google Scholar embolization from the carotid stump to the ipsilateral intracranial circulation via the ECA branches and ophthalmic artery, hemodynamic TIA, and cardiac embolism. Embolization from the contralateral ICA stenosis was considered unlikely because not one cerebral event occurred ipsilateral to the right carotid stenosis. Hemodynamic TIA are usually associated with changes in posture, exercise, or light-headedness, none of which were noted in this patient. Similarly, cardiac embolism was considered unlikely because the patient had no signs, symptoms, or history of cardiac disease, and a chest x-ray film and transthoracic echocardiogram were normal. Most important, one would not have expected all 26 events to affect only one vascular territory in the brain. Accordingly, by process of exclusion, it was assumed that the most likely cause was embolization from the residual carotid stump. Treatment options thereafter included surgical or endovascular exclusion of the stump. In view of the patient’s anatomy and because he had already undergone carotid surgery, endovascular exclusion was the preferred option. The left common carotid artery was selectively catheterized with a 5F vertebral catheter (Terumo, Tokyo, Japan) via right common femoral artery puncture. Pre-reconstruction selective angiography confirmed a swirling contrast motion within the stump, which had an irregular superior surface (Fig 1). With roadmapping, an angled 0.035 hydrophilic guide wire (Terumo) was carefully manipulated into the ECA, averting any wire contact with the stump surface. An 8 × 50-mm wall graft endoprosthesis (Boston Scientific, Natick, Mass) was positioned across the stump and released. Measurements for sizing the prosthesis were taken from the diagnostic angiogram. A 6-mm × 4-cm angioplasty balloon (Smash; Boston Scientific) was dilated in the distal part of the wall graft to ensure adequate release. The wall graft (Fig 2) filled the tapered contours of the wider common carotid artery and narrower ECA, with no evidence of contrast material leakage into the excluded stump. The patient was discharged home on the second postoperative day, but returned on the seventh postoperative day after having a brief episode of expressive dysphasia only, with no hemimotor or sensory symptoms, which resolved within 30 minutes. Duplex ultrasound scans showed no abnormality within or adjacent to the wall graft and transcranial Doppler ultrasound scans again showed no evidence of ongoing embolization. In view of this, systemic anticoagulation was performed. Subsequent review at 1 and 3 months after stump exclusion found the patient to be entirely asymptomatic. Duplex ultrasound scans confirmed patency of the ECA, with no evidence of any contrast leakage around the prosthesis or into the stump. Stump syndrome is a rare cause of cerebral vascular events,1Barnett H.J. Peerless S.J. Kaufmann J.C. “Stump” on internal carotid artery a source for further cerebral embolic ischemia.Stroke. 1978; 9: 448-456Crossref PubMed Scopus (170) Google Scholar but should be considered in the occasional patient with recurrent symptoms in the presence of ipsilateral ICA occlusion. Although sporadic cases have demonstrated the benefit of surgical exclusion of the stump, few large studies have been reported,3Kumar S.M. Wang J.C.C. Barry M.C. Farrell L. Kelly C.J. Fitzgerald P.H. et al.Carotid stump syndrome outcome from surgical management.Eur J Vasc Endovasc Surg. 2001; 21: 214-219Abstract Full Text PDF PubMed Scopus (24) Google Scholar and many vascular surgeons have probably never seen or treated the condition. In Leicester, more than 1200 carotid endarterectomies have been performed over the last decade, but only two cases of stump syndrome have been treated surgically. The current case typifies many of the diagnostic and management problems confronting the surgeon. First, it was not possible to be absolutely sure, before intervention, whether the cause was stump syndrome, transhemispheric embolization via reversed flow in the left anterior cerebral artery, hemodynamic, or cardioembolic. Angiography did, however, exclude significant disease in the aortic arch and proximal common carotid artery. The right (contralateral) ICA was 50% to 60% stenosed, and although there was some evidence of crossover flow into the left anterior cerebral artery, IADSA did not demonstrate filling of the left middle cerebral artery after selective injection of contrast medium into the right carotid artery. Cardiac embolism remained a possibility, but one would not have