Hintergrund und Fragestellung: Patienten und Methodik: Ergebnisse: Folgerung: Background and Objective: Patients and Methods: Results: Conclusions:

upper back discomfort was admitted to the hospital. Physical examination was unremarkable and a chest radiograph was normal. A computed tomographic (CT) scan confirmed acute aortic dissection type B without ischemic complications (Panel A, white arrows show dissection membrane). The patient was treated with aggressive blood-pressure control in the intensive care unit. Measurement of serum lactate, GOT Vascular Medicine 2006; 11: 133–134

BACKGROUND:Carotid endarterectomy is effective in stroke prevention for patients with severe symptomatic carotid-artery stenosis, and carotid-artery stenting has been widely used as alternative treatment. Since equivalence or superiority has not been convincingly shown for either treatment, we aimed to compare the two. METHODS:1200 patients with symptomatic carotid-artery stenosis were randomly assigned within 180 days of transient ischaemic attack or moderate stroke (modified Rankin scale score of < or =3) carotid-artery stenting (n=605) or carotid endarterectomy (n=595). The primary endpoint of this hospital-based study was ipsilateral ischaemic stroke or death from time of randomisation to 30 days after the procedure. The non-inferiority margin was defined as less than 2.5% on the basis of an expected event rate of 5%. Analyses were on an intention-to-treat basis. This trial is registered at Current Controlled Trials with the international standard randomised controlled trial number ISRCTN57874028. FINDINGS:1183 patients were included in the analysis. The rate of death or ipsilateral ischaemic stroke from randomisation to 30 days after the procedure was 6.84% with carotid-artery stenting and 6.34% with carotid endarterectomy (absolute difference 0.51%, 90% CI -1.89% to 2.91%). The one-sided p value for non-inferiority is 0.09. INTERPRETATION:SPACE failed to prove non-inferiority of carotid-artery stenting compared with carotid endarterectomy for the periprocedural complication rate. The results of this trial do not justify the widespread use in the short-term of carotid-artery stenting for treatment of carotid-artery stenoses. Results at 6-24 months are awaited.

(MD-CT) revealed a 5.0 4.0 2.7 cm tumor of soft tissue density, heterogeneous contrast medium enhancement derivation from the infrarenal vena cava and infiltrating the surrounding tissue. Panel A shows contrast-enhanced CT in the axial (a) and coronal (b) reconstructed view demonstrating an abdominal mass (arrow). A primary leiomyosarcoma of the vena cava inferior was assumed. Staging using CT thorax and bone scintigraphy presented no evidence of metastatic spread. Phlebography of the vena cava inferior confirmed an obstruction of lumen (Panel B, arrow) with prominent lumbar veins for collateral venous blood flow via azygos and hemiazygos veins. For surgical planning, multiphasic magnetic resonance angiography (CE-MRA) (Panel C, arrow) was performed to evaluate the degree of vascular involvement (local tumor infiltration and renal vessel involvement), but tumor involvement of renal venous vasculature was still uncertain. Therefore, computer-assisted surgical planning using the three-dimensional (3D) surface rendering technique was performed based on multiphasic CE-MRA raw data (Panel D). The virtual imaging techniques allowed an intra-luminal view and revealed left and right renal veins without direct tumor involvement (Panel D). Results of computer-assisted planning are as follows: vena cava (blue) and tumor (hatched) (Panel D, left) have been Vascular Medicine 2005; 10: 55–57

Epidemiology Foot lesions are the single most commonly mismanaged problem of patients with diabetes mellitus and associated renal disease. They are often incorrectly considered to be a minor clinical problem, yet not infrequently they impact upon patient survival. What Is the Epidemiology of Foot Lesions in Diabetes? The cumulative lifetime frequency of amputations in type 1 and type 2 diabetic patients overall is approximately 15% both in Europe and in the United States (1,2). In Germany, two of three patients undergoing amputation suffer from diabetes, and the direct annual cost from this procedure amounts to 3 billion DM (approximately $1.5 billion U.S. dollars) (3). Amputation is a much-feared tragedy in the life of a diabetic patient, and the tragedy is compounded by the fact that a great number of amputations are either unnecessary or unnecessarily aggressive. Above-ankle amputation carries a perioperative mortality of 20%, and more than one-third of the patients remain unable to care for themselves. The best evidence that appropriate management prevents an excess of amputations comes from Sweden (4) and the United Kingdom (5), where so-called "Foot Clinics" with appropriate interdisciplinary care for patients with diabetic foot lesions reduced amputations, particularly above-ankle