title: Use of niacin, statins, and resins in patients with combined hyperlipidemia.
abstract: Patients in the original Familial Atherosclerosis Treatment Study (FATS) cohort were subgrouped into those with triglyceride levels < or = 120 mg/dL (n = 26) and those with triglyceride levels > or = 190 mg/dL (n = 40). Their therapeutic responses to niacin plus colestipol, lovastatin plus colestipol, colestipol alone, or placebo were determined. Therapeutic response was also determined in the same 2 triglyceride subgroups (n = 12 and n = 27, respectively) of patients selected for low levels of high-density lipoprotein (HDL) cholesterol and coronary artery disease. These triglyceride criteria were chosen to identify patient subgroups with high likelihood of "pattern A" (normal-size low-density lipoprotein [LDL] particles and triglyceride < or = 120 mg/dL) or "pattern B" (small dense LDL and triglyceride > or = 190 mg/dL). Our findings in these small patient subgroups are consistent with the emerging understanding that coronary artery disease patients presenting with high triglyceride levels have lower HDL-C, smaller less buoyant LDL-C, and greater very low-density lipoprotein (VLDL) cholesterol and VLDL apolipoprotein B, and are more responsive to therapy as assessed by an increase in HDL-C and reduction in triglycerides, VLDL-C, and VLDL apolipoprotein B. In the FATS high-triglyceride subgroup with these characteristics, a tendency toward greater therapeutic improvement in coronary stenosis severity was observed among those treated with either of the 2 forms of intensive cholesterol-lowering therapy. This improvement is associated with therapeutic reduction of LDL-C and elevation of HDL-C, but also appears to be associated with drug-induced improvement in LDL buoyancy.
authors.affiliation: Department of Medicine, University of Washington School of Medicine, Seattle 98195, USA.
authors.forename: B G
authors.initials: BG
authors.lastname: Brown
authors.forename: A
authors.initials: A
authors.lastname: Zambon
authors.forename: D
authors.initials: D
authors.lastname: Poulin
authors.forename: A
authors.initials: A
authors.lastname: Rocha
authors.forename: V M
authors.initials: VM
authors.lastname: Maher
authors.forename: J W
authors.initials: JW
authors.lastname: Davis
authors.forename: J J
authors.initials: JJ
authors.lastname: Albers
authors.forename: J D
authors.initials: JD
authors.lastname: Brunzell
mesh_terms: D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D001053:Apolipoproteins / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D002986:Clinical Trials as Topic; D015331:Cohort Studies; D003084:Colestipol / Q000008:administration & dosage*; D003327:Coronary Disease / Q000209:etiology; D004359:Drug Therapy, Combination; D006801:Humans; D006950:Hyperlipidemia, Familial Combined / Q000097:blood / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000008:administration & dosage*; D008148:Lovastatin / Q000008:administration & dosage*; D009525:Niacin / Q000008:administration & dosage*; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D001053:Apolipoproteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D014280:Triglycerides; D009525:Niacin; D008148:Lovastatin; D003084:Colestipol