Weltweit steigt die Prävalenz der peripheren arteriellen Verschlusskrankheit (pAVK) und insbesondere die der kritischen Extremitätenischämie. Letztere ist das Endstadium der arteriellen Verschlusskrankheit und mit erhöhter Mortalität, erhöhtem Amputationsrisiko und beeinträchtigter Lebensqualität assoziiert. Menschen mit Diabetes mellitus und kritischer Ischämie bilden eine besondere Subgruppe unter dieser Klientel. Diabetische Ulzerationen und Wundinfektionen erhöhen das Amputationsrisiko erheblich. Darüber hinaus stellen die diabetische Mikro- und Makroangiopathie, die isolierte Unterschenkel-pAVK und die starke Kalzifizierung der betroffenen Gefäße eine zusätzliche Herausforderung dar. Dementsprechend erfordert die Revaskularisation bei Diabetespatienten komplexe chirurgische und endovaskuläre Strategien. Aufgrund ihrer erhöhten periprozeduralen Mortalität nach chirurgischen Rekonstruktionen führte die Entwicklung neuer endovaskulärer Techniken zu einem Paradigmenwechsel in der Behandlung dieser Hochrisikopatienten. Vor diesem Hintergrund ist die endovaskuläre Technik als Therapie der Wahl für Menschen mit Diabetes und pAVK anzusehen. Der vorliegende Beitrag soll zur Klärung und Präsentation neuer Entwicklungen im Bereich der endovaskulären Therapie des diabetischen Fußsyndroms beitragen.

As populations in western countries continue to age, the prevalence of peripheral arterial disease (PAD) and especially chronic limb-threatening ischemia (CLTI) also increases. CLTI is the most advanced stage of limb ischemia and is associated with high mortality, increased risk of amputation, and impaired quality of life. Patients with diabetes and CLTI represent a challenging subgroup. Diabetic ulcerations and wound infections significantly increase the risk of amputation. In addition, the presence of micro-/macroangiopathy, of heavily calcified vascular disease and isolated tibial/pedal occlusions often require complex surgical and endovascular procedures. Given the increased periprocedural morbidity among patients with diabetes following bypass grafting, the introduction of novel endovascular techniques has led to a paradigm shift in the treatment of these high-risk patients. Thus, endovascular treatment is currently considered the primary treatment strategy for patients with diabetes and PAD. Aim of this article is to present the advances of endovascular therapy for patients with diabetic foot syndrome.

Background Dysfunctional mitochondria have an influence on inflammation and increased oxidative stress due to an excessive production of reactive oxygen species. The mitochondrial DNA copy number (mtDNA-CN) is a potential biomarker for mitochondrial dysfunction and has been associated with various diseases. However, results were partially contrasting which might have been caused by methodological difficulties to quantify mtDNA-CN. Objective We aimed to investigate whether mtDNA-CN is associated with peripheral arterial disease (PAD) as well as all-cause mortality and cardiovascular events during seven years of follow-up. Methods A total of 236 male patients with PAD from the Cardiovascular Disease in Intermittent Claudication (CAVASIC) study were compared with 249 age- and diabetes-matched controls. MtDNA-CN was measured with a well-standardized plasmid-normalized quantitative PCR-based assay determining the ratio between mtDNA-CN and nuclear DNA. Results Individuals in the lowest quartile of mtDNA-CN had a twofold increased risk for PAD which, however, was no longer significant after adjusting for leukocytes and platelets. About 67 of the 236 patients had already experienced a cardiovascular event at baseline and those in the lowest mtDNA-CN quartile had a 2.34-fold increased risk for these events (95% CI 1.08-5.13). During follow-up, 37 PAD patients died and 66 patients experienced a cardiovascular event. Patients in the lowest mtDNA-CN quartile had hazard ratios of 2.66 (95% CI 1.27-5.58) for all-cause-mortality and 1.82 (95% CI 1.02-3.27) for cardiovascular events compared with the combined quartile 2-4 (adjusted for age, smoking, CRP, diabetes, prevalent cardiovascular disease, leukocytes and platelets). Conclusion This investigation supports the hypothesis of mitochondrial dysfunction in peripheral arterial disease and shows an association of low mtDNA-CNs with all-cause-mortality and prevalent and incident cardiovascular disease in PAD patients with intermittent claudication.

15 % der abdominalen Aortenaneurysmen (AAA) sind juxtarenal. Wegen ihrer Ausdehnung bis zu den Nierenarterien ist die Versorgung komplexer als im Falle von infrarenalen Aneurysmen. Um eine zufriedenstellende Ausschaltung der Aneurysmen zu erreichen, müssen oft die Nierenarterien oder sogar die Viszeralarterien in die Versorgung einbezogen werden. Das Ziel dieser Zusammenfassung ist eine Übersicht über die gegenwärtigen Therapieoptionen mit einem Hauptaugenmerk auf der endovaskulären Versorgung mittels FEVAR („fenestrated endovascular aortic repair“). Entscheidende technische Aspekte für die Durchführung einer FEVAR werden detailliert beschrieben. Des Weiteren werden Optionen der Notfallversorgung wie die sm(„surgeon-modified“)-FEVAR vorgestellt.

