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Conclusion The most relevant risk factors for development of CS are age, history of previous AMI, evidence of prior coronary revascularization and multivessel disease compared to AMI patients without CS.

Goliasch, H. Blessberger, J. Wojta, K. Maurer, Ch. Mannhalter, R. Department of Internal Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna Background Acute myocardial infarction at a young age is associated with high morbidity and long-term mortality.

The NADPH oxidase system as a main source of reactive oxygen species in vascular cells has been implicated in development and progression of coronary artery disease.

The homozygote c. In the adjusted logistic regression analysis, we detected a protective effect of the c. In the adjusted model the association was more pronounced with an odds ratio of 0.

Furthermore we could not detect a significant effect for these polymorphisms in the logistic regression analysis. Discussion The present study suggests a protective association between the c.

Jarai, K. Huber, R. Mehran, G. Dangas, G. Stone 3rd Med. However, limited data are available on the association of initial BNP concentrations with frequent co-morbidities left ven- tricular function, anemia, renal dysfunction observed in patients with acute STEMI.

Furthermore, the bleeding risk of patients with high admission BNP levels has also not been investigated yet. Results Patients with higher initial BNP levels had significantly longer time from symptom onset to first balloon inflation min vs min and significantly longer door-to-balloon times min vs 89 min.

In multivariate survival analysis high concentrations of BNP were strong predictors of major bleeding, as well as early and late mortality and stroke but not of ischemic endpoints TVR, reinfarction or stent thrombosis.

Conclusions In the present study we could show that high admission concentrations of BNP are associated with anemia and reduced renal function at admission to the hospital with STEMI but are not related to left ventricular function.

According to the present results, patients with high admission concentrations of BNP are at significantly higher risk of worsening renal function after primary PCI.

The significant association of high BNP levels with bleeding-risk should be evaluated by future studies.

Kaulfersch, G. Grimm Department of Emergency Medicine, National Hospital Klagenfurt Introduction Coronary artery vasospasm, or smooth muscle constriction of the coronary artery, is an important cause of chest pain syndromes that can lead to myocardial infarction, ventricular arrhythmias, and sudden death.

If minimal or no angiographic evidence of coronary artery disease is found in a patient who has recently had angina at rest with transient ST-segment elevation, vasospastic angina is the more likely diagnosis.

Once the diagnosis of coronary artery vasospasm is made, calcium channel blockers and long-acting nitrates may be used for long-term prophylaxis and treatment.

Case Report We report on a 50 year old male patient presenting to the emergency department with acute coronary syndrome a total of 6 times within a 4 month period.

At first presentation ECG showed a prior undiagnosed left bundle branch block. Laboratory testing showed slightly elevated cardiac enzymes.

Coronary angiography revealed small vessel disease without significant stenosis. Angiographic imaging of the right coronary artery showed vasospasm of the proximal RCA.

The patient was treated with aspirin, clopidogrel, statins and amlodipin. One week later the patient was readmitted to our department with acute resting chest pain and significant ST-elevation in the posterior leads.

Angiographic imaging showed no significant stenosis or coronary spasm. CKMB was measured 10 times above normal.

With the assumption of the patient having vasospastic angina he was started on diltiazem 90 mg twice daily. After application of intracoronary nitrate the spasms dissolved with ST-segment resolution.

Diltiazem was increased to mg twice daily. Six weeks later the patient was readmitted with acute coronary syndrome without STsegment changes and slightly elevated cardiac enzymes.

Diltiazem was increased to 90 mg, 5-times daily and nitrates p. After intravenous nitrates were given, he was treated with diltiazem mg, 3-times daily and nitrates 40 mg, twice daily.

The last episode of resting angina was documented one month later. Since then a 12 month period the patient is symptom-free with maximum medical therapy consisting of calcium channel blockers and long-acting nitrates.

Discussion In patients presenting with acute coronary syndrome and haemodynamic stability initial medical treatment should include sublingual, topical, or intravenous nitrate therapy.

Once the diagnosis of coronary artery vasospasm is made, calcium channel blockers and long-acting nitrates may be used for long-term prophylaxis.

Maximum dose vasospastic medical therapy, as shown in our case, may be necessary until the patient achieves long term pain free intervals.

Kraus, J. Altenberger, J. Schuler, M. Two types of Kounis syndrome have been described. We report a case of 2 stepped life threatening Typ II Kounis syndrome leading to acute myocardial infarction following a first time intake of Ibuprofen and recurrence under acetylsalicylicacid ASS therapy.

Case Report A 53 year-old male presented because of acute shortness of breath und severe chest pain. ECG reveals ST- elevation in diaphragmal leads.

Angiography showed diffuse arteriosclerotic plaques and severe spasms in both coronary arteries. After intracoronary Nitroglycerin administration spasms resolved and symptoms improved.

Allergic asthma bronchiale was known for 3 yrs and the patient was on inhalative steroid therapy. Furthermore he suffered from chronic sinusitis and nasal polyps.

Chest pain and dyspnoe occurred 1,5 hours after intake of Ibuprofen mg because of headache. In the meanwhile, while recovering from STEMI, 2 episodes of severe chest pain, hypotension and STelevation in the inferior leads occurred.

The patient was treated with Morphine, Hydrocortisone mg and Diltiazem. Symptomes and ECG changes resolved within 30 minutes. After 7 days the patient was discharged free of symptoms.

NSAIDs, like Ibubrofen, inhibiting Cyclooxygenose 1 are able to cross react with ASS, and inhibit vasodilatatory prostaglandins and cause a predisposition to coronary spasms.

ASS can precipitate asthmatic attacks, and provoke coronary artery spasm. Most cells located in the shoulder region of coronary arterosclerotic plaques, play an important role in the pathophysiology of acute coronary syndrom and myocardial infarction due to allergic plaque rupture like in Kounis II syndromes.

The recurrence of ST -elevation on low dose ASS is probably an effect of the slow process of mast cell degranulation based on the massive reaction due to the Ibuprofen related allergic event.

Currently treatment for mast cell stabilisation is used to avoid mast cell degranulation. In this case ASS seems to play an important role to adhere the allergic reaction, on the other hand prescription of ASS is a Class I Indication for patients suffering myocardial infarction.

Trials have shown ASS desensitization to be feasible. Nevertheless with regard to the massive coronary spasm in this case a provocation test with ASS was not performed for ethical reasons.

We decided to maintain a clopidogrel alone regimen. An important, maybe live saving issue, is to instruct the patient to avoid Ibuprofen in the future.

Mair, T. Ploner, A. Hammerer-Lercher, P. Schratzberger, A. Griesmacher, O. We compared the diagnostic performances of hscTnT with the 4th generation cTnT assay during a period of 2 months in a real world emergency department ED treating mainly adults with medical or neurological emergencies to evaluate potential benefits for routine diagnosis.

It was only ordered in patients treated by internists or neurologists and measured by assays from Roche Diagnostics. Results There were patients with the chief complaint of chest pain and with dyspnea.

The remaining patients suffered from various internal diseases. The overall diagnostic performances for AMI diagnosis of both assay generations were comparable area under receiver operating characteristics curves [AUC] 0.

If for both assays the 99th percentile cut-off limit is used also the early sensitivities on admission are comparable, but the 4th cTnT assay generation looses AMI specificity at 0.

However, with the endpoint detection of any acute or chronic cardiac diseases hs-cTnT is significantly superior to the previous cTnT assay due to its better assay precision at the low measuring range, which cannot be outweighed by lowering the cut-off value of the 4th cTnT assay generation to 0.

Mair, K. Brendel, H. Ott, A. We therefore investigated the prevalence of ASA and clopidogrel low- or no responders in ACS patients with stent implantation on day 2 of coronary care unit CCU stay with pantoprazole treatment 40 mg per day.

In 89 patients drug-eluting and in the remaining patients bare metal stents were implanted. Patients received mg clopidogrel as a loading dose on the first day of hospital stay and 75 mg clopidogrel as maintenance dose per day.

Conclusions Given the low prevalence of clopidogrel 6. Roth, H. Herkner, W. Schreiber, Ch. Diese Studie beinhaltete allerdings nur Patienten, die in weiterer Folge an Intensivstationen behandelt wurden.

Aus diesem Grund soll der Effekt von systolischem Blutdruck bei Aufnahme bzw. Roth et al. Ucar-Altenberger, C.

Avanzini, W. Winkler, C. Wegner, F. Weidinger 2. Methode Eingeschlossen wurden alle Patienten, die im Jahr an unserer Abteilung akut koronarangiographiert wurden.

Suppan1, R. Riedl1, A. Berghold1, B. Pieske2, H. Brussee2, M. Grisold2, O. Luha2, N. Watzinger2 1II. Material und Methode Die Datenerfassung erfolgt standardisiert in den 3 steirischen Herzkatheterzentren.

Es handelt sich hierbei um eine retrospektive Analyse der erhobenen Daten. Tentzeris1, S. Farhan1, R. Jarai1, E.

Samaha1, A. Geppert1, G. Unger1, J. Wojta2, K. Huber1 13rd Med. Methods In total, 1, consecutive patients, who underwent elective or acute PCI, were included in a prospective registry from January until December Forty nine patients had an angiographically proven acute occlusion of the LCX.

Time from presentation to 1st diagnostic angiogram, all-cause mortality and the combined endpoint allcause death and target vessel revascularisation were evaluated during a mean follow-up period of Clinical and angiographic characteristics such as age, gender, arterial hypertension, diabetes mellitus, hyperlipidaemia, previous myocardial infarction, renal dysfunction, heart failure, drug eluting stent implantation, stent length and stent diameter, respectively, were not significantly different between the 2 groups.

Time form presentation to angiogram was Four Seven For both groups clinical longterm outcome was statistically comparable but showed a trend to higher all-cause mortality in patients presenting with NSTEMI, in which diagnostic and therapeutic angiograms were performed delayed.

Patients with ACS and occluded LCX without ST-segment elevation might have a benefit of early revascularisation and should therefore be diagnosed earlier e.

Roth, Ch. Weiser, B. Heidinger, H. Schreiber, C. Former studies reported that this challenging goal usually requires high efforts.

The study was conducted from August, 23rd to September, 20th, The intervention was the availability of a dedicated ET. In the control group no ET was available.

The availability of the ET was randomized to three equally distributed shifts per day morning, day, night. The ET rotas were concealed for clinical staff.

Information about availability of ETs was marked with an alert sign at triage point and registration counter. To compare delay times we used a Mann-Whitney-U-test.

Results During the study period, in total patients received an ECG recording for different reasons. In the interventional group patients This represents a Risk Ratio of 5.

