Publications by authors named "Peter Marschang"

25 Publications

  • Page 1 of 1

Association of Food and Alcohol Consumption with Peripheral Atherosclerotic Plaque Volume as Measured by 3D-Ultrasound.

Nutrients 2020 Nov 30;12(12). Epub 2020 Nov 30.

Department of Internal Medicine III (Cardiology, Angiology), Medical University of Innsbruck, Anichstr. 35, A-6020 Innsbruck, Austria.

Background: Food patterns and alcohol consumption influence the risk for cardiovascular diseases (CVD) and a healthy nutrition is essential for the prevention of CVD. The aim of this study was to determine the influence of nutrition and alcohol consumption on peripheral atherosclerotic plaque volume (PV) using an innovative 3D ultrasound approach.

Methods: In this prospective, single centre study we included 342 patients with at least one cardiovascular risk factor or established CVD. PV in the carotid and femoral artery was measured using a semi-automatic software. Information on food and alcohol consumption of the participants was collected using an internationally acknowledged standardized questionnaire (DEGS1).

Results: Patients with low total PV consumed significantly more vegetables ( = 0.004) and vegetable juice ( = 0.019) per week compared to patients with high total PV. In contrast, patients with high total PV reported a higher alcohol consumption compared to patients with low total PV ( = 0.026). Patients without vascular disease, in particular cerebrovascular disease ( = 0.001) and peripheral arterial disease ( = 0.012), reported a significantly higher fish consumption per week. In the multivariate model, we found a significant negative association for vegetable consumption ( = 0.034) and female gender ( = 0.018) but a significant positive association for alcohol ( = 0.001), age ( < 0.001) the presence of vascular disease ( < 0.001) and cardiovascular risk factors ( < 0.001) with total PV.

Conclusion: In this study we were able to show an association of food and alcohol consumption with peripheral atherosclerotic PV measured by 3D-ultrasonography. Following a healthy nutritional lifestyle (vegetable consumption, no excessive alcohol consumption) and regular fish consumption appears to be associated with less peripheral atherosclerosis and decreased prevalence of vascular diseases, respectively.
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http://dx.doi.org/10.3390/nu12123711DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7760124PMC
November 2020

NGAL Correlates with Femoral and Carotid Plaque Volume Assessed by Sonographic 3D Plaque Volumetry.

J Clin Med 2020 Aug 31;9(9). Epub 2020 Aug 31.

Medical University of Innsbruck, University Hospital of Internal Medicine, Cardiology and Angiology, Anichstrasse 35, A-6020 Innsbruck, Austria.

Background/objectives: Inflammation represents a cornerstone in the development of atherosclerosis and early detection is essential to avoid cardiovascular events. Biomarkers like interleukin-1 beta, interleukin-6, or high sensitivity CRP (hs-CRP) have been investigated intensively in this field. Since they have several limitations, additional biomarkers are needed for cardiovascular risk stratification. The acute phase protein, neutrophil gelatinase-associated lipocalin (NGAL), modulates inflammation and is elevated in cardiovascular disease (CVD). Moreover, it contributes to plaque destabilization.

Methods: In this prospective, single-center study, we included 323 asymptomatic patients with at least one cardiovascular risk factor or established CVD. NGAL levels were measured in plasma samples using a commercially available ELISA. Carotid, femoral, and total atherosclerotic plaque volumes (PV) were measured using a 3D ultrasound system (Philips iU22). Patients were separated into a low ( = 243) and high ( = 80) total PV group.

Results: NGAL was significantly higher in patients with high total PV versus patients with low total PV. The NGAL amplitude for the prediction of high total PV was significantly higher when compared with hs-CRP. A high predictive value could also be observed for patients without established CVD.

Conclusion: NGAL seems to be a promising biomarker for the identification of asymptomatic patients with atherosclerotic disease.
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http://dx.doi.org/10.3390/jcm9092811DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7565934PMC
August 2020

Early onset of menopause is associated with increased peripheral atherosclerotic plaque volume and progression.

Atherosclerosis 2020 03 31;297:25-31. Epub 2020 Jan 31.

Department of Internal Medicine III (Cardiology and Angiology), Medical University of Innsbruck, Anichstr. 35, A-6020, Innsbruck, Austria.

Background And Aims: Cardiovascular disease (CVD) is the leading cause of death in western countries. One risk factor unique to women is the menopausal status. The aim of this study was to analyse the influence of the onset of menopause (MP) on the extent and progression of atherosclerotic plaque volume (PV).

