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Increased perivascular fat mass contributes to cardiometabolic risk (CMR). High peribrachial adipose tissue (PBAT) associates with insulin resistance independently of established CMR parameters. It is unknown to what extent periaortic adipose tissue (PAAT) may have a similar impact. In 95 participants, precise quantification of total adipose tissue, PBAT, PAAT, visceral adipose tissue (VAT), and liver fat (LF) content was performed by whole-body magnetic resonance imaging. Insulin sensitivity was determined by oral glucose tolerance test and carotid intima–media thickness (cIMT) by high-resolution ultrasound. In univariate analyses, PAAT correlated with PBAT (β = .65, P < .0001). A negative correlation of PAAT (β = −.35, P = .0002) and PBAT (β = −.43, P < .0001) with insulin sensitivity was observed. While in a stepwise forward regression analysis the relationship of PAAT with insulin sensitivity was no longer significant after adjustment for VAT, LF content, and other CMR factors ( P = 0.42), PBAT still correlated with insulin sensitivity ( r2 = .35, P = .01). The association between PAAT and cIMT (β = .49, P < .0001) remained significant after adjustment for these variables ( r2 = .42, P = .0001). Although PAAT and PBAT strongly correlate, PAAT is not associated with insulin resistance, but with cIMT. Therefore, PAAT and PBAT may act differently as possible modulators of insulin resistance and subclinical atherosclerosis.

Summary. Arteriovenous fistulae are defined as congenital or acquired abnormal direct communications between an artery and a vein leading to abnormal blood circulation. This report describes an unusual manifestation of an acquired peripheral arteriovenous fistula with a high shunt volume of 410 ml/min following a fracture of the 5th finger.

Aim: The visceral adiposity index (VAI) has been proposed as an estimate of visceral adipose tissue (VAT) mass and as an indicator of VAT dysfunction. Both parameters are associated with cardiometabolic risk, including insulin resistance. In this study, we investigated whether VAI is associated with subclinical atherosclerosis in subjects who were free of cardiovascular disease but were at risk of developing diabetes mellitus.Methods: A total of 731 adults with a median age of 47 years old without diabetes mellitus were included in this cross-sectional study. The anthropometric data, blood pressure, and lipid profiles of 398 women and 333 men were measured. All subjects underwent an oral glucose tolerance test, and carotid intima -media thickness (cIMT) was evaluated by ultrasound. Insulin resistance was estimated using the homeostatic model assessment of insulin resistance (HOMA-IR).Results: VAI and HOMA-IR (beta(st) = 0.44, p < 0.0001), VAI and cIMT (beta(st) = 0.17, p < 0.0001), and HOMA-IR and cIMT (beta(st) = 0.09, p = 0.0127) were correlated with each other. After adjusting for cofounding variables, VAI is still correlated with HOMA-IR (beta(st) = 0.42, p < 0.0001). Furthermore, VAI (beta(st) = 0.07, p = 0.0392) but not HOMA-IR (beta(st )= 0.03, p = 0.37) was correlated with cIMT independently of other established cardiovascular risk factors.Conclusion: The calculation of VAI may provide a better estimation of subclinical atherosclerosis than the calculation of HOMA-IR.

ZusammenfassungDas Auftreten sowohl der tiefen Beinvenenthrombose als auch einer Lungenarterienembolie wird bereits durch physiologische Mechanismen in der Schwangerschaft und im Wochenbett begünstigt. Es kommt neben vorbestehenden Risikofaktoren zu transienten Erscheinungen, die das Risiko für venöse thromboembolische Erkrankungen erhöhen. Die Klinik von Thromboembolien ist oft unspezifisch. Erprobte Diagnosealgorithmen bestehen in der Schwangerschaft nicht. Aufgrund der klinischen Relevanz ist jedoch eine Diagnosesicherung unerlässlich. Die Anamnese, Klinik und Labordiagnostik sind wesentliche Bestandteile in der Diagnosefin-dung, können aber alleine eine venöse Thromboembolie nicht ausschließen. Eine apparative Beurteilung der betroffenen Venen durch die Sonographie ist dabei die Untersuchungsmethode der Wahl. Die vorliegende Arbeit beschreibt die Diagnostik und Therapie venöser Thromboembolien in der Schwangerschaft.

Klippel-Trénaunay syndrome (KTS) is a rare congenital anomaly characterized by malformation of lymph and blood vessels as well as growth disturbance of soft tissue and bone. The clinical picture is variable and associated with an increased risk of thromboembolic events mediated by intravascular coagulopathy in venous malformations. Here, we report on a male patient with KTS suffering from recurrent deep vein thrombosis (DVT) and life-threatening bleeding due to consumptive coagulopathy. Furthermore, we describe the successful long-term anticoagulant management with rivaroxaban.

We report on a patient with acute dyspnea after several vertebral body interventions, among others a kyphoplasty, that was performed a few days earlier.In the computed tomography we prove a bilateral pulmonary embolism (cement and thrombus). There is no right heart failure. A deep vein thrombosis can be excluded by color-coded vascular ultrasound.The pulmonary embolism is due to bone cement. The cement material is also found paravertebral, intraspinal and intraneuroforaminal. By conservative treatment using therapeutic anticoagulation and analgesic medication, the patient showed a rapid clinical improvement.In patients with cardiopulmonary symptoms after vertebroplasty and kyphoplasty, pulmonary embolism due to bone cement should be considered as a possible cause. The therapy depends on the extent of the cement embolism and the symptoms of the patient.

The authors describe a case of an intrapancreatic gastroduodenal artery aneurysm in a pregnant woman. Successful endovascular therapy was performed for the first time in a visceral artery aneurysm during pregnancy as a bailout solution. The attributive risk to the fetus from scattered radiation during endovascular treatment did not exceed a critical level.