Background and aims: Peripheral artery disease (PAD) affects more than 200 million people worldwide. Increased low-density lipoprotein cholesterol (LDL-C)levels are a risk factor for PAD and the concentrations are influenced by proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 regulates the recycling of the LDL receptors to the cell membrane surface. Only a limited number of mostly small studies investigated the association between serum PCSK9 concentrations and PAD of different definition, which revealed contrasting results. Methods: Serum PCSK9, lipoprotein(a) [Lp(a)] and other lipoprotein concentrations were measured in male participants of the CAVASIC study, a case-control study of 248 patients with intermittent claudication and 251 age and diabetes-matched controls. Results: PAD patients had significantly higher PCSK9 concentrations when compared to controls (250 77 vs. 222 +/- 68 ng/mL, p < 0.001). Logistic regression analysis with adjustment for age revealed that an increase in PCSK9 concentrations of 100 ng/mL was associated with a 1.78-fold higher risk for PAD (95%CI 1.38-2.33, p = 1.43 x 10(-5)). The association attenuated, but was still significant when adjusting additionally for age, Lp(a)corrected LDL cholesterol, HDL cholesterol, high-sensitivity-CRP, statin treatment, hypertension, diabetes mellitus and smoking (OR = 1.49, 95%CI 1.03-2.18, p = 0.035). The strongest association was observed when both PCSK9 concentrations were above the median and Lp(a) concentrations were above 30 mg/dL (OR = 3.35, 95% CI 1.49-7.71, p = 0.0038). Conclusions: Our findings suggest an association of higher PCSK9 concentrations with PAD, which was independent of other lipid parameters and classical cardiovascular risk factors.

Juxtarenal abdominal aortic aneurysms (JAAA) represent approximately 15% of all AAA; however, due to extension to the renal arteries, management of JAAA is comparatively more challenging than that of AAA and frequently requires inclusion of the renal or even visceral arteries in the treatment plan. The aim of this report is to give an updated review of current treatment strategies, with a special emphasis on fenestrated endovascular aortic repair (FEVAR). The FEVAR technique is discussed in detail, highlighting the key aspects of these complex procedures. Furthermore, treatment possibilities for management of emergency JAAA, such as surgeon-modified (sm) FEVAR are also presented.

Die Frage nach dem optimalen Behandlungszeitpunkt bei Patienten mit symptomatischer Stenose der Arteria carotis interna scheint weiterhin nicht eindeutig beantwortet. Vieles deutet darauf hin, dass eine aufgebrochene Plaque in der ACI so schnell wie möglich entfernt werden soll, um weitere embolische Ereignisse zu verhindern und damit weiteren ischämischen Hirnschäden vorzubeugen.

Timing of treatment in carotid artery disease is still a matter of debate. So far there is controversial literature available concerning the safety of rapid treatment after a qualifying neurological event. Carotid endarterectomy turned out to be more effective in stroke prevention when carried out closer after the onset of symptoms. The initial "two weeks" cut off for surgery meanwhile turned into a "as soon as possible" treatment policy. In case of a cerebral infarction it seems reasonable, however, to delay surgery. Less evidence exists about the ideal timing of carotid artery stenting. Data analysis from the Carotid Stenosis Trialists' Collaboration showed that the early days after plaque rupture carry a high risk for periprocedural complications after carotid artery stenting. The analysis of a large register series showed, that carotid artery stenting carried a significantly higher risk for complications in patients with and without cerebral infarction when performed within 48 hours after the onset of symptoms.

OBJECTIVES:The timing of CEA for symptomatic internal carotid artery (ICA) stenosis remains a matter of controversy. Recent registry data showed a significantly increased risk, especially in the very early days after the onset of symptoms. In this study the outcome of CEA in the hyperacute phase has been investigated. METHODS:The outcome of CEA for symptomatic ICA stenosis between January 2004 and December 2013 has been retrospectively analyzed. Patients were divided into four timing groups: surgery within 0 and 2 days, between 3 and 7 days, 8 and 14 days, and thereafter. The post-operative 30 day stroke and death rates were assessed. RESULTS:A total of 761 symptomatic patients (40.1% with transient ischemic attack [TIA], 21.3% with amaurosis fugax, and 38.6% with ischemic stroke) were included, with an overall peri-operative stroke and death rate of 3.3%. A stroke and death rate of 4.4% (9/206) for surgery within 0 and 2 days, 1.8% (4/219) between 3 and 7 days, 4.4% (6/136) between 8 and 14 days, and 2.5% (5/200) in the period thereafter (p = .25 for the difference between the groups) was observed. The timing of surgery did not influence the peri-operative outcome in a multivariate regression analysis (OR 0.93 [0.63-1.36], p = .71). CONCLUSIONS:These data show that very urgent surgery in symptomatic patients can be performed without increased procedural risk. Given the fact that ruptured plaques with neurological symptoms carry the highest risk of a recurrent ischemic event in the first 2 days, treating patients as soon as possible to offer the highest benefit in stroke prevention is recommended.

Ionisierende Strahlung führt zu direkter Endothelschädigung mit dem Risiko der Plaqueformation im peripheren Gefäßsystem. Radiogene Plaques weisen im Vergleich zu arteriosklerotischen Plaques eine stabilere Morphologie auf. Kommt es nach Bestrahlungen im Karotisstromgebiet zu neurologischen Symptomen, so besteht eine klare Behandlungsindikation.