Methods: Postmenopausal women with at least one cardiovascular risk factor (CVRF) but without established CVD were included. Quantification of PV was performed in peripheral arteries using a three - dimensional (3D) ultrasound (US) technique. Follow-up examination to assess PV progression was performed after 19 (±8) months.

Results: 110 consecutive postmenopausal women (mean age 65.5) were included. Females with an earlier onset of MP (<45 years) had a significantly higher PV than those with an intermediate (45-52 years) or later onset of menopause (>52 years), irrespective of other CVRF (244 mm³ vs. 193 mm³ vs. 73 mm³, respectively, p = 0.023). In addition, women with an earlier onset of MP had a higher PV progression compared to women with an intermediate or late onset (40 mm³ vs. 35 mm³ vs. 8.5 mm³; p = 0.002, respectively). Moreover, these results were confirmed in multivariate regression, where only onset of MP (OR 0.88; 95%CI 0.81-0.96; p = 0.004) and age (OR 1.06; 95%CI 1.08-1.13; p = 0.025) were significant predictors for a higher atherosclerotic progression.

Conclusions: An earlier onset of MP was associated with an increase in atherosclerotic PV and accelerated progression, independent of other CVRF.
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http://dx.doi.org/10.1016/j.atherosclerosis.2020.01.023DOI Listing
March 2020

[Austrian Consensus on High Blood Pressure 2019].

Wien Klin Wochenschr 2019 Nov;131(Suppl 6):489-590

Universitätsklinik für Innere Medizin, Gemeinsame Einrichtung, Medizinische Universität Graz, Auenbruggerplatz 15, 8036, Graz, Österreich.

Elevated blood pressure remains a major cause of cardiovascular disease, disability, and premature death in Austria, with suboptimal rates of detection, treatment and control also in recent years. Management of hypertension is a common challenge for physicians with different spezializations. In an attempt to standardize diagnostic and therapeutic strategies and, ultimately, to increase the rate of patients with controlled blood pressure and to decrease the burden of cardiovascular disease, 13 Austrian medical societies reviewed the evidence regarding prevention, detection, workup, treatment and consequences of high blood pressure in general and in various clinical scenarios. The result is presented as the first national consensus on blood pressure. The authors and societies involved are convinced that a joint national effort is needed to decrease hypertension-related morbidity and mortality in our country.
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http://dx.doi.org/10.1007/s00508-019-01565-0DOI Listing
November 2019

Influence of Traditional Cardiovascular Risk Factors on Carotid and Femoral Atherosclerotic Plaque Volume as Measured by Three-Dimensional Ultrasound.

J Clin Med 2018 Dec 31;8(1). Epub 2018 Dec 31.

Department of Internal Medicine III (Cardiology, Angiology), Medical University of Innsbruck, Anichstr. 35, A-6020 Innsbruck, Austria.

Background: Atherosclerosis is a systemic multifocal disease with a preference for the branching points of the arteries. In this study, we quantitatively measured carotid and femoral plaque volume in subjects with cardiovascular risk factors (CVRF) and/or established atherosclerotic disease using a 3D ultrasound technique.

Methods: In this prospective, single-centre study, we included 404 patients (median age 64; 56.9% men) with at least one CVRF or established cardiovascular disease. Plaque volume was measured using 3D ultrasound equipped with an automated software.

Results: We found a strong correlation of plaque volume with CVRF and the number of vascular beds involved. The strongest associations with total and femoral plaque volume were noted for smoking, hypertension, age, as well as for the presence of peripheral arterial occlusive disease ( < 0.05). Carotid plaque volume was best predicted by hyperlipidaemia, hypertension, age, as well as the presence of cerebrovascular disease and coronary artery disease ( < 0.05).

Conclusion: We conclude that smoking appears to be associated with total and femoral plaque volume, whereas hyperlipidaemia seems to be associated with carotid plaque volume. Measurement of 3D plaque volume is a practical and reproducible technique with the potential to become an additional screening tool in cardiovascular risk stratification.
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http://dx.doi.org/10.3390/jcm8010032DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6352255PMC
December 2018

Dabigatran Added to Dual Antiplatelet Therapy to Treat a Left Ventricular Thrombus in an 87 Year Old Patient With Myocardial Infarction and Very High Bleeding Risk.

Front Pharmacol 2018 4;9:217. Epub 2018 Apr 4.

Angiology, Department of Internal Medicine III Cardiology, Innsbruck Medical University, Innsbruck, Austria.

