Several studies have shown cardiovascular benefit in treating
hypercholesterolemia with
HMG-CoA reductase inhibitor. However, in addition to the lowering of
cholesterol, the beneficial effects of this inhibitor reflect other pharmacological activities. Whether these beneficial effects are partly mediated by changes in fibrinolytic factors remains to be proven, since clinical studies on the effects of
HMG-CoA reductase inhibitors on fibrinolytic factors have not yielded consistent results. The purpose of this study was to evaluate the effects of
fluvastatin on fibrinolytic factors in hypercholesterolemic patients. After 6 weeks on a low-fat, low-
cholesterol diet, 23 outpatients known to have primary
hypercholesterolemia with
low density lipoprotein cholesterol (
LDL-C) > or = 130 mg/dl with at least 2 risk factors or fasting
LDL-C > or = 160 mg/dl were selected for the study. Venous blood samples were collected at baseline and at 8 weeks after
fluvastatin therapy (40 mg/day) to measure of
tissue plasminogen activator (t-PA),
plasminogen activators inhibitor-1 (PAI-1),
fibrinogen,
D-dimer and
lipid profile. After 8 weeks of
therapy,
fluvastatin reduced serum
cholesterol by 11% (261.9 mg/dl vs 233.2 mg/dl, P < 0.01) and
LDL-C by 22% (191.9 mg/dl vs 149.3 mg/dl, P < 0.01).
D-dimer was significantly decreased (0.38 ng/L vs 0.28 ng/L, P = 0.02) and tPA,
PAI-1 and
fibrinogen tended to decrease after
therapy.
Fluvastatin therapy improved fibrinolytic profile; the result of this study may in part explain the benefit of
HMG-CoA reductase inhibitor on cardiovascular system other than
lipid lowering.