The European Society for Vascular Surgery (ESVS) appointed the AAA Guidelines Committee to write the current clinical practice guidelines document for surgeons and physicians who are involved in the care of patients with abdominal aortic aneurysms (AAAs). Guideline development was recommended in 1990 by the Institute of Medicine to improve decision making for specific patients’ circumstances and to decrease the variability in appropriate and inappropriate health care between providers.1Committee to Advise the Public Health Service on Clinical Practice Guidelines, Institute of Medicine Field M.J. Lohr K.N. Clinical practice guidelines: directions of a new program. National Academy Press, Washington, DC1990Google Scholar, 2Field M. Lohr K. Guidelines for clinical practice: from development to use. National Academy Press, Washington, DC1992Google Scholar Appropriate decision-making is critical to achieving excellent outcomes. Abdominal aortic aneurysm disease is complex and has significant clinical practice variability, although a valid evidence base is available to guide recommendations. The significant increase in the quantity of scientific literature concerning abdominal aortic aneurysmal disease published in recent years along with the number of technical and medical advances enables guideline recommendations with more certainty and supporting evidence than before. Potential increases in health care costs and risks due to industry and public-driven use of novel treatment options make the current guidelines increasingly important.3Dubois R.W. Dean B.B. Evolution of clinical practice guidelines: evidence supporting expanded use of medicines.Dis Manag. 2006; 9: 210-223Google Scholar, 4Sood R. Sood A. Ghosh A.K. Non–evidence-based variables affecting physicians’ test-ordering tendencies: a systematic review.Neth J Med. 2007; 65: 167-177Google Scholar, 5Manchanda P. Honka E. The effects and role of direct-to-physician marketing in the pharmaceutical industry: an integrative review.Yale J Health Policy Law Ethics. 2005; 5: 785-822Google Scholar, 6Win H.K. Caldera A.E. Maresh K. Lopez J. Rihal C.S. Parikh M.A. et al.EVENT Registry Investigators. Clinical outcomes and stent thrombosis following off-label use of drug-eluting stents.JAMA. 2007; 297: 2001-2009Google Scholar Many clinical situations of patients with AAAs have not been the subject of randomised clinical trials. Patient care, however, needs to be delivered and decisions have to be made in these situations. Therefore, this document also provides guidance for decisions when extensive level I evidence is not available and recommendations are determined on the basis of the currently available best evidence for these situations. By providing information about the relevance and validity of the quality of evidence, the reader will be able to locate the most important and evidence-based information relevant to the individual patient.7Fonarow G.C. Abraham W.T. Albert N.M. Stough W.G. Gheorghiade M. Greenberg B.H. et al.OPTIMIZE-HF Investigators and Hospitals. Association between performance measures and clinical outcomes for patients hospitalized with heart failure.JAMA. 2007; 297: 61-70Google Scholar To optimise the implementation of the current document, the length of the guidelines has been kept as short as possible to enable prompt access to the guideline information. This clinical guidelines document is supposed to be a guide, not a document of rules, and allows flexibility for specific patients’ circumstances. This is the resulting clinical practice guidelines document and provides recommendations for clinical care of patients with abdominal aortic aneurysms including pre-operative, perioperative and post-operative care. Patients with AAAs are defined as male or female patients with asymptomatic, symptomatic or ruptured AAA with fusiform dilatation. This document does not cover patients with a saccular, infected or mycotic AAA or pseudoaneurysmal aortic dilatation. The AAA Guidelines Committee met in September 2009 for the first time to discuss the purpose and methods. The AAA Guidelines Committee has been constituted with incorporation of members from different European countries, from academic and private hospitals, vascular and endovascular specialists and patients to maximise the support for the final guidelines document. Since Europe encompasses a variety of health care systems and political economies, health policy makers were not included.8The AGREE collaborationDevelopment and validation of an international appraisal instrument for assessing the quality of clinical practice guidelines: the AGREE project.Qual Saf Health Care. 2003; 12: 18-23Google Scholar The AAA Guidelines Committee performed a systematic literature search in MEDLINE, EMBASE and COCHRANE Library databases for each of the different topics that are discussed in this guidelines document. The Guidelines Committee used a grading schema based on levels of evidence and grades of recommendation according to the levels of evidence from the Oxford Centre For Evidence-Based Medicine.9Centre for Evidence-Based Medicine Levels of evidence.http://www.cebm.net/levels_of_evidence.aspGoogle Scholar The level of evidence classification provides information about the study characteristics supporting the recommendation and expert consensus, according to the categories shown in Table 1.Table 1Level of evidence classification. Open table in a new tab The recommendation grade indicates the strength of a recommendation. Definitions of the grades of recommendation are shown in Table 2.Table 2Grades of recommendationAConsistent level 1 studiesBConsistent level 2 or 3 studies or extrapolations from Level 1 studiesCLevel 4 studies or extrapolations from level 2 or 3 studiesDLevel 5 evidence or troublingly inconsistent or inconclusive studies of any level“Extrapolations" are where data are used in a situation that has potentially clinically important differences than the original study situation. Open table in a new tab “Extrapolations" are where data are used in a situation that has potentially clinically important differences than the original study situation. The AAA Guidelines Committee aimed to report as much as possible the calculated estimates of effects with their 95% confidence intervals. Every part of the guidelines document has been prepared by at least two members of the Committee and has been reviewed by the entire Committee. The initial guidelines document has been subsequently reviewed by the AAA Guidelines Review Committee. After incorporation of all comments and recommendations, the guidelines have been provided to the members of the ESVS. The final document has been approved by the ESVS. Abdominal aortic aneurysm (AAA), which comes from the Ancient Greek word ἀνεύρυσμα, means a dilatation or widening of the abdominal aorta. The most accepted definition of an AAA is based on the diameter of the abdominal aorta: an abdominal aortic diameter of 3.0 cm or more, which usually is more than 2 standard deviations above the mean diameter for both men and women, and is considered to be aneurysmal.10Steinberg I. Stein H.L. Arterosclerotic abdominal aortic aneurysms. report of 200 consecutive cases diagnosed by intravenous aortography.JAMA. 1966; 195: 1025Google Scholar, 11McGregor J.C. Pollock J.G. Anton H.C. The value of ultrasonography in the diagnosis of abdominal aortic aneurysm.Scott Med J. 1975; 20: 133-137Google Scholar, 12Wanhainen A. Thermudo R. Ahlström H. Lind L. Johansson L. Thoracic and abdominal aortic dimension in 70-years old men and women – a population-based whole-body MRI study.J Vasc Surg. 2008; 47: 504-512Google Scholar Other researchers have suggested defining abdominal aortic aneurysm as the maximum infra-renal aortic diameter being at least 1.5 times larger than the expected normal infra-renal aortic diameter to compensate for individual variation in the diameter of the adjacent aorta.13Sterpetti A. Schultz R. Feldhaus R. Cheng S. Peetz D. Factors influencing enlargement rate of small abdominal aortic aneurysms.J Surg Res. 1987; 43: 211-219Google Scholar, 14Collin J. Walton J. Araujo L. Lindsell D. Oxford screening programme for abdominal aortic aneurysm in men aged 65 to 74 years.Lancet. 1988; 2: 613-615Google Scholar, 15Sonesson B. Lanne T. Hansen F. Sandgren T. Infrarenal aortic diameter in the healthy person.Eur J Vasc Surg. 1994; 8: 89-95Google Scholar AAA can be defined as an abdominal aortic diameter of 3.0 cm or more in either anterior-posterior or transverse planes. Level 2c, Grade B. Population screening studies offer the best evidence regarding the prevalence of AAA. Several of these have been conducted as randomised trials to assess the benefits of screening (MASS, Western Australia, Viborg and Chichester, the latter being the only one to include women).16Scott R.A. Wilson N.M. Ashton H.A. Kay D.N. Influence of screening on the incidence of ruptured abdominal aortic aneurysm: 5-year results of a randomised controlled study.Br J Surg. 1995; 82: 1066-1070Google Scholar, 17Lindholt J.S. Juul S. Fasting H. Henneberg E.W. Screening for abdominal aortic aneurysms: single centre randomised controlled trial.BMJ. 2005; 330: 750-753Google Scholar, 18Norman P.E. Jamrozik K. Lawrence-Brown M.M. Le M.T. Spencer C.A. Tuohy R.J. et al.Population based randomised controlled trial on impact of screening on mortality from abdominal aortic aneurysm.BMJ. 2004; 329: 1259-1262Google Scholar, 19Multicentre Aneurysm Screening Study GroupThe Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial.The Lancet. 