amputations, by 50 to 80%. What Is the Epidemiology of Foot Lesions in Diabetic Patients with Renal Disease? In the United States, the rate of lower limb amputation in patients whose renal failure was attributed to diabetic nephropathy has recently risen to 14% (2). The risk is excessive in the diabetic patient with uremia: the rate is 10 times higher than in the diabetic population at large. When diabetic patients enter renal replacement programs, approximately 10% already have a history of above- or below-ankle amputation (6), and the proportion of patients requiring amputation on dialysis is approximately 4% per year. In an ongoing German study in patients with type 2 diabetes on dialysis (4D study), 16% of incident patients have a history of amputation for gangrene and 44% have a diagnosis of peripheral arterial disease (7). What Causes the Diabetic Foot Lesion? Diabetic foot lesions occur either as a consequence of ischemia from macroangiopathy (ischemic foot) or as a result of one aspect of microangiopathy, i.e., neuropathy with loss of sensory, autonomous, and motor innervation (neuropathic foot). The distinction between these two varieties is important, because the interventional strategies are completely different. In practice, however, the two causes often coexist (8,9,10). In the study of Reike (12), 34% of diabetic foot lesions were due to neuropathic, 21% to ischemic, and 40% to combined neuropathic plus ischemic lesions. The mechanisms through which macroangiopathy and neuropathy predispose to foot lesions and the exogenous factors that trigger the lesions are schematically summarized in Figure 1. The major clinical features that allow one to distinguish the neuropathic and the ischemic lesions are listed in Table 1. We also refer to some recent reviews (8,9,10,11,13).Figure 1.: Mechanisms leading to the diabetic foot lesion.Table 1: Diabetic patients with foot lesionIn patients with advanced diabetic nephropathy, diabetic foot lesions are particularly frequent and, conversely, diabetic nephropathy is found in no less than 50% and overt coronary heart disease in 49% of the patients with diabetic foot lesions. The association of diabetic foot lesions with advanced diabetic nephropathy may be explained by: (1) the long duration of diabetes, which predisposes to both nephropathy and foot lesions; (2) the particularly high risk of nephropathic patients to develop macroangiopathic or neuropathic complications; or (3) a combination of both. Whatever the explanation, diabetic foot lesions are particularly frequent in patients seen by the nephrologist. The high comorbidity in patients with diabetic foot lesions also explains the considerably worse prognosis in amputated compared with nonamputated patients on dialysis or after renal transplantation. The potential for full rehabilitation after amputation is poor in diabetic patients compared with nondiabetic amputees, and patients may lose self-management to a degree that necessitates institutional care (2). The Neuropathic Foot Lesion Diabetic peripheral neuropathy in patients with renal failure is aggravated by superimposed uremic peripheral neuropathy, thus explaining the particularly frequent and severe lesions in the uremic diabetic patient. Perception of pain is impaired ("the neuropathic foot is silent and the patient is silent"). Loss of protective sensation predisposes to episodes of cumulative unnoticed trauma. Patients may also wear damaging footwear because pain from injury is not perceived. Additional mechanisms are operative in the damage to the neuropathic foot. In particular, the equilibrium of muscular forces is disrupted by the atrophy of the anterior muscles of the lower leg and atrophy of the lumbrical and interosseous muscles, thus destabilizing the metatarsophalangeal joint (14). The forefoot is further exposed to unphysiologically high pressures because of the adductor varus position of the toes. All of this leads to foot deformity. Mechanical trauma is further aggravated by factors that reduce the viscoelasticity of the foot, e.g., stiffening of connective tissue and diminished joint mobility (as a result of nonenzymatic glycation), loss of fat tissue, and edema formation. Neuropathic lesions are also associated with impaired energy metabolism, fatty infiltration, and increased intracellular pH of plantar muscles (15). As a result, excessive shear forces and pressure are generated when the deformed foot of a patient with loss of sensation and with lower limb muscle dysfunction resulting from disturbed innervation hits the ground in an uncoordinated manner (16). The importance of an additional factor, i.e., faulty loading caused by reduced joint mobility and foot deformity, is illustrated by the observation of Fernando et al. (17) that metatarsal ulcers were found in 60% of diabetic patients who had neuropathy plus foot deformity, but in only 5% of patients who had neuropathy alone. Neuropathy further causes abnormalities of the skin