Platelet function tests in thrombotic cerebrovascular disorders.

Abstract

A variety of platelet function tests were performed in patients with four forms of obstructive cerebrovascular disease (CVD); transient ischemic attacks (TIA), reversible ischemic neurological deficit (RIND), cerebral infarct, and cerebral embolism of cardiac source in rheumatic valvular heart disease (RVHD). Platelet studies included platelet aggregation induced by ADP and ristocetin, spontaneous platelet aggregation, von Willebrand factor (VIII:vWF), platelet aggregation enhancing factor (PAEF), and percentage of large platelets (megathrombocytes). Serial testing was carried out in acute stroke patients. The effect of aspirin therapy was also evaluated. A clear difference in results was observed between patients with cardiogenic embolism and those with other forms of CVD. In patients with TIA, RIND, and cerebral infarct, platelet aggregation, both induced and spontaneous, was enhanced along with elevation of plasma VIII:vWF and PAEF, and increased percentage of megathrombocytes. In patients with cardiogenic embolism, however, these studies were negative except for percent megathrombocytes. This value was increased in the embolic patients with RVHD in comparison with non-embolic patients with RVHD. Increase in platelet aggregation to ADP and percent megathrombocytes developed slowly over a week following stroke. Induced and spontaneous platelet aggregation, and percent megathrombocytes could be normalized with 600 mg aspirin p.o. These studies suggest that a systemic increase of hyperaggregable platelets and of plasma activators of platelet function exists in thrombotic CVD and may be related to its pathogenesis, while local hemodynamic factors may be more important in the thrombogenesis of cardiogenic embolism.

Coagulation factors and the increased risk of stroke in nonvalvular atrial fibrillation.

“…5 Other authors have found no such correlation in healthy subjects later suffering cardiovascular events. 6 - 27 Uchiyama et al 28 found increased vWF:Ag levels in patients with thromboembolic but not embolic (rheumatic valvular heart disease) stroke.…”

Platelet GP IIIa Pl A and GP Ib Variable Number Tandem Repeat Polymorphisms and Markers of Platelet Activation in Acute Stroke

“…Although a number of studies have investigated the association of platelet activation with MI 10,11 and stroke, 7,8,24 the majority have been relatively small. Elevated levels of ␤-TG have been found in subjects with thromboembolic and cardioembolic stroke compared with those with small-vessel infarction and healthy control subjects 7 ; similarly Konstantopoulos et al 8 found increased shear-induced platelet aggregation and a persistent increase in the percentage of circulating activated platelets in subjects with large-vessel infarction compared with those with small-vessel infarction or control subjects.…”

“…Increased ADP-induced platelet aggregation and increased spontaneous platelet aggregation have also been found in subjects with transient ischemic attack or reversible ischemic neurologic deficit and cerebral infarction compared with healthy controls. 24 In the Caerphilly Collaborative Heart Disease Study, hypersensitivity to ADP was found in subjects with a past history of MI or ECG evidence of ischemic heart disease. 10 …”

Association of the Platelet Glycoprotein IIb HPA-3 Polymorphism With Survival After Acute Ischemic Stroke

“…[3][4][5] Platelet activation results in a conformational change in the glycoprotein (GP) IIb/IIIa receptors on the platelet surface, which facilitates binding of soluble fibrinogen and platelet aggregation. 6 GPIIb/IIIa (␣ IIb ␤ 3 ) is a member of the integrin family of cell adhesion molecules, 7 and its importance in the pathogenesis of cardiovascular disease has been highlighted by the clinical use of anti-GPIIb/IIIa agents.…”