Adiponectin Genotype, Blood Pressures, and Arterial Stiffness: The Cardiometabolic Risk in Chinese (CRC) Study.
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ABSTRACT:
SUBMITTER: Liang J
PROVIDER: S-EPMC8032032 | biostudies-literature | 2015 May
REPOSITORIES: biostudies-literature
Publications
Adiponectin Genotype, Blood Pressures, and Arterial Stiffness: The Cardiometabolic Risk in Chinese (CRC) Study.
Liang Jun J Qiu Qinqin Q Gong Ying Y Liu Xuekui X Dou Lianjun L Zou Caiyan C Wang Yu Y Qi Lu L
Journal of clinical hypertension (Greenwich, Conn.) 20150226 5
The authors examined whether the adiponectin gene (ADIPOQ) variant was associated with blood pressure and arterial stiffness in Chinese adults. A genome-wide association study of the adiponectin variant rs864265 in the ADIPOQ gene was genotyped in a total of 2364 participants. After adjustment for sex, age, body mass index (BMI), fasting glucose, and lipids, participants carrying the T allele of rs864265 showed a greater increase in carotid-femoral pulse wave velocity (cfPWV) and systolic blood ...[more]
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Project description:BackgroundPrevious studies have reported the separate association of arterial stiffness (AS) and blood pressure with peripheral arterial disease (PAD).ObjectivesThe aim of this study was to investigate the risk stratification capacity of AS on incident PAD beyond blood pressure status.MethodsA total of 8,960 participants from Beijing Health Management Cohort were enrolled at the first health visit between 2008 and 2018 and then followed until the incidence of PAD or 2019. Elevated AS was defined as brachial-ankle pulse-wave velocity (baPWV) >1,400 cm/s, including moderate stiffness (1,400 ≤ baPWV <1,800 cm/s) and severe stiffness (baPWV ≥1,800 cm/s). PAD was defined as ankle-brachial index <0.9. A frailty Cox model was used to calculate the HR, integrated discrimination improvement, and net reclassification improvement.ResultsDuring follow-up, 225 participants (2.5%) developed PAD. After adjusting for confounding factors, the highest risk for PAD was observed in the group with elevated AS and blood pressure (HR: 2.253; 95% CI: 1.472-3.448). Among participants with ideal blood pressure and those with well-controlled hypertension, PAD risk was still significant for severe AS. The results remained consistent in multiple sensitivity analyses. In addition, baPWV significantly improved the predictive capacity for PAD risk beyond systolic and diastolic blood pressures (integrated discrimination improvement 0.020 and 0.190, net reclassification improvement 0.037 and 0.303).ConclusionsThis study suggests the clinical importance of combined evaluation and control of AS and blood pressure for the risk stratification and prevention of PAD.
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Project description:ObjectiveTo utilized the baseline data of the Beijing Fangshan Family Cohort Study, and to estimate whether the association between a healthy lifestyle and arterial stiffness might be modified by genetic effects.MethodsProbands and their relatives from 9 rural areas in Fangshan district, Beijing were included in this study. We developed a healthy lifestyle score based on five lifestyle behaviors: smoking, alcohol consumption, body mass index (BMI), dietary pattern, and physical activity. The measurements of arterial stiffness were brachial-ankle pulse wave velocity (baPWV) and ankle-brachial index (ABI). A variance component model was used to determine the heritability of arterial stiffness. Genotype-environment interaction effects were performed by the maximum likelihood methods. Subsequently, 45 candidate single nucleotide polymorphisms (SNPs) located in the glycolipid metabolism pathway were selected, and generalized estimated equations were used to assess the gene-environment interaction effects between particular genetic loci and healthy lifestyles.ResultsA total of 6 302 study subjects across 3 225 pedigrees were enrolled in this study, with a mean age of 56.9 years and 45.1% male. Heritability of baPWV and ABI was 0.360 (95%CI: 0.302-0.418) and 0.243 (95%CI: 0.175-0.311), respectively. Significant genotype-healthy diet interaction on baPWV and genotype-BMI interaction on ABI were observed. Following the findings of genotype-environment interaction analysis, we further identified two SNPs located in ADAMTS9-AS2 and CDH13 might modify the association between healthy dietary pattern and arterial stiffness, indicating that adherence to a healthy dietary pattern might attenuate the genetic risk on arterial stiffness. Three SNPs in CDKAL1, ATP8B2 and SLC30A8 were shown to interact with BMI, implying that maintaining BMI within a healthy range might decrease the genetic risk of arterial stiffness.ConclusionThe current study discovered that genotype-healthy dietary pattern and genotype-BMI interactions might affect the risk of arterial stiffness. Furthermore, we identified five genetic loci that might modify the relationship between healthy dietary pattern and BMI with arterial stiffness. Our findings suggested that a healthy lifestyle may reduce the genetic risk of arterial stiffness. This study has laid the groundwork for future research exploring mechanisms of arterial stiffness.
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