and subcutaneous tissue, which predispose to bacterial invasion and necrosis with ulcer formation. Autonomic neuropathy gives rise to vasodilation and anhidrosis, causing dry skin with cracks and fissure formation, as well as capillary hypertension with edema formation. It is an error to ascribe all leg edema of a diabetic patient to renal failure. Hyperkeratosis and ulcers occur at sites exposed to maximal pressure loads, i.e., the metatarsal head (Figure 2), the tips of the toes, or the lateral aspect of the foot, if the latter is exposed to pressure from tightly fitting shoes. The hypoxic tissue with reduced vitality underneath a hyperkeratotic callus easily develops necrosis, ultimately resulting in ulcer formation (Mal perforant).Figure 2.: Neuropathic ulcer. (A) Deep callous ulcer of the lateral plantar forefoot resulting from faulty loading and massive increase of plantar pressure. (B) Same ulcer 3 d later after surgical removal of callous wall and relief of pressure by bed rest. (C) Complete healing 2 wk later.In advanced cases, major destruction of the foot skeleton architecture is triggered by trivial trauma. Acro-osteolysis, aseptic bone necrosis, and severe foot deformity may develop (Charcot's foot). This lesion in diabetic patients is similar to that seen in cases of syringomyelia, leprosy, and polyneuropathy. The Ischemic Foot Lesion Peripheral arterial disease is observed more frequently in diabetic compared with matched nondiabetic patients (18,19). When ultrasound Doppler assessment of pulses is used, peripheral artery disease is found in 30% of all diabetic patients (18), the prevalence being 15 to 20% in those 70 yr of age and increasing to more than 50% at age 80 and above. Lower limb atherosclerosis in the diabetic patient is characterized by preferential involvement of the lower leg, e.g., in 70% of diabetic patients compared with only 20% of nondiabetic patients who suffer from peripheral arterial disease. Involvement of the deep femoral artery is also typical of diabetes. Often, multiple arterial segments are stenosed. The majority of patients do not complain of claudication (Table 2). The risk factors predisposing to macroangiopathy and ischemic foot lesions are the same as the risk factors in nondiabetic patients, particularly smoking, but the diabetic patient has an excess risk for any given constellation of risk factors. Peripheral arterial disease is 2.5 to 6 times more frequent than in nondiabetic patients and occurs 10 yr earlier. An important role of uncontrolled hyperglycemia is suggested by several epidemiologic studies, and this may explain in part the higher risk in the diabetic patient.Table 2: Characteristics of peripheral arterial disease of the lower extremity in diabetes mellitusCalcification of the media of arteries is common in the diabetic patient and can be recognized by linear calcification on ultrasonography. Such calcification of the media is a risk predictor for severe atherosclerotic lesions of the intima. Media calcification makes measurements of arterial blood pressure unreliable and causes spuriously elevated values because of the reduced compressibility of the arteries. Exogenous Triggers The trigger event leading to the clinically manifest diabetic foot lesion in patients at risk (20) is very often trivial. Skin lesions resulting from high pressure are caused by excessively tight shoes, minor trauma, and/or inadequate foot care, e.g., removal of hyperkeratotic plaques with sharp instruments or inadvertent cuts during nail trimming. Trauma is often incurred when walking barefoot and treading on sharp objects. Neuropathic lesions usually start as hyperkeratotic plaques with necrosis underneath, whereas ischemic lesions usually start as superficial ulcers or blisters. Infection is a major aggravating factor. Ports of entry are often ingrowing nails, paronychia, fissures, and interdigital mycoses. One usually finds mixed infections with an average of five different microbes, usually staphylococci, including methicillin-resistant staphylococci (21), hemolytic or nonhemolytic streptococci, Gram-negative Escherichia coli, and anaerobes (9,22,23). The most feared complication is spread of infection to ligaments, tendons, and bones. This may lead to septic thrombosis and secondarily to gangrene even in the absence of macroangiopathy (20). The diagnosis of osteomyelitis by x-ray is difficult, particularly its differentiation from neuropathic changes, e.g., from Charcot's foot. Both complications cause osteolysis, fragmentation of bone, and osteoarticular destruction. Bone scintigraphy may be of some help to make the distinction. Examination of the Patient with Diabetic Foot Lesions Table 3 summarizes the necessary points. A history of trauma should be sought. One should look for tissue trauma from the pressure of tight-fitting shoes; shoes and socks should be inspected; one should examine nails, inspect for interdigital mycosis, hyperkeratotic plaques, minor