Center for Cardiovascular Diseases, Meizhou People's Hospital, Meizhou Academy of Medical Sciences, No. 63 Huangtang Road, Meijiang District, Meizhou, China.
Guangdong Provincial Engineering and Technology Research Center for Molecular Diagnostics of Cardiovascular Diseases, Meizhou People's Hospital, Meizhou Academy of Medical Sciences, Meizhou, China.
BMC Cardiovasc Disord. 2024 Jul 10;24(1):353. doi: 10.1186/s12872-024-04021-8.
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.
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.
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/m (BMI ≥ 24.0 kg/m vs. BMI 18.5-23.9 kg/m, 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.
In summary, BMI ≥ 24.0 kg/m, 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.
血脂异常是冠心病(CAD)的原因之一,载脂蛋白 E(APOE)基因多态性影响血脂水平。然而,APOE 基因多态性与早发性 CAD(PCAD,男性 CAD 患者<55 岁,女性<65 岁)风险之间的关系在不同的研究中结果不同。本研究旨在评估这种关系,并进一步评估 APOE 基因多态性与客家人群 PCAD 风险之间的关系。
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。采用聚合酶链反应(PCR)-芯片技术检测 APOE rs429358 和 rs7412 多态性。比较病例组和对照组之间 APOE 基因型和等位基因的分布。通过 logistic 回归分析获得 APOE 基因型与 PCAD 风险的关系。
PCAD 患者的 APOE ɛ3/ɛ4 基因型(18.9%比 10.2%,p=0.001)和 ε4 等位基因(11.1%比 7.0%,p=0.007)频率高于对照组。携带 ε2 等位基因的 PCAD 患者的 TG 水平高于携带 ε3 等位基因的患者,携带 ε2 等位基因的对照组的 HDL-C 水平高于携带 ε3 等位基因的对照组,LDL-C 水平低于携带 ε3 等位基因的对照组。回归 logistic 分析显示,BMI≥24.0kg/m2(BMI≥24.0kg/m2 比 BMI 18.5-23.9kg/m2,OR:1.763,95%CI:1.235-2.516,p=0.002)、吸烟史(是比否,OR:5.098,95%CI:2.910-8.930,p<0.001)、ɛ3/ɛ4 基因型(ɛ3/ɛ4 比 ɛ3/ɛ3,OR:2.203,95%CI:1.363-3.559,p=0.001)、ε4 等位基因(ε4 比 ε3,OR:2.125,95%CI:1.333-3.389,p=0.002)和 TC 水平(OR:1.397,95%CI:1.023-1.910,p=0.036)与 PCAD 相关。
综上所述,BMI≥24.0kg/m2、吸烟史、APOE ɛ3/ɛ4 基因型和 TC 水平是 PCAD 的独立危险因素。这意味着超重、有吸烟史和携带 APOE ɛ3/ɛ4 基因型的年轻人患 PCAD 的风险增加。