Effect of APOE genotype on lipid levels in patients with coronary heart disease during a 3-week inpatient rehabilitation program.
It has been suggested that the apolipoprotein E (APOE) genotype modifies the effect of dietary and pharmacological interventions for lowering lipid levels. We wanted to determine whether APOE genotyping information would be useful in making lipid-lowering treatment decisions in clinical practice. We included 981 patients with coronary heart disease (CHD) enrolled in an inpatient 3-week standardized rehabilitation program. Of these, 555 (57%) patients received continued statin therapy and 232 (24%) patients received newly initiated statin therapy. Dietary intervention was part of the program only for 194 (20%) patients. Total cholesterol (TC) and low-density lipoprotein cholesterol (LDLC) levels decreased in all the groups of patients during rehabilitation. The decreases were less pronounced among the APOE E2 carriers. However, the observed variation among the groups with respect to reduction of lipid levels was accounted for mainly by the initial lipid levels (30-47%) and only marginally on the APOE genotype (1%) . We therefore found no evidence that APOE genotyping will be useful in guiding dietary or pharmacological lipid-lowering treatment decisions.
Vossen
C Y
CY
Division of Clinical Epidemiology and Aging Research, German Cancer Research Center, Heidelberg, Germany. h.brenner@dkfz.de
Hoffmann
M M
MM
Hahmann
H
H
Wüsten
B
B
Rothenbacher
D
D
Brenner
H
H
D000328:Adult; D000368:Aged; D000483:Alleles; D053329:Apolipoprotein E2 / Q000235:genetics; D053318:Apolipoprotein E3 / Q000235:genetics; D053327:Apolipoprotein E4 / Q000235:genetics; D001057:Apolipoproteins E / Q000235:genetics*; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood*; D003327:Coronary Disease / Q000097:blood* / Q000150:complications / Q000235:genetics / Q000534:rehabilitation*; D003657:Decision Making; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage; D005260:Female; D000077340:Fluvastatin; D005838:Genotype; D005858:Germany; D006538:Heptanoic Acids / Q000008:administration & dosage; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006937:Hypercholesterolemia / Q000150:complications / Q000178:diet therapy / Q000188:drug therapy*; D007211:Indoles / Q000008:administration & dosage; D007297:Inpatients; D016014:Linear Models; D008148:Lovastatin / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D017035:Pravastatin / Q000008:administration & dosage; D011237:Predictive Value of Tests; D011725:Pyridines / Q000008:administration & dosage; D011758:Pyrroles / Q000008:administration & dosage; D019821:Simvastatin / Q000008:administration & dosage; D014280:Triglycerides / Q000097:blood
D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D011725:Pyridines; D011758:Pyrroles; D014280:Triglycerides; D000077340:Fluvastatin; D008148:Lovastatin; D000069059:Atorvastatin; D019821:Simvastatin; C086276:cerivastatin; D017035:Pravastatin