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Biomedical subjects

Bernd Eber

Publications and source records attributed to Bernd Eber.

At least 55 records · Page 3Linked to original sources
PubMed2003

[Platelet glycoprotein IIb/IIIa inhibitors in coronary artery disease].

BACKGROUND: Inhibition of platelet activity at the injured coronary plaque is a target for novel therapeutic strategies. One of these mechanisms is the blockade of the platelet surface membrane glycoprotein (GP) IIb/IIIa receptor, which binds circulating fibrinogen or von Willebrand factor and crosslinks platelets as the final common pathway to platelet aggregation. Intravenous agents directed against this receptor include the chimeric monoclonal antibody fragment abciximab, the peptide inhibitor eptifibatide and nonpeptide mimetics tirofiban and lamifiban. RESULTS: During percutaneous coronary intervention, an absolute reduction of 1.5-6.5% in the 30-day risk of death, myocardial infarction or repeat urgent revascularization has been observed, with some variability in treatment effect among the agents tested. Treatment effect is achieved early with every modality of revascularization and maintained over the long-term up to 3 years. Increased bleeding risk may be minimized by reduction and weight adjustment of concomitant heparin dosing. In the acute coronary syndromes without ST segment elevation, absolute 1.5-3.2% reductions in 30-day rates of death or myocardial infarction have been achieved with 2- to 4-day courses of eptifibatide or tirofiban. Clinical benefit accrues during the period of drug infusion and is durable. Treatment effect may be enhanced among patients undergoing early coronary revascularization, with evidence of stabilization before intervention and suppression of postprocedural ischemic events. CONCLUSION: Thus, blockade of the platelet GP IIb/IIIa receptor reduces ischemic complications when used as an adjunct to percutaneous coronary intervention or the management of acute ischemic syndromes.

Abciximab↗
PubMed2003

Systemic embolism from a large descending aortic thrombus.

With the advent of transesophageal echocardiography (TEE), thrombi of the aorta are becoming increasingly recognized as possible sources of systemic emboli. This report describes a 58-year-old woman with multiple unexplained peripheral emboli. A giant thrombus of the descending aorta has been identified as the source of systemic thromboembolism. The patient refused surgery and was treated successfully with long-term anticoagulation.

Anticoagulants↗
PubMed2003

Clinical and angiographic outcome after cutting balloon angioplasty.

The cutting balloon is a new device for coronary angioplasty, that, by the combination of incision and dilatation of the plaque, is believed to be promising for treatment of in-stent restenosis. The purpose of the study was to evaluate the safety and efficacy of CBA. We reviewed the immediate and 6-month follow-up angiographic and clinical outcome of 147 patients (109 men and 38 women) with a mean age of 67.3 +/- 10 undergoing this procedure at eight interventional centers in Austria. The target lesions treated with CBA were in-stent restenosis in 61% of patients, stenosis after balloon angioplasty in 8% of patients, and native lesions in 33% of patients. Sixty-five percent of the patients included had multivessel disease. Lesion type was A in 18% of patients, B1 in 31% of patients, B2 in 39% of patients, and C in 12% of patients. The degree of stenosis was 87% +/- 9%, the length of the target lesion treated with CBA was 8.8 +/- 5.1 mm. Target vessel was left circumflex artery in 22 cases, right coronary artery in 36 cases, and left anterior descending artery in 89 cases. The overall procedural success rate was 90.5%. "Stand-alone" CBA was performed in 63% of patients, the procedure was combined with coronary stenting in 16% of patients, and with balloon angioplasty in 21% of patients. Coronary complications occurred in eight cases (5.4%) with coronary dissection in seven (total dissection rate of 4.7%) and urgent bypass surgery in one case (0.7%). No further complications such as death, occlusion, or perforation of coronary arteries, embolization, or thrombosis were observed. Six-month clinical follow-up revealed q-wave myocardial infarction in 2.7% of patients, aortocoronary bypass surgery in 8.5% of patients, and repeated percutaneous coronary intervention in 17% of patients (11.5% with stenting). Six-month angiographic follow-up of patients with recurrent angina showed target lesion restenosis (> 50% diameter stenosis) in 14% of patients, late lumen loss with < or = 50% diameter stenosis in 6% of patients and progression of "other than target" lesions with > 50% diameter stenosis in 14% of patients. This series demonstrates the safety and feasibility of cutting balloon angioplasty in patients with complex coronary artery disease and in-stent restenosis.

Adult↗
PubMed2003

D-dimer in acute aortic dissection.