lesions, and look for deformities of the foot, particularly loss of the pedal arch with flat-footedness associated with downward movement of the metatarsal heads and hammer toe formation.Table 3: Examination of the patient with diabetic foot lesionsTo recognize tissue ischemia, it is useful to measure ankle, and, if possible, toe perfusion pressure by Doppler measurements. Arterial media calcifications and diminished arterial compressibility may give rise to spuriously high arterial pressure values, but when pressures are lower by 10 mmHg or more compared with brachial pressure, one should suspect arterial stenoses. Ankle pressure values <50 mmHg and toe pressure values <30 mmHg indicate critical ischemia. This can be confirmed by transcutaneous oxygen partial pressure measurements, with values <10 mmHg indicating critical ischemia. In the management of the diabetic foot lesion, it is of crucial importance to establish whether the patient complains of pain. The absence of pain indicates a neuropathic component but unfortunately does not exclude the concomitant presence of ischemia. Neurologic examination comprises eliciting reflexes, testing for thermal sensation, perception of vibration (quantitative tuning fork), and perception of touch and pain. Measurement of the dynamic distribution of foot pressure by pedography (Figure 3) is helpful to recognize faulty loading and to guide selection of proper footwear.Figure 3.: Pedographic pressure patterns (red = highest pressure). (Left) Normal pattern. (Middle and Right) Two diabetic patients with increased pressure in the forefoot area and reduced (middle) or deficient toe function (right)Acute Management of the Patient with Diabetic Gangrene Although there is little controlled information (24), patients should be hospitalized and managed according to recently standardized guidelines (25). The aims of management are: to control infection; to assess the potential need for revascularization; to assess the potential need for amputation; and to provide in the long-term adequate foot care and footwear to prevent recurrence (18,19,20). Table 4 summarizes treatment strategies in the patient with diabetic gangrene. Local administration of powders or ointments is contraindicated. Wound care should differ according to the stage of evolution. If correctable ischemia is present, this intervention has priority. Otherwise, surgical debridement, removal of necrotic tissue, and antiseptic measures are usually indicated. For neuropathic ulcers, an active approach is frequently necessary. One has then to remove callus and luxuriant growth and relieve pressure from massive tissue infiltration using broad incisions. If tendons and bones are affected, minimal surgery should be considered, e.g., resection of metatarsal heads and toes (26,27). Excessively aggressive surgery should be avoided. Generally for foot lesions with severe infection, we prefer open wound care and try to avoid attempts at amputation. If amputation is necessary, the defect should be covered with an interpolated flap if possible.Table 4: Treatment strategies in the patient with diabetic gangreneTo increase fibroblast proliferation, moist wound dressings should be applied later. To promote epithelialization, tulle gras wound contact dressings should be used subsequently. Ischemic gangrenous toes must be kept dry, and the surrounding skin must be cleaned. If at all possible, one should wait for spontaneous demarcation. Bacterial inflammation of ulcers and fissures usually results from mixed infections (9,22,23,28) including anaerobes. Bacterial cultures should be obtained because frequently microbes requiring specific antibiotics are found, e.g., pseudomonas or methicillin-resistant Staphylococcus aureus. The major antibiotics used currently for systemic treatment include quinolones, β-lactam antibiotics with or without clavulanic acid, cephalosporins, clindamycin, and metronidazole. The risk of failure is high in patients with fever and gangrene who often require amputation (29). In patients with below-ankle microamputation, follow-up care is necessary to ensure that pressure loads are properly redistributed in order to prevent reappearance of ulcers at new sites or in the opposite foot. Revascularization If one considers revascularization, some basic rules should be followed. First, minimal surgery should be tried whenever possible, i.e., as little reconstruction as possible, but as much as necessary. Second, if revascularization is feasible, it should precede local surgery measures such as fenestration, debridement, or microamputation, because wound healing is delayed and infections tend to be more progressive in ischemic tissues. Stenoses and occlusions can be treated either by the endovascular or open surgical approach. If several stenoses in series are present, it may be advisable to correct the most proximal stenosis (even if it is not critical) by endovascular techniques in combination with distal bypass