Comparing the effects of five different statins on the HDL subpopulation profiles of coronary heart disease patients.
We compared the effects of five different statins (atorvastatin, simvastatin, pravastatin, lovastatin, and fluvastatin) on the lipid, lipoprotein, and apolipoprotein (apo) A-I-containing high-density lipoprotein (HDL) subpopulation profiles of 86 coronary heart disease (CHD) patients. Patients with established CHD, and low density lipoprotein (LDL) cholesterol (C)>130 mg/dl, and triglyceride (TG)<400 mg/dl, were treated with atorvastatin 20, 40, and 80 mg/day and one of the other four statins at 20, 40, and when available 80 mg/day in increasing doses (4 weeks of each dose) in a randomized crossover fashion. There was an 8-week placebo controlled washout period between different drug treatments. All five statins on each dose resulted in significant reductions in total- and LDL-C compared to placebo treatment. There were also decreases in plasma TG and increases in HDL-C and apoA-I concentrations, but not all treatments changed these parameters significantly. Each statin except fluvastatin improved the HDL subpopulation profile by increasing the concentrations of the large, cholesterol-rich, LpA-I alpha-1 and prealpha-1 HDL subpopulations. CHD patients have significantly lower concentration of the large, LpA-I alpha-1 HDL particles compared to controls. Our data indicate that statins which are the most effective in lowering LDL-C and TG are also the most effective agents in modifying the HDL subpopulation profile in CHD patients towards the patterns found in healthy individuals. The order of efficacy of statins in increasing alpha-1 HDL subpopulation was: atorvastatin, simvastatin, pravastatin, lovastatin and fluvastatin.
Asztalos
Bela F
BF
Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Center on Aging at Tufts University and Division of Endocrinology, Metabolism, Diabetes, and Molecular Medicine, New England Medical Center, Boston, MA 02111, USA. basztalos@hnrc.tufts.edu
Horvath
Katalin V
KV
McNamara
Judith R
JR
Roheim
Paul S
PS
Rubinstein
Joel J
JJ
Schaefer
Ernst J
EJ
D000328:Adult; D000368:Aged; D016632:Apolipoprotein A-I / Q000187:drug effects* / Q000378:metabolism; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000187:drug effects* / Q000378:metabolism; D008078:Cholesterol, LDL / Q000187:drug effects* / Q000378:metabolism; D003327:Coronary Disease / Q000175:diagnosis / Q000188:drug therapy*; D018592:Cross-Over Studies; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage; D005260:Female; D000077340:Fluvastatin; D005500:Follow-Up Studies; D006538:Heptanoic Acids / Q000008:administration & dosage; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D007211:Indoles / Q000008:administration & dosage; D008148:Lovastatin / Q000008:administration & dosage; D008297:Male; D020714:Maximum Tolerated Dose; D008875:Middle Aged; D017035:Pravastatin / Q000008:administration & dosage; D011336:Probability; D011758:Pyrroles / Q000008:administration & dosage; D012016:Reference Values; D012720:Severity of Illness Index; D019821:Simvastatin / Q000008:administration & dosage; D016037:Single-Blind Method; D016896:Treatment Outcome
D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D011758:Pyrroles; D000077340:Fluvastatin; D008148:Lovastatin; D000069059:Atorvastatin; D019821:Simvastatin; D017035:Pravastatin