A left ventricular (LV) thrombus is detected in approximately 5-10% of patients after myocardial infarction (MI). If left untreated, these LV thrombi carry a significant risk of complications including embolic stroke. According to current guidelines, anticoagulation with vitamin K antagonists (VKA) is recommended to treat a LV thrombus. An 87 year old patient was referred to our department with non ST-elevation MI. Five months before, he had been diagnosed with a subacute ST elevation MI, which had been treated conservatively. Recently, a rectal neoplasia had been diagnosed, but not operated yet. The patient underwent coronary angiography with implantation of two drug eluting stents (Cre8) requiring dual antiplatelet therapy. During ventriculography an apical LV thrombus of 16 mm diameter was detected. Due to the high bleeding risk in this patient, VKA therapy with potentially fluctuating international normalized ratio (INR) values was considered unsuitable. Therefore, dabigatran at a dose of 110 mg bid was chosen as anticoagulation therapy. After 4 weeks, cardiac computed tomography was performed, which failed to detect the LV thrombus described previously. Notably, triple therapy with dabigatran, clopidogrel, and aspirin was well tolerated without evidence for bleeding. The surgical resection of the rectal neoplasm was performed 2 months later without bleeding complications. Anticoagulation is effective in patients with MI and a LV thrombus in reducing the risk of embolization and in dissolving the thrombus. Our case is complex due to the required triple therapy, very old age and significant bleeding risk of our patient due to the rectal neoplasia. Although only few reports are available for the use of non VKA oral anticoagulants (NOAC) in this indication, we chose dabigatran at a dose of 110 mg bid added to dual antiplatelet therapy for our patient. Besides the advantage of a predictable pharmacokinetic profile of NOAC in contrast to VKA, the effect of dabigatran can rapidly be reversed by idaruzicumab in the case of severe bleeding. Physicians should carefully weigh the risk of thromboembolic events versus the risk of bleeding when combining antiplatelet with anticoagulation therapy.
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http://dx.doi.org/10.3389/fphar.2018.00217DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5893831PMC
April 2018

Femoral access site closure without prior femoral angiography : A retrospective analysis.

Wien Klin Wochenschr 2018 Mar 24;130(5-6):197-203. Epub 2018 Jan 24.

Department of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Anichstr. 35, 6020, Innsbruck, Austria.

Aims And Background: Although guideline recommendations have shifted towards a transradial route, femoral puncture is still an established vascular access, especially for complex coronary interventions. The FemoSeal™ vascular closure device (FVCD) helps to reduce femoral compression time and access site complications after removal of the catheter sheath. To ensure safe use, an angiography of the femoral artery prior to FVCD deployment is recommended by the manufacturer. We postulate that omitting this angiography does not relevantly increase the risk for vascular complications.

Methods And Results: In this retrospective analysis of an all-comers population (n = 1923) including patients receiving a percutaneous coronary intervention (PCI), we could show that combined vascular complication rates without femoral angiography were low (primary endpoint 4.6%) and comparable to a randomized clinical trial that did perform angiography of the vascular access site in a cohort of patients receiving diagnostic coronary angiography only. In addition to this analysis, we could demonstrate that patients with an acute coronary syndrome, receiving periprocedural anticoagulation or anti-platelet therapy had an increased risk for the formation of arterial pseudoaneurysms; however, we did not observe any ischemic vascular event after FVCD deployment.

Conclusion: Closure of the femoral access site after coronary angiography using the FVCD can be safely performed without femoral angiography; however, due to an increased risk for the formation of pseudoaneurysms we recommend the transradial access in situations with increased bleeding risk.
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http://dx.doi.org/10.1007/s00508-018-1314-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5978917PMC
March 2018

Incidental finding of an absent left common carotid artery.

Vasa 2018 Feb 22;47(2):153-155. Epub 2017 Dec 22.

1 Department of Internal Medicine, Medical University of Innsbruck, Innsbruck, Austria.

We describe a case of a young woman evaluated for Raynaud's phenomenon in whom an extremely rare variation, the absence of the left common carotid artery, was incidentally detected as an isolated finding. The detection of vascular anomalies may be important for future endovascular or surgical interventions.
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http://dx.doi.org/10.1024/0301-1526/a000680DOI Listing
February 2018

Expression of a recombinant full-length LRP1B receptor in human non-small cell lung cancer cells confirms the postulated growth-suppressing function of this large LDL receptor family member.

Oncotarget 2016 10;7(42):68721-68733

Department of Internal Medicine, Medical University of Innsbruck, Innsbruck, Austria.

