Abnormal PFA-100 closure time is associated with increased platelet aggregation in patients presenting with chest pain.

Background: Antiplatelet therapy has been proven to be effective for both primary and secondary prevention of myocardial infarction, stroke, and cardiovascular death. However, a significant proportion of patients treated with aspirin experience ischemic events. A number of prospective studies have demonstrated that decreased responsiveness to antiplatelet therapy as measured by various methods, is strongly associated with an increase in clinical events.

Platelet functional implications of glycoprotein Ibalpha polymorphisms in African Americans.

The platelet glycoprotein Ibalpha is crucial in the binding of platelets to Von Willebrand Factor within areas of high stress. A single nucleotide polymorphism of GP Ibalpha gives rise to the Ko(a) (HPA-2b) and the -5C Kozak polymorphism. The presence of these polymorphisms has been associated with an increased risk for atherothrombotic disease.

Evaluation of platelet function in aspirin treated patients with CAD.

Background: Studies of platelet function in the acute coronary syndrome (ACS) have revealed both increased and unchanged platelet activation. To obtain a better understanding of platelet function in coronary artery disease in the setting of aspirin therapy, we performed platelet functional testing in patients with ACS and compared results to patients without CAD.

Methods: We measured platelet aggregation and activation in response to ADP and epinephrine in 80 age and gender matched hospitalized patients (40 with ACS, 40 with non-cardiac chest pain (NCCP)).

Heparin therapy leads to platelet activation and prolongation of PFA-100 closure time.

Background: Heparin is used in the treatment of venous and arterial thromboembolic events, including unstable angina. Once unfractionated heparin is discontinued during the acute phase of unstable angina, it has been demonstrated that the disease process may be reactivated within hours. It is hypothesized that this reactivation may be a result of direct platelet activation by heparin that can linger even after the drug itself has been stopped.