{"title":"Association between ApoA1 Gene, Plasma Lipid Profile, hsCRP Level, and Risk of Arterial Stiffness in Thai Elderly.","authors":"Pruttaya Supajaree, Suwannee Chanprasertyothin, Prapimporn Chattranukulchai Shantavasinkul, Piyamitr Sritara, Jintana Sirivarasai","doi":"10.1155/2022/4930033","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Apolipoprotein A1 (ApoA1) gene polymorphism is linked to high-density lipoprotein cholesterol (HDL-C) levels. Variations in this gene, along with dyslipidemia and inflammation, may increase the risk of vascular stiffness. This study aimed to investigate the link between ApoA1 rs670 genetic variations, various biochemical parameters, and the risk of arterial stiffness in older people.</p><p><strong>Methods: </strong>This population-based cross-sectional study included 355 participants (≥60 years) who completed a demographic and lifestyle information questionnaire. Clinical and anthropometric examination, biochemical analysis, and ApoA1 rs670 genotyping by real-time PCR were performed. The cardio-ankle vascular index (CAVI) was used to assess arterial stiffness.</p><p><strong>Results: </strong>Age, BMI, waist circumference, SBP, LDL-C, and high-sensitivity C-reactive protein (hs-CRP) were associated with high CAVI (≥9) among older people. The mean CAVI (8.19 ± 2.78) for the ApoA1 rs670 AA genotype was lower than that of the GG genotypes (8.94 ± 1.00, <i>p</i> < 0.05). These results are supported by HDL-C (OR = 0.47, 95% CI: 0.24-0.93; <i>p</i>=0.030) and high hs-CRP (OR = 0.30, 95% CI: 0.16-0.57; <i>p</i>=0.006) levels together with adjusted ORs of both variables.</p><p><strong>Conclusion: </strong>ApoA1 rs670 genetic variations involved in the synthesis, transport, and processing of HDLs, hypertension, and inflammation are linked to arterial stiffness. Further studies are required to clarify these mechanisms.</p>","PeriodicalId":7388,"journal":{"name":"Advances in Preventive Medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9303502/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in Preventive Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/2022/4930033","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: Apolipoprotein A1 (ApoA1) gene polymorphism is linked to high-density lipoprotein cholesterol (HDL-C) levels. Variations in this gene, along with dyslipidemia and inflammation, may increase the risk of vascular stiffness. This study aimed to investigate the link between ApoA1 rs670 genetic variations, various biochemical parameters, and the risk of arterial stiffness in older people.
Methods: This population-based cross-sectional study included 355 participants (≥60 years) who completed a demographic and lifestyle information questionnaire. Clinical and anthropometric examination, biochemical analysis, and ApoA1 rs670 genotyping by real-time PCR were performed. The cardio-ankle vascular index (CAVI) was used to assess arterial stiffness.
Results: Age, BMI, waist circumference, SBP, LDL-C, and high-sensitivity C-reactive protein (hs-CRP) were associated with high CAVI (≥9) among older people. The mean CAVI (8.19 ± 2.78) for the ApoA1 rs670 AA genotype was lower than that of the GG genotypes (8.94 ± 1.00, p < 0.05). These results are supported by HDL-C (OR = 0.47, 95% CI: 0.24-0.93; p=0.030) and high hs-CRP (OR = 0.30, 95% CI: 0.16-0.57; p=0.006) levels together with adjusted ORs of both variables.
Conclusion: ApoA1 rs670 genetic variations involved in the synthesis, transport, and processing of HDLs, hypertension, and inflammation are linked to arterial stiffness. Further studies are required to clarify these mechanisms.