We have previously found that the mass of perivascular adipose tissue (PVAT) correlates negatively with insulin sensitivity and post-ischaemic increase in blood flow. To understand how PVAT communicates with vascular vessels, interactions between perivascular, subcutaneous and visceral fat cells with endothelial cells (ECs) were examined with regard to inflammatory, metabolic and angiogenic proteins. To test for possible in vivo relevance of these findings, circulating levels of the predominant secretion product, hepatocyte growth factor (HGF), was measured in individuals carefully phenotyped for fat distribution patterns.Mono- and co-cultures of human primary fat cells with ECs were performed. mRNA expression and protein production were studied using Luminex, cytokine array, RealTime Ready and ELISA systems. Effects of HGF on vascular cells were determined by WST assays. In patients, HGF levels were measured by ELISA, and the mass of different fat compartments was determined by whole-body MRI.In contrast with other fat cell types, PVAT cells released higher amounts of angiogenic factors, e.g. HGF, acidic fibroblast growth factor, thrombospondin-1, serpin-E1, monocyte chemotactic protein-1 and insulin-like growth factor-binding protein -3. Cocultures showed different expression profiles from monocultures, and mature adipocytes differed from pre-adipocytes. HGF was preferentially released by PVAT cells and stimulated EC growth and smooth muscle cell cytokine release. Finally, in 95 patients, only PVAT, not visceral or subcutaneous mass, correlated independently with serum HGF levels (p = 0.03; r = 0.225).Perivascular (pre-)adipocytes differ substantially from other fat cells with regard to mRNA expression and protein production of angiogenic factors. This may contribute to fat tissue growth and atherosclerotic plaque complications. Higher levels of angiogenic factors, such as HGF, in patients with increased perivascular fat mass may have pathological relevance.

Aneurysms of the gluteal arteries are rare clinical findings. The majority of those aneurysms consist of pseudoaneurysms due to pelvic trauma [1–3]. True aneurysms of the gluteal arteries occur due to atherosclerosis, infections, polyarteritis nodosa, or are associated with arteriovenous malformations (AVM) [1]. AVMs are considered to be undifferentiated high-flow vascular malformations characterized by multiple abnormal communications between the arterial and venous system without an intervening capillary network [4–6]. AVMs can involve any area of the body; the extremities, head and neck, lung, and liver are most commonly affected [5, 6]. In the pelvic region, these lesions are rare and more often are acquired secondary to neoplasm, pelvic trauma, and surgical procedures or can be associated with congenital diseases, such as the Klippel-Trenauny syndrome or the Parks-Webber syndrome [6–8]. The following report will describe a case of congenital gluteal AVM associated with a giant true aneurysm of the ipsilateral inferior gluteal artery. Due to its size and the risk of rupture, the aneurysm demanded therapy that could be successfully performed with endovascular techniques.

Apelin is proposed to possess protective cardiovascular properties and may furthermore promote favorable effects on glucose metabolism. First data in humans seem to support this hypothesis. Therefore we aimed to assess the meaning of apelin as an early risk indicator in young subjects prone to atherosclerosis and type 2 diabetes. Furthermore we examined the association of apelin serum levels with insulin sensitivity/resistance and body fat distribution as probably dependent cardiovascular risk factors. We examined 344 individuals (f/m=216/128, mean age 46±1 years) with an increased risk for type 2 diabetes. Apelin-36 serum levels were measured via ELISA. Endothelial dysfunction and intima media thickness (IMT) were assessed using high resolution ultrasound. Visceral adipose tissue (VAT) was measured with an axial T1-weighted fast spin echo technique with a 1.5 T whole-body imager. According to the study population's age, FMD (6.4±0.2%) and IMT (0.56±0.01 mm) were within the expected ranges. Gender or age had no influence on serum apelin levels. When looked at early stages of atherosclerosis, we could not detect a significant correlation between apelin serum levels and FMD or IMT. Blood pressure as well was unaffected by serum apelin levels. Furthermore, neither parameters of insulin sensitivity like insulin sensitivity index (ISI), nor fat distribution like BMI, grade of adiposity, total adipose tissue or VAT were associated with apelin serum levels. We conclude that apelin serum levels do not add further information on the cardiovascular-, or diabetes risk pattern in a diabetes prone population.

In obesity, particularly increased visceral- (VAT), but not total (TAT) adipose tissue mass is a major source of proinflammatory cytokine expression and secretion. VAT, more than TAT, is associated with endothelial dysfunction (ED), which is an accepted risk factor for atherosclerosis. Consequently, we hypothesized that during a lifestyle intervention specifically a decrease in VAT, rather than TAT, is associated with improved ED and vascular adhesion molecules in type 2 diabetes prone subjects.Analyses were done in 189 individuals (age: 45.4±0.8 years) at increased risk of type 2 diabetes, who underwent a 9-month lifestyle intervention. ED expressed as flow mediated dilation (FMD) of the brachial artery, sE-selectin, sV-CAM, sI-CAM, TAT and VAT (measured by magnetic resonance tomography) was determined.There was a mean decrease in body weight (-3%, p0.0001), TAT (-7.6%, p0.0001) and VAT (-12.5%, p0.0001), while FMD increased (+9.1%, p=0.04). The change in FMD was not associated with change in body weight (p=0.35) or TAT (p=0.21) but with a decrease in VAT (r=-0.19, p=0.009). In a post hoc analysis, the subjects were divided by the median change in VAT into responders and non-responders. FMD increased only in the responders (from 6.2±0.4% to 8.0±0.5%, p=0.0005) but not in the non-responders (p=0.15). Also sE-selectin significantly decreased only in the responders (from 54±4 ng/ml to 47±3 ng/ml; p=0.03).During a lifestyle intervention, not weight loss or decrease in TAT, but decrease in VAT is associated with improved ED in individuals prone to type 2 diabetes. Therefore, primary cardiovascular prevention should focus specifically on reducing VAT rather than body weight alone.

OBJECTIVE. The purpose of this article is to illustrate multitechnique imaging findings in patients with primary and secondary vasculitides involving large and medium-sized vessels and their mimics.CONCLUSION. Large and medium-sized vessels are affected by many primary and secondary inflammatory disorders or mimicking conditions, often presenting similar imaging characteristics. Knowledge of distinctive imaging features such as location, length, and degree of vessel wall enhancement as well as the particular clinical settings will help the clinician in appropriately narrowing down the differential diagnosis.

