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Bad Schallerbach, Austria

Brammen L.,Medical University of Vienna | Steiner S.,University of Leipzig | Berent R.,Center for Cardiovascular Rehabilitation | Sinzinger H.,Institute for Nuclear Medicine
VASA. Zeitschrift für Gefässkrankheiten | Year: 2016

Early non-invasive imaging of atherosclerosis and in particular the detection of lesions at risk with high specificity could significantly affect cardiovascular morbidity and mortality. Conventional nuclear medicine approaches, in particular using autologous radiolabeled lipoproteins, can be related to histopathological findings; however, they fail to identify lesions at risk. Positron emission tomography (PET) tracers with much better physical properties have been examined, the most detailed information being available for F-18-deoxyglucose (FDG) and F-18-sodium fluoride (NaF). These two approaches are sensitive to different biochemical mechanisms, i.e. inflammation and microcalcification. Initial enthusiasm, in particular for F-18-FDG, has disappeared, although for F-18-NaF there is some hope, but this is not a breakthrough. No tracer is available so far that is able to identify a specific characteristic of a lesion prone to rupture. Other PET tracers in the pipeline have been examined, mainly in experimental models and only a few in patients, but they failed to contribute significantly to early lesion discovery and do not support great expectations. The key question is: Do we understand what we see? Moreover, methodological problems, a lack of standardization of imaging protocols and aspects of quantification provide a wide range for potential future improvements. While monitoring a therapeutic intervention seems to be possible for both F-18-FDG and F-18-NaF, highly specific early identification of lesions at risk by PET imaging is still far away. As of today, PET is not ready for routine clinical judgment of atherosclerotic lesions at risk to rupture. Even if all these problems can be solved, radiation exposure will still remain a concern, in particular for repeated studies. Source


Berent R.,Center for Cardiovascular Rehabilitation | Sinzinger H.,Institute for Diagnosis and Treatment of Atherosclerosis and Lipid Disorders ATHOS
Vasa - Journal of Vascular Diseases | Year: 2011

Based upon various platelet function tests and the fact that patients experience vascular events despite taking acetylsalicylic acid (ASA or aspirin), it has been suggested that patients may become resistant to the action of this pharmacological compound. However, the term "aspirin resistance" was created almost two decades ago but is still not defined. Platelet function tests are not standardized, providing conflicting information and cut-off values are arbitrarily set. Intertest comparison reveals low agreement. Even point of care tests have been introduced before appropriate validation. Inflammation may activate platelets, co-medication(s) may interfere significantly with aspirin action on platelets. Platelet function and Cox-inhibition are only some of the effects of aspirin on haemostatic regulation. One single test is not reliable to identify an altered response. Th erefore, it may be more appropriate to speak about "treatment failure" to aspirin therapy than using the term "aspirin resistance". Th ere is no evidence based justification from either the laboratory or the clinical point of view for platelet function testing in patients taking aspirin as well as from an economic standpoint. Until evidence based data from controlled studies will be available the term "aspirin resistance" should not be further used. A more robust monitoring of factors resulting in cardiovascular events such as inflammation is recommended. © 2011 by Hans Huber Publishers, Hogrefe AG, Bern. Source


Sinzinger H.,Institute for Diagnosis and Treatment of Lipid Disorders and Atherosclerosis ATHOS | Sinzinger H.,Wilhelm Auerswald Atherosclerosis Research Group ASF | Sinzinger H.,Medical University of Vienna | Berent R.,Center for Cardiovascular Rehabilitation
Thrombosis Journal | Year: 2012

Background: Postprandial hyperlipidemia and hyperglycemia have been related to cardiovascular events. Among different underlying mechanisms platelet activation seems to be responsible too. No comparable data between various tests in normo- vs. hyperlipidemics before and at different time intervals are available after a fat meal. We aimed to compare 9 of them within the same patients at several time points in postprandial hyperlipidemia.Results: For some tests baseline values between the groups were significantly different (TXB2, platelet sensitivity, sedimentation and WU-test). However, hyperlipidemia revealed a variable influence on the tests examined. Some of the available tests apparently sensitive to show platelet activation reflect the increase in triglycerides (TG), such as the sedimentation index. ADP-induced platelet aggregatory activity in count adjusted washed isolated platelet samples during postprandial hyperlipidemia indicates mildly enhanced platelet activity, but does not seem to induce significant changes in aggregation. In patients with severe hypertriglyceridemia (> 400 mg/dl fasting) changes in platelet function are more pronounced due to delayed decay and may last up to 16 hours paralleling TG reaching the prevalue. The overwhelming majority of platelet function tests do not significantly respond to postprandial hyperlipidemia. The correlation between the tests applied is poor. For standardization purpose, platelet aggregation tests, aimed to examine proaggregatory capacity in atherosclerosis, should only be performed at the same time of the day after a fasting period > 6 hours. The great variation in preanalytical work-up on comparison of various tests, large number of platelet tests available and their respective potential value are discussed.Conclusions: At present, the suspicion that platelet function is significantly activated in the postprandial period cannot be supported by any of the tests used. The information provided is valuable to know for which test and group of patients a fasting period of which duration is recommendable. © 2012 Sinzinger and Berent; licensee BioMed Central Ltd. Source