Conclusion Implementing an ECG technician in the ED is feasible to reach a higher percentage of patients within the recommended 10 minutes benchmark of guideline requirements compared to business as usual.

Havel, H. Ein wichtiges Zeitfenster stellt in dieser Hinsicht das Patientendelay dar, welches die Zeit zwischen Beginn des Brustschmerzes und Alarmierung des Rettungsdienstes zeigt.

Durch Massenmedienkampagnen kann das Patientendelay positiv beeinflusst werden. Juli und Anhand dieser wurde das Patientendelay des Jahres analysiert.

Inkludiert wurden alle Patienten, die in diesem Zeitraum ambulant oder durch den Rettungsdienst zugewiesen und mit Myokardinfarkt an unserer Abteilung vorstellig wurden.

August hospitalisiert wurden. Die demographische Daten zeigt Tabelle 4. Vogel, S. Farhan, S. Hahne, I. Kozanli, R. Huber 3rd Med. Department of Internal Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna Background and Aim Due to the fact that there is only few data on long-term mortality in patients with hyperglycemia hospitalized with acute coronary syndrome, this study aimed to show the impact of elevated admission glucose on 4-year mortality in patients with NSTE-ACS.

Vogel et al. Table 5: B. In patients the glucose level at admission was missing, another patients had evident diabetes and were excluded from the analyses.

A follow-up concerning all-cause mortality up to four years was obtained. Results Patient with hyperglycemia were older In-hospital mortality, as well as four-year mortality was higher in patients with hyperglycemia In a Cox proportional hazard model the admission glucose level was an independent predictor for 4-year mortality Table 5.

Conclusion An elevated glucose level in patients hospitalized with acute coronary syndrome without ST-segment elevation is associated with worse long-term outcome.

Wallner, M. Schmidjell, H. Lafenthaler, W. Goebel, J. Westreicher, L. Keiler, S. Karnitschnig, R. Ablauf im Herzkatheterlabor in praxisnahen Flow-Charts abzubilden.

Beer, G. Werba, S. Nickl, A. Mitterbauer, M. Zimmermann, L. Wutzlhofer, H. Ankersmit, M. Lichtenauer Christian Doppler Laboratory for the Diagnosis and Regeneration of Cardiac and Thoracic Diseases, Medical University Vienna Background Chemokines are multifunctional mediators that are involved in development and homeostatic, stem-cell survival, wound healing and immune responses, as well as triggering chemotaxis and angiogenesis.

Diagnostic analysis of cytokines and chemokines in serum or plasma has become an important issue in several disease conditions. However, cytokines and chemokines are usually not considered to be very stable after blood collection, which might therefore alter test results.

Thus, the aim of the pilot study was to obtain better knowledge about stability of these mediators in blood samples for interpretation of test results.

Wallner et al. Holzwart, D. Beer et al. Results Interestingly all examined mediators rise when samples were stored above room temperature for more than 4 hours in serum tubes.

Conclusions These data indicate that most cytokine and chemokine levels remain stable when analyzed within a short interval after venipuncture.

EDTA plasma seems to be the most suitable for stability reasons and should be used for analysis of these mediators. Cardiac metabolism of glucose is very tightly regulated to maintain the variable energy demand that is required by cardiac tissue.

Energy metabolism of the cardiac myocyte can be regulated within seconds up to a few minutes or chronically regulated within the time frame of hours to days.

However, in coronary heart disease, this activation becomes deleterious. In myocardial ischemia, inhibition or decreased gene expression of pyruvate dehydrogense kinase is necessary in order to shift myocardial metabolism towards the fetal phenotype, thus metabolising more glucose than fat in order to preserve myocardial integrity.

Methods Myocardial tissue probes derive from the right auricle of patients undergoing cardiac surgery. A small part of the right auricle is removed when the heart is put on extra-corporal circulation.

By doing so, we are able to compare ischemic and non-ischemic tissue of the same patient. Results In our microarray experiments, we find that, in particular, pyruvate dehydrogense kinase isoform 4 is significantly less expresses under nebivolol both during O2 perfusion and simulated ischemia, an effect practically negligible under atenolol.

Here, nebivolol also exhibits a unique cardio-protective property, different from standard beta-blockers.

We find that, without the influence of beta-blockers, there is no significant regulation of pyruvate dehydrogense kinase-expression during myocardial ischemia.

There is just a trend towards a decrease in pyruvate dehydrogense kinase-Gene expression. There is, however a significant difference between the expression of PDK during myocardial ischemia in the presence of atenolol 3.

Especially patients with angina may profit from this particular property of nebivolol over atenolol. Affymetrix-Microarrays wurden verwendet, um mehr als microRNAs zu analysieren.

Die diastolische Spannung und die Kontraktionskinetik blieben von Sunitinib unbeeinflusst. Im Expressionsmuster der analysierten microRNAs zeigte sich nach 24h kein Unterschied zwischen unbehandelten und mit Sunitinib inkubierten Kardiomyozyten.

Doleschal, P. Rainer, Z. Saad, K. Groschner, H. Pieske, D. Abbildung 6: B. Doleschal et al. Dzilic, M.

Kreibich, M. Hasun, A. Baumgartner, D. Santer, P. Moser, B. Podesser, K. IS and AAR were expressed as percentage of the left ventricle.

However, viable myocardium in the ischemic area AAR-IS was significantly larger in group 2 group 1: In this model, protective effects of different cardioplegic solutions can be evaluated.

Additionally, the decrease of CF after 2h of reperfusion suggests that damage of vital myocardium is further enhanced after a longer reperfusion time.

Thus, improvement of endothelial protection might be an interesting therapeutic target to gain better outcome in these highrisk patients.

Dziodzio1, A Juraszek1, D. Zimpfer1, V. Scheikl1, M. Stoiber1, M. Grimm2, H. Schima1, M. The aim of the study was to evaluate different sites of primary entry tears and the propagation of the dissecting membrane, ante- and retrograde, in an experimental model of acute type B aortic dissection.

Methods The entire thoracic aortic aorta including the supraaortic branches was harvested from 26 adult pigs. An intimal tear of 15 mm was created via contralateral incisions sites 20 mm downstream the origin of the left subclavian artery.

In 13 cases the dissection was created at the concavity and in 13 cases at the convexity. The aortic annulus was then sewn into a silicon ring of a driving chamber.

The distal aorta was connected to a tubing with adjustable resistance elements. The circulation was driven by the pneumatically driven Vienna heart to mimic aortic flow and pressure.

The median antegrade propagation length of the dissecting membrane was 65 mm. The median retrograde propagation length in primary entry tears at the convexity was 20 mm and was stopped by the left subclavian artery.

Conclusions In this experimental model of acute type B aortic dissection, we confirmed that many type B dissections do also have a retrograde component.

At the convexity, this component is stopped by the left subclavian artery as an anatomic barrier. At the concavity, the propagation of the dissecting membrane may extend up to the ascending aorta and may therefore cause retrograde type A dissection.

These findings may substantiate clinical need for treatment of type B dissections with a primary entry tear at the concavity. Gasser, A.

Holzwart, H. For example, a few regulatory T-cells control a wide spectrum of the inflammatory cascade.

Ischemic injury leads to left ventricular remodelling and oxidative stress and inflammation are key elements in this context. Leukocyte-derived markers such as myeloperoxidase MPO correlates with outcome in ischemic heart disease.

In our present work using microarray technique, we have found that, in T-cell mediated immunity generally, a noteworthy down-regulation is brought about by beta-blockers.

From our investigations we suspect that most important, unique pleiotropic effects of nebivolol may be centered around favourable effects upon T-cell mediated response to ischemia.

In our microarray experiments we found an upregulation of MPO expression in the presence of nebivolol as well as in the presence of atenolol both in hypoxic as well as in well oxygenated conditions, as can be seen below.

There is a differential regulation between different beta-blockers during myocardial ischemia, which warrant further investigation.

We believe that there are complex pleiotropic effects of beta-blockers on immunity. Such pleiotropic effects have received more attention recently.

Our preliminary results show that beta-blockers inhibit the expression of T-cell immunity related genes during experimental hypoxia and we find that during experimental ischemia, there is an up-regulation of MPO-expression.

In the light of JUPITER and other recent publications on modulating inflammation by pleiotropic effects of cardiovascular drugs, the specific property of immune modulation by beta-blockers in myocardial ischemia may warrant further attention.

However, a further detailed exploration on both expression and molecular level is certainly needed. Gasser, E. Some exciting developments help elaborate the regulation of PAK activity and identify downstream signalling targets.

Considering these recent findings, we investigate their regulation during experimental myocardial ischemia. Results After 30 minutes of myocardial hypoxia we find that there is no significant regulation of PDK-expression during myocardial ischemia.

There is just a trend towards a decrease in PAK4-Gene expression. There is, however, a significant difference between the expression of PAK4 during myocardial ischemia in the presence of nebivolol 0.

There is, however a significant difference between the expression of DDAH during myocardial ischemia in the presence of atenolol Conclusion In the present study we find that the myocardial expression of DDAH is reduced in the presence of nebivolol in both normoxia as well as hypoxia.

The measured decrease of DDAH seen under nebivolol but not with atenolol both during normoxia and hypoxia could be a measure for the increased availability of NO brought about by nebivolol as a feed back control.

This is of interest since several steps in the pathways of interaction have remained unclear as yet.

Figure 7: R. Gasser et al. The recent advances in understanding these new regulators PAK family and their targets could explain some of the cellular cardioprotective effects that have been attributed to beta-blockers during myocardial ischemia.

Specific cardioprotection of beta-blockers may thus at least partially be explained by PAKs decisive role played in myocardial integrity.

Wolbank2, S. Charwat1, K. Ali1, R. Hofer-Warbinek3, R. Huber4, G. ADMA is recognised as a plasma marker of increased cardiovascular risk but it is unclear whether it ever accumulates to sufficient levels to affect NO pathways.

On the other hand it is possible that a feed back mechanism exists which regulates DDAH expression upon the availability of NO.

In this context, it has to be mentioned that nebivolol can stimulate an increase of endothelial NO, which becomes available at the vascular smooth muscle and induces vaso-relaxation.

Nebivolol seems to interact with the endothelial NO pathway in two complementary ways: it increases NOS activity and reduces the NOscavenging radical superoxide anion, by re-directing deranged NOS activity.

We have previously shown the immediate decrease of the myocardial blood flow after intracoronary mesenchymal stem cell MSC delivery.

Methods Farm pigs were subjected to min occlusion of the mid left anterior descending coronary artery followed by reperfusion.