STUDY OBJECTIVE: Laboratory testing plays a minor role in the assessment of aortic dissection. Its main value is in the exclusion of other diseases. Following an incidental observation, we systematically investigated the relationship between elevated d-dimer levels and acute aortic dissection. DESIGN: We prospectively tested d-dimer levels in patients with suspected acute aortic dissection (10 patients). In addition, we investigated 14 patients who had received a confirmed diagnosis of thoracic aortic dissection during the previous 5 years, in whom d-dimer testing had been performed for differential diagnosis. Thirty-five patients with acute chest pain of other origin served as a control group. SETTING: Tertiary referral hospital. PATIENTS: Twelve patients had type A dissection (Stanford classification), and 12 patients had type B. MEASUREMENTS AND RESULTS: A d-dimer analysis was performed (Tina-quant assay; Roche Diagnostics; Mannheim, Germany) [normal limit of the assay, 0.5 micro g/mL]. The result of the d-dimer test was positive (ie, > 0.5 micro g/mL) in all patients (sensitivity of the test, 100%) with a mean value of 9.4 micro g/mL and a range of 0.63 to 54.7 micro g/mL. The degree of the elevation was correlated to the delay from the onset of symptoms to laboratory testing (mean, 12.6 h; range, 1 to 120 h) and showed a trend to the extent of the dissection, but not to the outcome (14 patients could be discharged; 10 patients died). CONCLUSIONS: Based on our observation, we suggest that testing for d-dimer should be part of the initial assessment of patients with chest pain, especially if aortic dissection is suspected. A negative test result makes the presence of the disease unlikely.

Acute Disease↗
PubMed2003

Genetic polymorphisms in cytokine and adhesion molecule genes in coronary artery disease.

Both inflammation and genetics play an important role in the pathogenesis of atherosclerosis and coronary artery disease. Epidemiological studies have investigated the association between coronary artery disease (CAD) and gene polymorphisms of the inflammatory molecules tumor necrosis factors (TNF) alpha and beta, transforming growth factors (TGF) beta-1 and beta-2, interleukin (IL)-1 and its receptor antagonist (IL-1ra), CD14 (the receptor for lipopolysaccharide), P- and E-selectins, and platelet endothelial cell adhesion molecule (PECAM)-1. Current evidence suggests that the TNF polymorphisms explored so far are not linked to CAD. The majority of studies conducted showed no significant association between TGFbeta-1 and coronary atherosclerosis, but the data currently available are somewhat controversial. Some polymorphisms may increase the risk of myocardial infarction (MI) within specific ethnic groups or in certain populations. The association between the IL-1 system and atherosclerosis is complex and may vary as a result of a number of factors, such as stage of disease, clinical phenotype, and possibly population characteristics. The E-selectin gene (SELE) Arg128, 98T, and Phe554 alleles may increase the risk of atherosclerosis, but not necessarily the risk of MI. This association seems to be more pronounced in younger patients. The PECAM1 Leu125Val and Ser563Asn polymorphisms may increase the risk of atherosclerosis but not necessarily of MI. This association may be especially important in patients with a low risk for developing atherosclerosis. Current data indicate that screening for CD14-260C/T genotypes is unlikely to be a useful tool for risk assessment and it remains unclear whether CD14 polymorphisms significantly increase the risk of MI. The associations between candidate gene polymorphisms and CAD are complex as a consequence of pleiotropy, variations with age, selection due to the high lethality of the disease, and interactions with other genes and environmental factors. Nonetheless, although the current data is preliminary and partly conflicting, it does provide some evidence that alterations in the genetics of the inflammatory system may modify the risk of CAD.

Animals↗
PubMed2003

Arterial stiffness and cardiovascular drugs.

Arterial stiffness is the most important cause of increasing systolic and pulse pressure, and for decreasing diastolic pressure with ageing. Many measures can be applied to quantify arterial stiffness, but all are approximations only, on account of the nonhomogenous structure of the arterial wall, its variability in different locations, at different levels of distending pressure, and with changes in smooth muscle tone. This article summarizes those indices with a focus on newer non-invasive methods and provides an overview of physiological, pathological and pharmacological influences on arterial hemodynamics. In the near future, the ability to detect and monitor subclinical arterial damage will improve cardiovascular risk stratification and act as a better guide in assessing the efficacy of therapeutic interventions than monitoring blood pressure alone. However, large-scale clinical trials are needed to prove the hypothesis that treatment of these new therapeutic targets will translate into clinical benefit, expressed in cardiovascular events or even mortality.

Age Factors↗