Low-density lipoprotein (LDL) receptor-related protein 1B (LRP1B), a member of the LDL receptor family, is frequently inactivated in multiple malignancies including lung cancer. LRP1B is therefore considered as a putative tumor suppressor. Due to its large size (4599 amino acids), until now only minireceptors or receptor fragments have been successfully cloned. To assess the effect of LRP1B on the proliferation of non-small cell lung cancer cells, we constructed and expressed a transfection vector containing the 13.800 bp full-length murine Lrp1b cDNA using a PCR-based cloning strategy. Expression of LRP1B was analyzed by quantitative RT-PCR (qRT-PCR) using primers specific for human LRP1B or mouse Lrp1b. Effective expression of the full length receptor was demonstrated by the appearance of a single 600 kDa band on Western Blots of HEK 293 cells. Overexpression of Lrp1b in non-small cell lung cancer cells with low or absent endogenous LRP1B expression significantly reduced cellular proliferation compared to empty vector-transfected control cells. Conversely, in Calu-1 cells, which express higher endogenous levels of the receptor, siRNA-mediated LRP1B knockdown significantly enhanced cellular proliferation. Taken together, these findings demonstrate that, consistent with the postulated tumor suppressor function, overexpression of full-length Lrp1b leads to impaired cellular proliferation, while LRP1B knockdown has the opposite effect. The recombinant Lrp1b construct represents a valuable tool to unravel the largely unknown physiological role of LRP1B and its potential functions in cancer pathogenesis.
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http://dx.doi.org/10.18632/oncotarget.11897DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356585PMC
October 2016

Acute myocardial infarction as a manifestation of systemic vasculitis.

Wien Klin Wochenschr 2016 Nov 13;128(21-22):841-843. Epub 2016 Sep 13.

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Anichstraße 35, 6020, Innsbruck, Austria.

Acute myocardial infarction (AMI) is one of the major causes of mortality and morbidity worldwide. In Central Europe, causes of AMI other than atherosclerosis are unusual. Coronary artery vasculitis is one potential non-atherosclerotic process causing AMI. Herein, the authors depict a very rare case of AMI as a clinical manifestation of polyarteritis nodosa (PAN), a necrotizing systemic vasculitis. A 49-year-old male patient presented to our clinic with abdominal pain and markedly elevated concentrations of C‑reactive protein, creatinine and high-sensitivity cardiac troponin T. Electrocardiography showed new repolarization abnormalities in aVF and III. Besides PAN-typical angiographic findings, including bilateral renal artery microaneuryms as well as different arterial occlusions, coronary angiography displayed a complete thrombotic occlusion of the right coronary artery without any other coronary pathology. The present case report demonstrates AMI as very rare but deleterious complication in patients suffering from PAN, and highlights that this life-threatening event can occur even at a very early stage of PAN-related coronary affection.
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http://dx.doi.org/10.1007/s00508-016-1051-4DOI Listing
November 2016

Secretoneurin gene therapy improves hind limb and cardiac ischaemia in Apo E⁻/⁻ mice without influencing systemic atherosclerosis.

Cardiovasc Res 2015 Jan 5;105(1):96-106. Epub 2014 Nov 5.

Department of Cardiology and Angiology, Medical University of Innsbruck, University Hospital of Internal Medicine III, Anichstraße 35, Innsbruck A-6020, Austria

Aims: Hypercholesterolaemia is a major risk factor for cardiovascular diseases and has been shown to influence angiogenesis in the hind limb ischaemia (HLI) model. The impaired up-regulation of angiogenic factors seems to be one of the underlying mechanisms for reduced vessel formation. Since we found that secretoneurin (SN) is up-regulated in hypoxic skeletal muscle cells and exerts beneficial effects in myocardial and HLI, we hypothesized that SN therapy might improve neovascularization in hypercholesterolaemic Apo E(-/-) (Apo E knockout) mice suffering from an impaired vascular response.

Methods And Results: For in vitro experiments, endothelial cells (ECs) were incubated with oxidized low-density lipoprotein (oxLDL) to mimic hypercholesterolaemia. EC function was impaired by oxLDL, but SN induced EC proliferation and in vitro tube formation under these conditions. In the HLI model, injection of SN plasmid resulted in a significant better outcome regarding blood flow recovery, amputation rate, and vessel density. In the myocardial infarction (MI) model, the SN group showed improvement in cardiac parameters. Aortic plaque area was not influenced by local SN injection. Interestingly, SN-induced recruitment of angiogenic monocytic cells was abolished under hypercholesterolaemia.

Conclusions: SN gene therapy exerts beneficial effects in cardiovascular animal models in Apo E(-/-) mice without influencing atherosclerosis and might qualify as a promising therapy for cardiovascular disorders.
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http://dx.doi.org/10.1093/cvr/cvu237DOI Listing
January 2015

Safety and feasibility of a diagnostic algorithm combining clinical probability, d-dimer testing, and ultrasonography for suspected upper extremity deep venous thrombosis: a prospective management study.