Myocardial blood flow MBF was measured by combination of pressure wire and special designed infusion catheter under maximal hyperemia caused by adenosine.

The global left ventricular ejection fraction EF was measured 1-month post cell therapy by using magnet resonance imaging MRI. MicroCT of the infarcted hearts were performed using cast preparation method to visualize the microvascularization 1 month after MSC delivery.

Results The baseline parameter, such as number of delivered cells, heart rate, blood pressure and weight were similar in the two groups.

MBF decreased immediately after intracoronary delivery, while no significant change in tissue perfusion could be detected using the percutaneous intramyocardial delivery mode.

Fluorescence immunochemistry indicated higher level of myocardial expression of different homing tenascin, cadherin and integrin and angiogenic factors FGF-2 and VEGF in the infarcted area and at the border zone, in the intramyocardial group.

Increase in EF was significantly higher in the intramyocardial group, as compared to the animals in the intracoronary delivery group 0. MicroCT presented a higher capillary density in the infarcted area in the intramyocardial group as compared to a heart of intracoronary delivery group.

Conclusions Intracoronary stem cell delivery led to increased myocardial expression of MMP2 and reduced CXCR4 expression with attenuated functional recovery of the infarcted heart.

Hemetsberger, W. Sperker, C. Strehblow, C. Csonka, I. Pavo, D. Glogar, J. Waltenberger, M. The aim of the present study was to evaluate the association between intimal inflammation and intimal apoptosis in relation to neointimal development after intracoronary administration of Ac-YVad.

Terminal transferase-mediated dUTP nick end labeling TUNEL was carried out to calculate the percentage of the number of apoptotic cells in relation to the total number of intimal cells.

Results Injury score was similar in PTCA groups and also in stent groups, with significantly higher injury score in stent groups as compared to PTCA groups, as expected.

Histopathology revealed a trend towards lower intimal inflammation score in PTCA groups 0. Hohendanner, N. MacQuaide, G.

Antoons, B. Pieske, K. Sipido, F. Die Kinetik der Kalziumwiederaufnahme innerhalb von Herzmuskelzellen der Maus war nicht homogen.

Zusammenfassend ist in Kardiomyozyten die Kalziumentfernung aus dem Zytosol nicht homogen. Holfeld, D. Zimpfer, J. Dumfarth, C. Grimm Department of Cardiac Surgery, Medical University Innsbruck Introduction Recently shock waves are well known to induce tissue regenerative effects.

Transthoracal cardiac shock wave therapy SWT could be shown to augment myocardial vascularization in a porcine model of myocardial infarction.

SWT even improves myocardial perfusion and causes relief of angina symptoms in humans with severe coronary artery disease. Nevertheless the underlying mechanism remains largely unknown.

Cardiac function was evaluated using echocardiography. Angiogenesis was evaluated by analysis of several RNA and protein expressions.

Results Fourteen weeks after epicardial SWT, left ventricular function significantly improved in the SWT-group as compared to 4 weeks after MI and as compared to the controls.

Quantitative histology revealed more vital cells and more endothelial cells in the SWT group. In peripheral blood higher numbers of circulating endothelial progenitor cells could be detected in the treatment group.

Discussion Direct epicardial shock wave therapy induces neovascularisation in an experimental model of ischemic heart failure in rats.

High numbers of circulating endothelial progenitor cells can be found in the peripheral blood. These findings indicate that one of the main mechanisms of SWT may be recruitment of vessel forming cells.

Lichtenauer, G. Werba, M. Mildner, A. Baumgartner, A. Megerle, M. Podesser, H. Over the last decades research has focused on finding therapies to reduce inflammatory reactions after an ischaemic event.

Of relevance are reports showing that infusion of apoptotic leucocytes or anti-lymphocyte serum after AMI can reduce myocardial necrosis and preserves cardiac function.

In order to corroborate this therapeutic mechanism, the utilisation of immunosuppressive agents with a comparable mechanism such as anti-thymocyte globulin ATG was evaluated in this study.

Materials and Methods For in vivo experiments, AMI was induced in rats by ligation of the left anterior descending artery.

Untreated and sham operated animals served as controls. Histological evaluations were performed 3 days after AMI in order to analyze angiogenic cell populations in the infarcted myocardium.

Cardiac function was analyzed by echocardiography six weeks after induction of MI. Determination of infarction size was conducted by planimetry.

Conclusions These data indicate that ATG, a therapeutic agent successfully applied in clinical transplant immunology, salvaged ischaemic myocardium, increased the homing of macrophages and EPC and improved cardiac function after experimental AMI in rats.

Baumgartner, G. Werba, L. Beer, M. Clinical trials of cell based therapy after AMI evidenced only a moderate benefit. Of clinical relevance are reports that demonstrated that infusion of apoptotic cells lead to an initiation of immunosuppressive mechanisms.

Based on these reports, we hypothesized that injection of apoptotic cells into ischaemic myocardium reduces inflammatory reactions after AMI. Sham operated animals and rats injected with control medium or viable cells served as controls.

Tissue specimens were obtained 72 hours after induction of AMI to analyze the cellular infiltrate within the ischaemic myocardium.

Cardiac function was analyzed by echocardiography and infarction size was determined by planimetry after 6 weeks. Results Rats that were injected with irradiated apoptotic PBMC showed enhanced homing of macrophages and endothelial progenitor cells EPC within 72 hours as compared to controls.

Lichtenauer et al. Conclusions Based on these data we conclude that apoptotic cells induce the expression of pro-angiogenic factors necessary for attraction of regenerative cells to sites of ischaemia.

Intravenous and intramyocardial injection of apoptotic cell suspensions results in attenuation of myocardial remodelling after experimental AMI, preserves left ventricular function and increases homing of regenerative cells.

Lichtenauer, M. Mildner, M. Zimmermann, B. Podesser, W. Sipos, E. Tschachler, M. Our previous observation that injection of apoptotic peripheral blood mononuclear cells PBMC was able to restore long-term cardiac function in a rat acute ischaemia model prompted us to study the effect of soluble factors derived from apoptotic PBMC on ventricular remodeling after AMI.

Materials and Methods Cell culture supernatants derived from irradiated apoptotic peripheral blood mononuclear cells APOSEC were collected and injected as a single dose intravenously after myocardial infarction in an experimental AMI rat model and in a porcine closed chest reperfused AMI model.

Magnetic resonance imaging MRI and echocardiography were used to quantitate cardiac function. Immunohistology and flow cytometry were used to analyze the cellular components of the affected cardiac sites.

Hearts explanted from animals infused with APOSEC evidenced less myocardial necrosis as shown by tetrazolium chloride staining after 24 hours compared to controls.

Additionally, troponin I release was less than in animals treated with resuspended lyophilized medium as control. Figure 9: M. This effect seems to be due to the activation of pro-survival signalling cascades in the affected cardiomyocytes and to a higher presence of regenerative cells EPC and macrophages within the ischaemic tissue.

Muendlein, C. Saely, N. Stark, K. Geiger, S. Geller-Rhomberg, P. Rein, A. Vonbank, H. Potential links between these polymorphisms and coronary artery disease CAD are unclear and are addressed in the present study.

Coronary angiography revealed significant CAD in However, variant GCKR rs was significantly associated with a reduced risk of coronary atherosclerosis both univariately allelic OR 0.

Because this association is independent from fasting glucose, the polymorphism appears to be linked to CAD via non-glucose mechanisms.

Pavo, A. Poovathinkal, A. Posa, S. Charwat, S. Wolbank, G. Maurer, M. In our present experiment we have investigated the chemotactic signal of MSC for hematopoietic stem and progenitor cell HPC recruitment.

Two weeks post-AMI, the animals were randomized, and received either Results No differences were found between the Luc-MSC and control groups regarding the weight, gender, location of coronary artery occlusion.

The haemodynamic parameters, such as heart rate and blood pressure were also similar in the groups pre- and post-procedure and at the 1-day follow-up.

Myocardial expression of CXCR4 was significantly elevated at the injections site of infarction 0. Conclusion Intracardially injected MSC contribute to recruitment and homing of the autologous hematopoietic stem and progenitor cells, probably due to their paracrine effect, expressing chemotactic signals for cardiac accumulation of HSC.

Poovathinkal, I. Posa, G. Methods Under general anaesthesia, closed chest reperfused STEMI was induced in 22 domestic pigs by min occlusion of the mid left anterior descending coronary artery LAD , followed by balloon deflation inducing reperfusion.

The pigs were then allowed to recover. The total number of circulating leukocytes were measured, and the percentage proportion of the mononuclear cells were calculated by qualitative differential blood analysis.

Similarly, the absolute number of PB mononuclear cells increased too. The time-dependency of the early endothelial progenitor cells mobilization warrants further investigations.

Primessnig, P. Rainer, M. Wallner, R. Gasser, H. Trauner, B. Schwarzl et al. Schwarzl1, P. Steendijk2, St. Huber1, H. Obermayer-Pietsch1, B.

Pieske1, H. Experimental data also indicate a positive inotropic effect of MH. However, increased noradrenalin levels and shivering in awake and anaesthetized patients might reflect sympathetic activation, which would be an adverse side effect of MH after cardiac arrest.

We aimed to study, whether or not MH further excites sympathetic activation after resuscitation. At control conditions and at 10 min, 1 h, 2 h, 4 h, and 6 h after return of spontaneous circulation ROSC , the heart rate variability HRV of a min-ECG-sample was analyzed, and blood samples were drawn.

The high-frequent-fraction HF, 0. Adrenaline, noradrenaline and dopamine levels were measured via commercial RIA-kits.

Figure M. Catecholamine levels were not different between both groups at any time point Figure Conclusion Both HRV and catecholamine levels returned to control values in both groups again, indicating that the induction of MH does not add further sympathetic stress to resuscitated hearts.

Thus, beneficial effects of MH on cardiac function do not rely on an increased sympathetic tone. Steendijk2, S. Truschnig-Wilders1, B.

In normal and resuscitated porcine hearts, MH exerts a positive inotropic effect and reduces whole body oxygen demand. Hypothesis The induction of MH is a beneficial intervention in acute ischemic heart failure.

Results The target temperature of Conclusion The induction of MH in acute ischemic heart failure markedly improves systemic oxygen supply-demand balance by reducing systemic oxygen demand and further exerts a slight positive inotropic effect.

These data warrant clinical studies of MH as a rescue intervention in acute heart failure and cardiogenic shock. Stojkovic, C.

