TY - JOUR
T1 - Comparison of Treatment of Severe High-Density Lipoprotein Cholesterol Deficiency in Men With Daily Atorvastatin (20 mg) Versus Fenofibrate (200 mg) Versus Extended-Release Niacin (2 g)
AU - Alrasadi, Khalid
AU - Awan, Zuhier
AU - Alwaili, Khalid
AU - Ruel, Isabelle
AU - Hafiane, Anouar
AU - Krimbou, Larbi
AU - Genest, Jacques
PY - 2008/11/15
Y1 - 2008/11/15
N2 - To determine whether available lipid-modifying medication can increase high-density lipoprotein (HDL) cholesterol in well-defined genetic or familial HDL-deficiency states, we studied 19 men with HDL deficiency (HDL cholesterol <5th percentile for age and gender) 55 ± 10 years of age. Concomitant risk factors included diabetes (n = 3) and hypertension (n = 7) and 8 patients had coronary artery disease. Molecular analysis revealed that 4 patients had a mutation in the ABCA1 gene. Patients were assigned to sequentially receive atorvastatin 20 mg/day, fenofibrate 200 mg/day, and extended-release niacin 2 g/day for 8 weeks, with a 4-week washout period between each treatment. Patients in whom a statin was required, according to current treatment guidelines, were kept on atorvastatin throughout the study. Baseline HDL cholesterol level was 0.63 ± 0.12 mmol/L (24 ± 5 mg/dl), triglycerides 2.01 ± 0.98 mmol/L (180 ± 86 mg/dl), and low-density lipoprotein (LDL) cholesterol 2.29 ± 0.95 mmol/L (94 ± 39 mg/dl). Mean percent changes in HDL cholesterol on atorvastatin, fenofibrate, and niacin were -6% (p = NS), +6% (p = NS), and +22% (p <0.05), respectively. Furthermore, niacin significantly increased the large α-1 apolipoprotein A-I-containing HDL subspecies (12 to 17 nm). In conclusion, niacin was the only effective drug to increase HDL cholesterol. The absolute increase in HDL cholesterol, ∼0.10 mmol/L (3.9 mg/dl), is of uncertain clinical significance. Biomarkers of HDL-mediated cellular cholesterol efflux were not changed by niacin therapy. Atorvastatin or fenofibrate had little effect on HDL cholesterol; atorvastatin decreased the total cholesterol/HDL cholesterol ratio by 26%. Fenofibrate did not change HDL cholesterol levels and caused an increase in LDL cholesterol. Aggressive LDL cholesterol lowering may be the strategy of choice in such patients.
AB - To determine whether available lipid-modifying medication can increase high-density lipoprotein (HDL) cholesterol in well-defined genetic or familial HDL-deficiency states, we studied 19 men with HDL deficiency (HDL cholesterol <5th percentile for age and gender) 55 ± 10 years of age. Concomitant risk factors included diabetes (n = 3) and hypertension (n = 7) and 8 patients had coronary artery disease. Molecular analysis revealed that 4 patients had a mutation in the ABCA1 gene. Patients were assigned to sequentially receive atorvastatin 20 mg/day, fenofibrate 200 mg/day, and extended-release niacin 2 g/day for 8 weeks, with a 4-week washout period between each treatment. Patients in whom a statin was required, according to current treatment guidelines, were kept on atorvastatin throughout the study. Baseline HDL cholesterol level was 0.63 ± 0.12 mmol/L (24 ± 5 mg/dl), triglycerides 2.01 ± 0.98 mmol/L (180 ± 86 mg/dl), and low-density lipoprotein (LDL) cholesterol 2.29 ± 0.95 mmol/L (94 ± 39 mg/dl). Mean percent changes in HDL cholesterol on atorvastatin, fenofibrate, and niacin were -6% (p = NS), +6% (p = NS), and +22% (p <0.05), respectively. Furthermore, niacin significantly increased the large α-1 apolipoprotein A-I-containing HDL subspecies (12 to 17 nm). In conclusion, niacin was the only effective drug to increase HDL cholesterol. The absolute increase in HDL cholesterol, ∼0.10 mmol/L (3.9 mg/dl), is of uncertain clinical significance. Biomarkers of HDL-mediated cellular cholesterol efflux were not changed by niacin therapy. Atorvastatin or fenofibrate had little effect on HDL cholesterol; atorvastatin decreased the total cholesterol/HDL cholesterol ratio by 26%. Fenofibrate did not change HDL cholesterol levels and caused an increase in LDL cholesterol. Aggressive LDL cholesterol lowering may be the strategy of choice in such patients.
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U2 - 10.1016/j.amjcard.2008.07.010
DO - 10.1016/j.amjcard.2008.07.010
M3 - Article
C2 - 18993152
AN - SCOPUS:55249084748
SN - 0002-9149
VL - 102
SP - 1341
EP - 1347
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 10
ER -