Koppensteiner R, Minar E, Ehringer H
First Department of Medicine, University of Vienna, Austria.
Atherosclerosis. 1990 Jul;83(1):53-8. doi: 10.1016/0021-9150(90)90130-b.
To assess the effect of lovastatin on blood rheology, the hemorheological determinants fibrinogen, red cell aggregation, plasma viscosity, hematocrit and platelet aggregation (spontaneous and ADP-induced) were studied in 15 patients with type II hyperlipoproteinemia in the course of treatment with lovastatin. Prior to therapy, fibrinogen (Fgen), red cell aggregation (RCA-S, RCA-L) and plasma viscosity (PV) as well as cholesterol (Chol) and triglycerides (Tg) were increased in the hyperlipemic patients compared with healthy normolipemic controls (Fgen: 319.3 +/- 65 vs. 269.8 +/- 48 mg/dl; RCA-S: 7.93 +/- 1 vs. 6.62 +/- 1, RCA-L: 9.86 +/- 1 vs. 7.8 +/- 1 arbitrary units; PV: 1.75 vs. 1.63 mPa/s; Chol: 317.0 +/- 32 vs. 176.5 +/- 21 mg/dl; Tg: 154.5 +/- 88 vs. 72.8 +/- 16 mg/dl; all P less than 0.05). Three months of treatment with lovastatin resulted in a marked decrease in red cell aggregation and plasma viscosity, parallel to a fall in cholesterol (the following pretreatment values were monitored after a standard lipid-lowering diet; RCA-S: 7.59 +/- 1 vs. 6.65 +/- 0.9, RCA-L: 9.34 +/- 1 vs. 8.15 +/- 1 arbitrary units; PV: 1.74 vs. 1.65 mPa/s; Chol: 309.8 +/- 41 vs. 217.1 +/- 30 mg/dl; all P less than 0.01); fibrinogen however, remained unchanged throughout the treatment period (346.4 +/- 73.3 vs. 330.5 +/- 70.2 mg/dl, n.s.). No differences were seen in hematocrit and platelet aggregability between hyperlipemic patients and controls and no changes occurred in these parameters during the study.(ABSTRACT TRUNCATED AT 250 WORDS)