Kaun, G. Maurer, K. Huber, J. Wojta, S. Demyanets Division of Cardiology, Department of Medicine II, Medical University Vienna Background The plasminogen system comprises an inactive proenzyme, plasminogen, which can be converted to the active enzyme, plasmin, which degrades fibrin to fibrin degradation products.

Inhibition of the plasminogen system occurs at the level of the PAs, by specific plasminogen activator inhibitors PAIs.

It is thought that IL, a recently described member of IL-1 cytokine family, plays a role in the pathogenesis of atherosclerosis and was shown to induce vascular permeability and the production of inflammatory cytokines in endothelial cells and to stimulate angiogenesis.

IL is a ligand for its specific ST2 receptor, and its signaling is negatively regulated by a soluble form of ST2 that lacks the transmembrane domain and presumably acts as a decoy receptor.

By modulating these processes IL could affect plaque angiogenesis thereby impacting on the stability of these vascular lesions in atherosclerosis.

Baumgartner, M. Hasun, M. Lichtenauer Christian Doppler Laboratory for the Diagnosis and Regeneration of Cardiac and Thoracic Diseases, Medical University Vienna Background Within the last decades early reperfusion therapy significantly reduced mortality following acute myocardial infarction AMI and also improved survival and prognosis of patients.

However, the development of chronic ischaemic heart disease and congestive heart failure represents one of the most frequent causes of hospitalization in developed countries.

We have previously shown that injection of apoptotic cells improves left ventricular function after acute experimental myocardial infarction in rats.

In this study we sought to investigate changes in the composition of the fibrotic scar tissue after AMI. Materials and Methods Cell suspensions of apoptotic cells were injected intravenously or intramyocardially after experimental AMI induced by coronary artery ligation in rats.

Immunohistological analysis was performed to analyze the cellular infiltrate in the ischaemic myocardium. Six weeks after induction of AMI the scar tissue was examined for the ratio of collagenous and elastic fibres.

Cardiac function was quantified by echocardiography. Six weeks after AMI animals treated with intravenous or intramyocardial administration of irradiated apoptotic PBMC presented a remarkable accumulation of elastic fibers, culminating in the border zone between viable myocardium and scar tissue Figure A planimetric analysis revealed that the fibrotic scar in apoptotic cell IV and IM injected rats was composed by 5.

Werba et al. Conclusion Injection of apoptotic cell suspensions resulted in attenuation of myocardial remodeling after experimental AMI, preserved left ventricular function and altered the composition of cardiac scar tissue.

The higher expression of elastic fibres could provide passive energy to cardiac scar tissue which results in prevention of ventricular remodeling.

Avanzini, B. Freudenthaler, A. Bastovansky, F. Weidinger, P. Wexberg 2. Table 6: P. Bartko et al. Reduced left ventricular contractility needs further evaluation of the amount of residual viability as revealed by 18FDG-PET to estimate the potential of functional improvement.

Bartko1, S. Graf1, A. Khorsand1, R. Rosenhek1, J. Bergler-Klein1, M. Dumesnil4, IG. Burwash3, R. Beanlands3, M. Clavel4, H. Baumgartner5, P.

Pibarot4, G. Subsequently we arranged segments into groups: viable normal and mismatch versus reduced viability match and scar and normal versus scar.

Sub-analysis showed normal segments and 22 scarred segments. PLS values for different viability states are shown in Table 6.

ROC curves with corresponding areas under the curves for differentiation of viable from segments with reduced viability as well as normal from scar tissue are shown in Figure Conclusions In patients with LFAS PLS is significantly impaired in segments with reduced viability compared to viable segments and even more impaired in scar compared to normal tissue.

Dobutamine administration improves differentiation of viable from segments with reduced viability by PLS with best performance at LDD levels.

PLS in the setting of DSE in patients with LFAS may provide a new tool to discriminate different states of viability, especially to differentiate scar from normal myocardial tissue.

Berger1, W. Dichtl1, M. Seger2, M. Hintringer1, O. Pachinger1, Ch. Baumgartner2, B. Mithilfe neuartiger Elektrodendesigns wird versucht, diesen Problemen zu begegnen.

Jude Medical Inc. Berger et al. Narbenarealen und der CS Anatomie planbar sein. Buchmayr, C. Steinwender, W. Wichert I.

Die Untersuchung erfolgte im Sinusrhythmus. Die Auswertung erfolgte unmittelbar nach Ende der Untersuchung. Hier erfolgte eine perkutane Koronarintervention.

Freudenthaler, M. Bastovansky, A. Get your limited edition tee now before its too late! Vom by Dout on Wie funktioniert das Ganze?

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Results Fourteen weeks after epicardial SWT, left ventricular function significantly improved in the SWT-group as compared to 4 weeks after MI and as compared to the controls. Int J Cancer 94 2 : Springer Medizin Verlag, HeidelbergS. Therefore, frequent assessment of cardiac function and close clinical observation has been considered essential in these patients. Conclusions Given the low prevalence of clopidogrel 6. Poovathinkal, A. Chest pain and dyspnoe occurred 1,5 hours after intake of Ibuprofen mg because of headache. Hangler, J. Cerny, J. Department of Gods Of ägypt Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Spiele Pai Gow Poker - Video Slots Online Aims Pre-treatment with clopidogrel results in a reduction of ischemic 2 Löwen in elective coronary interventions.

Mit dieser Methode wird die Blase direkt inspiziert und ein makroskopischer Tumor bzw. Hingegen ist die Knochenszintigrafie als nuklearmedizinische Untersuchung nur bei klinischer Symptomatik indiziert.

Magnetresonanztomographie und Computertomographie sind keine obligaten Untersuchungsmethoden, um die lokale Ausbreitung aufzuzeigen.

Abbildung - Zystoskopie der Harnblase 45 Einleitung 17 1. Dabei wird ca. Mittels elektrischen Stroms kann nun das erkrankte Gewebe mit Hilfe einer Schlinge unter optischer Kontrolle abgetragen werden.

Um den hohen Rezidivraten entgegenzuwirken, werden verschiedene Substanzen adjuvant in die Harnblase instilliert. Jedoch gibt es auch andere Daten, die zeigen, dass mit der Instillationstherapie die Rezidivrate bei dieser Gruppe gesenkt werden kann.

Im individuellen Fall kann demnach eine adjuvante Therapie gerechtfertigt sein und eine einmalige Gabe von Mitomycin C erfolgen 28, 47, Studien haben gezeigt, dass besonders diese Gruppe von der Instillationstherapie profitiert 10, In diesen Studien ist beschrieben worden, dass neben Mitomycin C und Epirubicin auch Gemcitabin verwendet werden kann.

Diese Zytostatika zeigen nur geringe Nebenwirkungen. Gemcitabin ist bislang noch als experimentell anzusehen Pansadoro et al.

Es kann zu Dysurie, Zystitiden und rezidivierenden Temperaturen kommen. Nach einer medianen Laparotomie und Inzision des Peritoneums wird die radikale Zystektomie mit der beidseitigen Entfernung der pelvinen Lymphknoten begonnen.

Eine Art der inkontinenten Harnableitung ist die Ureterkutaneostomie. Dabei wird der Ureter in die Haut implantiert. Diese Form kommt v.

Dabei wird zwischen Ureter und Haut ein Darmsegment interponiert. Diese Form wird v. Die Komplikationsraten halten sich in akzeptablen Grenzen 59, Dabei wird aus ca.

Seltener wird die Anlage eines katheterisierbaren Pouches, z. Dabei werden verschiedene Zytostatika kombiniert verabreicht. Genauer wird dazu im Abschnitt 1.

Sowohl Pectasides et al. Alternativ wird eine Kombination von Gemcitabin mit Cisplatin eingesetzt. Dies sind z. Die Ermittlung der Tumormarker stellt beim Patienten ein minimal invasives Verfahren dar Blutabnahme und ist im Vergleich zu bildgebenen Verfahren weniger belastend.

Physiologischerweise wird diese Art von Antigenen in der Embryo- und Fetalzeit exprimiert. Richtwert, Graubereich und Halbwertszeit sind in Tabelle angegeben.

Falsch positive Werte findet man bei Rauchern Einleitung 27 1. Dieser Tumormarker leitet sich vom LewisBlutgruppensystem ab.

Aber auch beim Gallengangskarzinom, Magenkarzinom und Colonkarzinom spielt es eine wichtige Rolle als Marker. Lymphknotenmetastasen in der Literatur beschrieben 54, 61, Nach Erhalt der histologischen Untersuchung wird eine Korrelation zum Tumorstadium erfolgen.

Alter oder Geschlecht. Material und Methoden 29 2 Material und Methoden Die prospektiven Untersuchungen wurden von der lokalen Ethikkommission positiv bewertet Nr.

Im Einzelnen waren dies sechs Patienten mit Material und Methoden 30 Plattenepithelkarzinom, drei Patienten mit Prostatakarzinom, jeweils zwei Patienten hatten ein in die Harnblase metastasiertes Mammakarzinom bzw.

Ein Patient litt an einem sarkomatoiden Karzinom. Ergab die Histologie einen benignen Befund, wie z. Material und Methoden 31 2. Ziel ist es, ein Signal am Epitop deutlich zu erkennen.

Deshalb wird heutzutage eher das Protein Streptavidin aus dem Pilz Streptomyces avidinii verwendet. Mittels Lichtmikroskop kann man das Antigen nun spezifisch in oder auf der Zelle nachweisen.

Das Enzym Peroxidase ist endogen in Blutzellen vorhanden. Material und Methoden 35 2. Dieser ist mit Biotin konjungiert.

Material und Methoden 36 8. Die Ergebnisse wurden drei Gruppen zugeordnet und dokumentiert. Dabei gab es ebenfalls drei Gruppen.

Tabelle stellt dies noch einmal grafisch dar. Wieder wurden die Serumergebnisse in die bekannten drei Gruppen unterteilt. Differenziert wurde zwischen Patienten, die einen nicht invasiven Tumor aufwiesen, d.

Auch dies ist in Tabelle grafisch dargestellt. Serumkonzentration von CEA u. CA 2. Material und Methoden 39 2.

Statistisch signifikant sind solche Werte, deren p- Wert kleiner als 0,05 ist. Ergebnisse 40 3 Ergebnisse 3. Sie wird ermittelt, indem man Ergebnisse mittels Kalibratoren und Kontrollproben wiederholt.

Dies waren insgesamt sechs Patienten mit Plattenepithelkarzinom, drei Patienten mit Prostatakarzinom, Ergebnisse 41 zwei Patienten mit einem in die Harnblase metastasierten Mammakarzinom, zwei mit einem endokrinen Tumor und ein Patient mit einem sarkomatoiden Karzinom.