2002; 360: 1531-1539Google Scholar Other evidence comes from the Rotterdam, Tromsø and other large epidemiological screening studies.20Pleumeekers H.J. Hoes A.W. van der Does E. van Urk H. de Jong P.T. Grobbee D.E. Aneurysms of the abdominal aorta in older adults. The Rotterdam Study.Am J Epidemiol. 1995; 142: 1291-1299Google Scholar, 21Singh K. Bonaa K.H. Jacobsen B.K. Bjork L. Solberg S. Prevalence and risk factors for abdominal aortic aneurysms in a population-based study: the Tromsø Study.Am J Epidemiol. 2001; 154: 236-244Google Scholar Prevalence rates vary according to age, gender and geographical location (Table 3). Level 1a. In keeping with ethnic and environmental risk factors, a screening study of US veterans (between 50 and 79 years old, n = 73,451) showed the highest prevalence of AAA ≥3.0 cm was 5.9% and was found in white male smokers between 50 and 79 years.22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar All the aneurysm population screening data (Table 3) are now dated and there is little contemporary information for 21st century prevalence, although there are some indications, at least in the USA, that the admission rate for aneurysm repair is declining.23Levin D.C. Rao V.M. Frangos A.J. Sunshine J.H. Endovascular repair vs open surgical repair of abdominal aortic aneurysms: comparative utilization trends from 2001 to 2006.J Am Coll Radiol. 2009; 6: 506-509Google Scholar Important risk factors for AAA are advanced age, male gender and smoking.20Pleumeekers H.J. Hoes A.W. van der Does E. van Urk H. de Jong P.T. Grobbee D.E. Aneurysms of the abdominal aorta in older adults. The Rotterdam Study.Am J Epidemiol. 1995; 142: 1291-1299Google Scholar, 21Singh K. Bonaa K.H. Jacobsen B.K. Bjork L. Solberg S. Prevalence and risk factors for abdominal aortic aneurysms in a population-based study: the Tromsø Study.Am J Epidemiol. 2001; 154: 236-244Google Scholar, 22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar, 23Levin D.C. Rao V.M. Frangos A.J. Sunshine J.H. Endovascular repair vs open surgical repair of abdominal aortic aneurysms: comparative utilization trends from 2001 to 2006.J Am Coll Radiol. 2009; 6: 506-509Google Scholar, 24Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Hye R.J. Makaroun M.S. et al.The aneurysm detection and management study screening program: validation cohort and final results. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators.Arch Intern Med. 2000; 160: 1425-1430Google Scholar, 25Vardulaki K.A. Walker N.M. Day N.E. Duffy S.W. Ashton H.A. Scott R.A. Quantifying the risks of hypertension, age, sex and smoking in patients with abdominal aortic aneurysm.Br J Surg. 2000; 87: 195-200Google Scholar, 26Steickmeier B. Epidemiology of aortic disease: aneurysm, dissection, occlusion.Radiologe. 2001; 41: 624-632Google Scholar, 27Scott R.A. Bridgewater S.G. Ashton H.A. Randomised clinical trial of screening for abdominal aortic aneurysm in women.Br J Surg. 2002; 89: 283-285Google Scholar, 28Wilmink T.B. Quick C.R. Day N.E. The association between cigarette smoking and abdominal aortic aneurysms.J Vasc Surg. 1999; 30: 1099-1105Google Scholar, 29Johansen K. Koepsell T. Familial tendency for abdominal aortic aneurysms.JAMA. 1986; 256: 1934-1936Google Scholar, 30van Vlijmen-van Keulen C.J. Pals G. Rauwerda J.A. Familial abdominal aortic aneurysm: a systematic review of a genetic background.Eur J Vasc Endovasc Surg. 2002; 24: 105-116Google Scholar, 31Larsson E. Granath F. Swedenborg J. Hultgren R. A population-based case-control study of the familial risk of abdominal aortic aneurysm.J Vasc Surg. 2009; 49: 47-50Google Scholar A positive family history for AAA especially in male first-degree relatives, is also associated with increased risk for AAA.29Johansen K. Koepsell T. Familial tendency for abdominal aortic aneurysms.JAMA. 1986; 256: 1934-1936Google Scholar, 30van Vlijmen-van Keulen C.J. Pals G. Rauwerda J.A. Familial abdominal aortic aneurysm: a systematic review of a genetic background.Eur J Vasc Endovasc Surg. 2002; 24: 105-116Google Scholar, 31Larsson E. Granath F. Swedenborg J. Hultgren R. A population-based case-control study of the familial risk of abdominal aortic aneurysm.J Vasc Surg. 2009; 49: 47-50Google Scholar Smoking is a strong risk factor (odds ratio >3.0 in all studies), the associated risk being much higher than for either coronary artery disease or stroke.20Pleumeekers H.J. Hoes A.W. van der Does E. van Urk H. de Jong P.T. Grobbee D.E. Aneurysms of the abdominal aorta in older adults. The Rotterdam Study.Am J Epidemiol. 1995; 142: 1291-1299Google Scholar, 21Singh K. Bonaa K.H. Jacobsen B.K. Bjork L. Solberg S. Prevalence and risk factors for abdominal aortic aneurysms in a population-based study: the Tromsø Study.Am J Epidemiol. 2001; 154: 236-244Google Scholar, 22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar, 24Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Hye R.J. Makaroun M.S. et al.The aneurysm detection and management study screening program: validation cohort and final results. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators.Arch Intern Med. 2000; 160: 1425-1430Google Scholar, 28Wilmink T.B. Quick C.R. Day N.E. The association between cigarette smoking and abdominal aortic aneurysms.J Vasc Surg. 1999; 30: 1099-1105Google Scholar Level 2a. Additionally, the following factors have been associated with AAA development: history of other vascular aneurysms,32Allardice J.T. Allwright G.J. Wafula J.M. Wyatt A.P. High prevalence of abdominal aortic aneurysm in men with peripheral vascular disease: screening by ultrasonography.Br J Surg. 1988; 75: 240-242Google Scholar, 33Shapira O.M. Pasik S. Wassermann J.P. Barzilai N. Mashiah A. Ultrasound screening for abdominal aortic aneurysms in patients with atherosclerotic peripheral vascular disease.J Cardiovasc Surg (Torino). 1990; 31: 170-172Google Scholar, 34MacSweeney S.T. O’Meara M. Alexander C. O’Malley M.K. Powell J.T. Greenhalgh R.M. High prevalence of unsuspected abdominal aortic aneurysm in patients with confirmed symptomatic peripheral or cerebral arterial disease.Br J Surg. 1993; 80: 582-584Google Scholar, 35Graham L.M. Zelenock G.B. Whitehouse Jr., W.M. Erlandson E.E. Dent T.L. Lindenauer S.M. et al.Clinical significance of arteriosclerotic femoral artery aneurysms.Arch Surg. 1980; 115: 502-507Google Scholar greater height,22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar coronary artery disease,22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar, 33Shapira O.M. Pasik S. Wassermann J.P. Barzilai N. Mashiah A. Ultrasound screening for abdominal aortic aneurysms in patients with atherosclerotic peripheral vascular disease.J Cardiovasc Surg (Torino). 1990; 31: 170-172Google Scholar cerebrovascular disease,34MacSweeney S.T. O’Meara M. Alexander C. O’Malley M.K. Powell J.T. Greenhalgh R.M. High prevalence of unsuspected abdominal aortic aneurysm in patients with confirmed symptomatic peripheral or cerebral arterial disease.Br J Surg. 1993; 80: 582-584Google Scholar atherosclerosis,22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar hypercholesterolemia,20Pleumeekers H.J. Hoes A.W. van der Does E. van Urk H. de Jong P.T. Grobbee D.E. Aneurysms of the abdominal aorta in older adults. The Rotterdam Study.Am J Epidemiol. 1995; 142: 1291-1299Google Scholar, 22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar and hypertension,21Singh K. Bonaa K.H. Jacobsen B.K. Bjork L. Solberg S. Prevalence and risk factors for abdominal aortic aneurysms in a population-based study: the Tromsø Study.Am J Epidemiol. 2001; 154: 236-244Google Scholar, 22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar, 35Graham L.M. Zelenock G.B. Whitehouse Jr., W.M. Erlandson E.E. Dent T.L. Lindenauer S.M. et al.Clinical significance of arteriosclerotic femoral artery aneurysms.Arch Surg. 1980; 115: 502-507Google Scholar, 36Baxter B.T. Terrin M.C. Dalman R.L. Medical management of small abdominal aortic aneurysms.Circulation. 2008; 117: 1883-1889Google Scholar although the data for some of these factors are inconsistent and studies may not have been subject to multivariate adjustment, so that spurious associations may have been reported. More recently, genome-wide association studies have demonstrated the association with variants on chromosome 9p21. The presence of rs7025486[A] in the DAB21P gene is associated with a 20% increased risk of developing AAA, odds ratio 1.21 [95%CI 1.14–1.28].37Helgadottir A. Thorleifsson G. Magnusson K.P. Grétarsdottir S. Steinthorsdottir V. Manolescu A. et al.The same sequence variant on 9p21 associates with myocardial infarction, abdominal aortic aneurysm and intracranial aneurysm.Nat Genet. 