5.4. Apolipoprotein E

5.4.1. Allele distribution

The apolipoprotein E allele distribution of the individuals in study IV is given in Table 4-4, and the allele frequencies of the male and the female CAD patients and controls are given in Table 5-3 and Table 5-4 respectively. This series included no patients with the apo E phenotype 2/2, and all the CAD patients with an e 2 allele were smokers.

Table 5-3. Lipid values and apolipoprotein E gene frequencies of male controls and patients with different extensions of coronary artery disease.

 Controls<50% stenosis1-vessel stenosis2-vessel stenosis3-vessel stenosisF-ratiop
N=33N=10N=19N=18N=51
Total cholesterol5.6 (0.9)5.8 (1.2)6.6 (1.1)6.1 (1.1)6.4 (1.3)1.690.158
LDL cholesterol3.7 (0.9)3.7 (1.2)4.5 (0.9)*4.8 (0.7)*4.5 (1.1)*3.310.013
HDL cholesterol1.2 (0.2)1.1 (0.3)1.1 (0.2)*1.0 (0.2)*1.0 (0.3)*8.050.0001
VLDL cholesterol0.3(0.1-2.5)0.5 (0.1-2.2)0.5* (0.2-1.9)0.5(0.2-1.1)0.6*(0.1-1.9)3.650.008
Total triglycerides1.3(0.4-5.5)1.4(0.8-4.8)1.8*(0.8-5.7)1.7*(0.9-2.8)1.8*(0.6-4.5)2.800.029
VLDL triglycerides0.7(0.1-4.6)0.9(0.4-4.2)1.2*(0.4-4.6)1.0*(0.4-2.1)1.1*(0.3-3.6)4.480.002
Lp(a)>35mg/dl (%)15202833331.680.79
e 40.290.150.340.170.23  
e 30.700.750.610.810.75  
e 20.0200.050.030.03  
The values for total, LDL and HDL- cholesterol are expressed as mmol/l, mean and (SD), and those for total triglycerides, VLDL cholesterol and VLDL triglycerides as mmol/l, median and range. For the statistical analyses, total cholesterol, LDL cholesterol, HDL cholesterol and total triglycerides were age-adjusted. Logarithmic transformation was done for the analyses of total triglycerides, VLDL cholesterol and VLDL triglycerides. * p<0.05 compared to controls.

Table 5-4. Lipid values and apolipoprotein E gene frequencies of female controls and patients with different extensions of coronary artery disease

 Controls<50% stenosis1-vessel stenosis2-vessel stenosis3-vessel stenosisF-ratiop
N=27N=8N=6N=7N=7
Total cholesterol5.6 (1.1)6.3 (2.2)6.2 (1.2)7.4 (1.4)6.8 (1.2)1.85 0.135
LDL cholesterol3.6 (1.0)4.1 (1.1)4.4 (1.1)5.0 (1.0)4.4 (1.3)1.89 0.127
HDL cholesterol1.6 (0.4)1.3 (0.4)1.1 (0.2)*1.3 (0.7)1.1 (0.3)*4.470.003
VLDL cholesterol0.2 (0.1-0.5)0.3 (0.1-2.2)0.3 (0.2-1.1)0.7* (0.2-1.2)1.0*xd (0.5-2.3)8.820.0001
Total triglycerides0.9 (0.4-1.9)1.5 (0.5-5.2)1.4 (1.0-2.9)2.0* (0.9-3.1)2.6*xd (1.5-5.6)8.720.0001
VLDLtriglycerides0.4 (0.1-1.1)0.7 (0.2-2.3)0.7* (0.5-1.8)1.6* (0.3-2.1)1.7*xd (1.2-3.7)11.670.0001
Lp(a) >35mg/dl (%)712133303.670.45
e40.190.1300.290.14  
e30.800.881.00.710.86  
e20.020000  
The values for total, LDL and HDL cholesterol are expressed as mmol/l, mean and (SD), and those for total triglycerides, VLDL cholesterol and VLDL triglycerides as mmol/l, median and range. For the statistical analyses, total cholesterol, LDL cholesterol, HDL cholesterol and total triglycerides were age-adjusted. Logarithmic transformation was done for the analyses of total triglycerides, VLDL cholesterol and VLDL triglycerides. d: p<0.05 compared to1vessel stenosis, x p<0.05 compared to moderate disease, * p<0.05 compared to controls.

5.4.2. Association of apo E phenotypes with lipid and lipoprotein concentrations

No statistically significant differences in the plasma total cholesterol, HDL cholesterol or triglyceride values of the CAD patients or the controls were observed in the different apo E groups (phenotypes 2/3 and 2/4, 3/3, and 4/3 and 4/4).

The apo E allele 4 was associated with higher cholesterol concentrations in VLDL and IDL, higher total plasma triglycerides and higher triglyceride concentration in VLDL, IDL and LDL. The protein-cholesterol ratio of LDL was higher and the cholesterol-triglyceride ratio lower in the individuals with an apo E 4 allele. Also, the apo B concentrations of the subjects with at least one apo E 4 allele were higher than those in the subjects with the apo E 3/3 phenotype.

5.4.3. Fractional catabolic rate of LDL in individuals with different apo E phenotypes

We were unable to detect a difference in the FCR of LDL between patients having the apo E 4 allele and those homozygous for apo E 3. However, in three of the four patients with apo E 4/4, the autologous particle was cleared at a slower rate than the homologous apo E 3/3.

5.4.4. Influence of apo E polymorphism on hypolipidemic drug response

The influence of the apo E polymorphism on the lipid-lowering capacity of RS-86505-007 was studied in patients receiving the drug 6 mg tid. The patients with the apo E phenotype 3/3 had larger reductions in total and LDL cholesterol compared to those with at least one e 4 allele, but these differences were not statistically significant (Table 5-5).

Table 5-5. Plasma total cholesterol, triglyceride, HDL cholesterol and LDL cholesterol concentrations before treatment and their mean reductions during treatment in patients receiving RS-86505-007 6 mg tid according to apolipoprotein E polymorphisms.

 Apo E
E 3/3 (N=14)E 4/*1 (N=8)
Tot.chol.8.09(0.61)7.78(1.08)
Dchol21.49(0.95)0.61(1.50)
Triglyceride1.44(0.70)1.37(0.46)
Dtrigly20.26(0.46)0.13(0.31)
HDL chol.1.59(0.44)1.63(0.21)
DHDL20.02(0.22)0.14(0.29)
LDL chol.5.85(0.63)5.53(1.07)
DLDL21.35(1.00)0.42(1.32)
The values are expressed as mmol/l (SD). The differences are not statistically significant. 1 E 4/* = subjects with E4/3 or E 4/4, 2D= change due to treatment.

The lipid concentrations of the patients did not differ statistically significantly in the apo E groups before or after colestipol and lovastatin treatment. Hypertriglyceridemia was only associated with a reduced HDL cholesterol level in the patients lacking the apo E 4.