Assessing Anticoagulation in Neonates With Congenital Diaphragmatic Hernia During Extracorporeal Membrane Oxygenation: Does Anti-Factor Xa or Thromboelastometry Provide Additional Benefit?

The optimal management of anticoagulation in neonatal/pediatric patients during extracorporeal membrane oxygenation (ECMO) has not been established yet and varies greatly among ECMO centers worldwide. Therefore, we aimed to assess whether the use of anti-factor Xa assay and/or thromboelastometry correlate better than activated clotting time with heparin dose in newborns with congenital diaphragmatic hernia during ECMO. We also examined whether these coagulation assays correlate with thrombotic and/or hemorrhagic complications, when the management of anticoagulation is based only on activated clotting time values.

Investigation of platelet adhesiveness in patients with coronary artery disease and acute myocardial infarction using the platelet adhesion assay (PADA).

Background: Increased platelet reactivity may contribute to the development of coronary artery disease and myocardial infarction. The aim of the present study was to assess platelet adhesiveness in different stages of coronary artery disease using the platelet adhesion assay (PADA). In addition, the acute effect of coronary angiography and stent implantation on platelet adhesiveness was examined.

Platelet and monocyte activation in acute ischemic stroke--is there a correlation with stroke etiology?

An upregulation of platelet CD40 ligand (CD40L) and CD62P has been described in atherosclerotic cardiovascular diseases and among patients with acute cerebral ischemia. Correlation between platelet and monocyte activation and the etiology of ischemic stroke were examined in 41 patients with acute ischemic stroke. Compared to 10 controls, all patients with stroke showed a significantly elevated platelet expression of CD40L (P < .

Sudden death: do cytokines and prothrombotic peptides contribute to the occurrence of ventricular fibrillation during acute myocardial infarction?

Sudden cardiac death (SCD) is frequently caused by ventricular fibrillation (VF) occurring in the course of acute myocardial infarction (AMI). It has not been investigated yet, to what extent markers of coagulation activation and inflammation differ between patients with and without VF in the acute phase of AMI.

Antithrombin alfa in hereditary antithrombin deficient patients: A phase 3 study of prophylactic intravenous administration in high risk situations.

During surgery and childbirth, patients with hereditary antithrombin (AT) deficiency are at high risk for thrombosis, and heparin prophylaxis may not be sufficiently efficacious. In these patients, exogenous AT may be used in association with heparin. A recombinant human AT (generic name: antithrombin alfa) has been developed.

High plasma levels of tissue inhibitor of metalloproteinase-1 (TIMP-1) and interleukin-8 (IL-8) characterize patients prone to ventricular fibrillation complicating myocardial infarction.

Background: Atherosclerotic plaques prone to cause thrombotic complications and plaque rupture account for the majority of fatal myocardial infarctions (MI), which may be complicated by ventricular fibrillation (VF). Matrix-degrading metalloproteinases (MMPs) and their inhibitors (TIMPs) are expressed in atherosclerotic lesions and contribute to plaque vulnerability. Interleukin-8 (IL-8) is one of the predominant chemokines interacting with MMPs and TIMPs and the coagulation system.

Diagnostic performance of mid-regional pro-adrenomedullin as an analyte for the exclusion of left ventricular dysfunction.

Aims: In ambulatory patients with coronary artery disease (CAD) we aimed to evaluate the diagnostic performance of mid-regional pro-adrenomedullin (MR-proADM) for the detection or exclusion of impaired left ventricular ejection fraction (LVEF).

Methods And Results: MR-proADM levels were measured in blood samples taken from 102 outpatients with CAD classified according to the New York Heart Association (NYHA) and Canadian Cardiovascular society (CCS) I-II. Increased levels of MR-proADM correlated with impaired LVEF (r=-0.

Midregional pro-atrial natriuretic peptide is a useful indicator for the detection of impaired left ventricular function in patients with coronary artery disease.

Aims: We compared the diagnostic performance of N-terminal pro-brain natriuretic peptide (NT-proBNP) with a newly developed assay for the midregional part of pro-atrial natriuretic peptide (MR-proANP) concerning the detection of impaired left ventricular ejection function (LVEF) among patients with coronary artery disease (CAD).

Methods And Results: Plasma levels of MR-proANP and NT-proBNP were determined in 102 consecutive patients with a history of ST-elevation myocardial infarction. Plasma levels of both markers were measured during a mean follow-up period of 687 days after acute myocardial infarction.

Alimentary lipemia enhances procoagulatory effects of inflammation in patients with a history of acute myocardial infarction complicated by ventricular fibrillation.

Introduction: Acute myocardial infarction, often occurring postprandially, can be complicated by ventricular fibrillation. The role of acute alimentary lipemia and inflammation in the occurrence of ventricular arrhythmias in acute myocardial infarction has not been described yet.

Methods And Results: Before and 2 h after consumption of a defined fatty meal, blood samples of 27 patients with a history of acute myocardial infarction (AMI) were incubated with lipopolysaccharide (LPS).

Assessment of markers of thrombin generation in patients with acute myocardial infarction complicated by ventricular fibrillation.

Background: In most cases, sudden cardiac death is triggered by ischemia-related ventricular tachyarrhythmias and accounts for 50% of deaths from cardiovascular disease in developed countries. Chronic elevation of indicators of coagulation activation has been found in patients with coronary heart disease, but a role of coagulation activation as a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (MI) has not been investigated.

Methods: We enrolled 50 patients with a history of MI, of whom 26 presented with VF in the acute phase of myocardial ischemia; 24 patients had an acute MI without ventricular tachyarrhythmias.

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).

Coagulation activation and expression of CD40 ligand on platelets upon in vitro lipopolysaccharide-challenge in patients with unstable angina.

Background: Elevated markers of inflammation and coagulation are found in patients with coronary heart disease. A role of inflammatory stimulation on coagulation time and expression of CD40 ligand on platelets in acute coronary syndromes has not been described yet.

Methods And Results: Whole blood samples of 9 patients with coronary heart disease and stable angina, 10 patients with unstable angina, 7 patients with acute myocardial infarction and 7 patients without coronary heart disease 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).

Receptor activator of nuclear factor kappaB ligand and osteoprotegerin regulate aortic valve calcification.

Objective: - Recent studies have suggested that valvular calcification in calcific aortic stenosis (AS) may be actively regulated. "Receptor Activator of Nuclear factor kappaB Ligand" (RANKL) and osteoprotegerin (OPG) are members of a cytokine system involved in bone turnover and vascular calcification. Their role in calcific AS is not known.