| Effects of apolipoprotein and low density lipoprotein receptor gene polymorphisms on lipid metabolism, and the lipid risk factors of coronary artery disease | ||
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The men with CAD had a more atherogenic plasma lipid profile than the controls. The patients had higher plasma total cholesterol (6.3 vs. 5.6 mmol/l, p=0.03), lower HDL cholesterol (1.0 vs. 1.2 mmol/l, p<0.001) and higher LDL cholesterol (4.5 vs. 3.7 mmol/l, p=0.003), but no difference could be detected between the Lp(a) concentrations (11.7 vs. 6.6 mg/dl). The patients also had higher plasma total triglyceride (1.7 vs. 1.3 mmol/l), VLDL cholesterol (0.5 vs. 0.3 mmol/l) and VLDL triglyceride (1.1 vs. 0.7 mmol/l) concentrations than their controls (p < 0.001 for all the differences). The lipid concentrations of the male patients with different extensions of CAD and the controls are given in Table 5-3. The LDL-to-HDL cholesterol ratio was higher in all the patient groups than in the controls (Figure 5-4).

Figure 5-4. The LDL-to-HDL cholesterol ratio (± SD) of the controls and the male and female patients with different extensions of coronary artery disease. C=controls, <50%=<50% luminal stenosis, 1V=one-vessel disease, 2V=two-vessel disease 3V=three-vessel disease. The women with one,- two- or three-vessel disease differ from the controls at p<0.05. The men with two- and three-vessel disease differ from the men with <50% stenosis at p<0.05.
The women with CAD also had a more atherogenic plasma lipid profile than the controls. The patients had higher plasma total cholesterol (6.7 vs. 5.6 mmol/l, p=0.04), lower HDL cholesterol (1.2 vs. 1.6 mmol/l, p<0.001) and higher LDL cholesterol (4.5 vs. 3.6 mmol/l, p=0.02), but no difference could be detected between the Lp(a) concentrations (7.6 vs. 9.7 mg/dl). The patients had significantly higher plasma total triglyceride (1.8 vs. 0.9 mmol/l), VLDL cholesterol (0.5 vs. 0.2 mmol/l) and VLDL triglyceride (1.1 vs. 0.4 mmol/l) concentrations than their controls, with p < 0.001 for all the differences. The lipid concentrations of the female patients with different extensions of CAD and the controls are given in Table 5-4. The female patients with severe CAD also had a higher LDL-to-HDL cholesterol ratio than the controls (Figure 5-4).
HDL cholesterol was lower in all the male patient groups compared to the corresponding female groups. The female patients with severe CAD had higher plasma total triglyceride, VLDL triglyceride and VLDL cholesterol values than the males, and the female patients with three-vessel disease had the highest VLDL cholesterol and VLDL triglyceride concentrations. There was no clustering of diabetes, hypertension or smoking in the male two- and three-vessel disease patients, whereas three of the women with two- or three-vessel disease had hypertension and four had diabetes with hypertension, five were ex-smokers and only three patients had no other known CAD risk factors.
The stepwise logistic procedure suggests that HDL and LDL cholesterol discriminate both male and female controls from patients with different extensions of CAD. The effect of VLDL cholesterol is abolished in the presence of smoking and hypertension, but VLDL triglycerides remain significant in females after adjustment for age, smoking, hypertension and apolipoprotein E phenotype (Table 5-8).
Table 5-8. Ranked stepwise logistic procedure on the lipids of male and female controls and patients as explanatory factors for the extension of CAD
| Odds ratio | 95% confidence intervals | |
|---|---|---|
| Males | ||
| HDL cholesterol | 0.03 | 0.007-0.13 |
| LDL cholesterol | 1.7 | 1.17-2.36 |
| Lipoprotein(a) | 1.01 | 1.0-1.02 |
| Females | ||
| HDL cholesterol | 0.12 | 0.02-0.75 |
| VLDL triglycerides | 45.5 | 2.14-964 |
| LDL cholesterol | 1.6 | 0.84-3.04 |
| Age, smoking, hypertension and apolipoprotein E phenotype were forced into the model. LDL cholesterol, HDL cholesterol, lipoprotein(a), VLDL cholesterol and VLDL triglycerides have been included in the stepwise procedure. | ||