The flow cytometer model markedly affects measurement of ex vivo whole blood platelet-bound P-selectin expression in patients with chest pain: are we comparing apples with oranges.

Surface expression of P-selectin is known to be a marker of platelet activation in patients with acute coronary syndromes. However, direct comparisons of flow cytometer data may be obscured by differences in methodology, artifactual platelet activation during washing procedures, choice of antibodies, absence of control measurements, and possible observer bias due to unblinded data collection. We sought to test the hypothesis that the model of flow cytometer represents another variable affecting P-selectin measurements.

Effects of a novel Mac-1 inhibitor, NPC 15669, on hemostatic parameters during preconditioned myocardial infarction.

NPC 15669, a member of the leumedins family, inhibits leukocyte adhesion to the endothelium by blockage of upregulation of a member of beta2 integrin family Mac-1 (CD11b/CD18). Inhibition of neutrophil-endothelial interactions may alter the course of myocardial reperfusion injury. However, the effects of NPC 15669 supplementation on the hemostatic profile during ischemia-reperfusion are unknown.

Depression, coronary events, platelet inhibition, and serotonin reuptake inhibitors.

There is substantial clinical evidence that the incidence of depression and mortality after acute coronary events are strongly related. As mediators of coronary thrombosis, platelets may represent a link between these events, and could be possibly targeted by therapy with serotonin reuptake inhibitors.

Plasma thromboxane and prostacyclin are linear related and increased in patients presenting with acute myocardial infarction.

The role of prostanoids in patients with ischemic heart disease including acute myocardial infarction (AMI) has been recognized. However, there is very limited knowledge of the baseline TXB2 and 6-keto-PGF1a plasma levels in patients with AMI before therapy has been administered. We compared plasma levels of TXB2 and 6-keto-PGF1a by enzyme immunoassay in 18 AMI patients before thrombolysis, with those of 13 healthy controls.

Clopidogrel: the future choice for preventing platelet activation during coronary stenting?

Ticlopidine has become an established therapy in patients with stroke, and during stenting in patients with coronary artery disease. Clopidogrel, another thienopyridine, is a safe and promising alternative, that irreversibly inhibits ADP-induced platelet aggregation, and reduces formation of both arterial and venous thrombi. In a recent, large, well-controlled trial (CAPRIE), clopidogrel has been shown to be superior to aspirin in terms of prevention of ischaemic stroke, myocardial infarction and death in patients with atherosclerotic vascular disease.

Soluble PECAM-1, but not P-selectin, nor osteonectin identify acute myocardial infarction in patients presenting with chest pain.

We sought to determine plasma levels of platelet/endothelial cell adhesion molecule-1 (PECAM-1), P-selectin, and platelet-derived osteonectin, and prospectively compare these data with the discharge diagnosis in patients presenting with chest pain in a community hospital Emergency Department. Soluble antigens were measured by ELISA in 44 subjects including patients with acute myocardial infarction (AMI) (n = 13), chest pain of noncardiac origin (n = 17), and compared to those of age- and sex-matched healthy controls (n = 14). Elevated soluble PECAM-1 (64.

Usefulness of soluble and surface-bound P-selectin in detecting heightened platelet activity in patients with congestive heart failure.

P-selectin is an important marker of platelet activation and may be up-regulated in patients with congestive heart failure (CHF). We sought to prospectively compare simultaneously determined platelet and soluble P-selectin in patients with CHF and in healthy controls. Matched soluble levels by enzyme-linked immmunosorbent assay, and platelet-bound expression by whole blood flow cytometry of P-selectin were measured in 22 patients with CHF and compared with 14 healthy controls.

Effect of thrombolytic therapy on platelet expression and plasma concentration of PECAM-1 (CD31) in patients with acute myocardial infarction.

Animal studies have shown that the administration of antibodies against platelet/endothelial cell adhesion molecule-1 (PECAM-1) before reperfusion can reduce infarct size. The purpose of the present study was to define the effects of thrombolytic therapy in acute myocardial infarction (AMI) patients on the platelet expression and plasma concentrations of PECAM-1 at prespecified time points after attempted reperfusion. The plasma concentration and platelet expression of PECAM-1 were determined in 23 AMI patients enrolled in the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO-III) trial before thrombolysis and at 3, 6, 12, and 24 hours thereafter and compared with 22 healthy controls.

Increased baseline levels of platelet P-selectin, and platelet-endothelial cell adhesion molecule-1 in patients with acute myocardial infarction as predictors of unsuccessful thrombolysis.

Background: Platelets play a pivotal role in the pathogenesis of acute myocardial infarction and their activation can cause thrombolysis to fail.

Methods: Baseline aggregation of platelets and expression of major surface receptors measured by flow cytometry were compared with clinical outcome after thrombolysis for 23 patients enrolled in the GUSTO-III trial.

Results: Failure to reperfuse (n = 3) and recurrent ischemia (n = 2) were observed in five patients who subsequently underwent emergency angioplasty.

Serial changes of soluble endothelin-1 levels during myocardial ischaemia-reperfusion. Effects of magnesium, diltiazem and a novel MAC-1 inhibitor.