To assess thyroid perfusion in patients with autoimmune thyroid diseases compared with that in healthy control subjects by using an arterial spin-labeling (ASL) magnetic resonance (MR) technique and to assess whether thyroid perfusion is associated with endocrine laboratory abnormalities.This study was approved by the local institutional review board. All participants gave written informed consent. Perfusion imaging of the thyroid gland was performed in 10 patients with Graves disease (GD) and 10 patients with Hashimoto thyroiditis (HT). Ten healthy individuals served as control subjects. Perfusion imaging was performed with a 1.5-T MR unit by using a flow-sensitive alternating inversion recovery-true fast imaging with steady-state precession technique. Perfusion maps of the entire thyroid gland were calculated on the basis of extended Bloch equations. Analysis of variance with a post hoc test (Tukey honestly significant difference) was performed to assess differences in perfusion between groups. Associations between perfusion and laboratory parameters were analyzed with univariate regression analysis.Mean thyroid perfusion was 1596 mL/min/100 g +/- 436 (standard deviation) in patients with GD, 825 mL/min/100 g +/- 264 in patients with HT, and 491 mL/min/100 g +/- 89 in healthy control subjects. Perfusion was significantly higher in patients with GD (P.0001) and those with HT (P.05) than in control subjects. A significant difference in thyroid perfusion was detected between the two autoimmune entities (P.0001). In patients with GD, significant associations were found between perfusion and serum concentrations of free thyroid hormones and anti-thyroid-stimulating hormone receptor antibodies (P.05 for all).Quantitative ASL perfusion imaging of the thyroid gland revealed significant perfusion differences in the autoimmune thyroid diseases GD and HT. Absolute quantification of thyroid perfusion may be useful in the clinical assessment of autoimmune thyroid disorders and when monitoring therapeutic treatment in GD.

To longitudinally assess the value of cardiac functional and viability imaging as a supplement to MR angiography in patients with atherosclerotic disease.Cardiac MRI was performed in 195 consecutive patients with symptomatic peripheral arterial disease. Of these, 186 patients were followed for 22 +/- 5 months for the presence of cardiac events (cardiac death, acute coronary syndrome and hospitalisation as a result of congestive heart failure).Myocardial viability imaging showed a high prevalence of known (n = 31) and occult myocardial infarctions (MI) (n = 26). Cardiac events occurred more often in patients with reduced ventricular function (ejection fraction (EF) less than 40%, cardiac event in 4/8 patients; EF 40-55%, cardiac event in 10/40 patients; EF greater than 55%, cardiac event in 15/138 patients) as well as in patients with occult MI (8/25 patients) and known MI (11/30 patients). In patients with normal function, the detection of a previous MI was of high relevance to prognosis.Both reduced EF and the presence of MI influence patients' prognoses. Performing cardiac MRI in this patient population may influence further patient management including intensified risk factor intervention.

Udgivelsesdato: 2008-Nov AIMS/HYPOTHESIS: Different ectopic fat depots, such as visceral or hepatic fat, are known to affect whole body insulin sensitivity. It has recently been hypothesised that differences in perivascular adipose tissue (PVAT) mass around resistance vessels may also contribute to insulin resistance, possibly via direct vascular effects leading to reduced capillary cross-sectional area in the muscle, which in turn affects muscular blood flow and glucose uptake. Based on this, the aim of the present study was to test whether PVAT around conduit arteries (i.e. the brachial artery) influences NO bioavailability, expressed as flow-mediated dilation (FMD), or insulin sensitivity in humans in vivo. METHODS: Insulin sensitivity was measured by OGTT in all 95 participants (59 women, 36 men; median age 47 years, range 19-66 years) and by the gold standard, a euglycaemic-hyperinsulinaemic clamp, in a randomly selected subgroup of 33 participants. Quantification of the different fat compartments, including PVAT around the brachial artery, was achieved by high-resolution magnetic resonance imaging (1.5 T). Blood flow and FMD were measured at the brachial artery using high-resolution (13 MHz) ultrasound, after 5 min of forearm occlusion. RESULTS: PVAT was negatively correlated with insulin sensitivity and the post-ischaemic increase in blood flow. The association between PVAT and insulin sensitivity (r = -0.54, beta = -0.37, p = 0.009) was independent of age, sex, visceral adipose tissue, liver fat, BMI and further cardiovascular risk factors. No correlation could be detected between PVAT and local endothelial function. However, we observed an independent association between PVAT and post-ischaemic increase in blood flow (r = -0.241; beta = -1.69; p = 0.02). CONCLUSIONS/INTERPRETATION: PVAT seems to play an independent role in the pathogenesis of insulin resistance. This may be due to direct vascular effects influencing muscular blood flow.

Monocyte-chemoattractant-protein (MCP)-1 and its receptor CCR2 have been shown to play a pivotal role in vascular inflammation and atherosclerotic plaque formation. However, it is currently unclear whether MCP-1/CCR2 triggered inflammation affects nitric oxide (NO)-bioavailability, hence influencing vascular function, a sign of early atherosclerosis. Therefore, we sought to investigate the association between serum levels of MCP-1 and NO-bioavailability, expressed as flow mediated dilation (FMD) in vivo, and the impact of CCR2 gene variations on FMD. We studied a German population of 242 prediabetic individuals (144 women, 98 men; mean age 45+/-0.8 years) via FMD by high-resolution ultrasound (13MHz). In order to replicate our findings, a second, independent population (n=115; 44 women, 77 men; mean age 48+/-1.0 years) (total=357 individuals) from Italy was studied. Vascular function in the Italian population was studied via intra-arterial application of acetylcholine. MCP-1 serum-levels were assessed by ELISA and CCR2 polymorphisms were determined by sequencing. MCP-1 serum levels showed no association with FMD (p=0.90), whereas the CCR2 promoter polymorphism was associated with elevated FMD (T/T: 5.6+/-0.3%; T/A: 6.7+/-0.4%; A/A: 8.3+/-0.8%; p=0.01) after adjusting for possible confounders. These results were confirmed in the independent Italian population (A/A: 97.1+/-20.3 vs. T/T: 60.5+/-5.6% forearm blood-flow increase; p