2008; 40: 217-224Google Scholar Black or Asian race and diabetes mellitus are negatively associated with AAA development.22Lederle F.A. Johnson G.R. Wilson S.E. Chute E.P. Littooy F.N. Bandyk D. et al.Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126: 441-449Google Scholar, 38Salem M.K. Rayt H.S. Hussey G. Rafelt S. Nelson C.P. Sayers R.D. et al.Should Asian men be included in abdominal aortic aneurysm screening programmes?.Eur J Vasc Endovasc Surg. 2009; 38: 748-749Google Scholar Level 2a-3b. The evidence for other risk factors including homocysteinemia, high levels of lipoprotein (a) and plasminogen activator inhibitor-1 is very weak.39Sofi F. Marcucci R. Giusti B. Pratesi G. Lari B. Sestini I. et al.High levels of homocysteine, lipoprotein (a) and plasminogen activator inhibitor-1 are present in patients with abdominal aortic aneurysm.Thromb Haemost. 2005; 94: 1094-1098Google Scholar Level 4b. The reported average growth rate of AAAs between 30 and 55 mm ranges from 0.2 to 0.3 cm per year. Larger AAA diameters are associated with higher AAA growth rates. A wide variation between patients has been reported consistently.40Thompson A.R. Cooper J.A. Ashton H.A. Hafez H. Growth rates of small abdominal aortic aneurysms correlate with clinical events.Br J Surg. 2010; 97: 37-44Google Scholar, 41Brady A.R. Thompson S.G. Fowkes F.G. Greenhalgh R.M. Powell J.T. Abdominal aortic aneurysm expansion: risk factors and time intervals for surveillance.Circulation. 2004; 110: 16-21Google Scholar, 42Schouten O. van Laanen J.H. Boersma E. Vidakovic R. Feringa H.H. Dunkelgrun M. et al.Statins are associated with a reduced infrarenal abdominal aortic aneurysm growth.Eur J Vasc Endovasc Surg. 2006; 32: 21-26Google Scholar, 43Brown P.M. Sobolev B. Zelt D.T. Selective management of abdominal aortic aneurysms smaller than 5.0 cm in a prospective sizing program with gender-specific analysis.J Vasc Surg. 2003; 38: 762-765Google Scholar, 44McCarthy R.J. Shaw E. Whyman M.R. Earnshaw J.J. Poskitt K.R. Heather B.P. Recommendations for screening intervals for small aortic aneurysms.Br J Surg. 2003; 90: 821-826Google Scholar, 45Santilli S.M. Littooy F.N. Cambria R.A. Rapp J.H. Tretinyak A.S. d’Audiffret A.C. et al.Expansion rates and outcomes for the 3.0-cm to the 3.9-cm infrarenal abdominal aortic aneurysm.J Vasc Surg. 2002; 35: 666-671Google Scholar, 46Lindholt J.S. Heegaard N.H. Vammen S. Fasting H. Henneberg E.W. Heickendorff L. Smoking, but not lipids, lipoprotein(a) and antibodies against oxidized LDL, is correlated to the expansion of abdominal aortic aneurysms.Eur J Vasc Endovasc Surg. 2001; 21: 51-56Google Scholar, 47Lindholt J.S. Juul S. Vammen S. Lind I. Fasting H. Henneberg E.W. Immunoglobulin A antibodies against Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysm.Br J Surg. 1999; 86: 634-638Google Scholar, 48Lindholt J.S. Heickendorff L. Antonsen S. Fasting H. Henneberg E.W. Natural history of abdominal aortic aneurysm with and without coexisting chronic obstructive pulmonary disease.J Vasc Surg. 1998; 28: 226-233Google Scholar, 49Stonebridge P.A. Draper T. Kelman J. Howlett J. Allan P.L. Prescott R. et al.Growth rate of infrarenal aortic aneurysms.Eur J Vasc Endovasc Surg. 1996; 11: 70-73Google Scholar Level 1b-2b. Several cohort studies have implicated that statins are associated with lower AAA growth rates.42Schouten O. van Laanen J.H. Boersma E. Vidakovic R. Feringa H.H. Dunkelgrun M. et al.Statins are associated with a reduced infrarenal abdominal aortic aneurysm growth.Eur J Vasc Endovasc Surg. 2006; 32: 21-26Google Scholar, 50Sukhija R. Aronow W.S. Sandhu R. Kakar P. Babu S. Mortality and size of abdominal aortic aneurysm at long-term follow-up of patients not treated surgically and treated with and without statins.Am J Cardiol. 2006; 97: 279-280Google Scholar, 51Schlösser F.J. Tangelder M.J. Verhagen H.J. van der Heijden G.J. Muhs B.E. van der Graaf Y. et al.SMART study groupGrowth predictors and prognosis of small abdominal aortic aneurysms.J Vasc Surg. 2008; 47: 1127-1133Google Scholar However, the largest and most carefully conducted study has not demonstrated any association between statins and AAA growth.52Ferguson C.D. Clancy P. Bourke B. Walker P.J. Dear A. Buckenham T. et al.Association of statin prescription with small abdominal aortic aneurysm progression.Am Heart J. 2010; 159: 307-313Google Scholar Smoking has been associated with aneurysm expansion.40Thompson A.R. Cooper J.A. Ashton H.A. Hafez H. Growth rates of small abdominal aortic aneurysms correlate with clinical events.Br J Surg. 2010; 97: 37-44Google Scholar, 46Lindholt J.S. Heegaard N.H. Vammen S. Fasting H. Henneberg E.W. Heickendorff L. Smoking, but not lipids, lipoprotein(a) and antibodies against oxidized LDL, is correlated to the expansion of abdominal aortic aneurysms.Eur J Vasc Endovasc Surg. 2001; 21: 51-56Google Scholar, 47Lindholt J.S. Juul S. Vammen S. Lind I. Fasting H. Henneberg E.W. Immunoglobulin A antibodies against Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysm.Br J Surg. 1999; 86: 634-638Google Scholar, 53Brady A.R. Thompson S.G. Greenhalgh R.M. Powell J.T. Cardiovascular risk factors and abdominal aortic aneurysm expansion: only smoking counts. US small aneurysm trial participants.Br J Surg. 2003; 90: 491-492Google Scholar, 54Chang J.B. Stein T.A. Liu J.P. Dunn M.E. Risk factors associated with rapid growth of small abdominal aortic aneurysms.Surgery. 1997; 121: 117-122Google Scholar, 55Vega de C.M. Gomez R. Estallo L. Rodriguez L. Baquer M. Barba A. Growth rate and associated factors in small abdominal aortic aneurysms.Eur J Vasc Endovasc Surg. 2006; 31: 231-236Google Scholar, 56Norman P. Spencer C.A. Lawrence-Brown M.M. Jamrozik K. C-reactive protein levels and the expansion of screen-detected abdominal aortic aneurysms in men.Circulation. 2004; 110: 862-866Google Scholar, 57Eriksson P. Jones K.G. Brown L.C. Greenhalgh R.M. Hamsten A. Powell J.T. Genetic approach to the role of cysteine proteases in the expansion of abdominal aortic aneurysms.Br J Surg. 2004; 91: 86-89Google Scholar Smoking cessation may be recommended to reduce the risk of AAA growth. Level 2b, Grade B. Data on the predictive value of hypertension,42Schouten O. van Laanen J.H. Boersma E. Vidakovic R. Feringa H.H. Dunkelgrun M. et al.Statins are associated with a reduced infrarenal abdominal aortic aneurysm growth.Eur J Vasc Endovasc Surg. 2006; 32: 21-26Google Scholar, 55Vega de C.M. Gomez R. Estallo L. Rodriguez L. Baquer M. Barba A. Growth rate and associated factors in small abdominal aortic aneurysms.Eur J Vasc Endovasc Surg. 2006; 31: 231-236Google Scholar, 58Simoni G. Beghello A. Buscaglia M. Ermirio D. Caprio J. [Growth rate of abdominal aortic aneurysms. Ultrasounds study and clinical outcome].Minerva Cardioangiol. 2002; 50: 371-377Google Scholar, 59Wilmink A.B. Hubbard C.S. Day N.E. Quick C.R. The incidence of small abdominal aortic aneurysms and the change in normal infrarenal aortic diameter: implications for screening.Eur J Vasc Endovasc Surg. 2001; 21: 165-170Google Scholar, 60Schewe C.K. Schweikart H.P. Hammel G. Spengel F.A. Zollner N. Zoller W.G. Influence of selective management on the prognosis and the risk of rupture of abdominal aortic aneurysms.Clin Investig. 1994; 72: 585-591Google Scholar age,41Brady A.R. Thompson S.G. Fowkes F.G. Greenhalgh R.M. Powell J.T. Abdominal aortic aneurysm expansion: risk factors and time intervals for surveillance.Circulation. 2004; 110: 16-21Google Scholar, 42Schouten O. van Laanen J.H. Boersma E. Vidakovic R. Feringa H.H. Dunkelgrun M. et al.Statins are associated with a reduced infrarenal abdominal aortic aneurysm growth.Eur J Vasc Endovasc Surg. 2006; 32: 21-26Google Scholar, 47Lindholt J.S. Juul S. Vammen S. Lind I. Fasting H. Henneberg E.W. Immunoglobulin A antibodies against Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysm.Br J Surg. 1999; 86: 634-638Google Scholar, 54Chang J.B. Stein T.A. Liu J.P. Dunn M.E. Risk factors associated with rapid growth of small abdominal aortic aneurysms.Surgery. 1997; 121: 117-122Google Scholar, 59Wilmink A.B. Hubbard C.S. Day N.E. Quick C.R. The incidence of small abdominal aortic aneurysms and the change in normal infrarenal aortic diameter: implications for screening.Eur J Vasc Endovasc Surg. 2001; 21: 165-170Google Scholar, 61Solberg S. Singh K. Wilsgaard T. Jacobsen B.K. Increased growth rate of abdominal aortic aneurysms in women. The Tromsø study.Eur J Vasc Endovasc Surg. 2005; 29: 145-149Google Scholar gender,41Brady A.R. Thompson S.G. Fowkes F.G. Greenhalgh R.M. Powell J.T. Abdominal aortic aneurysm expansion: risk factors and time intervals for surveillance.Circulation. 2004; 110: 16-21Google Scholar, 42Schouten O. van Laanen J.H. Boersma E. Vidakovic R. Feringa H.H. Dunkelgrun M. et al.Statins are associated with a reduced infrarenal abdominal aortic aneurysm growth.Eur J Vasc Endovasc Surg. 2006; 32: 21-26Google Scholar, 43Brown P.M. Sobolev B. Zelt D.T. Selective management of abdominal aortic aneurysms smaller than 5.0 cm in a prospective sizing program with gender-specific analysis.J Vasc Surg. 2003; 38: 762-765Google Scholar, 61Solberg S. Singh K. Wilsgaard T. Jacobsen B