The key role of endothelin-1 (ET-1) has been recognised in patients with ischaemic heart disease. However, the serial changes of ET-1 during both brief and prolonged ischaemia-reperfusion are poorly known. Serial changes of plasma ET-1 were measured during myocardial stunning (MS) and acute myocardial infarction (AMI).

Depressed plasma platelet-activating factor acetylhydrolase in patients presenting with acute myocardial infarction.

Cell membrane phospholipids, including platelet-activating factor (PAF), participate in the pathogenesis of acute myocardial infarction (AMI). The plasma level of PAF acetylhydrolase (AH) was determined in 18 patients at presentation with AMI before thrombolysis, and the administration of adjunctive therapy, and compared with 13 healthy controls. Plasma levels of PAF-AH were significantly lower in the AMI patients (23.

Heterogeneity of platelet aggregation and major surface receptor expression in patients with acute myocardial infarction.

Background: Platelets play an important role in the natural history of acute myocardial infarction (AMI).

Methods And Results: Platelet aggregation and receptor expression were studied in 23 patients with AMI before reperfusion therapy and compared with 10 healthy control subjects. Platelet aggregation was induced with 5 micromol/L adenosine 5'-diphosphate, 10 micromol/L ADP, 1 microg/mL collagen, 1 mg/mL thrombin, and 1.

Antecedent aspirin therapy inhibits baseline platelet activity in patients presenting with acute myocardial infarction. The GUSTO-III Platelet Substudy.

Aspirin therapy and platelet inhibition reduce the risk for the development of acute myocardial infarction (AMI). However, the effects of aspirin on baseline platelet activity in patients presenting with AMI are not known. We determined the effect of long-term aspirin use on baseline platelet activity in patients presenting with AMI, enrolled in the GUSTO-III Platelet Study.

Changes in hemostasis after parenteral magnesium in myocardial ischemia-reperfusion: from animal studies to clinical trials.

There has been some debate regarding the benefit of parenteral magnesium (Mg) in the treatment of acute myocardial infarction (AMI), due to conflicting results from animal studies and recent clinical trials. Several different hypotheses, proposing antiplatelet, and antithrombotic properties have been advanced to explain the cardioprotective properties of Mg during AMI. Although early clinical results were promising, there were serious flaws in the design and the logistics of small trials including out of date methodology, absence of control groups, and possible observer bias due to unblinded data collection.

Effects of reteplase and alteplase on platelet aggregation and major receptor expression during the first 24 hours of acute myocardial infarction treatment. GUSTO-III Investigators. Global Use of Strategies to Open Occluded Coronary Arteries.

Objectives: We sought to compare platelet characteristics after reteplase and alteplase therapy in the setting of the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO)-III trial.

Background: Platelet function may be impaired during thrombolysis in patients with an acute myocardial infarction. The effects of reteplase and alteplase on platelet aggregation and major surface antigen expression during the first 24 h of infarction therapy are unknown.

Plasma fibronectin during myocardial ischemia-reperfusion: effects of magnesium, diltiazem, and a novel Mac-1 inhibitor.

The important role of fibronectin (Fn) has been recognized in patients with ischemic heart disease. However, serial changes of Fn during both brief and prolonged ischemia-reperfusion are poorly known. Plasma Fn was measured during acute myocardial infarction (AMI) and myocardial stunning (MS), and in the absence of myocardial injury.

Soluble vascular cell adhesion molecule-1 and E-selectin in patients with acute myocardial infarction treated with thrombolytic agents.

Twenty-three patients enrolled in th GUSTO-III study underwent serial measurements of soluble vascular cell adhesion molecule-1 (VCAM-1) and E-selectin by enzyme-linked immunosorbent assay at prespecified time intervals. Soluble VCAM-1, but not E-selectin levels, were increased in patients with acute myocardial infarction, indicating that VCAM-1 may serve as a marker of increased endothelial activation in acute myocardial infarction.

Depressed platelet status in an elderly patient with hemorrhagic stroke after thrombolysis for acute myocardial infarction. GUSTO-III Investigators.

Background: Impaired platelet function has been reported in acute myocardial infarction (AMI) and stroke. However, prospective data on the changes of platelet status in patients before the occurrence of hemorrhagic stroke after thrombolytic therapy are unavailable.

Case Description: An 86-year-old male patient was among the 23 AMI patients enrolled in the platelet study for the GUSTO-III trial.

Effects of intracoronary diltiazem on certain hemostatic parameters during acute myocardial infarction in swine.

Controversy currently exists regarding the use of diltiazem in the treatment of acute myocardial infarction (AMI). due to conflicting results from clinical trials and animal studies. The purpose of this project was to evaluate the changes in the hemostatic profile during AMI following low dose intracoronary diltiazem infusion.

Bolus magnesium infusion in humans is associated with predominantly unfavourable changes in platelet aggregation and certain haemostatic factors.

Unlabelled: The purpose of this study was an attempt to extrapolate favorable observations on the effects of magnesium on platelets and haemostasis from animal models to humans. Intravenous magnesium in the treatment of acute myocardial infarction has been tested in several large clinical trials and remains controversial. The mechanism for the cardioprotective properties of magnesium is unknown.