scholarly journals Origins of Disparities in Cardiovascular Disease: Birth Weight, Body Mass Index, and Young Adult Systolic Blood Pressure in the National Longitudinal Study of Adolescent Health

2011 ◽  
Vol 21 (8) ◽  
pp. 598-607 ◽  
Author(s):  
Liana J. Richardson ◽  
Jon M. Hussey ◽  
Kelly L. Strutz
2014 ◽  
pp. S403-S409 ◽  
Author(s):  
O. AUZKÝ ◽  
R. DEMBOVSKÁ ◽  
J. MRÁZKOVÁ ◽  
Š. NOVÁKOVÁ ◽  
L. PAGÁČOVÁ ◽  
...  

Preclinical atherosclerosis may represent a risk factor for venous thromboembolism (VTE). In longitudinal study we followed longitudinally 96 patients (32 men) with thrombophilias with (n=51) and without (n=45) history of VTE. In both groups we studied the changes of preclinical atherosclerosis at peripherally located arteries detected by ultrasound. In addition, we assessed changes in selected risk factors of atherosclerosis. During the mean follow-up of 56.0±7.62 months we did not find significant change in preclinical atherosclerosis defined as Belcaro score in either group (–3 % in the VTE group vs 0 % in non VTE group). Significant increase in body mass index (1.03±1.98 kg*m-2, resp. 1.21±1.67 kg*m-2, p<0.01) and non-significant increase in systolic blood pressure were detected in both groups. Waist circumference increased significantly only in patients without VTE (4.11±7.84 cm, p<0.05). No differences in changes of risk factors under study between both groups were detected. In summary, patients with thrombophilia and history of VTE showed no evidence of greater progression of atherosclerosis or increase in traditional risk factors of atherosclerosis than patients with thrombophilia without history of VTE. Unfavorable changes of body mass index, waist circumference and systolic blood pressure were detected in both groups during study period.


Stroke ◽  
2012 ◽  
Vol 43 (6) ◽  
pp. 1478-1483 ◽  
Author(s):  
Rumi Tsukinoki ◽  
Yoshitaka Murakami ◽  
Rachel Huxley ◽  
Takayoshi Ohkubo ◽  
Xianghua Fang ◽  
...  

2018 ◽  
Author(s):  
Alice R Carter ◽  
Dipender Gill ◽  
Neil M Davies ◽  
Amy E Taylor ◽  
Taavi Tillmann ◽  
...  

Key PointsQuestionWhat is the role of body mass index, systolic blood pressure and smoking in mediating the effect of education on cardiovascular disease risk?FindingWe find consistent evidence that body mass index, systolic blood pressure and smoking mediate the effect of education, explaining up to 18%, 27% and 33% respectively. Including all three risk factors in a model together explains around 40% of the effect of education.MeaningIntervening on body mass index, systolic blood pressure and smoking would lead to reductions in cases of CVD attributable to lower levels of education. Over half of the effect of education on risk of cardiovascular disease is not mediated through these risk factors.ImportanceLower levels of education are causally related to higher cardiovascular risk, but the extent to which this is driven by modifiable risk factors also associated with education is unknown.ObjectiveTo investigate the role of body mass index, systolic blood pressure and smoking in explaining the effect of education on risk of cardiovascular disease outcomes.DesignMultivariable regression analysis of observational data and Mendelian randomization (MR) analysis of genetic data.SettingUK Biobank and international genome-wide association study consortia.ParticipantsPredominantly individuals of European ancestry.Main outcomes and measuresThe effects of education (per 1-standard deviation increase, equivalent to 3.6 years) on coronary heart disease, cardiovascular disease (all subtypes), myocardial infarction and stroke risk (all measured in odds ratio, OR), and the degree to which this is mediated through body mass index, systolic blood pressure and smoking.ResultsEach additional standard deviation of education associated with 13% lower risk of coronary heart disease (OR 0.87, 95% confidence interval [CI] 0.84 to 0.89) in observational analysis and 37% lower risk (OR 0.63, 95% CI 0.60 to 0.67) in Mendelian randomization analysis. As a proportion of the total risk reduction, body mass index mediated 15% (95% CI 13% to 17%) and 18% (95% CI 14% to 23%) in the observational and Mendelian randomization estimates, respectively. Corresponding estimates for systolic blood pressure were 11% (95% CI 9% to 13%) and 21% (95% CI 15% to 27%), and for smoking, 19% (15% to 22%) and 33% (95% CI 17% to 49%). All three risk factors combined mediated 42% (95% CI 36% to 48%) and 36% (95 % CI 16% to 63%) of the effect of education on coronary heart disease in observational and Mendelian randomization respectively. Similar results were obtained when investigating risk of stroke, myocardial infarction and all-cause cardiovascular disease.Conclusions and relevanceBMI, SBP and smoking mediate a substantial proportion of the protective effect of education on risk of cardiovascular outcomes and intervening on these would lead to reductions in cases of CVD attributable to lower levels of education. However, more than half of the protective effect of education remains unexplained and requires further investigation.


2016 ◽  
Vol 117 (3) ◽  
pp. 394-398 ◽  
Author(s):  
Vivek K. Prasad ◽  
Clemens Drenowatz ◽  
Gregory A. Hand ◽  
Carl J. Lavie ◽  
Xuemei Sui ◽  
...  

2014 ◽  
Vol 84 (12) ◽  
pp. 759-768 ◽  
Author(s):  
Tracy K. Richmond ◽  
Carly Milliren ◽  
Courtney E. Walls ◽  
Ichiro Kawachi

2020 ◽  
Author(s):  
Dipender Gill ◽  
Verena Zuber ◽  
Jesse Dawson ◽  
Jonathan Pearson-Stuttard ◽  
Alice R Carter ◽  
...  

Background: Higher body-mass index (BMI) and waist-to-hip ratio (WHR) increase the risk of cardiovascular disease, but the extent to which this is mediated by blood pressure, diabetes, lipid traits and smoking is not fully understood. Methods: Using consortia and UK Biobank genetic association summary data from 140,595 to 898,130 participants predominantly of European ancestry, MR mediation analysis was performed to investigate the degree to which genetically predicted systolic blood pressure (SBP), diabetes, lipid traits and smoking mediated an effect of genetically predicted BMI and WHR on risk of coronary artery disease (CAD), peripheral artery disease (PAD) and stroke. Results: The 49% (95% confidence interval [CI] 39%-60%) increased risk of CAD conferred per 1-standard deviation increase in genetically predicted BMI attenuated to 34% (95% CI 24%-45%) after adjusting for genetically predicted SBP, to 27% (95% CI 17%-37%) after adjusting for genetically predicted diabetes, to 47% (95% CI 36%-59%) after adjusting for genetically predicted lipids, and to 46% (95% CI 34%-58%) after adjusting for genetically predicted smoking. Adjusting for all the mediators together, the increased risk attenuated to 14% (95% CI 4%-26%). A similar pattern of attenuation was observed when considering genetically predicted WHR as the exposure, and PAD or stroke as the outcomes. Conclusions: Measures to reduce obesity will lower risk of cardiovascular disease primarily by impacting on downstream metabolic risk factors, particularly diabetes and hypertension. Reduction of obesity prevalence alongside control and management of its mediators is likely to be most effective for minimizing the burden of obesity.


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