Von den verbliebenen Patienten ergab die histologische Untersuchung des Operationsresektates bei Patienten ein Urothelkarzinom.

Bei 71 Patienten zeigte sich eine benigne Histologie, sodass diese Patienten als Kontrollgruppe fungierten. Der Median des Alters aller untersuchten Patienten betrug 69,3 Jahre.

Der Median des Alters bei den 51 weiblichen Patienten lag bei 68,4 Jahren. Die Tumorgruppe wurde in zwei Fraktionen aufgeteilt.

Die andere Gruppe zeigte histologisch ein muskelinvasives Tumorstadium, d. In diese Gruppe wurden insgesamt 38 Patienten eingeordnet. Jeweils 19 Patienten hatten einen pT2 Tumor bzw.

Dies ist in Abbildung graphisch dargestellt. Abbildung - Geschlechterverteilung zwischen Tumor- und Kontrollgruppe Ergebnisse 3.

In den Klammern ist jeweils die Standardabweichung angegeben. Die restlichen 17 Patienten zeigten ein muskelinvasives Tumorwachstum. Als graphische Darstellung dient Abbildung Siehe hierzu auch Abbildung Lymphogen bereits metastasierte Tumoren untereinander verglichen.

Siehe hierzu Abbildung Vergleiche hierzu auch Abbildung Insgesamt musste diese Diagnose bei neun Patienten gestellt werden.

Sie errechnet sich aus der Anzahl der richtig- positiv getesteten Werte geteilt durch die Summe der richtig- positiven und der falschnegativen Werte.

Sie errechnet sich aus der Anzahl der richtig- negativen Ergebnisse geteilt durch die Summe der richtig- negativen und der falsch- positiven Werte.

Ergebnisse 57 3. Dies ist vereinbar mit der serologischen Untersuchung. Ergebnisse 61 3. Dies entspricht der Grenze des Referenzwertes. Ergebnisse 64 3.

Der Patient wies ein Tumorstadium pT3-G3 auf. Der Patient wies ebenfalls einen pT3-G3 Tumor auf. Immunhistochemisch kann sich ein ganz anderes Bild darstellen.

Allerdings kann zudem festgehalten werden, dass sich das immunhistochemische Ergebnis mit der Aussage deckt, dass CA ansteigt, je schlechter differenziert der Tumor ist.

Die Signifikanz ist mit einem p- Wert von 0, deutlich Abbildung Siehe dazu auch Tabelle sowie die Abbildungen Bis heute existieren lediglich einzelne Fallberichte zu diesem Thema.

Unter anderem haben Inai et al. Dabei haben wir neben der Serumbestimmung der beiden Tumormarker auch eine immunhistochemische Gewebeuntersuchung vorgenommen und die Ergebnisse untereinander korreliert.

Diskussion 74 Untersuchungen von Margel et al. Die Arbeitsgruppe um Chuang et al. CEA und CA haben sich in der Diagnostik gastrointestinaler Tumoren bereits im klinischen Alltag etabliert und werden hier auch mit Erfolg eingesetzt.

Dazu haben wir prospektiv die Serumkonzentrationen der Tumormarker mit dem histologischen Ergebnis korreliert. Das prospektiv untersuchte Patientenkollektiv bestand insgesamt aus Personen, die mit dem Verdacht auf einen malignen Befund der Harnblase in der urologischen Klinik vorstellig wurden.

Die Ergebnisse wurden dann mit dem Tumorstadium korreliert. Patienten mit einem histologisch benignen Befund dienten als Kontrollgruppe.

Albers P: Harnableitung nach Zystektomie. In: J Urol , In: Curr Opin Urol, , Sep; 17 5 In: Cancer Res, , 5. A systematic Review. In: BJU Int. In: Urologe B , ; In: Ann Oncol.

No abstract available. In: Oncology. Epub Aug 4. Anhang II 9. In: Urology, ; In: Int J Cancer, 86, Burch JD, Rohan T. In: Int J Cancer, 44, 4 : In: Urol Int ; BTA quantitative assay and NMP22 testing compared with urine cytology in the detection of transitional cell carcinoma of the bladder.

Urol Int. In: Scand J Urol Nephrol, , Anhang III In: Br J Cancer ; Cristina M, Villanueva et al. In: Am. In: Crit Rev Oncol Hematol ; Duffy, MJ: Carcinoembryonic antigen as a marker for colorectal cancer: is it clinically useful?

In: Clin Chem, ; 47 4 : Anhang IV In: Der Onkologe, , 9; In: Cancer, 45 7 Suppl , In: Eur Urol, , Fortuny J, Kogevinas M et al.

In: BMC Urol. Gasser T: Basiswissen Urologie. Springer Medizin Verlag, Heidelberg , S. In: J Urol, , Anhang V In: J Urol, , 4 : In: Cancer Invest.

Review In: Eur J Surg Oncol. Epub Nov 9. In: J Urol, , 2 : In: Semin. Cancer Biol, , 9 2 : 81 Anhang VI In: Der Urologe, , Hegele A: Harnblasenkarzinom- State of the Art.

In: Pharma Fokus Onkologie, 5. The predefined primary endpoint of Table 1: C. Adlbrecht et al. Patient characteristics with or without available 24h ECG were similar Table 1.

Beta-blocker medication was not associated with SVES in regression analysis standardized beta 0. However, SVES increased. Distelmaier, C.

Adlbrecht, J. Jakowitsch, O. Wagner, Ch. Gerner, I. Lang, M. Kubicek Division of Cardiology, Department of Medicine II, Medical University Vienna Aims Thrombotic occlusion of an epicardial coronary artery upon atherosclerotic plaque rupture is considered the ultimate and key step in acute myocardial infarction AMI.

The pathophysiological mechanisms of coronary thrombus formation in AMI are still not fully deciphered. Methods and Results We have analyzed soluble and particulate thrombus material aspirated from the ruptured plaque site of nondiabetic patients with ST-elevation myocardial infarction using proteomic techniques.

When culprit site derived plasma was compared to systemic plasma we observed a prominent differential regulation of complement cascade components and a decrease of anti-thrombotic pigment epithelial derived factor PEDF.

ELISA showed PEDF, which is known to have a protective role in atherothrombosis to be relatively decreased at the culprit site with a level of expression that is inversely correlated with local matrix metalloproteinase 9 MMP-9 activities.

In vitro, culprit site plasma displayed enhanced proteolytic activity towards PEDF. Edlinger, H. Alber, K. Pachinger, H.

Schuchlenz, P. Siostrzonek, F. Department of Internal Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna Aims Pre-treatment with clopidogrel results in a reduction of ischemic events in elective coronary interventions.

Data on upstream clopidogrel in the setting of primary percutaneous coronary intervention PCI is limited.

Multiple logistic regression analysis including major confounding factors and stratified for the participating centres was performed to investigate the independent effect of pre-treatment with clopidogrel on in-hospital mortality.

On univariate analysis, clopidogrel pre-treatment was associated with a reduced in-hospital mortality 3. After adjustment for major confounders in multivariate analysis, clopidogrel pre-treatment remained a strong and independent predictor of in-hospital mortality OR 0.

Conclusion Clopidogrel pre-treatment before arrival at the PCI centre is associated with reduced in-hospital mortality compared with peri-interventional treatment in a real world setting of primary PCI.

Petener, G. Grimm, H. Krappinger, O. Pachinger, F. Roithinger, G. Zenker, F. This may lead to missed opportunities for prompt reperfusion therapy.

Baseline characteristics, treatment, culprit artery distribution and in-hospital outcome were compared. Results The prevalence of total occlusion was In patients with total occlusion, the culprit lesion was more frequently located in the arteries supplying the infero-lateral territory circumflex, CX; right coronary artery, RCA compared to patients with patent arteries CX: Eitel, S.

Desch, G. Schuler, H. Variable Table 3: G. Currently, the risk factors for development of CS are poorly determined.

Results Patients in CS were significantly older Neither smoking, nor the presence of hypertension, hyperlipidemia, diabetes or anterior wall infarctions showed higher risk for CS, but patients with CS had higher rates of prior AMI, percutaneous coronary intervention and coronary artery bypass grafts, had higher degrees of multi vessel disease and showed less rates of sinus rhythm at presentation Table 3.

Conclusion The most relevant risk factors for development of CS are age, history of previous AMI, evidence of prior coronary revascularization and multivessel disease compared to AMI patients without CS.

Goliasch, H. Blessberger, J. Wojta, K. Maurer, Ch. Mannhalter, R. Department of Internal Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna Background Acute myocardial infarction at a young age is associated with high morbidity and long-term mortality.

The NADPH oxidase system as a main source of reactive oxygen species in vascular cells has been implicated in development and progression of coronary artery disease.

The homozygote c. In the adjusted logistic regression analysis, we detected a protective effect of the c. In the adjusted model the association was more pronounced with an odds ratio of 0.

Furthermore we could not detect a significant effect for these polymorphisms in the logistic regression analysis.

Discussion The present study suggests a protective association between the c. Jarai, K. Huber, R. Mehran, G. Dangas, G.

Stone 3rd Med. However, limited data are available on the association of initial BNP concentrations with frequent co-morbidities left ven- tricular function, anemia, renal dysfunction observed in patients with acute STEMI.

Furthermore, the bleeding risk of patients with high admission BNP levels has also not been investigated yet.

Results Patients with higher initial BNP levels had significantly longer time from symptom onset to first balloon inflation min vs min and significantly longer door-to-balloon times min vs 89 min.

In multivariate survival analysis high concentrations of BNP were strong predictors of major bleeding, as well as early and late mortality and stroke but not of ischemic endpoints TVR, reinfarction or stent thrombosis.

Conclusions In the present study we could show that high admission concentrations of BNP are associated with anemia and reduced renal function at admission to the hospital with STEMI but are not related to left ventricular function.

According to the present results, patients with high admission concentrations of BNP are at significantly higher risk of worsening renal function after primary PCI.

The significant association of high BNP levels with bleeding-risk should be evaluated by future studies. Kaulfersch, G. Grimm Department of Emergency Medicine, National Hospital Klagenfurt Introduction Coronary artery vasospasm, or smooth muscle constriction of the coronary artery, is an important cause of chest pain syndromes that can lead to myocardial infarction, ventricular arrhythmias, and sudden death.

If minimal or no angiographic evidence of coronary artery disease is found in a patient who has recently had angina at rest with transient ST-segment elevation, vasospastic angina is the more likely diagnosis.

Once the diagnosis of coronary artery vasospasm is made, calcium channel blockers and long-acting nitrates may be used for long-term prophylaxis and treatment.

