The Midspan studies.
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Cardiovascular Diseases↗
Biomedical subjects
Mark N Upton
Publications and source records attributed to Mark N Upton.
The accuracy of the Framingham risk-score in different socioeconomic groups: a prospective study.
BACKGROUND: The primary prevention of cardiovascular disease involves using the Framingham risk score to identify high risk patients and then prescribe preventive treatments. AIM: To examine the performance of the Framingham risk score in different socioeconomic groups in a population with high rates of cardiovascular disease. DESIGN OF STUDY: A prospective study. SETTING: West of Scotland. METHOD: The observed 10-year cardiovascular disease and coronary heart disease mortality rates in 5626 men and 6678 women free from cardiovascular disease from the Renfrew/Paisley Study were compared with predicted rates, stratified by socioeconomic class and by area deprivation score. RESULTS: The ratio of predicted to observed cardiovascular mortality rate in the 12 304 men and women with complete risk factor information was 0.56 (95% confidence interval [CI] = 0.52 to 0.60), a relative underestimation of 44%. Cardiovascular disease mortality was underestimated by 48% in manual participants (predicted over observed = 0.52, 95% CI = 0.48 to 0.56) compared to 31% in the non-manual participants (predicted over observed = 0.69, 95% CI = 0.60 to 0.81, P = 0.0005). Underestimation was also worse in participants from deprived areas (P = 0.0017). Only 4.8% of individuals had a 10-year cardiovascular risk of >40% (equivalent to >30% 10-year coronary risk), and 81% of deaths occurred in the rest. If the Framingham score had been recalibrated for manual and non-manual members of this population, an additional 3611 individuals mainly from manual social classes would have reached the treatment threshold. CONCLUSION: Currently recommended risk scoring methods underestimate risk in socioeconomically deprived individuals. The likely consequence is that preventive treatments are less available to the most needy.
Adult↗
Inverse association between birth weight and C-reactive protein concentrations in the MIDSPAN Family Study.
OBJECTIVE: Inflammation markers and low birth weight each predict elevated risk of cardiovascular events and type 2 diabetes. However, potential associations between the low-grade inflammatory response as represented by C-reactive protein (CRP) concentrations and low birth weight have been sparsely examined. METHODS AND RESULTS: In the MIDSPAN Family Study, 1663 individuals had birth weight data and CRP concentrations measured as adults (age 30 to 59). The relationship between these parameters was examined after adjusting for factors known to influence CRP concentrations inclusive of age, body mass index, smoking, socio-economic deprivation, and hormone use in women. After adjusting for potential confounders, there was a negative association between birth weight and CRP, whereby a 1-kg increase in birth weight is associated with a 10.7% decrease in CRP (95% CI: 3.0% to 17.8% decrease). There was no strong evidence that the effects differed in men and women (P=0.32). CONCLUSIONS: Low birth weight contributes to elevated CRP concentration in adult life. Future studies are required to determine to what extent this association reflects catch-up centile crossing, in utero programming, or genetic factors.
Adult↗
Maternal and personal cigarette smoking synergize to increase airflow limitation in adults.
Susceptibility of the lungs to cigarette smoke is poorly understood. It is not known whether maternal smoking increases chronic obstructive pulmonary disease (COPD) risk. In 1998 we reported an inverse association between maternal smoking (prerecorded) and FEV(1) in adults. Because FEV(1) and FVC are strongly correlated, it is unclear whether the association in question reflects a link with lung volume, airflow limitation, or both. We extended our original analysis to investigate whether maternal and personal smoking synergize to increase airflow limitation. We estimated residual FEV(1) to express FEV(1) variation that was not associated with FVC. Maternal smoking was inversely associated with FVC and FEV(1) irrespective of personal smoking. It was inversely associated with FEV(1)/FVC, forced midexpiratory flow rates (FEF(25-75) [mean forced expiratory flow during the middle half of the FVC], FEF(25-75)/FVC), and residual FEV(1) in current smokers but not in never or former smokers (heterogeneity p = 0.016, 0.024, 0.021, and 0.016, respectively). We tested the clinical relevance of findings in ever smokers without asthma: 10 cigarettes/day maternal smoking increased prevalent COPD by 1.7 (95% confidence interval: 1.2-2.5) after adjustment for covariates. Maternal smoking impairs lung volume irrespective of personal smoking and appears to synergize with personal smoking to increase airflow limitation and COPD.
Adult↗
The Y chromosome effect on blood pressure in two European populations.
Higher blood pressure (BP) in males compared with females is well documented and is thought to be influenced in part by the Y chromosome. To examine whether there is an association between BP and a polymorphic HindIII biallelic marker in the nonrecombining region of the Y chromosome, we genotyped 155 males from a Polish study group and 762 males from a Scottish study group. We also tested for possible interaction between the Y chromosome and a mutation in the steroidogenic factor binding site of the aldosterone synthase gene by genotyping the same group from Scotland. There was no significant difference in age or body mass index between 2 Y chromosome genotypes in both study groups. Men with the HindIII(+) genotype had significantly higher systolic and diastolic pressures than those with the HindIII(-) genotype in both the Polish and Scottish studies. This difference between the genotypes was 5.27 mm Hg (P=0.0014) and 3.14 mm Hg (P=0.0005) for adjusted systolic BP and 2.6 mm Hg (P=0.0045) and 1.44 mm Hg (P=0.0084) for adjusted diastolic BP in the Polish and the Scottish studied, respectively. On binary logistic regression analysis, males with the HindIII(+)/TT SF1 genotype combination had an odds ratio for elevated BP of 3.92 (CI 1.21 to 12.68, P=0.023). Our results indicate that the Y chromosome harbors a locus or loci that contribute to BP variation in hypertensive and normotensive men. The polymorphism in the aldosterone synthase gene may interact with the Y chromosome to increase the odds of an individual's developing higher BP.
Adult↗