BACKGROUND:Timing of surgery remains a controversial subject with some concerns persisting that the benefit of early carotid endarterectomy (CEA) offsets the perioperative risks. We investigated the neurological outcome of patients with symptomatic internal carotid artery (ICA) stenosis after surgery in relation to the timing of treatment.METHODS:From January 2005 to June 2010, 468 patients (n = 349 male, 74.6%, median age 71 years) underwent CEA for symptomatic stenosis. Perioperative morbidity and mortality rates were assessed in the 30 days' follow-up.RESULTS:The median time interval between index event and CEA was 7 days; the overall stroke and death rate reached 3.4%. There was no difference in the 30 days' rate of stroke /death rate, depending on the timing of surgery (n = 5/241, 2.1% in patients treated within 1 week vs. n = 10/215, 4.7% in patients treated thereafter, p = 0.12). Patients with a postoperative neurological deterioration had more often an ischaemic infarction on preoperative cerebral computed tomography (CCT) compared with those without deterioration (n = 6/15, 40.0% vs. n = 39/441, 9.0%, p = 0.003). Logistic regression analysis showed that patients with preoperative infarction on CCT had the highest risk for postoperative neurological deterioration.CONCLUSION:An infarction on the preoperative CCT leads to an increased risk for a postoperative deterioration after CEA. Patients should be treated at an early point in time with bland CCTs.

