S1 guidelines: Lipedema.

The present, revised guidelines on lipedema were developed under the auspices of and funded by the German Society of Phlebology (DGP). The recommendations are based on a systematic literature search and the consensus of eight medical societies and working groups. The guidelines contain recommendations with respect to diagnosis and management of lipedema. The diagnosis is established on the basis of medical history and clinical findings. Characteristically, there is a localized, symmetrical increase in subcutaneous adipose tissue in arms and legs that is in marked disproportion to the trunk. Other findings include edema, easy bruising, and increased tenderness. Further diagnostic tests are usually reserved for special cases that require additional workup. Lipedema is a chronic, progressive disorder marked by the individual variability and unpredictability of its clinical course. Treatment consists of four therapeutic mainstays that should be combined as necessary and address current clinical symptoms: complex physical therapy (manual lymphatic drainage, compression therapy, exercise therapy, and skin care), liposuction and plastic surgery, diet, and physical activity, as well as psychotherapy if necessary. Surgical procedures are indicated if - despite thorough conservative treatment - symptoms persist, or if there is progression of clinical findings and/or symptoms. If present, morbid obesity should be therapeutically addressed prior to liposuction.

S1-Leitlinie Lipödem.

Die vorliegende überarbeitete Leitlinie zum Lipödem wurde unter der Federführung der Deutschen Gesellschaft für Phlebologie (DGP) erstellt und finanziert. Die Inhalte beruhen auf einer systematischen Literaturrecherche und dem Konsens von acht medizinischen Fachgesellschaften und Berufsverbänden. Die Leitlinie beinhaltet Empfehlungen zu Diagnostik und Therapie des Lipödems. Die Diagnose ist dabei auf der Basis von Anamnese und klinischem Befund zu stellen. Charakteristisch ist eine umschriebene, symmetrisch lokalisierte Vermehrung des Unterhautfettgewebes an den Extremitäten mit deutlicher Disproportion zum Stamm. Zusätzlich finden sich Ödeme, Hämatomneigung und eine gesteigerte Schmerzhaftigkeit der betroffenen Körperabschnitte. Weitere apparative Untersuchungen sind bisher besonderen Fragestellungen vorbehalten. Die Erkrankung ist chronisch progredient mit individuell unterschiedlichem und nicht vorhersehbarem Verlauf. Die Therapie besteht aus vier Säulen, die individuell kombiniert und an das aktuelle Beschwerdebild angepasst werden sollten: komplexe physikalische Entstauungstherapie (manuelle Lymphdrainage, Kompressionstherapie, Bewegungstherapie, Hautpflege), Liposuktion und plastisch-chirurgische Interventionen, Ernährung und körperliche Aktivität sowie ggf. additive Psychotherapie. Operative Maßnahmen sind insbesondere dann angezeigt, wenn trotz konsequent durchgeführter konservativer Therapie noch Beschwerden bestehen bzw. eine Progredienz des Befundes und/oder der Beschwerden auftritt. Eine begleitend zum Lipödem bestehende morbide Adipositas sollte vor einer Liposuktion therapeutisch angegangen werden.

Reproducibility of 3-dimensional ultrasound readings of volume of carotid atherosclerotic plaque.

BACKGROUND: Non-invasive 3-dimensional (3D) ultrasound (US) has emerged as the predominant approach for evaluating the progression of carotid atherosclerosis and its response to treatment. The aim of this study was to investigate the quality of a central reading procedure concerning plaque volume (PV), measured by 3D US in a multinational US trial. METHODS: Two data sets of 45 and 60 3D US patient images of plaques (mean PV, 71.8 and 39.8 mul, respectively) were used. PV was assessed by means of manual planimetry. The intraclass correlation coefficient (ICC) was applied to determine reader variabilities. The repeatability coefficient (RC) and the coefficient of variation (CV) were used to investigate the effect of number of slices (S) in manual planimetry and plaque size on measurement variability. RESULTS: Intra-reader variability was small as reflected by ICCs of 0.985, 0.967 and 0.969 for 3 appointed readers. The ICC value generated between the 3 readers was 0.964, indicating that inter-reader variability was small, too. Subgroup analyses showed that both intra- and inter-reader variabilities were lower for larger than for smaller plaques. Mean CVs were similar for the 5S- and 10S-methods with a RC of 4.7 microl. The RC between both methods as well as the CVs were comparatively lower for larger plaques. CONCLUSION: By implementing standardised central 3D US reading protocols and strict quality control procedures highly reliable ultrasonic re-readings of plaque images can be achieved in large multicentre trials.

Effect of angiotensin receptor blockade on central haemodynamics in essential hypertension: results of a randomised trial.