Insulin resistance, as well as vascular disease, both share a relevant genetic background taking the influence of a positive family history of these disorders. On the other hand, insulin resistance is associated with a proatherosclerotic disturbance in nitric oxide dependent vasodilation, probably contributing to the link between these two disorders. We examined the association between nitric oxide dependent vasodilation (measured with high resolution ultrasound at 13 MHz) and three relevant NO-synthase (eNOS)-polymorphisms in 200 insulin resistant subjects participating in the Tuebinger Lifestyle Intervention Program (TULIP). This study revealed that carriers of the eNOS intron 4 polymorphism (aa 2.16%; ab 24.2%; bb 73.2%) show significantly worse endothelial, and thereby eNOS dependent vasodilation (p=0.03, multivariate ANOVA), as compared to wildtype carriers. The 5' UTR T-786C and the G894 T polymorphism did not show any influence on eNOS-activity. In subjects at increased risk to develop type 2 diabetes, the eNOS intron 4 polymorphism is independently associated with endothelial function as indicated by disturbed endothelial NO production. Due to the high prevalence and the relatively strong effect, this polymorphism might help to identify subjects at increased risk for atherosclerosis associated with overweight and insulin resistance.

Circulating trimethylamine N-Oxide (TMAO) levels predict cardiovascular disease (CVD), possibly by impacting on cholesterol metabolism and oxidative stress. Because hepatic TMAO production is regulated by insulin signalling and it is unclear whether and to what extent circulating TMAO levels associate with CVD risk, independently of insulin resistance and its important determinants fatty liver and visceral obesity, we have now addressed this question in 220 subjects who participated in the Tübingen Lifestyle Intervention Program. Visceral fat mass (r = 0.40, p 20%). We provide novel information that increased serum TMAO levels associate with increased cIMT, independently of established cardiovascular risk markers, including insulin resistance, visceral obesity and fatty liver. Furthermore, the decrease of cIMT during a lifestyle intervention may be related to the decrease of TMAO levels.

The authors report on a case of arterial embolism caused by bone entrapment of the popliteal artery due to a protrusion of a hydroxyl-apatite wedge. The wedge had been placed 4 years earlier during the course of a valgus osteotomy procedure. Thrombolytic therapy was performed, and the wedge was removed. Because causes for arterial embolism vary, the knowledge of its underlying mechanism is necessary to avoid recurring events. Bone entrapment after knee surgery is a differential diagnosis that should be taken into account, even years after surgery.

We report on two pregnant women with dyspnoe and thoracic pain in the context of an ovarian hyperstimulation syndrome.Both patients had pleural effusions. The first patient was diagnosed with pulmonary embolism via computer tomography. In the second patient, thrombosis of the upper part of the body including intracranial thrombosis was revealed via magnetic resonance and ultrasound imaging. In both cases, thrombosis was caused by ovarian hyperstimulation.Therapy included anticoagulation with low molecular weight heparin and a drainage of the pleural effusions. One patient had an abortion in the 8th week of pregnancy, the second patient gave birth to two healthy children.Ovarian hyperstimulation syndrome is a potentially life-threatening disease, which should be considered as a differential diagnosis of causes of thromboembolic events in early pregnancy.

Abstract. Background: There is a widely approved influence of novel risk factors like the body fat distribution and the associated metabolic syndrome, subclinical inflammation, insulin resistance and prediabetic disturbances in glucose metabolism on the progression of atherosclerosis. Former studies examining normal values for intima-media thickness (IMT) did not consider all of these new study results in detail. We therefore aimed to assess an update on age- and gender-specific normal values for IMT accounting for these novel risk factors. Patients and methods: We evaluated IMT by high-resolution ultrasound (13 MHz) on the far wall of the common carotid artery in 801 subjects without cardiovascular disease (428 women aged 46.2±12.9 years; 373 men aged 47.3±13.3 years). After precise evaluation and exclusion of 14 cardiovascular risk factors, 90% limits of IMT were determined by parametric statistics. Results: The reference limits of IMT according to the age classes 18-29, 30-39, 40-49 and 50-59 years were estimated as 0.47, 0.59, 0.67 and 0.70 mm in women and 0.47, 0.62, 0.72 and 0.80 mm in men. Conclusions: Age and gender-specific normal values for IMT are lower than reported in former studies after additionally accounting for novel cardiovascular risk factors. The still widely regarded upper IMT limit of 1 mm must be strictly regarded as obsolete.

Background: The metabolic effects of adiponectin, including insulin sensitivity, seem to become stronger with increasing adiposity. Adiposity may also affect the relationship of adiponectin concentrations with serum lipid profile; markers of inflammation, atherosclerosis, and endothelial function; and ectopic fat accumulation. Methods: We measured plasma adiponectin concentrations, serum lipids, and serum markers of inflammation, atherosclerosis, and endothelial function in 242 Caucasians without type 2 diabetes. We also measured visceral adipose tissue with magnetic resonance tomography and liver and intramyocellular fat with 1H magnetic resonance spectroscopy. Results: We divided the study participants into 2 groups: lean [mean (SE) total body fat, 26% (0.6%); n = 119] and obese [36% (0.6%); n = 123]. In the obese group, plasma adiponectin concentrations showed a strong positive association with concentrations of HDL cholesterol (P 0.10). High visceral adipose tissue was a strong predictor of low adiponectin concentrations, particularly in the obese group, and attenuated many of the significant relationships. Conclusions: High adiponectin plasma concentrations are associated with favorable lipid profiles, decreased subclinical inflammation, decreased markers of atherosclerosis and endothelial function, and low ectopic fat accumulation, particularly in obese persons. Adiponectin may also have a concentration-related effect on the relationship between visceral adipose tissue and these metabolic characteristics, especially in obese persons.

