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Rate of decline of forced vital capacity predicts future arterial hypertension: the Coronary Artery Risk Development in Young Adults Study.

ABSTRACT: Lung function studies in middle-aged subjects predict cardiovascular disease mortality. We studied whether greater loss of forced vital capacity (FVC) early in life predicted incident hypertension. The sample was 3205 black and white men and women in the Coronary Artery Risk Development in Young Adults Study examined between 1985 and 1986 (Coronary Artery Risk Development in Young Adults year 0, ages 18-30 years) and 2005-2006 and who were not hypertensive by year 10. FVC was assessed at years 0, 2, 5, 10, and 20. Proportional hazard ratios and linear regression models predicted incident hypertension at years 15 or 20 (n=508) from the change in FVC (FVC at year 10 - peak FVC, where peak FVC was estimated as the maximum across years 0, 2, 5, and 10). Covariates included demographics, center, systolic blood pressure, FVC maximum, smoking, physical activity, asthma, and body mass index. Unadjusted cumulative incident hypertension was 25% in the lowest FVC loss quartile (Q1; median loss: 370 mL) compared with 12% cumulative incident hypertension in those who achieved peak FVC at year 10 (Q4). Minimally adjusted hazard ratio for Q1 versus Q4 was 2.21 (95% CI: 1.73-2.83), and this association remained significant in the fully adjusted model (1.37; 95% CI: 1.05-1.80). Decline in FVC from average age at peak (29.4 years) to 35 years old predicted incident hypertension between average ages 35 and 45 years. The findings may represent a common pathway that may link low normal FVC to cardiovascular disease morbidity and mortality.

SUBMITTER: Jacobs DR

PROVIDER: S-EPMC3269403 | biostudies-literature | 2012 Feb

REPOSITORIES: biostudies-literature

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Rate of decline of forced vital capacity predicts future arterial hypertension: the Coronary Artery Risk Development in Young Adults Study.

Jacobs David R DR Yatsuya Hiroshi H Hearst Mary O MO Thyagarajan Bharat B Kalhan Ravi R Rosenberg Sharon S Smith Lewis J LJ Barr R Graham RG Duprez Daniel A DA

Hypertension (Dallas, Tex. : 1979) 20111227 2

Lung function studies in middle-aged subjects predict cardiovascular disease mortality. We studied whether greater loss of forced vital capacity (FVC) early in life predicted incident hypertension. The sample was 3205 black and white men and women in the Coronary Artery Risk Development in Young Adults Study examined between 1985 and 1986 (Coronary Artery Risk Development in Young Adults year 0, ages 18-30 years) and 2005-2006 and who were not hypertensive by year 10. FVC was assessed at years 0 ...[more]

PMID: 22203738

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Project description:BACKGROUND:Forced Vital Capacity (FVC) is an important predictor of all-cause mortality in the absence of chronic respiratory conditions. Epidemiological evidence highlights the role of early life factors on adult FVC, pointing to environmental exposures and genes affecting lung development as risk factors for low FVC later in life. Although highly heritable, a small number of genes have been found associated with FVC, and we aimed at identifying further genetic variants by focusing on lung development genes. METHODS:Per-allele effects of 24,728 SNPs in 403 genes involved in lung development were tested in 7,749 adults from three studies (NFBC1966, ECRHS, EGEA). The most significant SNP for the top 25 genes was followed-up in 46,103 adults (CHARGE and SpiroMeta consortia) and 5,062 children (ALSPAC). Associations were considered replicated if the replication p-value survived Bonferroni correction (p<0.002; 0.05/25), with a nominal p-value considered as suggestive evidence. For SNPs with evidence of replication, effects on the expression levels of nearby genes in lung tissue were tested in 1,111 lung samples (Lung eQTL consortium), with further functional investigation performed using public epigenomic profiling data (ENCODE). RESULTS:NCOR2-rs12708369 showed strong replication in children (p = 0.0002), with replication unavailable in adults due to low imputation quality. This intronic variant is in a strong transcriptional enhancer element in lung fibroblasts, but its eQTL effects could not be tested due to low imputation quality in the eQTL dataset. SERPINE2-rs6754561 replicated at nominal level in both adults (p = 0.036) and children (p = 0.045), while WNT16-rs2707469 replicated at nominal level only in adults (p = 0.026). The eQTL analyses showed association of WNT16-rs2707469 with expression levels of the nearby gene CPED1. We found no statistically significant eQTL effects for SERPINE2-rs6754561. CONCLUSIONS:We have identified a new gene, NCOR2, in the retinoic acid signalling pathway pointing to a role of vitamin A metabolism in the regulation of FVC. Our findings also support SERPINE2, a COPD gene with weak previous evidence of association with FVC, and suggest WNT16 as a further promising candidate.

Project description:RationaleBlack Africans have reduced FVC compared with white persons, but the prevalence and determinants of reduced values are not well understood.ObjectivesTo evaluate the prevalence and factors leading to reduced FVC in a Nigerian population and to examine current theories regarding the determinants of this difference.MethodsWe studied the ventilatory function of 883 adults aged 40 years or older participating in the Burden of Obstructive Lung Disease Study in Ile-Ife, Nigeria. Respondents completed pre- and post-bronchodilator spirometry test and provided information on their smoking history, respiratory symptoms, risk factors, and diagnoses, including anthropometric details. We used standard categories to define body mass index as either underweight, normal, overweight, or obese. We defined reduced FVC as a post-bronchodilator FVC below the lower limit of normal using National Health and Nutrition Examination Survey (NHANES) equations, Global Lung Function Initiative 2012 equations, and local reference equations based on nonsmoking study participants without a respiratory diagnosis. We fit multivariate linear regression models to FVC as a continuous measure, adjusting for age, sex, height, and other confounders.ResultsThe prevalence of reduced FVC was 70.4% for men and 72.8% for women when using NHANES values for white Americans, 17.8% for men and 14.4% for women using NHANES equations for African Americans, and 15.5% for men and 20.5% for women using the Global Lung Function Initiative 2012 equations. Using the equations derived from nonsmoking respondents in the survey without a respiratory diagnosis, the prevalence of reduced FVC was less than 4% for both men and women. FVC was lower in participants who had less than 7 years of education (FVC, -96 ml; 95% confidence interval [CI], -172 to -19), were underweight (FVC, -269 ml; 95% CI, -464 to -73), were overweight (FVC, -132 ml; 95% CI, -219 to -46), and were obese (FVC, -222 ml; 95% CI, -332 to -112).ConclusionsThere is a wide variation in the prevalence of reduced FVC based on the reference standard used. This variation is not satisfactorily explained by factors thought to affect FVC within individual populations. However, the prevalence strongly associates with both education level and body mass index in this population, regardless of the specific standard used.

Dataset Information

Rate of decline of forced vital capacity predicts future arterial hypertension: the Coronary Artery Risk Development in Young Adults Study.

Publications

Rate of decline of forced vital capacity predicts future arterial hypertension: the Coronary Artery Risk Development in Young Adults Study.

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