OBJECTIVE: Angiotensin-converting enzyme (ACE) inhibitors have been shown to lower central augmentation index (cAI), an index of arterial wave reflection, more than beta-blockers. We tested whether this is also true for long-term treatment with an angiotensin receptor blocker (ARB). METHODS: One-hundred and fifty-six subjects with essential hypertension were randomised to treatment with either irbesartan or atenolol. cAI and central blood pressure (BP) were determined by pulse wave analysis from the radial and the carotid artery after six and after 18 months treatment. RESULTS: Peripheral and central systolic and diastolic BP were reduced to a similar extent in the two groups. cAI was reduced with irbesartan, but increased with atenolol (derived from the carotid artery: -6+/-10 vs. -4+/-12% after six months, p<0.001; -4+/-12 vs. +1+/-11% after 18 months; p=0.011). Furthermore, central to peripheral pulse pressure (PP) amplification was unaffected by treatment with irbesartan, but decreased with atenolol. CONCLUSIONS: Although treatment with irbesartan and atenolol similarly decreased peripheral and central BP, only treatment with irbesartan had beneficial effects on arterial wave reflection and preserved PP amplification. These haemodynamic effects may at least partly explain the reported differential effects of ARB versus beta-blocker treatment on cardiovascular mortality in patients with essential hypertension.

[Acute peripheral arterial occlusive disease]. / Akute periphere arterielle Verschlusskrankheit.

Acute lower limb ischemia is not infrequently associated with limb loss 10-30%) or death of the affected patient (15-30%). Thus, acute lower limb ischemia is an emergency. There are two categories of acute arterial occlusion: embolism (70-80%) and thrombosis (20-30%). Early diagnosis is a prerequisite for optimal management. Initial clinical examination is the crucial point: it makes the diagnosis of acute ischemia, localizes the level of occlusion, collects etiologic information and allows for assessing the local and general impact of ischemia on the patient. If sensation and motor function are present, viability of the limb is not threatened (incomplete limb ischemia), and good results can be obtained by utilizing anticoagulation and delayed elective revascularization, if the latter is indicated. If the patient, however, presents symptoms of a complete limb ischemia (paralysis or anesthesia is present), then ultimate limb loss is likely. Most patients present with subtle findings and lack classic symptoms, which makes the diagnosis difficult. The standard office-based tests to determine the presence of acute peripheral vascular disease are calculation of the ankle-brachial index and color duplex sonography. Up to now, digital subtraction angiography is used as standard of reference for definitive localization of the occlusion before revascularization. Magnetic resonance arteriography may be helpful when symptoms or findings do not correlate with the noninvasive ultrasound methods. Therapeutic choices are high-dose heparin therapy, surgical removal of the clot, mechanical interventional thrombectomy, and/or catheter-directed thrombolysis - the ultimate choice being dependent on the particular status of the patient. Patients with severe ischemia require immediate surgical intervention. In patients with contraindications to surgical management or incomplete ischemia, interventional revascularization is the therapy of primary choice. Successful outcome is dependent on careful clinical assessment and a prompt multidisciplinary approach to revascularization.

Carotid intima-media thickness and plaque volume changes following 2-year angiotensin II-receptor blockade. The Multicentre Olmesartan atherosclerosis Regression Evaluation (MORE) study.

OBJECTIVE: The Multicentre Olmesartan atherosclerosis Regression Evaluation (MORE) study was a double-blind trial in patients with hypertension at increased cardiovascular risk with carotid wall thickening and a defined atherosclerotic plaque that used non-invasive 2- and 3-dimensionaL (D) ultrasound (US), to compare the effects of a 2-year treatment based on either olmesartan medoxomil or atenolol on common carotid (CC) intima-media thickness (IMT) and plaque volume (PV). METHODS: A total of 165 patients (with systolic/diastolic blood pressure 140-180/ 90-105 mmHg) were randomized to receive either olmesartan (20-40 mg/day) or atenolol (50-100 mg/day). US was performed at baseline and 28, 52 and 104 weeks. The primary efficacy outcome was the change from baseline ( Delta) in CC-IMT assessed by 2D US. Secondary outcomes included Delta PV assessed by 3D US and blood pressure (BP). RESULTS: Olmesartan and atenolo produced comparable significant reductions in CC-IMT; mean Delta IMT (SEM) was -0.090 (0.015) mm for oLmesartan and -0.082 (0.014) mm for atenolol. Mean Delta PV was -4.4 (2.3) microl and 0.1 (1.5) microl in the olmesartan and atenolol treated subjects, respectively, without significant between-treatment differences. In the subgroup of patients with baseLine PV > or = median (33.7 microl), significant between-treatment differences existed in Delta PV (p = 0.023), because PV regressed significantly with olmesartan (Delta PV: -11.5 (4.4) microl) but not with atenolol ( Delta PV: 0.6 (2.5) microl). In these patients BP reductions were comparabLe. CONCLUSIONS: Carotid IMT and BP decreased similarly with olmesartan and atenolol, but only olmesartan reduced the volume of larger atherosclerotic plaques.