techniques. Adequate imaging of vasculature before therapy is necessary, bearing in mind the risk of acute renal failure after administration of a radiocontrast agent in diabetic nephropathy. In the future, carbon dioxide and nuclear magnetic resonance angiography may become the procedure of choice (30). The interventional strategy depends on the level and extension of the arterial lesion. Iliac Arteries The best results are achieved in patients with short proximal occlusions that are susceptible to percutaneous transluminal arterioplasty (PTA) with or without stents (Figure 4). Novel advanced prosthesis, e.g., stent grafts under regional or local anesthesia, may permit stenting even of more extended occlusions.Figure 4.: (A and B) Female diabetic patient, 48 year old, with occlusion of the left common iliac artery before (A) and after (B) treatment with balloon angioplasty.If iliac artery stenoses or occlusions are associated with lesions at the inguinal level, or if the percutaneous endovascular approach has been unsuccessful, open surgery is required. In patients with unilateral occlusion of the iliac artery, we have successfully used extra-anatomical femoral or iliaco-femoral cross-over bypass. In patients with bilateral pelvic artery occlusion, one can use either bifurcation bypass or axillo-bifemoral graft bypass. Femoral Arteries If the superficial femoral artery is occluded and the origin of the deep femoral artery is stenosed, perfusion may be sufficiently improved by correcting the deep femoral artery alone. Unfortunately, in diabetic patients one often finds, in addition, atherosclerotic lesions in the periphery of the deep femoral artery, so that collateral formation to the popliteal artery may not be sufficient. In this case, superficial femoral artery bypass to the popliteal artery is recommended. For short stenoses or occlusions of the superficial femoral artery, PTA is the procedure of first choice. Currently, the success rate for stents at the level of the femoral artery is unsatisfactory. Stents should not be used except to correct occluding dissection complicating PTA, but stent-reinforced vascular prostheses are currently under evaluation and may change the practice in the future. For occlusions exceeding 10 to 15 cm in length, open bypass surgery should be performed. When the superficial femoral artery is reconstructed and the distal anastomosis is located above the knee, bypass prostheses should be used to save veins for future reconstructions. If the anastomosis is located at or below the level of the popliteal artery, an autologous venous bypass is the preferred approach. Popliteal Artery Occlusions at the level of the popliteal artery and trifurcation, i.e., the point of origin of tibial and peroneal arteries, should be treated exclusively with autologous venous bypass. If the long saphenous vein is not suitable, the short saphenous vein can be used. Some surgeons use arm veins, but this should be discouraged in view of the potential future need for hemodialysis access. Another possibility is the in situ venous bypass technique, i.e., the use of the local veins, if the diameter of the saphenous vein is <4 mm. Peroneal and Tibial Arteries If the pedal arteries are patent, correction by popliteopedal venous or even lower tibiopedal bypass is possible. Correction with PTA is an extremely difficult issue because, although insertion of stents is technically feasible, the reocclusion rate is extremely high and it is therefore contraindicated. Postoperatively, medication with platelet aggregation inhibitors (low dose aspirin and/or clopidogrel) is mandatory in all patients with peripheral reconstructions. In selected cases, warfarin therapy can be used (31), but if large fluctuations of international normalized ratio occur, e.g., because of patient noncompliance, paradoxically even a prothrombotic tendency may be created. Prophylaxis (Foot Care and Shoe Selection) Prophylaxis of the diabetic foot syndrome cannot be achieved without adequate education and motivation of the patient. It has been shown that implementation of an adequate education program can reduce by half the number of leg amputations even without revascularization procedures. Table 5 summarizes prophylactic measures to prevent diabetic foot problems.Table 5: Prophylactic measures to prevent diabetic foot problemsProper fitting of footwear, i.e., shoes and in-soles, is a cornerstone of primary and secondary prevention. A step-care approach according to the risk category should be followed. As long as there are no deformities, properly fitted in-soles are sufficient for pressure relief. Enough space especially in the forefoot of the shoes is mandatory. Patients with deformities, severe neuropathy, peripheral vascular disease, or a history of foot ulcer need specially fitted shoes. Often a stiff sole and a forefoot roll are necessary. For patients with acute forefoot ulcers, a therapeutic half shoe for total pressure relief is required.

