Assessing prognosis by quantifying FcγRIIa on fixed platelets.

FcγRIIa amplifies platelet activation and higher platelet FcγRIIa identifies patients at greater risk of subsequent cardiovascular events. We report the accuracy and precision of a modified test to quantify FcγRIIa on previously fixed platelets (pFCG test). An antibody clone (5G1) was developed after exposure of mice to formaldehyde treated FcγRIIa.

Pharmacokinetic and pharmacodynamic profiles of a novel phospholipid-aspirin complex liquid formulation and low dose enteric-coated aspirin: results from a prospective, randomized, crossover study.

Low dose enteric-coated aspirin (EC-ASA) is routinely used for secondary cardiovascular event prevention. However, absorption of EC tablets is poor, which can result in subtherapeutic antiplatelet effects. Phospholipid-aspirin liquid filled capsules (PL-ASA) are a novel FDA-approved immediate-release formulation designed to reduce gastrointestinal (GI) injury by limiting direct contact with the stomach lining.

Influence of Lipid Excipients on Platelet Function and the Pharmacodynamic Effects of Aspirin.

The combination of pharmaceutical lipid excipients with aspirin in a novel liquid oral formulation (Vazalore) limits gastrointestinal toxicity of aspirin. This study was performed to determine whether the lipid excipients influence the pharmacodynamic effects of aspirin and whether the excipients directly affect platelet function. The pharmacodynamic effects of aspirin were assessed over a range of concentrations designed to exert limited to maximal inhibition of cyclooxygenase-1 (COX1) necessary for thromboxane A2 production.

Assessment of Cardiovascular Risk by the Combination of Clinical Risk Scores Plus Platelet Expression of FcγRIIa.

Platelet expression of FcγRIIa was quantified after myocardial infarction (MI) and we found that patients with high platelet FcγRIIa expression (>11,000/platelet) had a fourfold greater risk of subsequent MI, stroke, and death. This analysis of the original cohort of 197 patients was designed to determine whether platelet expression of FcγRIIa could be used in combination with clinical risk scores (GRACE [Global Registry of Acute Coronary Events] and DAPT [Dual Antiplatelet Therapy]) to refine cardiovascular risk assessment. Platelet expression of FcγRIIa quantified with the use of flow cytometry was broadly distributed in patients stratified into high and low risk groups based on clinical risk scores.

Variation in platelet expression of FcγRIIa after myocardial infarction.

FcγRIIa amplifies platelet activation and greater platelet expression of FcγRIIa identifies patients at greater risk of subsequent cardiovascular events. Thus, platelet expression of FcγRIIa may be useful to guide therapy. Because platelet function tests are impacted by preparative procedures and substantial intra-individual variability, we examined the impact of these factors on platelet expression of FcγRIIa in blood from healthy subjects and in patients after myocardial infarction (MI).

Augmentation of megakaryocyte expression of FcgammaRIIa by interferon gamma.

Objective: The purpose of this study was to identify factors that alter expression of FcgammaRIIa by megakaryocytes.

Methods And Results: Effects of selected cytokines and growth factors on megakaryocyte expression of FcgammaRIIa were assessed with phorbol 12-myristate 13-acetate (PMA)-differentiated human erythroleukemia (HEL) cells and with thrombopoietin-differentiated CD34 stem cells and compared with those obtained with myelocytic cell lines and a monocytic cell lines. Expression of FcgammaRIIa was quantified with the use of Western blots and real-time reverse transcriptase-polymerase chain reaction.

Contributions of young platelets and of previously activated platelets to platelet reactivity in patients with coronary artery disease.

Introduction: We sought to determine why some patients with coronary artery disease have more platelets that do not activate (express P-selectin on their surface) despite exposure in vitro to high concentrations of agonists and whether this finding is associated with altered platelet reactivity.

Methods: We assessed platelet activation and the proportion of young platelets with the use of flow cytometry in blood from 50 patients with coronary artery disease undergoing cardiac catheterization. Ultrastructural characteristics of platelets isolated with the use of a fluorescence activated cell sorter were assessed with the use of electron microscopy.