Ann Intern Med 2014 Apr;160(7):451-7

Background: Although well-established for suspected lower limb deep venous thrombosis, an algorithm combining a clinical decision score, d-dimer testing, and ultrasonography has not been evaluated for suspected upper extremity deep venous thrombosis (UEDVT).

Objective: To assess the safety and feasibility of a new diagnostic algorithm in patients with clinically suspected UEDVT.

Design: Diagnostic management study. (ClinicalTrials.gov: NCT01324037) SETTING: 16 hospitals in Europe and the United States.

Patients: 406 inpatients and outpatients with suspected UEDVT.

Measurements: The algorithm consisted of the sequential application of a clinical decision score, d-dimer testing, and ultrasonography. Patients were first categorized as likely or unlikely to have UEDVT; in those with an unlikely score and normal d-dimer levels, UEDVT was excluded. All other patients had (repeated) compression ultrasonography. The primary outcome was the 3-month incidence of symptomatic UEDVT and pulmonary embolism in patients with a normal diagnostic work-up.

Results: The algorithm was feasible and completed in 390 of the 406 patients (96%). In 87 patients (21%), an unlikely score combined with normal d-dimer levels excluded UEDVT. Superficial venous thrombosis and UEDVT were diagnosed in 54 (13%) and 103 (25%) patients, respectively. All 249 patients with a normal diagnostic work-up, including those with protocol violations (n = 16), were followed for 3 months. One patient developed UEDVT during follow-up, for an overall failure rate of 0.4% (95% CI, 0.0% to 2.2%).

Limitations: This study was not powered to show the safety of the substrategies. d-Dimer testing was done locally.

Conclusion: The combination of a clinical decision score, d-dimer testing, and ultrasonography can safely and effectively exclude UEDVT. If confirmed by other studies, this algorithm has potential as a standard approach to suspected UEDVT.

Primary Funding Source: None.
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http://dx.doi.org/10.7326/M13-2056DOI Listing
April 2014

[Periprocedual management of vitamin K antagonist's with low molecular weight heparins during invasive procedures--Consensus of experts].

Wien Klin Wochenschr 2013 Jul;125(13-14):412-20

AKH Wien, Univ.-Klinik für Innere Medizin I, Währinger Gürtel 18–20, 1090 Wien, Österreich.

Interruption of an ongoing therapy with vitamin K antagonists (VKAs) is necessary in almost all patients undergoing major surgery. The purpose of the following expert recommendations is to provide easy to use guidance for the periprocedural management of patients on VKAs based on current evidence from the literature. Management of anticoagulation during the time of interruption of VKAs is based on balancing the thromboembolic (TE) risk of underlying conditions against the bleeding risk of the surgical procedure. VKAs should be stopped 3–7days prior to surgery. Low molecular weight heparin (LMWH) is used to cover (“bridge”) the progressive pre-operative loss of anticoagulation and the slow post-operative onset of anticoagulant activity of VKAs. Patients with high risk of TE should receive a therapeutic dose of LMWH, patients with a moderate risk of TE should receive half of this dose. Patients with a low risk of TE do not need bridging therapy with LMWH. In case of an uneventful postoperative course, patients with a therapeutic pre-operative dose should be treated post-operatively with the same dose, starting on day 4 in case of major surgery and on day 2 in case of minor procedures. Patients with a half-therapeutic preoperative dose should be treated post-operatively with the same dose, starting on day 3 in case of major surgery and on day 1 in case of minor procedures. Therapy with VKAs should be re-instituted on the second post-operative day based on the preoperative dosage. Procedure-related post-operative thromboprophylaxis should be given irrespective of these recommendations on days without “bridging” anticoagulation.
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http://dx.doi.org/10.1007/s00508-013-0390-7DOI Listing
July 2013

Prevalence of hypovitaminosis D and folate deficiency in healthy young female Austrian students in a health care profession.

Eur J Nutr 2012 Dec 25;51(8):1021-31. Epub 2011 Nov 25.

Department of Pharmacology and Toxicology, Institute of Pharmacy, Peter-Mayrstr 1, 6020 Innsbruck, Austria.

Purpose: We performed a single-day cross-sectional study to assess the prevalence of vitamin D deficiency as well as folate status in healthy young female volunteers well educated with respect to health information.

