Effects of Atorvastatin versus Fenofibrate on lipoprotein profiles, low-density lipoprotein subfraction distribution, and hemorheologic parameters intype 2 diabetes mellitus with mixed hyperlipoproteinemia
Rja. Frost et al., Effects of Atorvastatin versus Fenofibrate on lipoprotein profiles, low-density lipoprotein subfraction distribution, and hemorheologic parameters intype 2 diabetes mellitus with mixed hyperlipoproteinemia, AM J CARD, 87(1), 2001, pp. 44-48
Citations number
22
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Diabetic dyslipoproteinemia characterized by hypertriglyceridemia, low high
-density lipoprotein (HDL) cholesterol, and often elevated low-density lipo
protein (LDL) cholesterol with predominance of small, dense LDL is a strong
risk factor for atherosclerosis. It is unclear whether fibrate or statin t
herapy is more effective in these patients. We compared atorvastatin (10 mg
/day) with fenofibrate (200 mg/day), each for 6 weeks separated by a 6-week
washout period in 13 patients (5 men and 8 women; mean age 60.0 +/- 6.8 ye
ars; body mass index 30.0 +/- 3.0 kg/m(2)) with type 2 diabetes mellitus (h
emoglobin A(1c) 7.3 +/- 1.1%) and mixed hyperlipoproteinemia (LDL cholester
ol 164.0 +/- 37.8 mg/dl, triglycerides 259.7 +/- 107 mg/dl, HDL cholesterol
48.7 +/- 11.0 mg/dl) using a randomized, crossover design. Lipid profiles,
LDL subfraction distribution, fasting plasma viscosity, red cell aggregati
on, and fibrinogen concentrations were determined before and after each dru
g. Atorvastatin decreased all LDL subfractions (LDL cholesterol, -29%; p <0
.01) including small, dense LDL. Fenofibrate predominantly decreased trigly
ceride concentrations (triglycerides, -39%; p <0.005) and induced a shift,
in LDL subtype distribution from small, dense LDL (-31%) to intermediate-de
nse LDL (+36%). The concentration of small, dense LDL was comparable during
therapy to both drugs (atorvastatin 62.8 +/- 19.5 mg/dl, fenofibrate 63.0
+/- 18.1 mg/dl). Both drugs induced an increase in HDL cholesterol (atorvas
tatin +10%, p <0.05; fenofibrate +11%, p = 0.06). In addition, fenofibrate
decreased fibrinogen concentration (-15%, p <0.01) associated with a decrea
se in plasma viscosity by 3% (p <0.01) and improved red cell aggregation by
15% (p <0.05), whereas atorvastatin did not affect any hemorheologic param
eter. We conclude that atorvastatin and fenofibrate con improve lipoprotein
metabolism in type 2 diabetes. However, the medications affect different a
spects of lipoprotein metabolism. (C) 2001 by Excerpta Medico, Inc.