Single low density lipoprotein (LDL) fibrinogen apheresis has shown beneficial effects in the treatment of patients with sudden sensorineural hearing loss (SSHL). Pathophysiologically, a microcirculatory disorder of the inner ear, probably caused by disturbed endothelial function, is discussed as a final common pathway of a variety of SSHL etiologies. Thus, we carried out a prospective pilot study on the efficacy of Rheopheresis on vascular function in these patients, embedded into an ongoing randomized controlled multicenter trial investigating the efficacy of Rheopheresis for the treatment of SSHL. Potential modulation of systemic endothelial dysfunction by Rheopheresis was examined by measuring flow-associated vasodilatation of the brachial artery (according to the criteria of the American College of Cardiology) in a small group of patients suffering from SSHL (N = 6, 5m/1f, mean age 56 ± 11 years) within the last 3 days. At baseline, five of the six patients with acute hearing loss showed endothelial dysfunction as evidenced by diminished flow-mediated vasodilatation (FMD

We report on a 57-year-old male patient with typical claudication localised in the right thigh, following aortic valve replacement. The ankle brachial index under resting conditions is within normal range on both sides. A conspicuous monomorphic double-humped peripheral Doppler flow pattern with an early systolic notch extending to the baseline can be registered in all the arteries of the right lower limb. The flow patterns of all other peripheral arteries are properly configured and of triphasic morphology. As the underlying cause of the pathologically altered Doppler flow morphology, aortic dissection Type A can be detected, extending from the former cannulation site of the ascending aorta into the right common iliac artery. Its dissection membrane functionally occludes the right common iliac artery in the early systole, the effect being brief and reversible. The pathogenesis of this morphologically altered Doppler flow pattern and potential differential diagnoses are discussed in this case report, also considering the current literature.

Disturbances in nitric oxide (NO) metabolism resulting in endothelial dysfunction play a central role in the pathogenesis of atherosclerosis in hypercholesterolemia and in individuals with type 2 diabetes. It is unclear whether lipid lowering therapy with HMG-CoA-reductase inhibitors might improve endothelial function in subjects with type 2 diabetes as it is demonstrated in non-diabetic subjects with hypercholesterolemia. We examined the influence of 0.2 mg and 0.8 mg cerivastatin on endothelial function in a multicenter, randomised, double-blind, and three-arm placebo-controlled clinical trial. Endothelial function was assessed by nitric oxide-dependent flow mediated vasodilatation (FMD) of the brachial artery. A total of 103 patients with type 2 diabetes were enrolled in the study. Bayer Company undertook a voluntary action to withdraw cerivastatin from market, therefore the study was terminated earlier. At this point 77 patients were randomised, of which 58 completed the study (mean age 60 +/- 8 years, HbA1c 7.4 +/- 0.9 %). At baseline mean FMD was disturbed in all three therapy arms (5.18 +/- 2.31 % in the placebo group, 3.88 +/- 1.68 in the 0.2-mg cerivastation group, and 4.86 +/- 2.25 in the 0.8-mg cerivastatin group). Despite a significant reduction in cholesterol and LDL-cholesterol-levels after 12 weeks of treatment (decrease in LDL-cholesterol - 26.8 +/- 13.9 % in the 0.2-mg group and - 40.3 +/- 16.0 % in the 0.8-mg group, p = 0.0001, ANCOVA) there was no difference in flow mediated vasodilatation (p = 0.52 and p = 0.56 vs. placebo, respectively, ANCOVA). HbA1c, CRP, and HDL-cholesterol did not change during the study. Furthermore no difference in safety profile between cerivastatin and placebo was found. Despite a significant improvement in lipid profile under statin therapy, no improvement of endothelial dysfunction in terms of nitric oxide bioavailability could be detected.

AIMS Glimepiride has the lowest ratio of insulin release to glucose decrease compared with other sulphonylureas. This prompted us to study in vitro and in vivo in a placebo-controlled study the effect of glimepiride on the redox-sensitive transcription factor nuclear factor-kappa B (NF-kappaB). METHODS Fifteen patients with type 2 diabetes on glibenclamide with a stable HbA1c over the last 6 months were included. After sampling for determination of baseline values, 10 patients were changed to an equivalent dose of glimepiride, while the placebo group was maintained at glibenclamide plus placebo. The glimepiride dose in these patients was adjusted so that no change in glucose control occurred, allowing for direct comparison. The others were kept on glibenclamide and received additional placebo. After 4 weeks of glimepiride or glibenclamide plus placebo, a second blood sample was taken. Mononuclear cells were isolated and assayed in a tissue-culture-independent electrophoretic mobility shift assay (EMSA)-based detection system for NF-kappaB binding activity, and by Western Blot for nuclear localization of NF-kappaB-p65, the cytoplasmic content of IkappaBalpha and the NF-kappaB-controlled haemoxygenase-1. Glimepiride dose-dependent inhibition of carboxymethyllysin (CML) albumin or tumour necrosis factor alpha (TNFalpha)- and H2O2-induced activation of NF-kappaB binding were determined, using isolated peripheral blood mononuclear cells from healthy volunteers, and transcriptional activity of bovine aortic endothelial cells either left untreated or induced with CML albumin incubated with or without glimepiride. Furthermore, in-vitro studies were implemented to demonstrate radical quenching properties of glimepiride in the cell-free 2,2'-azo-bis(2-aminopropane)-dihydrochloride system. RESULTS Baseline glucose and HbA1c remained stable in the patients switched from glibenclamide to a corresponding dose of glimepiride or kept on glibenclamide plus placebo. While in the group of patients only taking glibenclamide plus placebo the NF-kappaB binding activity did not change significantly (p = 0.58), the NF-kappaB binding activity in the group of patients taking glimepiride was reduced from 19.3 relative NF-kappaB-p65-equivalents to 15.5 relative NF-kappaB-p65-equivalents (p = 0.04). The nuclear translocation of NF-kappaB-p65 was reduced from 100% at baseline to 58% after 4 weeks (p = 0.04); the cytoplasmic localization of NF-kappaB-p65 increased from 100% to 129% (p = 0.03) and the cytoplasmic content of IkappaBalpha increased from 100% to 109% (p = 0.06). The redox-sensitive haemoxygenase-1 antigen was reduced from 100% to 82% (p = 0.04). To prove directly that glimepiride reduces NF-kappaB activation, we isolated peripheral blood mononuclear cells (PBMC) from healthy volunteers. In vitro, glimepiride reduced TNFalpha-(1 nmol/l) and CML albumin (800 nmol/l)-induced NF-kappaB activation dose dependently, being half maximal at 120 micromol/l. H2O2-mediated NF-kappaB activation was only partially reduced. In addition, glimepiride reduced NF-kappaB-dependent gene expression using a NF-kappaB-driven luciferase reporter system. Finally, a cell-free detection system showed that glimepiride has radical quenching properties. CONCLUSION Glimepiride can affect the activation of the redox-sensitive transcription factor NF-kappaB in vitro and in vivo.

