Platelet-vessel wall interaction: from the bedside to molecules.

This paper is an overview of the progress made in the field of platelet-vessel wall interaction during the past three quarters of a century. (I) "Prehistoric" era (1918-1948): description of Thrombasthenia by 3 European clinicians (Glanzmann, Switzerland, 1918), Hereditary Pseudohemophila (von Willebrand, Finland 1926) and Congenital Hereditary Platelet Dystrophy (Bernard and Soulier, France 1948). (II) Physiopathological era (1957-1972) based on the understanding of these 3 disorders: abnormality of platelet adhesion to the vessel wall in von Willebrand (vW) and Bernard Soulier syndrome (BSS), abnormality of platelet aggregation in thrombasthenias (GT). Breakthrough was made by I.M. Nilsson et al in vWD in Aåland Islands with the recognition of a plasmatic anomaly, later confirmed by Cornu et al to be different from factor VIII deficiency. (III) The third and crucial development (glycoprotein era) (1974-1981) came from the discovery by Nurden & Caen (1974-1975) of GPIIb-IIIa defect in GT and of GPIb-IX in BSS. Polyclonal antibodies against GPIIb-IIIa and GPIb-IX inhibit clearly ex vivo platelet aggregation and adhesion respectively. On everted rabbit subendothelium platelet, adhesion was abnormal in BSS whichever shear stress and at high shear stress in vWD. (IV) The molecular biology era (1984-1995) with the exquisite recognition of gene or protein anomalies in the above mentioned disorders together with the cloning of the 3 genes [for vW factor (vWF) (GPIb-IX, GPIIb, and GPIIIa]. (V) We are at the dawn of the more crucial era, the antithrombotic therapy acting either on the GPIb-vWF complex or on the GPIIb-IIIa.(ABSTRACT TRUNCATED AT 250 WORDS)