Publications by authors named "Martin E Beyer"

Aim: The aim of the present study was to investigate the effect of GPIIb/IIIa inhibition with eptifibatide and tirofiban on the expression of cellular adhesion molecules on monocytes at different temperatures.

Materials And Methods: Circulation of blood from six volunteers was performed in an extracorporal circulation model at 36°C and 18°C for 30 min. The blood of each donor was prepared either with addition of eptifibatide or tirofiban, or was left untreated as control.

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Deep hypothermic circulatory arrest (DHCA) is a common technique used to protect vital organs during surgical interventions on the thoracic aorta or during surgery for complex congenital heart disease. Activated leukocytes are key mediators of inflammatory responses during ischemia. Intercellular crosstalk between leukocytes, platelets and endothelial cells is mediated by cell adhesion molecules.

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Aim: The aim of the present study was to investigate the effect of different hypothermic temperatures on the expression of cellular adhesion molecules on leukocytes.

Materials And Methods: Circulation of blood from six volunteers was performed in an extracorporeal circulation model at 36°C, 28°C and 18°C for 30 minutes. Expression of CD11b, CD54 and CD162 on monocytes was measured using flow cytometry.

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Background: Thrombogenicitiy of drug-eluting stents is a matter of controversial debate. The aim of this study was to evaluate the thrombogenicity of sirolimus-eluting stents (SES) compared to bare metal stents (BMS) in a standardised in vitro model.

Materials And Methods: Nine SES and nine BMS were implanted in tubing loops and nine loops without stent served as controls.

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Background: The interaction among inflammation, Hemostasis, and fibrinolysis plays a major role in the genesis of coronary artery disease (CAD). The aim of the study was to compare the effect of clopidogrel plus aspirin versus aspirin alone on cellular adhesion molecules on leukocytes, soluble adhesion molecules, and molecular markers of coagulation and fibrinolysis in patients with CAD.

Methods: In this randomized, placebo-controlled, and double-blind study, 42 patients with chronic angina pectoris were included.

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The main aim of the present study was to investigate the direct inotropic effects of stimulation of the endothelin (ET) receptor ETA under in vivo conditions. It is well known that ETA receptor stimulation causes pronounced vasoconstriction. The ET-1-induced coronary vasoconstriction may lead to myocardial ischaemia and, consequently, to cardiodepressor effects that may mask the direct positive inotropic effect of ETA receptor stimulation.

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Background: In severe acute coronary syndromes (ACS) elevation of markers of inflammation and acute phase reaction (APR) like C-reactive protein (CRP) as well as a release of troponin have been reported. Using a high sensitivity troponin T (TnT) test we investigated whether an APR occurs in ACS only in the presence of ischemic myocardial damage.

Methods: In 85 patients with ACS C-reactive protein (CRP), serum amyloid A (SAA), fibrinogen, thrombin antithrombin III complexes (TAT) and kallikrein were determined vs.

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Endothelin-1 (ET-1) is a potent vasoconstrictor, and ET(A) receptors mainly mediate this effect. Elevated plasma levels of ET-1 are observed in patients with coronary heart disease. The release of this peptide from the damaged endothelium may play a role in the initiation and maintenance of myocardial ischaemia.

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Elevated C-reactive protein (CRP) can identify patients with coronary artery disease who are prone to future acute events. We investigated whether elevated CRP is related to the activation of the terminal complement cascade in 66 patients with unstable angina pectoris (UAP), in 45 patients with stable angina pectoris, and in 42 controls. CRP, additional acute phase reactants, the terminal complement complex (sC5b-9), leukocytes, and troponin T were measured.

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