Methods: We assessed dietary intake of vitamin D and calcium, serum concentrations of 25-OH-vitamin D(3), folate, red blood cell folate and other dietary, laboratory, and lifestyle parameters in 215 young healthy women (age 18-30 years) on a single day at the end of the winter months. Primary aim was to investigate the prevalence of hypovitaminosis D. Folic acid status was a secondary study aim.

Results: Mean daily ingestion of vitamin D was 2.25 μg/day with a daily calcium intake of 749 mg/day. 6.9% had hypovitaminosis D (25-OH-vitamin D(3) <30 nmol/L) and 89.3% were vitamin D insufficient (<75 nmol/L). Preplanned subpopulation comparison (lower vs. upper quartile) revealed a significant negative correlation (P = 0.048) between plasma PTH and 25-OH-vitamin D(3) levels. Fifteen individuals (6.9%) were folic acid deficient (<140 ng/mL RBC folate). Only 9.3% reached RBC folate concentrations regarded as optimal for the prevention of fetal neural tube defects (>400 ng/mL).

Conclusions: The prevalence of hypovitaminosis D in healthy young women trained in health care professions is low but 89.3% can be classified as vitamin D insufficient in spring. Folate status can also be considered not sufficient. Considering the emerging role of higher vitamin D plasma levels for many health conditions, a timely correction of vitamin D status in the general Austrian population appears appropriate.
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http://dx.doi.org/10.1007/s00394-011-0281-5DOI Listing
December 2012

Symptomatic upper extremity deep vein thrombosis as a complication of ambulatory blood pressure monitoring.

Thromb Haemost 2008 Oct;100(4):711-2

Clinical Division of General Internal Medicine, Clinical Department of Internal Medicine, Innsbruck Medical University, Anichstrasse 35, Innsbruck, Austria.

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October 2008

Dabigatran versus enoxaparin after total hip replacement.

Lancet 2007 Dec;370(9604):2002; author reply 2003-4

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http://dx.doi.org/10.1016/S0140-6736(07)61858-3DOI Listing
December 2007

Reduction of soluble P-selectin by statins is inversely correlated with the progression of coronary artery disease.

Int J Cardiol 2006 Jan;106(2):183-90

Clinical Division of General Internal Medicine, Clinical Department of Internal Medicine, Innsbruck Medical University, Austria.

Background: Cell adhesion molecules (CAM) play an important role in the pathogenesis of atherosclerosis by mediating the binding of leukocytes to the endothelium. Soluble CAM isoforms are known to be elevated in the sera of patients suffering from coronary artery disease (CAD).

Methods: We measured the concentrations of soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, P-selectin, platelet endothelial cell adhesion molecule-1, and highly sensitive C-reactive protein (hs-CRP) in the blood of 47 CAD patients before and 6 months after starting statin therapy and in 16 untreated CAD patients. The progression of CAD was monitored by calculating the coronary calcium score using electron beam computed tomography.

Results: Soluble P-selectin (92+/-11 ng/ml vs. 59 +/- 4 ng/ml, p < 0.0001) and hs-CRP (0.92 +/- 0.14 mg/dl vs. 0.42 +/- 0.11 mg/dl, p < 0.001) decreased significantly in the statin-treated group compared to baseline levels. None of the other proteins studied showed significant changes. In contrast to hs-CRP, the reduction of soluble P-selectin concentrations correlated directly with the lowering of total cholesterol (r(2) = 0.236, p < 0.005) and inversely with the progression of CAD (r(2) = 0.393, p < 0.0001).

Conclusions: Our results suggest P-selectin as an additional marker for the beneficial action of statins in patients with CAD.
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http://dx.doi.org/10.1016/j.ijcard.2005.01.042DOI Listing
January 2006

Postprandial, but not postabsorptive low-density lipoproteins increase the expression of intercellular adhesion molecule-1 in human aortic endothelial cells.

Atherosclerosis 2006 May 24;186(1):101-6. Epub 2005 Aug 24.

Clinical Division of General Internal Medicine, Clinical Department of Internal Medicine, Innsbruck Medical University, Anichstr. 35, A-6020 Innsbruck, Austria.

