Objective: To develop and validate a prediction model for airflow obstruction (AO) in older Chinese.Methods.Design: Multivariable logistic regression analysis in large population cohort of Chinese... Show moreObjective: To develop and validate a prediction model for airflow obstruction (AO) in older Chinese.Methods.Design: Multivariable logistic regression analysis in large population cohort of Chinese aged >50 years.Participants: Model development: 8762 Chinese aged >= 50 years were selected from the early phase recruits to the Guangzhou Biobank Cohort Study (GBCS) (recruited from September 2003 to May 2006). Internal validation: 100 bootstrap samples drawn with replacement from the development sample. External validation: 8395 Chinese aged >= 50 years from later phase GBCS (recruited from September 2006 to January 2008).Outcomes: AO was defined by a forced expiratory volume in 1 s/forced vital capacity ratio < lower limits of normal.Results: 839 (9.6%) and 764 (9.1%) individuals had AO in the development and temporal validation samples respectively. The predictors in the prediction model included sex, age, body mass index groups, smoking status, presence of respiratory symptoms, and history of asthma. Model development and validation was stratified by sex. Model performance including calibration (calibration-in-the-large -0.017 vs. -0.157; and calibration slope 0.88 vs. 1.02), discrimination (C-statistic 0.72 vs. 0.63 with 95% confidence interval 0.69-0.75 vs. 0.62-0.73) and clinical usefulness (decision curve analysis) in the external temporal validation sample were more satisfactory in men than that in women. Prediction models with risk thresholds (13% in men and 7% in women) and easy-to-use nomograms were developed to assess the probability of AO.Conclusion: The diagnostic models based on readily available epidemiologic and clinical information with satisfactory performance can assist physicians to identify older individuals at high risk of AO and may improve the efficiency of spirometry for active case finding. Further validation beyond the Chinese population is warranted. Show less
Background Whether triglyceride-mediated pathways are causally relevant to coronary heart disease is uncertain. We studied a genetic variant that regulates triglyceride concentration to help judge... Show moreBackground Whether triglyceride-mediated pathways are causally relevant to coronary heart disease is uncertain. We studied a genetic variant that regulates triglyceride concentration to help judge likelihood of causality. Methods We assessed the -1131T>C (rs662799) promoter polymorphism of the apolipoprotein A5 (APOA5) gene in relation to triglyceride concentration, several other risk factors, and risk of coronary heart disease. We compared disease risk for genetically-raised triglyceride concentration (20 842 patients with coronary heart disease, 35 206 controls) with that recorded for equivalent differences in circulating triglyceride concentration in prospective studies (302 430 participants with no history of cardiovascular disease; 12 785 incident cases of coronary heart disease during 2.79 million person-years at risk). We analysed -1131T>C in 1795 people without a history of cardiovascular disease who had information about lipoprotein concentration and diameter obtained by nuclear magnetic resonance spectroscopy. Findings The minor allele frequency of -1131T>C was 8% (95% CI 7-9). -1131T>C was not significantly associated with several non-lipid risk factors or LDL cholesterol, and it was modestly associated with lower HDL cholesterol (mean difference per C allele 3.5% [95% CI 2.6-4.6]; 0.053 mmol/L [0.039-0.068]), lower apolipoprotein AI (1.3% [0.3-2.3]; 0.023 g/L [0.005-0.041]), and higher apolipoprotein B (3.2% [1.3-5.1]; 0.027 g/L [0.011-0.043]). By contrast, for every C allele inherited, mean triglyceride concentration was 16.0% (95% CI 12.9-18.7), or 0.25 mmol/L (0.20-0.29), higher (p=4.4x10(-24)). The odds ratio for coronary heart disease was 1.18 (95% CI 1.11-1.26; p=2.6x10(-7)) per C allele, which was concordant with the hazard ratio of 1.10 (95% CI 1.08-1.12) per 16% higher triglyceride concentration recorded in prospective studies. -1131T>C was significantly associated with higher VLDL particle concentration (mean difference per C allele 12.2 nmol/L [95% CI 7.7-16.7]; p=9.3x10(-8)) and smaller HDL particle size (0.14 nm [0.08-0.20]; p=7.0x10(-5)), factors that could mediate the effects of triglyceride. Interpretation These data are consistent with a causal association between triglyceride-mediated pathways and coronary heart disease. Show less