expected all of the cerebral events to be localized to one vascular territory. Accordingly, it was concluded that stump syndrome was the most likely cause. Having determined the most likely diagnosis, what was the optimal mode of treatment? The patient had had a second cluster of symptoms despite 4 weeks of clopidogrel therapy. Although formal anticoagulation remained an option, in view of the repeated events within such a short period it was decided to undertake stump exclusion. Therapeutic options included surgical or endovascular exclusion. Factors mitigating against a surgical approach included the patient’s anatomy, ie, short, wide neck, and history of carotid endarterectomy. Both were believed to increase the risks for cranial nerve injury and operative stroke. The alternative was endovascular exclusion. To our knowledge, this is the first case in which a carotid stump has been excluded with endovascular placement of a covered stent. Postoperatively the patient had another TIA, which resolved rapidly. We have not been able to demonstrate an embolic source for this, and it may have arisen from transient platelet thrombus at the proximal or distal limits of the wall graft. In view of this, formal anticoagulation was carried out. No other symptoms have occurred during follow-up, and the stent has remained patent with no evidence of any contrast material leakage into the stump or stenosis on duplex scan surveillance. Although efforts were made preoperatively to exclude an alternative cause to stump syndrome, that the patient had a further TIA after stent placement raises the question as to whether the diagnosis was correct and whether his symptoms might have stopped with anticoagulation therapy alone. Clearly, neither question can now be answered retrospectively. No further events have occurred, but this might also have been the situation if systemic warfarin therapy had not been introduced after stent insertion. In conclusion, stump syndrome is a rare condition that has previously required treatment with surgical exploration and stump exclusion. Endovascular exclusion with a covered stent is, however, a new alternative to surgical intervention. In: “Endovascular treatment of carotid stump syndrome” (Naylor AR, Bell PR, Bolia A.: J Vasc Surg 2003;38:593-5)Journal of Vascular SurgeryVol. 38Issue 5PreviewCarotid stump syndrome is a rare cause of transient ischemic attacks/stroke and is usually treated by open surgery and exclusion of the stump from the circulation. An alternative method for treatment, deploying a covered stent to exclude the stump, was successfully utilized in a highly symptomatic patient who had previously undergone carotid endarterectomy. Endovascular exclusion of the symptomatic carotid stump is an alternative to operative surgery. Full-Text PDF Open Archive

Background: Cytokines are the primary mediators of inflammation and also influence matrix metalloproteinase expression, both of which are important in development of abdominal aortic aneurysm (AAA). A significant, but as yet unknown, familial factor contributes to the pathogenesis of AAA. Many cytokine genes contain polymorphic sites, some of which affect cytokine production in vitro. Cytokine gene polymorphisms may therefore influence the pathogenesis of AAA. The purpose of this study was to determine whether there is any association between cytokine gene polymorphisms and AAA. Methods and Results: This case-control study comprised 100 patients with AAA and 100 age-matched and sex-matched control subjects. For each case and control subject in the study, genotypes at the following cytokine gene polymorphic loci were determined: interleukin (IL)-1β +3953, IL-6 −174, IL-10 −1082, IL-10 −592, and tumor necrosis factors-α −308. Allele and genotype frequencies were compared between AAA and control groups, and odds ratios (OR) were calculated for the presence of AAA with each allele at each locus examined as risk factors. The IL-10 −1082 A allele was significantly more common in the AAA group than the control group (P =.03). The OR for the IL-10 −1082 A allele as a risk factor for AAA was 1.8 (95% confidence interval, 0.9-3.6). Discussion: These associations suggest a significant role for IL-10 in the pathogenesis of AAA. This association of AAA with the IL-10 −1082 A allele is also biologically plausible; the IL-10 −1082 A allele is associated with low IL-10 secretion, and it may be that AAA develops in patients who are unable to mount the same anti-inflammatory response as those who do not have AAA. (J Vasc Surg 2003;37:999-1005.)