Platelets intravascular coagulation and fibrinolysis in hyperlipidaemias: relationship to thrombo-embolic complications.

Abstract

ABSTRACT. Platelet function, intra‐vascular coagulation (IVC) and fibrinolysis were studied in 85 patients with Type II hyperlipo‐proteinaemia, 36 with Type IV hypertriglyce‐ridaemia and 36 normal subjects. The effects of clofibrate and nicotinic acid therapy on their plasma lipid concentrations, platelet behaviour, IVC and fibrinolysis were also evaluated. Untreated Type II patients had platelet hyperreactivity to aggregating agents and increased nucleotide release. Their platelet phospholipid content was quantitatively and qualitatively altered. The mechanism of platelet hyperreactivity appears to be related to their ability to convert AA to cyclic endoperoxides and thromboxanes. Although both groups of common hyperlipidaemias had accelerated activation of the blood coagulation systems, the Type II patients had worse blood alterations than the Type IV patients did. Furthermore, our data also suggests that in hypercholesterolaemia platelets appear to mediate these blood changes. Clofibrate treatment in Type II patients improved the platelet reactivity, reversed IVC and stimulated fibrinolysis without altering their plasma lipid levels. In contrast, in Type IV patients, clofibrate therapy significantly lowered plasma triglycerides but did not alter the blood coagulation changes nor did it stimulate fibrinolysis. Thrombo‐embolic complications were common in both groups of hyperlipida etnias but more so in Type II patients. A correlation therefore appears to exist between laboratory evidence of platelet reactivity and IVC and increased incidence of thromboembolic complications.Taken together, these observations suggest that anti‐platelet drugs may be useful in the prevention of thrombo‐embolic complications in Type II patients. In contrast, in hypertriglyceridaemia, impairment of the fibrinolytic system is the likely mechanism by which these thrombotic events occur. Unfortunately, simple preventive treatments to stimulate fibrinolysis are not yet available.