q Hintergrund: Die aktuelle Atherosklerosetheorie sieht in Storungen der endothelialen Stickoxid-(NO-)Produktion eine Schlusselrolle in Bezug auf die Thrombogenitat der Gefaswand und einen Triggermechanismus morphologischer Veranderungen im Prozess zur stenosierenden Plaque. Entsprechend der bislang vorliegenden Studienlage durfte der Diagnostik einer gestorten endothelialen NO-Bioverfugbarkeit auch eine relevante prognostische Bedeutung in der Primarpravention kardiovaskularer Erkrankungen zukommen. Die Erfassung einer gestorten NO-Produktion kann risikolos, nichtinvasiv mit konventionellem hochauflosendem Ultraschall durchgefuhrt werden. Gerade bei Diabetikern wird analog dazu einer vorliegenden Mikroalbuminurie ein erhohtes Risiko kardiovaskularer Erkrankungen zugeschrieben. Unklar ist die Frage, ob eine Mikroalbuminurie damit als Ausdruck einer globalen endothelialen Dysfunktion aufzufassen ist oder ob andere Partialfunktionen des Endothels, wie die NO-Produktion, bereits vor Auftreten einer erhohten Albuminausscheidung gestort sind. q Probanden und Methodik: Daher wurde an 129 Probanden (56 Typ-2-Diabetiker und 73 Nichtdiabetiker) der Zusammenhang von endothelialer Vasotonusregulation (endotheliale NO-Produktion) mit dem Grad der renalen Albuminausscheidung untersucht. Die endotheliale NO-Produktion wurde als flussmediierte Vasodilatation (FMD) der Arteria brachialis mit einer 13-MHz-Linearsonde gemessen. Verglichen wurden Probanden mit gestorter endothelialer NO-Produktion (FMD 5%). q Ergebnisse: Bei normaler Albuminausscheidung (< 20 μg/min bzw. < 20 mg/l) konnten weder fur die Gruppe der Typ-2-Diabetiker noch fur die Gruppe der Nichtdiabetiker Unterschiede in der Albuminausscheidungsrate fur Probanden mit gestorter versus normaler FMD festgestellt werden (Diabetiker 4,8 ± 5,5 vs. 4,6 ± 5,1 mg/l bzw. Nichtdiabetiker 5,1 ± 2,6 vs. 4,9 ± 2,7 μg/min). Dabei waren die Gruppen ausgeglichen bezuglich der Pravalenz anderer Risikofaktoren des metabolischen Syndroms (systolischer/diastolischer Blutdruck, Glucosestoffwechsel, Lipidstatus). Auch ergab der Vergleich der FMD von Probanden mit bereits vorliegender Mikroalbuminurie (20–200 μg/min bzw. 20–200 mg/l, n = 18) gegenuber normoalbuminurischen Probanden (n = 111) weder fur die Gruppe der Diabetiker (FMD Median 4,3% [Spannweite 1,8–7,6] vs. 5,0% [Spannweite 1,1–9,1%]) noch fur die Gruppe der Nichtdiabetiker (FMD Median 4,7% [Spannweite 3,1–13,3%] vs. 5,2% [Spannweite −1,2–31,6%]) einen relevanten Unterschied. Allerdings zeigten sich hier die klassischen Risikofaktoren von relevantem Einfluss. So wiesen insbesondere in der Gruppe der Nichtdiabetiker Probanden mit Mikroalbuminurie bereits hohere Blutdruckwerte (p = 0,05) und einen hoheren Bodymass-Index (p < 0,01) auf. q Schlussfolgerung: Die dargestellten Ergebnisse fuhren zu dem Schluss, dass beide Testverfahren (Bestimmung der Albuminausscheidung und der endothelabhangigen Vasodilatation) zwei voneinander unabhangige Storungen der Gefaswand erfassen. Zudem konnen entsprechend den Ergebnissen Storungen der endothelialen NO-Produktion bereits vor erhohten Albuminausscheidungsraten vorliegen. Im Sinne einer echten Fruhdiagnostik kardiovaskularer Risikogruppen sollte deshalb die periphere Endothelfunktionstestung erganzend zur Bestimmung der renalen Albuminausscheidung durchgefuhrt werden.

We report on a 58-year-old male patient with abdominal and right-sided flank pain, who presented with the picture of an acute abdominal emergency.Laboratory tests revealed evidence of an inflammation and a hematuria. In the Doppler duplex ultrasound and computed tomography, chronic idiopathic periaortitis was diagnosed. The inflammatory-fibrosing disease resulted in urine retention and rupture of the fornix of the right kidney.After surgical implementation of an ureteral stent and initiation of immunosuppressive therapy, it came to an improvement of the symptoms.In the differential diagnosis of an acute abdominal emergency, diseases of the aorta should be taken into account. Especially in male patients with anatomical complications it is important to exclude an inflammatory-fibrosing disease.

