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Abstract：
OBJECTIVE: Dyslipidemia is one of the causes of coronary heart disease (CAD), and apolipoprotein E (APOE) gene polymorphism affects lipid levels. However, the relationship between APOE gene polymorphisms and premature CAD (PCAD, male CAD patients with ≤ 55 years old and female with ≤ 65 years old) risk had different results in different studies. The aim of this study was to assess this relationship and to further evaluate the relationship between APOE gene polymorphisms and PCAD risk in the Hakka population.
METHODS: This study retrospectively analyzed 301 PCAD patients and 402 age matched controls without CAD. The APOE rs429358 and rs7412 polymorphisms were genotyped by polymerase chain reaction (PCR) -chip technique. The distribution of APOE genotypes and alleles between the case group and the control group was compared. The relationship between APOE genotypes and PCAD risk was obtained by logistic regression analysis.
RESULTS: The frequency of the APOE ɛ3/ɛ4 genotype (18.9% vs. 10.2%, p = 0.001) and ε4 allele (11.1% vs. 7.0%, p = 0.007) was higher in the PCAD patients than that in controls, respectively. PCAD patients with ɛ2 allele had higher TG level than those with ɛ3 allele, and controls carried ɛ2 allele had higher HDL-C level and lower LDL-C level than those carried ɛ3 allele. Regression logistic analysis showed that BMI ≥ 24.0 kg/m2 (BMI ≥ 24.0 kg/m2 vs. BMI 18.5-23.9 kg/m2, OR: 1.763, 95% CI: 1.235-2.516, p = 0.002), history of smoking (Yes vs. No, OR: 5.098, 95% CI: 2.910-8.930, p < 0.001), ɛ3/ɛ4 genotype (ɛ3/ɛ4 vs. ɛ3/ɛ3, OR: 2.203, 95% CI: 1.363-3.559, p = 0.001), ε4 allele (ε4 vs. ε3, OR: 2.125, 95% CI: 1.333-3.389, p = 0.002), and TC level (OR: 1.397, 95% CI: 1.023-1.910, p = 0.036) were associated with PCAD.
CONCLUSIONS: In summary, BMI ≥ 24.0 kg/m2, history of smoking, APOE ɛ3/ɛ4 genotype, and TC level were independent risk factors for PCAD. It means that young individuals who are overweight, have a history of smoking, and carried APOE ɛ3/ɛ4 genotype had increased risk of PCAD.
METHODS: This study retrospectively analyzed 301 PCAD patients and 402 age matched controls without CAD. The APOE rs429358 and rs7412 polymorphisms were genotyped by polymerase chain reaction (PCR) -chip technique. The distribution of APOE genotypes and alleles between the case group and the control group was compared. The relationship between APOE genotypes and PCAD risk was obtained by logistic regression analysis.
RESULTS: The frequency of the APOE ɛ3/ɛ4 genotype (18.9% vs. 10.2%, p = 0.001) and ε4 allele (11.1% vs. 7.0%, p = 0.007) was higher in the PCAD patients than that in controls, respectively. PCAD patients with ɛ2 allele had higher TG level than those with ɛ3 allele, and controls carried ɛ2 allele had higher HDL-C level and lower LDL-C level than those carried ɛ3 allele. Regression logistic analysis showed that BMI ≥ 24.0 kg/m2 (BMI ≥ 24.0 kg/m2 vs. BMI 18.5-23.9 kg/m2, OR: 1.763, 95% CI: 1.235-2.516, p = 0.002), history of smoking (Yes vs. No, OR: 5.098, 95% CI: 2.910-8.930, p < 0.001), ɛ3/ɛ4 genotype (ɛ3/ɛ4 vs. ɛ3/ɛ3, OR: 2.203, 95% CI: 1.363-3.559, p = 0.001), ε4 allele (ε4 vs. ε3, OR: 2.125, 95% CI: 1.333-3.389, p = 0.002), and TC level (OR: 1.397, 95% CI: 1.023-1.910, p = 0.036) were associated with PCAD.
CONCLUSIONS: In summary, BMI ≥ 24.0 kg/m2, history of smoking, APOE ɛ3/ɛ4 genotype, and TC level were independent risk factors for PCAD. It means that young individuals who are overweight, have a history of smoking, and carried APOE ɛ3/ɛ4 genotype had increased risk of PCAD.
摘要：
目的:血脂异常是冠心病(CAD)的病因之一,载脂蛋白E（APOE）基因多态性影响血脂水平。然而,APOE基因多态性与早熟CAD(PCAD，在不同的研究中，≤55岁的男性CAD患者和≤65岁的女性CAD患者）的风险具有不同的结果。这项研究的目的是评估这种关系，并进一步评估APOE基因多态性与客家人人群PCAD风险之间的关系。
方法：本研究回顾性分析了301例PCAD患者和402例年龄匹配的无CAD对照者。通过聚合酶链反应（PCR）芯片技术对APOErs429358和rs7412多态性进行基因分型。比较病例组与对照组的APOE基因型和等位基因分布。通过logistic回归分析获得APOE基因型与PCAD风险的关系。
结果：APOE^3/^4基因型的频率（18.9%vs.10.2%,p=0.001）和ε4等位基因（11.1%vs.7.0%,p=0.007）在PCAD患者中高于对照组，分别。与?2等位基因的PCAD患者的TG水平高于?3等位基因的患者,和对照组相比，携带2等位基因的人具有更高的HDL-C水平和更低的LDL-C水平。回归Logistic分析显示BMI≥24.0kg/m2(BMI≥24.0kg/m2vs.BMI18.5-23.9kg/m2，OR：1.763，95%CI：1.235-2.516，p=0.002），吸烟史（是vs.不,OR：5.098，95%CI：2.910-8.930，p<0.001），3/4基因型3/4与3/3，OR：2.203，95%CI：1.363-3.559，p=0.001），ε4等位基因(ε4vs.ε3，OR：2.125，95%CI：1.333-3.389，p=0.002），TC水平(OR:1.397,95%CI:1.023-1.910,p=0.036)与PCAD相关。
结论：总之，BMI≥24.0kg/m2，吸烟史，APOE^3/^4基因型，TC水平是PCAD的独立危险因素。这意味着超重的年轻人，有吸烟史,携带APOE的3/4基因型增加了PCAD的风险。
方法：本研究回顾性分析了301例PCAD患者和402例年龄匹配的无CAD对照者。通过聚合酶链反应（PCR）芯片技术对APOErs429358和rs7412多态性进行基因分型。比较病例组与对照组的APOE基因型和等位基因分布。通过logistic回归分析获得APOE基因型与PCAD风险的关系。
结果：APOE^3/^4基因型的频率（18.9%vs.10.2%,p=0.001）和ε4等位基因（11.1%vs.7.0%,p=0.007）在PCAD患者中高于对照组，分别。与?2等位基因的PCAD患者的TG水平高于?3等位基因的患者,和对照组相比，携带2等位基因的人具有更高的HDL-C水平和更低的LDL-C水平。回归Logistic分析显示BMI≥24.0kg/m2(BMI≥24.0kg/m2vs.BMI18.5-23.9kg/m2，OR：1.763，95%CI：1.235-2.516，p=0.002），吸烟史（是vs.不,OR：5.098，95%CI：2.910-8.930，p<0.001），
结论：总之，BMI≥24.0kg/m2，吸烟史，APOE^3/^4基因型，TC水平是PCAD的独立危险因素。这意味着超重的年轻人，有吸烟史,携带APOE的3/4基因型增加了PCAD的风险。