Effect of irbesartan versus atenolol on left ventricular mass and voltage: results of the CardioVascular Irbesartan Project.

Regression of hypertensive left ventricular hypertrophy (LVH) is associated with improved prognosis. The aim of this trial was to compare the effects of irbesartan versus atenolol on LVH in subjects with essential hypertension. Because electrocardiographic and echocardiographic parameters of LVH carry disparate prognostic information, both methods were applied in this trial. In the randomized, double-blind, multicenter trial CardioVascular Irbesartan Project, 240 patients with essential hypertension were treated with irbesartan or atenolol for 18 months. Voltage criteria used for LVH were Sokolow index, Cornell index, Cornell voltage x QRS duration product and Lewis index. In parallel, left ventricular mass (LVM) was determined by 2-dimensional guided M-mode echocardiography. After 6 and 18 months, reductions of LVM and voltage criteria for LVH were only found in subjects treated with irbesartan. However, a reduction of LVM was only detectable in subjects within the highest quartile of baseline LVM but not overall. In contrast, reductions of voltage criteria for LVH were detectable after 6 and 18 months even within commonly used normal limits. In conclusion, treatment of hypertension with irbesartan resulted in a significant reduction in the voltage criteria for LVH, although an effect on LVM was only seen in subjects with high baseline LVM. In contrast, atenolol did not lead to reductions in electrocardiographic or echocardiographic parameters of LVH. Because voltage criteria for LVH have been shown to predict cardiovascular outcome independently from LVM, we suggest that both methods should be used to accurately assess the benefits of antihypertensive treatment.

Comparison of the effects of losartan and atenolol on common carotid artery intima-media thickness in patients with hypertension: results of a 2-year, double-blind, randomized, controlled study.

BACKGROUND: Hypertension induces progressive pathologic changes in the arterial wall. Experimental findings suggest that these changes, which include intima-media thickening, may be mediated, at least in part, by angiotensin II (AII). OBJECTIVE: The Losartan Vascular Regression Study (LAARS) was a double-blind, parallel-group, randomized, controlled, multicenter study designed to compare the effects of the AII antagonist losartan and the beta-blocker atenolol on ultrasonographically determined intimamedia thickness (IMT) of the common carotid artery (CCA) in patients with mild to moderate essential hypertension. METHODS: The primary end point of the study was the yearly rate of change (YRC) from baseline of the mean IMT of the CCA (CCA-IMT(mean)) averaged over 2 years of treatment. Secondary end points included IMT of the common femoral artery and sitting systolic and diastolic blood pressures (SiSBP/SiDBP). Safety assessments of losartan and atenolol were made by statistical and clinical review of the incidence of adverse experiences as well as review of vital signs and laboratory values. A total of 414 patients with essential hypertension were screened for study inclusion at 36 study centers in Germany and Brazil. Patients received losartan (50 mg once daily) or atenolol (50 mg once daily) for 24 months. Target blood pressure (SiSBP/SiDBP <140/<90 mm Hg) was achieved by adding hydrochlorothiazide 12.5 mg once daily, doubling the dose of study drug, or adding an open-label calcium channel blocker sequentially, as needed. RESULTS: Of the original 414 patients screened, 280 hypertension patients (SiDBP 95-115 mm Hg), aged 35 to 65 years, with an IMT of 0.8 to 1.5 mm of the right or left CCA, were randomized to treatment with either losartan (n = 142) or atenolol (n = 138). Both losartan and atenolol therapy produced comparable reductions in CCA-IMTmean over 24 months compared with baseline; the average YRC was -0.038 +/- 0.004 mm/y (P < or = 0.001) for losartan and -0.037 +/- 0.004 mm/y (P < or = 0.001) for atenolol. There were no significant differences between groups. Losartan showed a greater reduction of femoral artery IMT than did atenolol; the average YRC was -0.024 mm/y (P < or = 0.05) for losartan and -0.017 mm/y for atenolol (P = NS), with no significant difference between groups. Both agents produced similar significant reductions in SiSBP and SiDBP and were generally well tolerated. Approximately 7% of losartan patients had drug-related clinical adverse events, compared with 12% of atenolol patients. CONCLUSIONS: The findings of LAARS, the first large study with an AII antagonist that examined IMT, suggest that AII antagonism reverses the early stages of vascular hypertrophy in patients with hypertension. Further studies are needed to delineate the relative importance of AII antagonism versus blood pressure reduction per se in mediating the beneficial vascular effects of losartan.