Since the introduction of endovascular aneurysm repair (EVAR) in 1991, the endovascular therapy with newest stent grafts has assumed a prominent role in the clinical management of abdominal aortic aneurysms (AAA) with a superior perioperative mortality of EVAR and an equivalent mid-term outcome, compared to open surgery. Newest techniques using chimney or periscope grafts and customized fenestrated and branched stent grafts allow the endovascular treatment of complex pararenal AAA. This article reviews EVAR in the treatment of AAA, evidence based results and advanced indication by newest interventional techniques and technical developments. Key Points: • EVAR has become standard treatment of abdominal aortic aneurysm with equivalent results to open surgery. • Technical advancements and the introduction of newest stent grafts continually expand the indication of EVAR. • Chimney- and periscope grafts as well as custom-made prothesis systems allow endovascular treatment of complex para- and suprarenal aneurysms. Citation Format: • Ketelsen D, Thomas C, Schmehl J et al. Endovascular Aneurysm Repair of Abdominal Aortic Aneurysms: Standards, Technical Options and Advanced Indications. Fortschr Rontgenstr 2014; 186: 337 – 347

A 56 year old male developed bilateral massive adrenal haemorrhage (BMAH) resulting in chronic adrenal insufficiency in the course of heparin-induced thrombocytopenia (HIT)-syndrome. Thrombosis of the central adrenal vein (CAV) with subsequent adrenal haemorrhagic infarction is the most probable cause of the rare association of HIT and BMAH. The exorbitantly high catecholamine plasma levels within the CAV in addition to immunogenic platelet activation are discussed as possible underlying pathophysiological mechanisms.

UNLABELLED The non-invasive evaluation of endothelial dysfunction with high-resolution ultrasound has become a widely accepted tool in determination of high-risk subjects for early atherosclerosis. Furthermore it is often used as intermediate outcome in intervention studies. AIM We examined the influence of examiner experience on intra- and inter-individual variability in the measurement of flow-associated vasodilation (FAD) independent of automated analysis systems. METHOD FAD was measured on two occasions in 7 and 8 subjects respectively (mean age 32 +/- 3 years) by two investigators after different prior training procedures with a 13 MHz linear transducer (LA14A, ESAOTE Biomedica). RESULTS The intra-individual variability expressed as median absolute difference in the measurements of FAD was 1.1 % (range from 0.03 % to 3.2 %) for examiner one with an experience of more than 50 FAD measurements through former studies and 2.9 % (range from 1.6 % to 9.2 %) for examiner two with only 10 training examinations under supervision. By a further training period of two months, with an increase of examinations of additional 20 measurements by both examiners, the intra-observer variability could be dropped to 0.9 % (range from 0.03 % to 1.3 %) for examiner two (p = 0.0025) with no significant change for examiner one (median 0.6 % with a range from 0.14 % to 3.7 %). As expected, the inter-individual variability was not influenced by this further training (median 1.0 % with a range of 0.5 % to 3.6 % versus a median of 1.6 % with a range from 0.15 % to 7.5 %). CONCLUSION 30 training measurements of FAD under supervision should be regarded as minimum requirement for valid determination of endothelial function. The reachable result for the intra-observer variability is thereby within the range of computed analysis systems.

Background: Endothelial dysfunction (ED) is regarded as an early step in the development of atherosclerosis. Recent experimental data showed a crosstalk between endothelial NO-synthase activity and thyrotropin production. Therfore we studied whether basal TSH can predict flow associated vasodilation (FAD) in a cohort of healthy young subjects with normal TSH levels. Patients and methods: FAD was evaluated in 60 normotensive and normoglycemic subjects (mean age 34 years; range 18–50). The mean thyroptropin level was 1.43 ± 0.11 muU/ml (range 0.18–3.52 muU/ml). Results: Comparing subjects in the upper, middle and lower tertile of TSH (2.38 ± 0.14 muU/ml, 1.23 ± 0.04 muU/ml and 0.65 ± 0.06 muU/ml respectively) there was no difference in terms of the classical cardiovascular risk factor profiles (24 h blood pressure, HDL- and LDL-cholesterol, triglycerides, oral glucose load and body fat content). Regarding the vascular parameters, we could neither find an independent association with FAD (7.0 ± 1.1%, 6.4 ± 1.0% and 5.8 ± 1.1% respectively) nor with endothelial independent vasodilation (after application of glycerol trinitrate GTN, 17.3 ± 1.9%, 18.4 ± 1.7% bzw. 17.5 ± 1.6% respectively) between the groups. Furthermore, we could not find a significant association between free thyroid hormones (fT3/ fT4) and FAD or GTN-induced vasodilation. Conclusion: TSH has no predictive value towards endothelial dysfunction in subjects with thyrotropin levels within the normal range.

Diabetes mellitus and impaired glucose tolerance are linked to increased cardiovascular morbidity and mortality. Vascular disease is directly associated with plasma glucose levels, and reduction of these levels forestalls to a certain extent the vascular complications of diabetes, such as myocardial infarction, nephropathies, and retinopathies. In addition to hyperglycemia, there are other risk factors that play a prominent role, such as hypertension, hyperlipidemia, and genetic factors. Endothelial dysfunction is one of the major factors in the development of cardiovascular disease. The vascular endothelium regulates the blood flow by tightly controlling the coagulation system, cell-cell interaction, and vascular tone. These functions are disturbed in diabetic patients. In diabetics, endothelin-1 levels are increased, leading to vasoconstriction. Endothelin levels are directly related to plasma glucose levels. In addition, the endothelial cell-NO axis is disturbed. NO release and function are impaired. This seems to be dependent upon hyperglycemia and genetic factors. Impaired NO function also results in vasoconstriction. Furthermore, enhanced vascular permeability is seen in diabetics. This appears to be related to impaired endothelial cell relaxation and reactive oxygen species as well as advanced glycosylated end products (AGEs). The complex changes seen in diabetes and even prediabetes are therefore related to numerous derailments related to endothelial dysfunction, and no single therapeutic approach is likely to solve the problem of vascular complications.