Auer J.,General Hospital Braunau | Leitner A.,General Hospital Wels | Berent R.,Center for Cardiovascular Rehabilitation | Lamm G.,General Hospital St. Polten | And 2 more authors.
Atherosclerosis | Year: 2010

Background: Although drug-eluting stents (DES) reduce restenosis rates relative to bare-metal stents (BMS), recent reports have indicated that the use of DES may be associated with an increased risk of stent thrombosis. Our study focused on the effect of stent type on clinical outcomes in a " real world" setting. Methods: 889 patients undergoing percutaneous coronary intervention (PCI) with either DES (Cypher or Taxus; n= 490) or BMS (n= 399) were enrolled in a prospective single center registry. The outcome analysis covered a period of up to 3.2 years (mean 2.7 years ± 0.5 years) and was based on 65 deaths, 27 myocardial infarctions, 76 clinically driven target lesion revascularizations (TLR), and 15 angiographically confirmed cases of definite stent thrombosis and was adjusted for differences in baseline characteristics. Results: In total 1277 stents (613 BMS and 664 DES) were implanted in 1215 lesions. Despite a significantly different unadjusted death rate (10.1% and 5.1% in BMS and DES patients, respectively; p<. 0.05), the patient groups did not differ significantly in the risk of myocardial infarction during 2.7 years of follow-up. After adjustment for differences in baseline characteristics between groups, the difference in the cumulative incidence of death did not remain statistically significant (p= 0.22). Target lesion revascularizations occurred significantly less frequently in patients with DES compared to individuals after BMS implantation (5.9% and 11.8% in patients with DES and BMS, respectively; p<. 0.05). The rate of angiographically confirmed stent thrombosis was 2.1% in patients with DES and 1.1% in BMS patients (p= 0.31). There was a significantly lower unadjusted event rate (including deaths, myocardial infarction, target lesion revascularization, and stent thrombosis) in patients with drug-eluting stents than in those with bare-metal stents (16.4% and 25.8%, respectively), with 9.4 fewer such events per 100 patients (unadjusted hazard ratio [HR], 0.64; 95% confidence interval [CI], 0.46 to 0.87). After adjustment, the relative risk for all outcome events in patients with drug-eluting stents was 0.79 (95% CI, 0.67 to 0.95). However, the adjusted relative risk for death and myocardial infarction did not differ significantly between groups (adjusted relative risk in patients with drug-eluting stents 0.94 (95% CI, 0.77 to 1.37)). Conclusions: In this real-world population, the beneficial effect of first generation DES in reducing the need for new revascularization compared with BMS extends to more than 2.5 years without evidence of a worse safety profile. The minor risk of stent thrombosis and myocardial infarction within this period after implantation of DES seems unlikely to outweigh the benefit of these stents. © 2009 Elsevier Ireland Ltd. Source


Eder A.,University of Vienna | Koegl E.,University of Vienna | Von Duvillard S.P.,Norwegian School of Sport Sciences | Von Duvillard S.P.,Center for Cardiovascular Rehabilitation | And 2 more authors.
Archives of Oral Biology | Year: 2012

Arachidonic acid (AA) is metabolized to eicosanoids and isoprostanes (IPs) via different pathways. The presence of granuloma in apical periodontitis (AP) is linked with inflammation and the synthesis of metabolites of AA. Objective: We investigated the conversion rate of 14C labelled arachidonic acid (14C-AA), the lipoxygenases (LOX) products and the endogenous synthesis of eicosanoids and IPs in extracted granuloma. Furthermore, we assessed if there are markers for bone destruction and the influence of cigarette smoking. Patients and methods: In 46 patients with symptoms and corresponding radiological signs of AP, teeth were extracted including the periapical granuloma. The endogenous synthesis of eicosanoids and IPs, the conversion rate of 14C-AA and LOX products in extracted granuloma were analyzed. Results: We found that smoking increases significantly the synthesis of IPs and LOX-metabolites in granuloma. Furthermore, smoking may have contributed to significant differences in qualitative and quantitative profile of eicosanoids, IPs and the conversion rate of 14C-AA independent of the size of the granuloma. Conclusions: Our data demonstrate that in smokers with granuloma due to AP products of lipid peroxidation as 8-iso-PGF 2α and products of the LOX-pathway are increased at the expense of cyclooxygenase products. The size of granuloma did not influence the amount of synthesized eicosanoids, IPs or LOX-metabolites out of 14C-AA whereas cigarette smoking was a significantly influencing and modifiable risk factor. © 2012 Elsevier Ltd. Source

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