Apolipoprotein E E3/E4 genotype is associated with an increased risk of premature coronary artery disease.


Journal

BMC cardiovascular disorders
ISSN: 1471-2261
Titre abrégé: BMC Cardiovasc Disord
Pays: England
ID NLM: 100968539

Informations de publication

Date de publication:
10 Jul 2024
Historique:
received: 31 03 2024
accepted: 27 06 2024
medline: 11 7 2024
pubmed: 11 7 2024
entrez: 10 7 2024
Statut: epublish

Résumé

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 In summary, BMI ≥ 24.0 kg/m

Identifiants

pubmed: 38987708
doi: 10.1186/s12872-024-04021-8
pii: 10.1186/s12872-024-04021-8
doi:

Substances chimiques

Apolipoprotein E3 0
Apolipoprotein E4 0
ApoE protein, human 0
Apolipoproteins E 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

353

Informations de copyright

© 2024. The Author(s).

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Auteurs

Youqian Li (Y)

Center for Cardiovascular Diseases, Meizhou People's Hospital, Meizhou Academy of Medical Sciences, No. 63 Huangtang Road, Meijiang District, Meizhou, China. d_yoyo@163.com.
Guangdong Provincial Engineering and Technology Research Center for Molecular Diagnostics of Cardiovascular Diseases, Meizhou People's Hospital, Meizhou Academy of Medical Sciences, Meizhou, China. d_yoyo@163.com.

Wei Zhong (W)

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.

Changjing Huang (C)

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.

Junyin Peng (J)

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.

Hanlin Li (H)

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.

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