Endovascular stent-graft repair is a less invasive technique than traditional open aortic reconstruction for strictly selected patients with descending thoracic aortic aneurysms. To prevent distal migration of the device as a result of the propulsive flow during systole, it is helpful to induce temporary asystole for > or = 20 s while the stent-graft is placed in the thoracic aorta.We report here a case study of a patient who was given a bolus dose of 60 mg of adenosine to induce temporary asystole. Placement of the stent-graft was successfully performed during the temporary asystole. After 45 s the patient returned to normal sinus rhythm. He was extubated 4 h after the conclusion of surgery and was discharged after 1 week.Induction of temporary asystole with bolus adenosine to facilitate placement of stent-grafts in the thoracic aorta is a simple, easy and effective method of avoiding distal device migration.

The treatment of infrarenal aortic aneurysms by means of transluminally placed endovascular prostheses reflects significant progress in the field of vascular surgery. In the case of infrarenal aortic aneurysm it is possible to achieve technically successful implantation of such a prosthesis in well over 90 % of cases. The rate of clinical success, meaning lasting effective exclusion of the aortic aneurysm, cannot (yet) be definitively determined, since no long-term results are so far available. Secondary leaks are observed in at least 10 % of all patients, making a further therapy necessary (endorepair, conversion, embolization). Further development of endovascular prostheses will include optimization of the aortal/iliac attachment of the prostheses, a better configuration and the development of long-lasting materials that can be used for endovascular prostheses.

Background. The deposition of protein Z was investigated in atherosclerotic vascular lesions of patients with diabetes mellitus or atherosclerotic vascular disease without diabetes in comparison to controls.Patients and methods: Protein Z antigen was evidenced by immunohistochemistry in arteries of 5 healthy control patients, 11 diabetic patients with arterio-occlusive disease and 7 patients suffering from arterio-occlusive disease without diabetes. For immunohistochemistry, a commercially available antibody was taken as first antibody, and Immunopositivity was evaluated independently by two investigators (J. G.; I. K.) as negative (0), positive (+) and strongly positive (++). The results were assessed by the Whitney-Mann-Wilcoxon test.Results: Macrovascular endothelial cells were stained positive for protein Z in all arteries studied. Arteries of controls did not show significant immunopositivity in cells other than macrovascular endothelial cells, while the microvascular endothelial cells of control arteries were largely negative.The proliferating subendothelial space in atherosclerotic vascular lesions showed significant immunopositivity for protein Z. In contrast to control arteries, the microvascular endothelial cells of the proliferating areas stained positive. The staining pattern of the subendothelial space was similar in atherosclerotic vessels independent of the risk factor for atherosclerosis. Plaques were immunopositive for protein 5 too.Conclusions: Protein Z is present in atherosclerotic vascular lesions of diabetic and non-diabetic patients, but not in the subendothelial space and microvascular endothelial cells of healthy controls. Since protein Z-positivity was detected in microvascular endothelium as well as In extra-vascular deposits around plaques, it may play a role in the development of these lesions.

