Platelet changes in thrombosis

Daniel, Sandra E (1979) Platelet changes in thrombosis. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

Platelet differences have been demonstrated between patients,studied long after recovery from the acute effects of a myocardial infarction or deep vein thrombosis or suffering from intermittent claudication, and control subjects. These differences have been utilised to develop statistical functions with the ability to discriminate between the control and patient groups. The functions have been tested using further sets of data from similar subject groups and those designed to discriminate between myocardial infarction patients and controls, and between claudicant patients and controls, have been validated. It has been postulated that these patients are at risk of further similar thrombotic problems, that the observed platelet differences reflect this risk, and that the validated discriminant functions may therefore be reclassified as Risk Functions. It has been suggested that these Risk Functions could be of practical value in identifying at risk members of the general population. The Vein/Control discriminant function could not be validated suggesting differences in platelet involvement in arterial and venous thrombosis. The prime predictor variable for all the validated Risk Functions was the Heparin Thrombin Clotting Time. The changes found in this parameter, and in the other measurements comprising the Risk Functions, appeared to reflect platelet hyperactivation in arterial thrombotic disease as here defined. Changes in dietary fat ingestion produced changes in the Heparin Thrombin Clotting Time and thus in thrombotic risk as assessed by the Risk Function. Polyunsaturated fat ingestion caused the clotting time to change in a direction away from that demonstrated in the thrombotic patients and saturated fat ingestion produced a change in direction toward that found in the patients. The lipid lowering agent, clofibrate, was shown similarly to effect a change in the Heparin Thrombin Clotting Time in a direction away from that found in thrombosis.

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