[Dyslipidemia, lipid lowering drugs and thrombosis]

Many abnormalities of haemostasis have been described in hyperlipidaemias. They are especially marked in hypertriglyceridaemia with raised factor VII, PAI-1 and, sometimes, fibrinogen levels. The hypercholesterolaemias are associated with a raised haematocrit and blood viscosity. Changes in platelet aggregation are inconstant and consist of platelet activation in vivo and increased reactivity ex vivo. The origin of these disturbances has not been clearly established. Some, like the hyperfibrinogenaemia or platelet activation, are perhaps only secondary to the vascular disease caused by the dyslipidaemia. The effect of lipid-lowering therapy on these abnormalities varies according to the class of drug. Several fibrate-derivatives decrease fibrinogen, factor VII, PAI-1 levels and platelet activation. The resins have little effect on the parameters of haemostasis. The statins reduce platelet activation in and ex vivo, and, inconsistently, correct blood hyperviscosity. It is to early to attribute clinical importance to the effects on haemostasis of lipid-lowering drugs. Although it has been demonstrated that some statins have a rapid preventive action after only several months' treatment, on myocardial infarction and coronary deaths, it is also true that resins, which do not affect haemostatic parameters, are also effective in preventing coronary events. The most widely accepted mode of action of lipid-lowering drugs is the stabilisation of atheromatous plaques.