SPREADING OF PLATELETS - A MORPHOLOGICAL MARKER FOR PLATELET REACTIVITY IN PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Platelet-surface contact is the first step in thrombus formation. Plat elet spreading makes this initial contact irreversible. On the other h and plasma lipids and fibrinogen have been described to activate plate lets or promote adhesion. We therefore investigated whether platelet s preading under stagnation-point flow conditions correlated with plasma concentrations of cardiovascular risk factors such as fibrinogen and high density lipoprotein (HDL)-cholesterol, Platelet rich plasma (PRP) from patients with peripheral arterial occlusive disease and healthy controls was examined by means of the Stagnation-Point Flow Adhesio- A ggregometer (SPAA). The SPAA comprises a microscopic setup with a flow chamber that permits direct observation and quantitation of platelet deposition onto standardized surfaces. After the flow experiments the deposited platelets were analyzed morphometrically for the degree of s preading expressed as inverse circularity (1/C). 1/C was correlated ov er 2 x 2 tables of fibrinogen combined with plasma levels of HDL-chole sterol, each of which was divided into a low and high value group. The patient and control group differed significantly with regard to 1/C, i.e. patient platelets demonstrated more adhesive platelets with a mor e extensive degree of spreading. 1/C was inversely correlated with HDL -cholesterol and showed significant differences between the patient an d the control group. Increased 1/C values were found when associated w ith high fibrinogen levels and simultaneously with low HDL-cholesterol concentrations. Platelet spreading shows a correlation with increased levels of independent plasmatic risk factors for thrombosis in PAOD p atients. Obtained during stagnation-point flow, spreading seems to be a morphological marker for platelet hyperreactivity.