The magnitude of postprandial lipemia has been identified as independent risk factor for the development of coronary artery disease. To test the effect of postprandial versus postabsorptive low-density lipoproteins (LDL) on the expression of adhesion molecules, LDL were isolated from healthy subjects before and 4h after ingestion of a standardized fatty test meal. We used flow cytometry and Northern blotting to quantify cell adhesion molecules in human aortic endothelial cells (HAEC). The adherence of leukocytes to HAEC was analyzed using a monocyte adhesion assay. Incubation of HAEC with postprandial, but not postabsorptive LDL induced a two-fold increase in the surface expression of intercellular adhesion molecule-1 (ICAM-1), but not of E-selectin or vascular cell adhesion molecule-1. In addition, increased amounts of ICAM-1 transcripts were found in HAEC treated with postprandial LDL. The adhesion of monocytes to HAEC was enhanced after pretreatment with postprandial, but not with postabsorptive LDL. We conclude that postprandial, but not postabsorptive LDL increase the surface expression of ICAM-1 in HAEC apparently by de novo protein synthesis leading to increased adhesion of monocytes. The upregulation of ICAM-1 by postprandial LDL may explain part of the proatherogenic effect of high postprandial lipemia.
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http://dx.doi.org/10.1016/j.atherosclerosis.2005.07.014DOI Listing
May 2006

Normal development and fertility of knockout mice lacking the tumor suppressor gene LRP1b suggest functional compensation by LRP1.

Mol Cell Biol 2004 May;24(9):3782-93

Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

LRP1b and the closely related LRP1 are large members of the low-density lipoprotein receptor family. At the protein level LRP1b is 55% identical to LRP1, a multifunctional and developmentally essential receptor with roles in cargo transport and cellular signaling. Somatic LRP1b mutations frequently occur in non-small cell lung cancer and urothelial cancers, suggesting a role in the modulation of cellular growth. In contrast to LRP1, LRP1b-deficient mice develop normally, most likely due to its restricted expression pattern and functional compensation by LRP1 or other receptors. LRP1b is expressed predominantly in the brain, and a differentially spliced form is present in the adrenal gland and in the testis. Despite the presence of a potential furin cleavage site and in contrast to LRP1, immunoblotting for LRP1b reveals the presence of a single 600-kDa polypeptide species. Using a yeast two-hybrid approach, we have identified two intracellular proteins, the postsynaptic density protein 95 and the aryl hydrocarbon receptor-interacting protein, that bind to the intracellular domain of LRP1b. In addition, we have found several potential ligands that bind to the extracellular domain. Analysis of LRP1b knockout mice may provide further insights into the role of LRP1b as a tumor suppressor and into the mechanisms of cancer development.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC387731PMC
http://dx.doi.org/10.1128/mcb.24.9.3782-3793.2004DOI Listing
May 2004

Coaxing the LDL receptor family into the fold.

Cell 2003 Feb;112(3):289-92

Department of Molecular Genetics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.

Low-density-lipoprotein (LDL) receptor family members control diverse developmental and physiological pathways. In this issue of Cell, both Culi and Mann and Hsieh et al. report on Boca/MESD, a highly conserved chaperone required for transport of LDLR family proteins to the cell surface. Together with recent insights into the atomic structure of the LDL receptor, they shed new light on the synthesis and trafficking of this important class of multifunctional receptors.
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http://dx.doi.org/10.1016/s0092-8674(03)00073-4DOI Listing
February 2003

Mouse models as tools for dissecting disorders of lipoprotein metabolism.

Semin Cell Dev Biol 2003 Feb;14(1):25-35

Department of Molecular Genetics, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390-9046, USA.

The overexpression of proteins as transgenes or by adenovirus-mediated gene transfer as well as the disruption of genes by homologous DNA recombination in the mouse provide powerful tools to dissect the role of individual proteins in complex biological pathways. These and similar techniques have been widely used to characterize the function of most of the players involved in lipoprotein metabolism. These models are expected to greatly advance the finding of new therapeutic strategies for the treatment of disorders of lipoprotein metabolism.
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http://dx.doi.org/10.1016/s1084-9521(02)00169-6DOI Listing
February 2003

Association between increased iron stores and impaired endothelial function in patients with hereditary hemochromatosis.

J Am Coll Cardiol 2002 Dec;40(12):2189-94

Department of Internal Medicine, University Hospital, Innsbruck, Austria.

Objectives: We studied associations between iron status and early functional and structural vascular abnormalities in patients with hereditary hemochromatosis (HH).

Background: Iron may be involved in atherogenesis, and patients bearing a genetic mutation associated with HH are possibly at risk of developing coronary heart disease.

Methods: We studied the vascular properties of 41 HH patients who had homozygosity for the C282Y mutation, along with 51 age-matched control subjects, by determination of endothelium-dependent dilation (EDD) of the brachial artery and intima-media thickness (IMT) of the carotid artery.

