Sir, Malle and Sattler's excellent review links lipids with the release of serotonin from platelets.' It is therefore, of interest that correlations between serum cholesterol and intraplatelet/plasma serotonin concentrations have been reported.'-* Moreover, reducing serum cholesterol and low density lipoprotein (LDL) concentrations normalised previously decreased intraplatelet serotonin levels.2 Serotonin enhances platelet aggregation, may act as a vasoconstrictor in atheromatous arteries5 and stimulates vascular smooth muscle proliferation in cell cultures.6 Serotonin also enhances the growth promoting effects of platelet derived growth factor ( PDGF).6 Therefore, if lipids modify serotonin status, these effects may turn out to be yet another link between lipids and atherogenesis/ thrombogenesis. Malle and Sattler' discuss the binding of lipid fractions to platelets and their effect on platelet activity. The binding interactions between various lipid fractions as well as between fibrinogen and lipids were also considered. These interactions may explain how lipid lowering agents influence platelet activity since these drugs do not equally alter the same lipid fractions. Thus, HMGCoA reductase inhibitors (e.g. fluvastatin, lovastatin, pravastatin, simvastatin) mainly reduce serum LDL levels whereas fibrates (e.g. ciprofibrate, bezafibrate, fenofibrate, gemfibrozil ) mainly reduce very low density lipoprotein and increase high density lipoprotein concentration~.~ However, fibrates usually also reduce plasma fibrinogen concentration and third generation fibrates (ciprofibrate, fenofibrate) have a substantial LDL-lowering effect.' More attention should be directed to assessing the effects of lipid fractions on platelets, in particular the release of intraplatelet products. The effect of lipid lowering drugs on coagulation and fibrinolysis also need to be well documented.