EFFECT OF LOVASTATIN ON HEMORHEOLOGY IN TYPE-II HYPERLIPOPROTEINEMIA

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 < 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 < 0.01); fibrinogen however, remained uncharged throughout the treatment period (346.4 ± 73.3 vs. 330.5 ± 70.2 mg/dl, n.s.). No differences wereseen in hematocrit and platelet aggregability between hyperlipemic patients and controls and no changes occurred in these parameters during the study. Our data suggest that treatment with lovastatin improves blood rheology in patients with type II hyperlipoproteinemia by lowering abnormally raised plasma viscosity and red cell aggregation; these effects are most likely due to the decrease in cholesterol as fibrinogen remained unaffected by lovastatin therapy. © 1990.