A. Van De Wiel

Although strokes belong to the group of cardiovascular disorders, there is no clear association between LDL and/or HDL levels and 'stroke' as an entity. However, there is ample evidence that statins reduce stroke risk in selected patient groups such as survivors of myocardial infarction. This apparent paradox can be explained on the one hand by the heterogeneity of strokes as a group and on the other hand by the specific characteristics of statins. There are strong indications for a relationship between blood lipid profiles and types of stroke that have atherosclerosis as the underlying pathogenetic mechanism. Apart from their ability to reduce LDL levels significantly, statins have a number of other properties, which influence the process of atherosclerosis at various stages. Future and ongoing trials have to prove which patients at risk for stroke will benefit most from the preventive use of statins.

In contrast to a reduced risk of coronary heart disease (CHD) with light to moderate alcohol consumption, heavy alcohol intake and binge drinking are associated with increased cardiovascular mortality. Alcohol has an acute and profound effect on fibrinolysis that may be relevant to the pathogenesis of CHD.The short‐term effects of a low (two glasses, 250 mL, 20 g ethanol) and a high (six glasses, 750 mL, 60 g ethanol) intake of red wine were studied in male volunteers and compared to the intake of mineral water. To find a threshold for inhibition of fibrinolysis and to study a binge effect, a second experiment was performed comparing the intake of four (500 mL, 40 g ethanol) and eight (1000 mL, 80 g ethanol) glasses of red wine with mineral water. Plasminogen activator inhibitor‐1 (PAI‐1), tissue‐type plasminogen activator (t‐PA), plasmin–antiplasmin (PAP) complexes and clot lysis time were measured.In contrast to the circadian rhythm with an enhanced fibrinolysis in the evening that was found in the mineral water group, an intake above four glasses of wine inhibited fibrinolysis significantly. After the intake of two glasses no significant disturbance of the circadian rhythm was observed. Five hours after the consumption of six glasses of wine, a dramatic increase occurred of PAI‐1 antigen (77 ± 42 μg L⁻¹ vs. − 5 ± 10 μg L⁻¹ in the mineral water controls; P < 0·001) and PAI‐1 activity (27 ± 15 U mL⁻¹ vs. − 2 ± 3 U mL⁻¹ in mineral water controls; P < 0·001). Despite a rise in t‐PA antigen, t‐PA activity dropped (− 0·5 ± 0·2 U mL⁻¹ vs. − 0·1 ± 0·2 in controls; P < 0·001) as did PAP complexes (− 103 ± 55 μg L⁻¹ vs. − 26 ± 57 μg L⁻¹ in controls; P < 0·01). After the consumption of eight glasses of wine, the clot lysis assay indicated continued inhibition of fibrinolysis the following morning.Drinking a large amount of alcohol in the evening results in an acute inhibition of fibrinolysis, persisting the following morning. This may predispose to accelerated atherosclerosis and set the stage for thrombotic coronary events, explaining the higher cardiovascular mortality risk in binge drinkers.

The effect of pretransfusion incubation of platelets at 37 degrees C was assessed because of the controversial reports about its relevance. A dual-label technique (111indium and 114mindium) was applied in 10 healthy subjects receiving warmed and unwarmed autologous platelets simultaneously. Fresh platelet concentrates were infused into five subjects, whereas the other five subjects received stored platelet concentrates. The mean platelet volume decreased in all platelet concentrates during incubation, reflecting the restoration of the discoid shape of the platelets. The mean decrease was 0.35 fL (P = .003). However, the initial recovery and the mean platelet life-span were not improved by this procedure. It was concluded that there is no evidence that brief warming of platelets has any beneficial effect on platelet viability in healthy volunteers.