Case Report We report on a 50 year old male patient presenting to the emergency department with acute coronary syndrome a total of 6 times within a 4 month period.

At first presentation ECG showed a prior undiagnosed left bundle branch block. Laboratory testing showed slightly elevated cardiac enzymes.

Coronary angiography revealed small vessel disease without significant stenosis. Angiographic imaging of the right coronary artery showed vasospasm of the proximal RCA.

The patient was treated with aspirin, clopidogrel, statins and amlodipin. One week later the patient was readmitted to our department with acute resting chest pain and significant ST-elevation in the posterior leads.

Angiographic imaging showed no significant stenosis or coronary spasm. CKMB was measured 10 times above normal.

With the assumption of the patient having vasospastic angina he was started on diltiazem 90 mg twice daily. After application of intracoronary nitrate the spasms dissolved with ST-segment resolution.

Diltiazem was increased to mg twice daily. Six weeks later the patient was readmitted with acute coronary syndrome without STsegment changes and slightly elevated cardiac enzymes.

Diltiazem was increased to 90 mg, 5-times daily and nitrates p. After intravenous nitrates were given, he was treated with diltiazem mg, 3-times daily and nitrates 40 mg, twice daily.

The last episode of resting angina was documented one month later. Since then a 12 month period the patient is symptom-free with maximum medical therapy consisting of calcium channel blockers and long-acting nitrates.

Discussion In patients presenting with acute coronary syndrome and haemodynamic stability initial medical treatment should include sublingual, topical, or intravenous nitrate therapy.

Once the diagnosis of coronary artery vasospasm is made, calcium channel blockers and long-acting nitrates may be used for long-term prophylaxis.

Maximum dose vasospastic medical therapy, as shown in our case, may be necessary until the patient achieves long term pain free intervals.

Kraus, J. Altenberger, J. Schuler, M. Two types of Kounis syndrome have been described. We report a case of 2 stepped life threatening Typ II Kounis syndrome leading to acute myocardial infarction following a first time intake of Ibuprofen and recurrence under acetylsalicylicacid ASS therapy.

Case Report A 53 year-old male presented because of acute shortness of breath und severe chest pain. ECG reveals ST- elevation in diaphragmal leads.

Angiography showed diffuse arteriosclerotic plaques and severe spasms in both coronary arteries. After intracoronary Nitroglycerin administration spasms resolved and symptoms improved.

Allergic asthma bronchiale was known for 3 yrs and the patient was on inhalative steroid therapy. Furthermore he suffered from chronic sinusitis and nasal polyps.

Chest pain and dyspnoe occurred 1,5 hours after intake of Ibuprofen mg because of headache. In the meanwhile, while recovering from STEMI, 2 episodes of severe chest pain, hypotension and STelevation in the inferior leads occurred.

The patient was treated with Morphine, Hydrocortisone mg and Diltiazem. Symptomes and ECG changes resolved within 30 minutes. After 7 days the patient was discharged free of symptoms.

NSAIDs, like Ibubrofen, inhibiting Cyclooxygenose 1 are able to cross react with ASS, and inhibit vasodilatatory prostaglandins and cause a predisposition to coronary spasms.

ASS can precipitate asthmatic attacks, and provoke coronary artery spasm. Most cells located in the shoulder region of coronary arterosclerotic plaques, play an important role in the pathophysiology of acute coronary syndrom and myocardial infarction due to allergic plaque rupture like in Kounis II syndromes.

The recurrence of ST -elevation on low dose ASS is probably an effect of the slow process of mast cell degranulation based on the massive reaction due to the Ibuprofen related allergic event.

Currently treatment for mast cell stabilisation is used to avoid mast cell degranulation. In this case ASS seems to play an important role to adhere the allergic reaction, on the other hand prescription of ASS is a Class I Indication for patients suffering myocardial infarction.

Trials have shown ASS desensitization to be feasible. Nevertheless with regard to the massive coronary spasm in this case a provocation test with ASS was not performed for ethical reasons.

We decided to maintain a clopidogrel alone regimen. An important, maybe live saving issue, is to instruct the patient to avoid Ibuprofen in the future.

Mair, T. Ploner, A. Hammerer-Lercher, P. Schratzberger, A. Griesmacher, O. We compared the diagnostic performances of hscTnT with the 4th generation cTnT assay during a period of 2 months in a real world emergency department ED treating mainly adults with medical or neurological emergencies to evaluate potential benefits for routine diagnosis.

It was only ordered in patients treated by internists or neurologists and measured by assays from Roche Diagnostics. Results There were patients with the chief complaint of chest pain and with dyspnea.

The remaining patients suffered from various internal diseases. The overall diagnostic performances for AMI diagnosis of both assay generations were comparable area under receiver operating characteristics curves [AUC] 0.

If for both assays the 99th percentile cut-off limit is used also the early sensitivities on admission are comparable, but the 4th cTnT assay generation looses AMI specificity at 0.

However, with the endpoint detection of any acute or chronic cardiac diseases hs-cTnT is significantly superior to the previous cTnT assay due to its better assay precision at the low measuring range, which cannot be outweighed by lowering the cut-off value of the 4th cTnT assay generation to 0.

Mair, K. Brendel, H. Ott, A. We therefore investigated the prevalence of ASA and clopidogrel low- or no responders in ACS patients with stent implantation on day 2 of coronary care unit CCU stay with pantoprazole treatment 40 mg per day.

In 89 patients drug-eluting and in the remaining patients bare metal stents were implanted. Patients received mg clopidogrel as a loading dose on the first day of hospital stay and 75 mg clopidogrel as maintenance dose per day.

Conclusions Given the low prevalence of clopidogrel 6. Roth, H. Herkner, W. Schreiber, Ch. Diese Studie beinhaltete allerdings nur Patienten, die in weiterer Folge an Intensivstationen behandelt wurden.

Aus diesem Grund soll der Effekt von systolischem Blutdruck bei Aufnahme bzw. Roth et al. Ucar-Altenberger, C. Avanzini, W. Winkler, C. Wegner, F.

Weidinger 2. Methode Eingeschlossen wurden alle Patienten, die im Jahr an unserer Abteilung akut koronarangiographiert wurden. Suppan1, R. Riedl1, A.

Berghold1, B. Pieske2, H. Brussee2, M. Grisold2, O. Luha2, N. Watzinger2 1II. Material und Methode Die Datenerfassung erfolgt standardisiert in den 3 steirischen Herzkatheterzentren.

Es handelt sich hierbei um eine retrospektive Analyse der erhobenen Daten. Tentzeris1, S. Farhan1, R. Jarai1, E.

Samaha1, A. Geppert1, G. Unger1, J. Wojta2, K. Huber1 13rd Med. Methods In total, 1, consecutive patients, who underwent elective or acute PCI, were included in a prospective registry from January until December Forty nine patients had an angiographically proven acute occlusion of the LCX.

Time from presentation to 1st diagnostic angiogram, all-cause mortality and the combined endpoint allcause death and target vessel revascularisation were evaluated during a mean follow-up period of Clinical and angiographic characteristics such as age, gender, arterial hypertension, diabetes mellitus, hyperlipidaemia, previous myocardial infarction, renal dysfunction, heart failure, drug eluting stent implantation, stent length and stent diameter, respectively, were not significantly different between the 2 groups.

Time form presentation to angiogram was Four Seven For both groups clinical longterm outcome was statistically comparable but showed a trend to higher all-cause mortality in patients presenting with NSTEMI, in which diagnostic and therapeutic angiograms were performed delayed.

Patients with ACS and occluded LCX without ST-segment elevation might have a benefit of early revascularisation and should therefore be diagnosed earlier e.

Roth, Ch. Weiser, B. Heidinger, H. Schreiber, C. Former studies reported that this challenging goal usually requires high efforts.

The study was conducted from August, 23rd to September, 20th, The intervention was the availability of a dedicated ET.

In the control group no ET was available. The availability of the ET was randomized to three equally distributed shifts per day morning, day, night.

The ET rotas were concealed for clinical staff. Information about availability of ETs was marked with an alert sign at triage point and registration counter.

To compare delay times we used a Mann-Whitney-U-test. Results During the study period, in total patients received an ECG recording for different reasons.

In the interventional group patients This represents a Risk Ratio of 5. Conclusion Implementing an ECG technician in the ED is feasible to reach a higher percentage of patients within the recommended 10 minutes benchmark of guideline requirements compared to business as usual.

Havel, H. Ein wichtiges Zeitfenster stellt in dieser Hinsicht das Patientendelay dar, welches die Zeit zwischen Beginn des Brustschmerzes und Alarmierung des Rettungsdienstes zeigt.

Durch Massenmedienkampagnen kann das Patientendelay positiv beeinflusst werden. Juli und Anhand dieser wurde das Patientendelay des Jahres analysiert.

Inkludiert wurden alle Patienten, die in diesem Zeitraum ambulant oder durch den Rettungsdienst zugewiesen und mit Myokardinfarkt an unserer Abteilung vorstellig wurden.

August hospitalisiert wurden. Die demographische Daten zeigt Tabelle 4. Vogel, S. Farhan, S. Hahne, I.

Kozanli, R. Huber 3rd Med. Department of Internal Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna Background and Aim Due to the fact that there is only few data on long-term mortality in patients with hyperglycemia hospitalized with acute coronary syndrome, this study aimed to show the impact of elevated admission glucose on 4-year mortality in patients with NSTE-ACS.

Vogel et al. Table 5: B. In patients the glucose level at admission was missing, another patients had evident diabetes and were excluded from the analyses.

A follow-up concerning all-cause mortality up to four years was obtained. Results Patient with hyperglycemia were older In-hospital mortality, as well as four-year mortality was higher in patients with hyperglycemia In a Cox proportional hazard model the admission glucose level was an independent predictor for 4-year mortality Table 5.

Conclusion An elevated glucose level in patients hospitalized with acute coronary syndrome without ST-segment elevation is associated with worse long-term outcome.

Wallner, M. Schmidjell, H. Lafenthaler, W. Goebel, J. Westreicher, L. Keiler, S. Karnitschnig, R. Ablauf im Herzkatheterlabor in praxisnahen Flow-Charts abzubilden.

Beer, G. Werba, S. Nickl, A. Mitterbauer, M. Zimmermann, L. Wutzlhofer, H. Ankersmit, M. Lichtenauer Christian Doppler Laboratory for the Diagnosis and Regeneration of Cardiac and Thoracic Diseases, Medical University Vienna Background Chemokines are multifunctional mediators that are involved in development and homeostatic, stem-cell survival, wound healing and immune responses, as well as triggering chemotaxis and angiogenesis.