Coral reef aorta is a rare, unique entity with extensive calcification of the entire aorta, mainly the supra- and juxtarenal part. The main symptoms are lower limb claudication, hypertension, deterioration of renal function and angina abdominalis.We report a case of successful treatment of a patient with a coral reef aorta by an ascending aorta to iliac artery bypass graft. Five years later the descending aorta was found to be completely occluded with visceral and distal perfusion via the bypass only.

Chronische Verschlussprozesse der A. subclavia oder des Truncus brachiocephalicus sind meist arteriosklerotischer Genese. Je nach Sitz der Stenose kann es zu zerebralen Symptomen im Sinn eines „Subclavian-steal-Syndroms“ oder zu peripheren Beschwerden mit dem Bild einer Armclaudicatio kommen. Neben bildgebenden Verfahren (DSA, MRA, CTA) spielen die genaue Anamneseerhebung sowie die klinische Untersuchung in der Diagnostik eine besondere Rolle. Aus chirurgischer Sicht stehen sowohl Bypassverfahren als auch Transpositionseingriffe zur Verfügung. Die perkutane Dilatation, ggf. mit Stentimplantation, findet zunehmende Anwendung.

Increased plasma concentrations of apolipoprotein A-IV (apoA-IV) in chronic renal disease suggest a metabolic role of the kidney for this antiatherogenic protein. Therefore, we investigated patients with various forms of proteinuria and found increased serum concentrations of apoA-IV in 124 nephrotic patients compared with 274 controls (mean 21.9 ± 9.6 vs. 14.4 ± 4.0 mg/dl; P < 0.001). Decreasing creatinine clearance showed a strong association with increasing apoA-IV levels. However, serum albumin levels significantly modulated apoA-IV levels in patients with low creatinine clearance, resulting in lower levels of apoA-IV in patients with low compared with high albumin levels (21.4 ± 8.6 vs. 29.2 ± 8.4 mg/dl; P = 0.0007). Furthermore, we investigated urinary apoA-IV levels in an additional 66 patients with a wide variety of proteinuria and 30 controls. Especially patients with a tubular type of proteinuria had significantly higher amounts of apoA-IV in urine than those with a pure glomerular type of proteinuria and controls (median 45, 14, and 0.6 ng/mg creatinine, respectively). We confirmed these results in affected members of a family with Dent's disease, who are characterized by an inherited protein reabsorption defect of the proximal tubular system. In summary, our data demonstrate that the increase of apoA-IV caused by renal impairment is significantly modulated by low levels of serum albumin as a measure for the severity of the nephrotic syndrome. From this investigation of apoA-IV in urine as well as earlier immunohistochemical studies, we conclude that apoA-IV is filtered through the normal glomerulus and is subsequently reabsorbed mainly by proximal tubular cells.

