Apolipoprotein E Genotype and Coronary Heart Disease in a Mongolian Cohort: An Exploratory Case-Control Study
Ochgerel Dogsom1, Ariunzul Punsaldulam2, Odonchimeg Dogsom3
1Department of Psychopathology Clinic, National Center Mental Health of Mongolia, Ulaanbaatar, Mongolia.
Insights
The apolipoprotein E (APOE) genotype is linked to coronary heart disease (CHD) risk in Mongolians. Specific APOE genotypes, like ε2/ε3, may reduce CHD odds, independent of cholesterol levels.
Area of Science:
- Genetics
- Cardiovascular Medicine
- Population Health
Background:
- Investigating the link between apolipoprotein E (APOE) gene variations and coronary heart disease (CHD) risk.
- Focusing on a specific Mongolian clinical cohort.
Purpose of the Study:
- To determine the association between APOE gene polymorphisms and CHD risk in a Mongolian population.
- To explore the role of genetic factors in cardiovascular disease risk assessment.
Main Methods:
- A hospital-based case-control study involving 63 CHD patients and 61 healthy controls.
- Assessment of anthropometric measurements, lipid profiles, and APOE genotypes.
- Multivariable logistic regression analysis to identify risk factors.
Main Results:
- Significant differences in APOE genotype distribution between CHD cases and controls (P = .009).
- The APOE ε2/ε3 genotype was associated with significantly lower odds of CHD (OR = 0.29, P = .007).
- Higher high-density lipoprotein cholesterol and lower total cholesterol observed in the CHD group.
Conclusions:
- A significant association exists between APOE genotype and CHD in the Mongolian population.
- APOE polymorphisms may influence CHD risk independently of absolute cholesterol levels.
- Emphasizes the need for population-specific cardiovascular risk assessment considering genetic factors.
Background:
To investigate the association between apolipoprotein E (APOE) gene polymorphisms and coronary heart disease (CHD) risk within a localized Mongolian clinical cohort.
Methods:
This hospital-based case–control study recruited 63 patients with angiographically confirmed CHD and 61 sex-matched healthy controls. Anthropometric measurements and lipid profiles and pathways for APOE genotypes were strictly assessed. This exploratory hospital-based case–control study was not designed as a nationally representative population-based survey, and participant recruitment was limited to a single tertiary referral center in Mongolia.
Results:
High-density lipoprotein cholesterol levels were significantly higher in the case group than in the control group (1.56 ± 0.14 vs. 1.33 ± 0.18 mmol/L, P < .001), while total cholesterol was significantly lower in cases than in controls (3.91 ± 0.60 vs. 5.34 ± 0.80 mmol/L, P < .001). The distribution of APOE genotypes (ε2/ε3, ε3/ε3, ε3/ε4, and ε4/ε4) differed significantly between the case and control groups (P = .009). Both systolic and diastolic blood pressure significantly correlated with waist circumference (P = .026). Multivariable logistic regression revealed that the ε2/ε3 genotype was associated with significantly lower odds of disease (odds ratio [OR] = 0.29, P = .007, 95% CI: 0.12-0.71), whereas ε4-related findings were highly imprecise due to sparse genotype counts and lacked statistical significance (OR = 1.07, P = .930, 95% CI: 0.23-5.02).
Conclusion:
This study showed a significant association between the APOE genotype and CHD in a Mongolian population. These findings highlight the importance of considering qualitative aspects of lipid metabolism, rather than total cholesterol alone, and suggest that genetic factors, including APOE polymorphisms, may contribute to CHD risk independently of absolute cholesterol levels, underscoring the need for population-specific cardiovascular risk assessment.
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