Diagnostic analysis of cytokines and chemokines in serum or plasma has become an important issue in several disease conditions. However, cytokines and chemokines are usually not considered to be very stable after blood collection, which might therefore alter test results.

Thus, the aim of the pilot study was to obtain better knowledge about stability of these mediators in blood samples for interpretation of test results.

Wallner et al. Holzwart, D. Beer et al. Results Interestingly all examined mediators rise when samples were stored above room temperature for more than 4 hours in serum tubes.

Conclusions These data indicate that most cytokine and chemokine levels remain stable when analyzed within a short interval after venipuncture.

EDTA plasma seems to be the most suitable for stability reasons and should be used for analysis of these mediators. Cardiac metabolism of glucose is very tightly regulated to maintain the variable energy demand that is required by cardiac tissue.

Energy metabolism of the cardiac myocyte can be regulated within seconds up to a few minutes or chronically regulated within the time frame of hours to days.

However, in coronary heart disease, this activation becomes deleterious. In myocardial ischemia, inhibition or decreased gene expression of pyruvate dehydrogense kinase is necessary in order to shift myocardial metabolism towards the fetal phenotype, thus metabolising more glucose than fat in order to preserve myocardial integrity.

Methods Myocardial tissue probes derive from the right auricle of patients undergoing cardiac surgery. A small part of the right auricle is removed when the heart is put on extra-corporal circulation.

By doing so, we are able to compare ischemic and non-ischemic tissue of the same patient. Results In our microarray experiments, we find that, in particular, pyruvate dehydrogense kinase isoform 4 is significantly less expresses under nebivolol both during O2 perfusion and simulated ischemia, an effect practically negligible under atenolol.

Here, nebivolol also exhibits a unique cardio-protective property, different from standard beta-blockers.

We find that, without the influence of beta-blockers, there is no significant regulation of pyruvate dehydrogense kinase-expression during myocardial ischemia.

There is just a trend towards a decrease in pyruvate dehydrogense kinase-Gene expression. There is, however a significant difference between the expression of PDK during myocardial ischemia in the presence of atenolol 3.

Especially patients with angina may profit from this particular property of nebivolol over atenolol. Affymetrix-Microarrays wurden verwendet, um mehr als microRNAs zu analysieren.

Die diastolische Spannung und die Kontraktionskinetik blieben von Sunitinib unbeeinflusst. Im Expressionsmuster der analysierten microRNAs zeigte sich nach 24h kein Unterschied zwischen unbehandelten und mit Sunitinib inkubierten Kardiomyozyten.

Doleschal, P. Rainer, Z. Saad, K. Groschner, H. Pieske, D. Abbildung 6: B. Doleschal et al. Dzilic, M. Kreibich, M.

Hasun, A. Baumgartner, D. Santer, P. Moser, B. Podesser, K. IS and AAR were expressed as percentage of the left ventricle.

However, viable myocardium in the ischemic area AAR-IS was significantly larger in group 2 group 1: In this model, protective effects of different cardioplegic solutions can be evaluated.

Additionally, the decrease of CF after 2h of reperfusion suggests that damage of vital myocardium is further enhanced after a longer reperfusion time.

Thus, improvement of endothelial protection might be an interesting therapeutic target to gain better outcome in these highrisk patients.

Dziodzio1, A Juraszek1, D. Zimpfer1, V. Scheikl1, M. Stoiber1, M. Grimm2, H. Schima1, M. The aim of the study was to evaluate different sites of primary entry tears and the propagation of the dissecting membrane, ante- and retrograde, in an experimental model of acute type B aortic dissection.

Methods The entire thoracic aortic aorta including the supraaortic branches was harvested from 26 adult pigs.

An intimal tear of 15 mm was created via contralateral incisions sites 20 mm downstream the origin of the left subclavian artery.

In 13 cases the dissection was created at the concavity and in 13 cases at the convexity. The aortic annulus was then sewn into a silicon ring of a driving chamber.

The distal aorta was connected to a tubing with adjustable resistance elements. The circulation was driven by the pneumatically driven Vienna heart to mimic aortic flow and pressure.

The median antegrade propagation length of the dissecting membrane was 65 mm. The median retrograde propagation length in primary entry tears at the convexity was 20 mm and was stopped by the left subclavian artery.

Conclusions In this experimental model of acute type B aortic dissection, we confirmed that many type B dissections do also have a retrograde component.

At the convexity, this component is stopped by the left subclavian artery as an anatomic barrier. At the concavity, the propagation of the dissecting membrane may extend up to the ascending aorta and may therefore cause retrograde type A dissection.

These findings may substantiate clinical need for treatment of type B dissections with a primary entry tear at the concavity.

Gasser, A. Holzwart, H. For example, a few regulatory T-cells control a wide spectrum of the inflammatory cascade.

Ischemic injury leads to left ventricular remodelling and oxidative stress and inflammation are key elements in this context.

Leukocyte-derived markers such as myeloperoxidase MPO correlates with outcome in ischemic heart disease. In our present work using microarray technique, we have found that, in T-cell mediated immunity generally, a noteworthy down-regulation is brought about by beta-blockers.

From our investigations we suspect that most important, unique pleiotropic effects of nebivolol may be centered around favourable effects upon T-cell mediated response to ischemia.

In our microarray experiments we found an upregulation of MPO expression in the presence of nebivolol as well as in the presence of atenolol both in hypoxic as well as in well oxygenated conditions, as can be seen below.

There is a differential regulation between different beta-blockers during myocardial ischemia, which warrant further investigation. We believe that there are complex pleiotropic effects of beta-blockers on immunity.

Such pleiotropic effects have received more attention recently. Our preliminary results show that beta-blockers inhibit the expression of T-cell immunity related genes during experimental hypoxia and we find that during experimental ischemia, there is an up-regulation of MPO-expression.

In the light of JUPITER and other recent publications on modulating inflammation by pleiotropic effects of cardiovascular drugs, the specific property of immune modulation by beta-blockers in myocardial ischemia may warrant further attention.

However, a further detailed exploration on both expression and molecular level is certainly needed.

Gasser, E. Some exciting developments help elaborate the regulation of PAK activity and identify downstream signalling targets.

Considering these recent findings, we investigate their regulation during experimental myocardial ischemia. Results After 30 minutes of myocardial hypoxia we find that there is no significant regulation of PDK-expression during myocardial ischemia.

There is just a trend towards a decrease in PAK4-Gene expression. There is, however, a significant difference between the expression of PAK4 during myocardial ischemia in the presence of nebivolol 0.

There is, however a significant difference between the expression of DDAH during myocardial ischemia in the presence of atenolol Conclusion In the present study we find that the myocardial expression of DDAH is reduced in the presence of nebivolol in both normoxia as well as hypoxia.

The measured decrease of DDAH seen under nebivolol but not with atenolol both during normoxia and hypoxia could be a measure for the increased availability of NO brought about by nebivolol as a feed back control.

This is of interest since several steps in the pathways of interaction have remained unclear as yet. Figure 7: R. Gasser et al. The recent advances in understanding these new regulators PAK family and their targets could explain some of the cellular cardioprotective effects that have been attributed to beta-blockers during myocardial ischemia.

Specific cardioprotection of beta-blockers may thus at least partially be explained by PAKs decisive role played in myocardial integrity.

Wolbank2, S. Charwat1, K. Ali1, R. Hofer-Warbinek3, R. Huber4, G. ADMA is recognised as a plasma marker of increased cardiovascular risk but it is unclear whether it ever accumulates to sufficient levels to affect NO pathways.

On the other hand it is possible that a feed back mechanism exists which regulates DDAH expression upon the availability of NO. In this context, it has to be mentioned that nebivolol can stimulate an increase of endothelial NO, which becomes available at the vascular smooth muscle and induces vaso-relaxation.

Nebivolol seems to interact with the endothelial NO pathway in two complementary ways: it increases NOS activity and reduces the NOscavenging radical superoxide anion, by re-directing deranged NOS activity.

We have previously shown the immediate decrease of the myocardial blood flow after intracoronary mesenchymal stem cell MSC delivery.

Methods Farm pigs were subjected to min occlusion of the mid left anterior descending coronary artery followed by reperfusion. Myocardial blood flow MBF was measured by combination of pressure wire and special designed infusion catheter under maximal hyperemia caused by adenosine.

The global left ventricular ejection fraction EF was measured 1-month post cell therapy by using magnet resonance imaging MRI. MicroCT of the infarcted hearts were performed using cast preparation method to visualize the microvascularization 1 month after MSC delivery.

Results The baseline parameter, such as number of delivered cells, heart rate, blood pressure and weight were similar in the two groups.

MBF decreased immediately after intracoronary delivery, while no significant change in tissue perfusion could be detected using the percutaneous intramyocardial delivery mode.

Fluorescence immunochemistry indicated higher level of myocardial expression of different homing tenascin, cadherin and integrin and angiogenic factors FGF-2 and VEGF in the infarcted area and at the border zone, in the intramyocardial group.

Increase in EF was significantly higher in the intramyocardial group, as compared to the animals in the intracoronary delivery group 0. MicroCT presented a higher capillary density in the infarcted area in the intramyocardial group as compared to a heart of intracoronary delivery group.

Conclusions Intracoronary stem cell delivery led to increased myocardial expression of MMP2 and reduced CXCR4 expression with attenuated functional recovery of the infarcted heart.

Hemetsberger, W. Sperker, C. Strehblow, C. Csonka, I. Pavo, D. Glogar, J. Waltenberger, M. The aim of the present study was to evaluate the association between intimal inflammation and intimal apoptosis in relation to neointimal development after intracoronary administration of Ac-YVad.

Terminal transferase-mediated dUTP nick end labeling TUNEL was carried out to calculate the percentage of the number of apoptotic cells in relation to the total number of intimal cells.

Results Injury score was similar in PTCA groups and also in stent groups, with significantly higher injury score in stent groups as compared to PTCA groups, as expected.

Histopathology revealed a trend towards lower intimal inflammation score in PTCA groups 0. Hohendanner, N. MacQuaide, G.

Antoons, B. Pieske, K. Sipido, F. Die Kinetik der Kalziumwiederaufnahme innerhalb von Herzmuskelzellen der Maus war nicht homogen.

Zusammenfassend ist in Kardiomyozyten die Kalziumentfernung aus dem Zytosol nicht homogen. Holfeld, D. Zimpfer, J. Dumfarth, C.

Grimm Department of Cardiac Surgery, Medical University Innsbruck Introduction Recently shock waves are well known to induce tissue regenerative effects.