Patients with peripheral arterial disease including those with intermittent claudication have a high risk for cardiovascular and cerebrovascular morbidity and mortality. The outcome of patients with intermittent claudication is less limited by local complications in the leg than by the systemic complications of coronary and cerebral vessels. About 30 % of these patients will die within 5 years, three-quarters of them due to vascular events. Analyses using data of the KORA Study 2004/2005 (F3), a follow-up examination of the participants of the MONICA Survey 1994/95 (S3), will try to identify biochemical as well as genetic risk factors for peripheral arterial disease. The anti-atherogenic apolipoprotein A-IV will be one of our candidates of interest.

In etwa 25% liegt ischämischen zerebralen Schlaganfällen eine arteriosklerotische Veränderung der extrakraniellen A. carotis zugrunde. In der speziellen Diagnostik hat die Duplexsonographie die Angiographie weitgehend abgelöst. Es stehen zwei gleichwertige Operationstechniken zur Verfügung, die Längsendarterektomie mit Patchplastik und die Eversionsendarteriektomie.

PURPOSE:To assess the relationship between outcome of carotid surgery and wait after ischemic stroke.METHODS:We retrospectively analysed data from patients undergoing carotid endarterectomy after ischemic stroke. We investigated the time interval between the event and endarterectomy in relation to surgical results and complications.RESULTS:Between January 2000 and December 2003, 104 patients were scheduled to undergo carotid endarterectomy after a recent stroke. Endarterectomy was performed within 6 h in seven patients (6.7%); within 4 weeks in 29 (27.9%); 4 weeks or more in 62 (59.6%) and six (5.8%) patients received no further therapy. Perioperative complications among patients treated within 4 weeks were 3.4% and were comparable to those treated after 4 weeks (4.8%). However, more than 12% of the patients awaiting operation experienced a new cerebrovascular event (ischemic stroke or carotid occlusion), most of them occurred in the 3rd or 4th week after the initial event.CONCLUSION:Our data indicates, that carotid endarterectomy can be performed with a comparable risk within a short delay after stroke. In addition severe cerebrovascular events occurring within the waiting period may be avoided.