Secondary prevention of atherosclerosis, especially before the onset of symptoms, appears desirable and could be possible with a serum marker detecting atherosclerosis. Circulating, shedded forms of adhesion molecules may serve as such because their expression is upregulated in atherosclerotic plaques. In 52 patients with peripheral arterial vascular disease (Fontaine class IIa, 7 patients; class IIb, 29 patients; and class III, 16 patients), the extent of atherosclerosis was evaluated on the basis of angiograms of a large portion of the arterial system. The area diseased by atherosclerosis was determined by the percentage of vessel wall irregularities of the following calculated segments: aorta (distal from the kidney arteries), common iliac artery, external iliac artery, common femoral artery, lateral circumflex femoral artery, and popliteal artery. The maximal surface area that could exhibit atherosclerotic changes was 250 cm2. The serum concentration of circulating vascular cell adhesion molecule-1 (VCAM-1) correlated with the extent of atherosclerosis (r = .8, P < .001). In contrast, circulating intercellular adhesion molecule-1, E-selectin, P-selectin, and thrombomodulin (as markers for endothelial cell damage) did not correlate with the extent of atherosclerosis. Furthermore, circulating VCAM-1 could be used to indicate stages of atherosclerosis with a high degree of statistical significance. The potential bias of factors such as age, diabetes mellitus, hypercholesterolemia, arterial hypertension, renal failure, and history of myocardial infarction on the correlation of circulating VCAM-1 with the extent of atherosclerosis could be excluded by multivariate analysis. These findings suggest an important role of VCAM-1 in atherosclerosis and may serve as the basis for further evaluation of circulating VCAM-1 as a potential serum marker for atherosclerosis.

PURPOSE To compare the degree of carotid artery stenosis in angiography and CT angiography with the degree of stenosis measured in an intact eversion endarterectomy specimen. METHODS Preoperative angiograms (intraarterial DSA, 512 x 512 matrix) and CT-angiograms (24 sec spiral scan, slice thickness 2 mm, pitch 1.5) were taken in 12 patients with symptomatic carotid stenosis. Evaluation of the degree of stenosis was performed according to the NASCET ("distal" degree) and ECST ("local" degree) methods. These data were compared with measurements of the surgical specimens. RESULTS The median "local" degree of stenosis in angiograms was 81.5% (range: 70-99%), in CT angiograms 83% (59-94%) and in specimens 85.5% (65-96%). The "distal" degree of stenosis was 79% (50-99%) in angiograms, 85.5% (55-99%) in CT angiograms and 81% (52-95%) in specimens. CT angiography slightly overestimated the degree of stenosis compared with the specimen, whereas angiography slightly underestimated the true degree of stenosis. However, these differences were not statistically significant. CONCLUSION CT angiography is able to predict the degree of internal carotid stenosis when compared with an intact surgical specimen. It is as accurate as the "gold standard" of invasive angiography.

The cellular interactions of advanced glycation end products (AGEs), which have been hypothesized to contribute to the development of vascular lesions, occur, at least in part, through their binding to a novel integral membrane protein, the receptor for AGEs (RAGE). Studies of human vascular segments show that endothelial RAGE expression at the antigen and mRNA level was variable and usually at low levels in samples from healthy individuals. In contrast, patients with a range of peripheral occlusive vascular diseases, with or without underlying diabetes, demonstrated prominent enhancement of endothelial RAGE expression. Smooth muscle cells and nerves in the vessel wall showed constitutively high levels of RAGE expression that were unchanged with aging (from 1 to 92 years) or by the presence of vascular disease. These data suggest that RAGE is likely to have ligands other than AGEs, and that multiple factors in addition to AGEs impact on its expression. Taken together, our findings suggest that RAGE may contribute to the pathogenesis of a range of vascular disorders.

Berichtet wird über 356 nachuntersuchte Operationen an der A. subclavia in den letzten 15 Jahren. 128 Patienten erhielten eine Subclavia-Carotis-Transposition, 228 Patienten wurden mit einem Bypass versorgt. An Operationsfolgen verstarb nur ein Patient der Bypass-Gruppe. Neurologische Komplikationen traten selten, aber ebenfalls nur in der Bypass-Gruppe auf. Dagegen werden technische Schwierigkeiten bei der Transposition der A. subclavia hervorgehoben. Bei der Transposition wird nur eine Anastomose erforderlich. Beim Vergleich der beiden Techniken überwiegen die Vorteile für die Transposition.