Results: Male HH patients who were not receiving phlebotomy therapy showed a reduced EDD and increased IMT compared with controls and HH patients receiving therapy. In female HH patients, irrespective of treatment status, vascular parameters were not different from those of controls, and none of these patients had severe iron overload. In HH patients, increased iron load was significantly associated with reduced EDD and increased IMT. Moreover, we found a positive correlation between body iron stores and indicators of oxidative stress. When previously untreated male HH patients were re-investigated after intensive phlebotomy therapy, a significant improvement in EDD was observed (2.6 +/- 1.3% before vs. 5.5 +/- 2.1% after treatment, p = 0.0015).

Conclusions: Impaired endothelial function and increased IMT are associated with iron overload, with subsequent induction of oxidative stress, and are not linked to a genetic disability in HH patients. Consequent iron-depletion therapy normalizes endothelial function and may thus reduce the increased risk of cardiovascular events. Female patients may be at a reduced risk, presumably due to continuous iron loss by menstruation.
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http://dx.doi.org/10.1016/s0735-1097(02)02611-6DOI Listing
December 2002

Transendothelial migration of leukocytes and signalling mechanisms in response to the neuropeptide secretoneurin.

Regul Pept 2002 Apr;105(1):35-46

Department of Internal Medicine, Division of General Internal Medicine, Faculty of Medicine, University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria.

Secretoneurin (SN), a newly discovered neuropeptide, may be implicated in inflammatory responses as it was shown to modulate leukocyte, endothelial and mesenchymal cell functions. Neutrophils placed above pulmonary arterial or venous endothelial monolayers migrated through this cellular barrier in response to apical or basal stimulation with SN in a dose-dependent manner. At optimal concentrations of 10(-6) to 10(-8) M, SN was nearly equally effective in stimulating neutrophil transmigration as was tumor necrosis factor-alpha at 10 ng/ml or a chemotactic gradient of formyl-Met-Leu-Phe (10(-8) M). Stimulation of transendothelial migration appears to be specific, since a trypsin digest of SN was ineffective and excess concentrations of anti-SN antibodies completely abolished the effect. Inhibition of cyclooxygenase or nitric oxide synthase did not affect the action of SN. Preincubation of endothelial cells with pertussistoxin (PTx) or choleratoxin (CTx), and the presence of staurosporine significantly inhibited transmigration, suggesting that SN uses a signalling pathway that is coupled to G-proteins and protein kinase C in endothelium. Moreover, SN treatment resulted in transient elevation of cytoplasmatic calcium concentration in endothelial cells. These data support the hypothesis that SN might contribute to neurogenic inflammation in vivo and reveal signalling mechanisms of SN in endothelial cells.
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http://dx.doi.org/10.1016/s0167-0115(01)00379-2DOI Listing
April 2002

Effect of insulin therapy on endothelium-dependent dilation in type 2 diabetes mellitus.

Am J Cardiol 2002 Feb;89(4):431-4

Department of Internal Medicine, University of Innsbruck, Anichstrasse 35, 6020, Innsbruck, Austria.

Endothelial dysfunction is an early marker of atherosclerosis occurring in patients with type 2 diabetes mellitus. Endothelium-dependent dilation (EDD) has been shown to improve by combined therapy of insulin and metformin. Studies on endothelium-independent vasodilatory capacity, however, have had controversial results. We sought to investigate the vascular reactivity--EDD and endothelium-independent dilation--and their changes induced by the addition of insulin therapy to patients with type 2 diabetes mellitus pretreated with diet and oral hypoglycemic drugs. We therefore performed vascular studies in 21 poorly controlled type 2 diabetic patients and 11 nondiabetic control subjects by using high resolution ultrasound of the brachial artery. After 3 months of additional insulin therapy, vascular and laboratory measurements including C-reactive protein and parameters of glucose and lipoprotein metabolism were repeated. At baseline, EDD was significantly impaired in diabetic patients compared with controls (2.7 +/- 2.2% vs 7.0 +/- 1.8%, p <0.001), whereas endothelium-independent dilation was normal in both groups. After insulin therapy, EDD increased from 2.7 +/- 2.2% to 5.0 +/- 2.8% (p <0.001) in diabetic patients. All other vascular parameters did not change over the treatment period. The absolute change in EDD showed a significant negative correlation with the change in hemoglobin A(1c) (r = -0.67, p <0.001) and with fasting blood glucose (r = -0.84, p <0.001) levels. In contrast, there was no correlation between EDD and the observed changes in lipid and C-reactive protein levels. Our findings demonstrate that insulin therapy has beneficial effects on vascular function, resulting in enhanced EDD, most probably due to an improved glycemic control as the underlying mechanism.
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http://dx.doi.org/10.1016/s0002-9149(01)02266-4DOI Listing
February 2002