Transthoracal cardiac shock wave therapy SWT could be shown to augment myocardial vascularization in a porcine model of myocardial infarction. SWT even improves myocardial perfusion and causes relief of angina symptoms in humans with severe coronary artery disease.

Nevertheless the underlying mechanism remains largely unknown. Cardiac function was evaluated using echocardiography. Angiogenesis was evaluated by analysis of several RNA and protein expressions.

Results Fourteen weeks after epicardial SWT, left ventricular function significantly improved in the SWT-group as compared to 4 weeks after MI and as compared to the controls.

Quantitative histology revealed more vital cells and more endothelial cells in the SWT group. In peripheral blood higher numbers of circulating endothelial progenitor cells could be detected in the treatment group.

Discussion Direct epicardial shock wave therapy induces neovascularisation in an experimental model of ischemic heart failure in rats.

High numbers of circulating endothelial progenitor cells can be found in the peripheral blood. These findings indicate that one of the main mechanisms of SWT may be recruitment of vessel forming cells.

Lichtenauer, G. Werba, M. Mildner, A. Baumgartner, A. Megerle, M. Podesser, H. Over the last decades research has focused on finding therapies to reduce inflammatory reactions after an ischaemic event.

Of relevance are reports showing that infusion of apoptotic leucocytes or anti-lymphocyte serum after AMI can reduce myocardial necrosis and preserves cardiac function.

In order to corroborate this therapeutic mechanism, the utilisation of immunosuppressive agents with a comparable mechanism such as anti-thymocyte globulin ATG was evaluated in this study.

Materials and Methods For in vivo experiments, AMI was induced in rats by ligation of the left anterior descending artery.

Untreated and sham operated animals served as controls. Histological evaluations were performed 3 days after AMI in order to analyze angiogenic cell populations in the infarcted myocardium.

Cardiac function was analyzed by echocardiography six weeks after induction of MI. Determination of infarction size was conducted by planimetry.

Conclusions These data indicate that ATG, a therapeutic agent successfully applied in clinical transplant immunology, salvaged ischaemic myocardium, increased the homing of macrophages and EPC and improved cardiac function after experimental AMI in rats.

Baumgartner, G. Werba, L. Beer, M. Clinical trials of cell based therapy after AMI evidenced only a moderate benefit.

Of clinical relevance are reports that demonstrated that infusion of apoptotic cells lead to an initiation of immunosuppressive mechanisms.

Based on these reports, we hypothesized that injection of apoptotic cells into ischaemic myocardium reduces inflammatory reactions after AMI.

Sham operated animals and rats injected with control medium or viable cells served as controls. Tissue specimens were obtained 72 hours after induction of AMI to analyze the cellular infiltrate within the ischaemic myocardium.

Cardiac function was analyzed by echocardiography and infarction size was determined by planimetry after 6 weeks. Results Rats that were injected with irradiated apoptotic PBMC showed enhanced homing of macrophages and endothelial progenitor cells EPC within 72 hours as compared to controls.

Lichtenauer et al. Conclusions Based on these data we conclude that apoptotic cells induce the expression of pro-angiogenic factors necessary for attraction of regenerative cells to sites of ischaemia.

Intravenous and intramyocardial injection of apoptotic cell suspensions results in attenuation of myocardial remodelling after experimental AMI, preserves left ventricular function and increases homing of regenerative cells.

Lichtenauer, M. Mildner, M. Zimmermann, B. Podesser, W. Sipos, E. Tschachler, M. Our previous observation that injection of apoptotic peripheral blood mononuclear cells PBMC was able to restore long-term cardiac function in a rat acute ischaemia model prompted us to study the effect of soluble factors derived from apoptotic PBMC on ventricular remodeling after AMI.

Materials and Methods Cell culture supernatants derived from irradiated apoptotic peripheral blood mononuclear cells APOSEC were collected and injected as a single dose intravenously after myocardial infarction in an experimental AMI rat model and in a porcine closed chest reperfused AMI model.

Magnetic resonance imaging MRI and echocardiography were used to quantitate cardiac function. Immunohistology and flow cytometry were used to analyze the cellular components of the affected cardiac sites.

Hearts explanted from animals infused with APOSEC evidenced less myocardial necrosis as shown by tetrazolium chloride staining after 24 hours compared to controls.

Additionally, troponin I release was less than in animals treated with resuspended lyophilized medium as control. Figure 9: M. This effect seems to be due to the activation of pro-survival signalling cascades in the affected cardiomyocytes and to a higher presence of regenerative cells EPC and macrophages within the ischaemic tissue.

Muendlein, C. Saely, N. Stark, K. Geiger, S. Geller-Rhomberg, P. Rein, A. Vonbank, H. Potential links between these polymorphisms and coronary artery disease CAD are unclear and are addressed in the present study.

Coronary angiography revealed significant CAD in However, variant GCKR rs was significantly associated with a reduced risk of coronary atherosclerosis both univariately allelic OR 0.

Because this association is independent from fasting glucose, the polymorphism appears to be linked to CAD via non-glucose mechanisms. Pavo, A. Poovathinkal, A.

Posa, S. Charwat, S. Wolbank, G. Maurer, M. In our present experiment we have investigated the chemotactic signal of MSC for hematopoietic stem and progenitor cell HPC recruitment.

Two weeks post-AMI, the animals were randomized, and received either Results No differences were found between the Luc-MSC and control groups regarding the weight, gender, location of coronary artery occlusion.

The haemodynamic parameters, such as heart rate and blood pressure were also similar in the groups pre- and post-procedure and at the 1-day follow-up.

Myocardial expression of CXCR4 was significantly elevated at the injections site of infarction 0. Conclusion Intracardially injected MSC contribute to recruitment and homing of the autologous hematopoietic stem and progenitor cells, probably due to their paracrine effect, expressing chemotactic signals for cardiac accumulation of HSC.

Poovathinkal, I. Posa, G. Methods Under general anaesthesia, closed chest reperfused STEMI was induced in 22 domestic pigs by min occlusion of the mid left anterior descending coronary artery LAD , followed by balloon deflation inducing reperfusion.

The pigs were then allowed to recover. The total number of circulating leukocytes were measured, and the percentage proportion of the mononuclear cells were calculated by qualitative differential blood analysis.

Similarly, the absolute number of PB mononuclear cells increased too. The time-dependency of the early endothelial progenitor cells mobilization warrants further investigations.

Primessnig, P. Rainer, M. Wallner, R. Gasser, H. Trauner, B. Schwarzl et al. Schwarzl1, P. Steendijk2, St.

Huber1, H. Obermayer-Pietsch1, B. Pieske1, H. Experimental data also indicate a positive inotropic effect of MH. However, increased noradrenalin levels and shivering in awake and anaesthetized patients might reflect sympathetic activation, which would be an adverse side effect of MH after cardiac arrest.

We aimed to study, whether or not MH further excites sympathetic activation after resuscitation. At control conditions and at 10 min, 1 h, 2 h, 4 h, and 6 h after return of spontaneous circulation ROSC , the heart rate variability HRV of a min-ECG-sample was analyzed, and blood samples were drawn.

The high-frequent-fraction HF, 0. Adrenaline, noradrenaline and dopamine levels were measured via commercial RIA-kits. Figure M. Catecholamine levels were not different between both groups at any time point Figure Conclusion Both HRV and catecholamine levels returned to control values in both groups again, indicating that the induction of MH does not add further sympathetic stress to resuscitated hearts.

Thus, beneficial effects of MH on cardiac function do not rely on an increased sympathetic tone. Steendijk2, S. Truschnig-Wilders1, B.

In normal and resuscitated porcine hearts, MH exerts a positive inotropic effect and reduces whole body oxygen demand.

Hypothesis The induction of MH is a beneficial intervention in acute ischemic heart failure. Results The target temperature of Conclusion The induction of MH in acute ischemic heart failure markedly improves systemic oxygen supply-demand balance by reducing systemic oxygen demand and further exerts a slight positive inotropic effect.

These data warrant clinical studies of MH as a rescue intervention in acute heart failure and cardiogenic shock. Stojkovic, C.

Kaun, G. Maurer, K. Huber, J. Wojta, S. Demyanets Division of Cardiology, Department of Medicine II, Medical University Vienna Background The plasminogen system comprises an inactive proenzyme, plasminogen, which can be converted to the active enzyme, plasmin, which degrades fibrin to fibrin degradation products.

Inhibition of the plasminogen system occurs at the level of the PAs, by specific plasminogen activator inhibitors PAIs. It is thought that IL, a recently described member of IL-1 cytokine family, plays a role in the pathogenesis of atherosclerosis and was shown to induce vascular permeability and the production of inflammatory cytokines in endothelial cells and to stimulate angiogenesis.

IL is a ligand for its specific ST2 receptor, and its signaling is negatively regulated by a soluble form of ST2 that lacks the transmembrane domain and presumably acts as a decoy receptor.

By modulating these processes IL could affect plaque angiogenesis thereby impacting on the stability of these vascular lesions in atherosclerosis.

Baumgartner, M. Hasun, M. Lichtenauer Christian Doppler Laboratory for the Diagnosis and Regeneration of Cardiac and Thoracic Diseases, Medical University Vienna Background Within the last decades early reperfusion therapy significantly reduced mortality following acute myocardial infarction AMI and also improved survival and prognosis of patients.

However, the development of chronic ischaemic heart disease and congestive heart failure represents one of the most frequent causes of hospitalization in developed countries.

We have previously shown that injection of apoptotic cells improves left ventricular function after acute experimental myocardial infarction in rats.

In this study we sought to investigate changes in the composition of the fibrotic scar tissue after AMI. Materials and Methods Cell suspensions of apoptotic cells were injected intravenously or intramyocardially after experimental AMI induced by coronary artery ligation in rats.

Immunohistological analysis was performed to analyze the cellular infiltrate in the ischaemic myocardium. Six weeks after induction of AMI the scar tissue was examined for the ratio of collagenous and elastic fibres.

Cardiac function was quantified by echocardiography. Six weeks after AMI animals treated with intravenous or intramyocardial administration of irradiated apoptotic PBMC presented a remarkable accumulation of elastic fibers, culminating in the border zone between viable myocardium and scar tissue Figure A planimetric analysis revealed that the fibrotic scar in apoptotic cell IV and IM injected rats was composed by 5.

Werba et al. Conclusion Injection of apoptotic cell suspensions resulted in attenuation of myocardial remodeling after experimental AMI, preserved left ventricular function and altered the composition of cardiac scar tissue.

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