Impaired Interaction (Adhesion-Aggregation) of Platelets with the Subendothelium in Storage-Pool Disease and after Aspirin Ingestion

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Abstract
Possible defects in the interaction of platelets with the subendothelial surface were evaluated in six patients with storage-pool disease, nine patients with von Willebrand's disease and seven normal subjects who ingested aspirin. Citrated blood was perfused through a chamber containing everted segments of rabbit aorta previously denuded of endothelium by means of a balloon catheter. With normal blood, 83.3 ± 1.9 per cent (S.E.M.) of the surface was covered by adherent platelets. Platelet adhesion was normal after aspirin ingestion (89.7 ± 4.6 per cent) and decreased in some patients with storage-pool disease. The most striking defect in both circumstances was the virtual absence of platelet thrombi. In contrast, decreased adhesion (57.3 ± 3.4 per cent), but normal thrombus formation, was characteristic of von Willebrand's disease. These types of defects in platelet adhesion and aggregation may account for the hemostatic defects in a variety of bleeding disorders. The findings further suggest the possible usefulness of aspirin as an antithrombotic agent. (N Engl J Med 293:619–623, 1975)