Out of hospital extracorporeal life support (ECLS) implantation in cardiogenic shock after cardiac arrest.

We report the use of out-of-hospital extracorporeal life support (ECLS) in a 62-year-old patient with severe cardiogenic shock after cardiac arrest. The patient was successfully stabilized using the ECLS system in the pre-hospital setting. Hospital discharge with a good neurological outcome was possible after 23days.

Expansion of the Multi-Link Frontier™ coronary bifurcation stent: micro-computed tomographic assessment in human autopsy and porcine heart samples.

Background: Treatment of coronary bifurcation lesions remains challenging, beyond the introduction of drug eluting stents. Dedicated stent systems are available to improve the technical approach to the treatment of these lesions. However dedicated stent systems have so far not reduced the incidence of stent restenosis.

Enhanced expression of platelet CD40-ligand by in vitro lipopolysaccharide-challenge in patients with ventricular fibrillation complicating acute myocardial infarction.

Background: Acute myocardial infarction can be complicated by ventricular arrhythmias due to electrophysiological changes in the ischemic myocardium, but the exact predisposing factors causing ventricular fibrillation during myocardial infarction still remain unclear. A role of inflammatory stimulation on platelets as a potential risk factor for ventricular fibrillation during acute myocardial infarction has not been described yet.

Methods And Results: Whole blood samples of 21 patients with a history of acute myocardial infarction (AMI) and ventricular fibrillation (VF) were incubated with lipopolysaccharide (LPS).

Enhanced coagulation activation by in vitro lipopolysaccharide challenge in patients with ventricular fibrillation complicating acute myocardial infarction.

Background: Indicators of coagulation and inflammation are elevated in patients with coronary heart disease. A role of coagulation activation in ventricular fibrillation during acute myocardial infarction has not been described.

Methods And Results: Whole blood samples of 21 patients with a history of acute myocardial infarction complicated by ventricular fibrillation and whole blood samples of 18 patients without ventricular fibrillation were incubated with lipopolysaccharide (LPS).

Magnetic resonance imaging findings in patients with Brugada syndrome.

Introduction: Cardiac magnetic resonance imaging (CMR) is a powerful diagnostic tool for evaluating cardiac structure and function. Recently, right ventricular wall-motion abnormalities were described using electron beam tomography in patients with Brugada syndrome. In the present study, we prospectively evaluated CMR findings in patients with Brugada syndrome compared to matched controls.

Anti-hirudin antibodies alter pharmacokinetics and pharmacodynamics of recombinant hirudin.

Recombinant hirudin (r-hirudin) is a potent direct thrombin inhibitor with immunogenic properties. Anti-hirudin antibodies (aHAb) are detected in up to 74% of patients treated with r-hirudin for more than 5 days. aHAb may alter the pharmacokinetics and pharmacodynamics of r-hirudin.

Stabilization of monocyte chemoattractant protein-1-mRNA by activated protein C.

The activated protein C (APC) pathway has been suggested to be a common link between coagulation and inflammation. APC may function to restore hemostasis via modulation of cytokine expression. We investigated the effect of APC on the endothelial expression of monocyte chemoattractant protein-1 (MCP-1), a chemokine that is controlled by the activation of central proinflammatory transcription factors, such as nuclear factor-kappa B (NF-kappaB).

Biological relevance of anti-recombinant hirudin antibodies--results from in vitro and in vivo studies.

This article provides an overview of the clinically relevant characteristics of antibodies directed toward recombinant (r) hirudin, with emphasis on the different ways in which these antibodies may influence pharmacokinetics and pharmacodynamics of r-hirudin. A high incidence of anti-hirudin antibody (AHAb) formation, mainly of the immunoglobulin G (IgG) subclass, was reported in up to 74% of patients treated with r-hirudin for more than 5 days. Like other drug-induced antibodies, AHAb may be responsible for accumulation or neutralization of the drug.