Studienziel: Die endothelial Dysfunktion (ED) gilt als frühfunktioneller, die Intima-Media-Dicke (IMT) als frühmorphologischer Marker der Atherogenese. Gibt es ein einfaches, nichtinvasives, routinemaßig einsetzbares Ver-fahren zur Darstellung des Atherosklerosestatus, welches die frühfunktionellen Veränderungen z.B. bei Typ II-Diabetikern mitberücksichtigt? Methode: Wir untersuchten mittels hochauflosendem Ultraschall bei 25 Typ II-Diabetikern und gematchten Kontrollpersonen die periphere Endothelfunktion (ausgedrückt durch die flußassoziierte Vasodilatation nach Ischämie = FAD %) und die endothelunabhangige Vasodilatation nach Gabe von 400 μg Glyceroltrinitrat (Postnitro %) an der A. brachialis sowie die IMT an der A. carotis communis. Ergebnisse (Mittelwerte ± SD): Die Typ II-Diabetiker zeigen eine deutliche Endothelschadigung (FAD %: 3,8 ±3,3 vs. 6,9 ± 4,4%, p = 0,01) sowie eine bereits verdickte IMT (0,72 ±0,14 vs. 0,62 ± 0,10 mm, p > 0,01). Die Vasodilatation nach Nitrogabe als Ausdruck eines prinzipiell noch dilatierfähigen Gefäßsystems unterscheidet sich nicht von der der Gesunden (Postnitro %: 14,3 ±9,4 vs. 14,9 ±8,5%, p = ns). Schlußfolgerung: Die hier verwendete diagnostische Trias ermöglicht die Darstellung des Atherosklerosestatus unter Berücksichtigung der frühfunktionellen Störungen bei Typ II-Diabetikern.

We report on a young female patient with flank pain and a swelling of the lower limb of the left side.In magnetic resonance angiography as well as Doppler-duplex ultrasound an iliofemoral phlebothrombosis of the left side due to vena cava inferior hypoplasia with collateral circulation was diagnosed. Oral contraception could play a role as a trigger. The patient also presented activated protein C resistance/ heterozygous factor V Leiden mutation.According to the CaVenT study we treated the patient successfully with catheter-directed thrombolysis. Follow-ups presented a patency of the iliofemoral vein.In young patients with short duration of a proximal deep vein thrombosis and after exclusion of contraindications a catheter-directed lysis should be considered as a treatment option. The differential diagnostic of a (bilateral) ilio-femoral vein thrombosis in young patients should include an anomaly of the venous system.

Anamnese und klinischer Befund: Wir berichten uber einen Patienten mit akuter Dyspnoe nach mehreren Wirbelkorpereingriffen, unter anderem einer Kyphoplastie, die wenige Tage zuvor erfolgte. Untersuchungen: Computertomografisch kann eine eine bilaterale Lungenarterienembolie (Zement und Thrombus) nachgewiesen werden. Der rechte Ventrikel ist nicht belastet. Eine tiefe Beinvenenthrombose kann mittels Farbduplexsonografie ausgeschlossen werden. Diagnose, Therapie und Verlauf: Ursache fur die Lungenembolie ist Knochenzement. Das Material wird zudem paravertebral, intraspinal und intraneuroforaminal gefunden. Unter einer konservativen Therapie mittels therapeutischer Antikoagulation und analgetischer Medikation bessert sich der Patient klinisch rasch. Folgerung: Bei Patienten mit kardiopulmonalen Symptomen nach einer Vertebro- oder Kyphoplastie sollte eine durch Knochenzement vermittelte Lungenarterienembolie in Betracht gezogen werden. Die Therapie richtet sich nach der Symptomatik des Patienten und dem Ausmas der Zementembolie.

Background: In patients with arterial hypertension, increased blood pressure (BP) variability contributes to end organ damage independently from mean levels of arterial BP. Increased BP variability has been linked to alterations in autonomic function including sympathetic overdrive. We hypothesized that catheter-based renal sympathetic denervation (RDN) confers beneficial effects on BPV. Methods and Results: Eleven consecutive patients with therapy-refractory arterial hypertension (age 68.9±7.0 years; baseline systolic BP 189±23mmHg despite medication with 5.6±2.1 antihypertensive drugs) underwent bilateral RDN. Twenty-four hour ambulatory blood pressure monitoring (ABPM) was performed before RDN and six months thereafter. BPV was primarily assessed by means of standard deviation of 24-hour systolic arterial blood pressures (SDsys). Secondary measures of BPV were maximum systolic blood pressure (MAXsys) and maximum difference between two consecutive readings of systolic BP (deltamaxsys) over 24 hours. Six months after RDN, SDsys, MAXsys and deltamaxsys were significantly reduced from 16.9±4.6mmHg to 13.5±2.5mmHg (p=0.003), from 190±22mmHg to 172±20mmHg (p

Antidiabetic thiazolidinediones (TZDs) improve endothelial function in patients with or without type 2 diabetes. The present randomised, placebo-controlled, double-blind study examined the time course of a single dose of rosiglitazone on flow-mediated endothelium-dependent vasodilation (FMD), metabolic parameters, and its effect on inflammatory markers in non-diabetic men. Forty non-obese, healthy men with normal glucose tolerance were randomised to a single dose of rosiglitazone (8 mg) or placebo, and FMD was assessed at baseline as well as after 6 h and 24 h. Rosiglitazone did not significantly affect blood glucose and insulin levels or lipid parameters after 6 and 24 h compared with placebo. Treatment with rosiglitazone significantly increased FMD after 6 h from 4.3% (3.3; 4.9) to 7.6% (5.6; 9.2) ( p

We report on a patient with known hypertension, who presented to his general practitioner with severe thoracic pain of sudden onset. The aches had started during a dental treatment. Immediately, the patient was admitted to hospital by the general practitioner because myocardial ischemia was suspected.Neither the electrocardiogram nor the laboratory findings (creatin kinase, troponin I) argued for an acute coronary syndrome. Since the plasma D-dimer level was increased and the transthoracic echocardiography showed discrete signs of right ventricular strain, pulmonary embolism could not be ruled out. Because of the high intensity of pain and for further diagnostics the patient underwent a contrast medium-enhanced computed tomography (CT).The contrast medium-enhanced CT showed a type B acute aortic dissection. According to the current guidelines for the treatment of type B aortic dissection, a conservative therapeutic regimen was applied. Antihypertensive therapy was escalated. Furthermore, the patient transiently received analgesic drugs. After three weeks the patient was released from hospital without pain and with physiologic blood pressure under intensified antihypertensive therapy. A follow up examination three months after the acute aortic dissection showed a constant aortic diameter. Therefore, surgical treatment was not indicated.This case report illustrates a typical clinical picture of acute aortic dissection and gives an overview about its epidemiology, classification, pathogenesis, and prognosis. Furthermore, the diagnostic opportunities and the current guidelines for the treatment of acute aortic dissection are discussed.