Correction: Accelerometer measured physical activity and the incidence of cardiovascular disease: Evidence from the UK Biobank cohort study

To examine associations of unhealthy lifestyle and genetics with risk of all-cause mortality, cardiovascular disease (CVD) mortality, myocardial infarction (MI) and stroke. We used data on 76,958 adults from the UK Biobank prospective cohort study. Favourable lifestyle included no overweight/obesity, not smoking, physical activity, not sedentary, healthy diet and adequate sleep. A Polygenic Risk Score (PRS) was derived using 300 CVD-related single nucleotide polymorphisms. Cox proportional hazard ratios (HR) were used to model effects of lifestyle and PRS on risk of CVD and all-cause mortality, stroke and MI. New CVD (n = 364) and all-cause (n = 2408) deaths, and stroke (n = 748) and MI (n = 1140) events were observed during a 7.8 year mean follow-up. An unfavourable lifestyle (0–1 healthy behaviours) was associated with higher risk of all-cause mortality (HR: 2.06; 95% CI: 1.73, 2.45), CVD mortality (HR: 2.48; 95% CI: 1.64, 3.76), MI (HR: 2.12; 95% CI: 1.65, 2.72) and stroke (HR:1.74; 95% CI: 1.25, 2.43) compared to a favourable lifestyle (≥4 healthy behaviours). PRS was associated with MI (HR: 1.35; 95% CI: 1.27, 1.43). There was evidence of a lifestyle-genetics interaction for stroke (p = 0.017). Unfavourable lifestyle behaviours predicted higher risk of all-cause mortality, CVD mortality, MI and stroke, independent of genetic risk.

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Osteoporosis and Its Association With Cardiovascular Disease, Respiratory Disease, and Cancer: Findings From the UK Biobank Prospective Cohort Study

Mayo Clinic Proceedings ◽

10.1016/j.mayocp.2021.07.019 ◽

2022 ◽

Vol 97 (1) ◽

pp. 110-121

Author(s):

Irene Rodríguez-Gómez ◽

Stuart R. Gray ◽

Frederick K. Ho ◽

Fanny Petermann-Rocha ◽

Paul Welsh ◽

...

Keyword(s):

Cardiovascular Disease ◽

Cohort Study ◽

Respiratory Disease ◽

Prospective Cohort Study ◽

Prospective Cohort ◽

Uk Biobank ◽

The Uk

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Accelerometer measured physical activity and the incidence of cardiovascular disease: Evidence from the UK Biobank cohort study

PLoS Medicine ◽

10.1371/journal.pmed.1003487 ◽

2021 ◽

Vol 18 (1) ◽

pp. e1003487

Author(s):

Rema Ramakrishnan ◽

Aiden Doherty ◽

Karl Smith-Byrne ◽

Kazem Rahimi ◽

Derrick Bennett ◽

...

Keyword(s):

Physical Activity ◽

Cardiovascular Disease ◽

Lower Risk ◽

Cox Regression ◽

Moderate Intensity ◽

Inverse Association ◽

Uk Biobank ◽

Reverse Causality ◽

Vigorous Intensity ◽

The Uk

Background Higher levels of physical activity (PA) are associated with a lower risk of cardiovascular disease (CVD). However, uncertainty exists on whether the inverse relationship between PA and incidence of CVD is greater at the highest levels of PA. Past studies have mostly relied on self-reported evidence from questionnaire-based PA, which is crude and cannot capture all PA undertaken. We investigated the association between accelerometer-measured moderate, vigorous, and total PA and incident CVD. Methods and findings We obtained accelerometer-measured moderate-intensity and vigorous-intensity physical activities and total volume of PA, over a 7-day period in 2013–2015, for 90,211 participants without prior or concurrent CVD in the UK Biobank cohort. Participants in the lowest category of total PA smoked more, had higher body mass index and C-reactive protein, and were diagnosed with hypertension. PA was associated with 3,617 incident CVD cases during 440,004 person-years of follow-up (median (interquartile range [IQR]): 5.2 (1.2) years) using Cox regression models. We found a linear dose–response relationship for PA, whether measured as moderate-intensity, vigorous-intensity, or as total volume, with risk of incident of CVD. Hazard ratios (HRs) and 95% confidence intervals for increasing quarters of the PA distribution relative to the lowest fourth were for moderate-intensity PA: 0.71 (0.65, 0.77), 0.59 (0.54, 0.65), and 0.46 (0.41, 0.51); for vigorous-intensity PA: 0.70 (0.64, 0.77), 0.54 (0.49,0.59), and 0.41 (0.37,0.46); and for total volume of PA: 0.73 (0.67, 0.79), 0.63 (0.57, 0.69), and 0.47 (0.43, 0.52). We took account of potential confounders but unmeasured confounding remains a possibility, and while removal of early deaths did not affect the estimated HRs, we cannot completely dismiss the likelihood that reverse causality has contributed to the findings. Another possible limitation of this work is the quantification of PA intensity-levels based on methods validated in relatively small studies. Conclusions In this study, we found no evidence of a threshold for the inverse association between objectively measured moderate, vigorous, and total PA with CVD. Our findings suggest that PA is not only associated with lower risk for of CVD, but the greatest benefit is seen for those who are active at the highest level.

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A model of lifetime health outcomes in cardiovascular disease based on clinical trials and large cohorts

European Heart Journal ◽

10.1093/eurheartj/ehab724.3149 ◽

2021 ◽

Vol 42 (Supplement_1) ◽

Author(s):

R Wu ◽

C Williams ◽

I Schlackow ◽

J Zhou ◽

J Emberson ◽

...

Keyword(s):

Physical Activity ◽

Cardiovascular Disease ◽

Life Expectancy ◽

Remaining Life ◽

Uk Biobank ◽

Cvd Risk ◽

Micro Simulation ◽

History Of ◽

Remaining Life Expectancy ◽

The Uk

Abstract Background and purpose Cardiovascular disease (CVD) risk of individuals depends on their socio-demographic characteristics, clinical risk factors, and treatments, and strongly influences their quality of life and survival. Individual-based long-term disease models, which aim to more accurately calculate the lifetime consequences, can help to target treatments, develop disease management programmes, and assess the value of new therapies. We present a new micro-simulation CVD model. Methods This micro-simulation model was developed using individual participant data from the Cholesterol Treatment Trialists' collaboration (CTT: 118,000 participants; 15 trials) and calibrated (with added socioeconomic deprivation, ethnicity, physical activity, mental illness, cancer and incident diabetes) in the UK Biobank cohort (UKB: 502,000 participants). Parametric survival models estimated risks of key endpoints (myocardial infarction (MI), stroke, coronary revascularisation (CRV), diabetes, cancer and vascular (VD) and nonvascular death (NVD) using participants' age, sex, ethnicity, physical activity, socioeconomic deprivation, smoking history, lipids, blood pressure, creatinine, previous cardiovascular diseases, diabetes, mental illness and cancer at entry and non-fatal incidents of the key endpoints during follow-up. The model integrates the risk equations and enables annual projection of endpoints and survival over individuals' lifetimes. The model was used to project remaining life expectancy across UK Biobank participants. Results Nonfatal cardiovascular events and age were the major determinants of CVD risk and, together with incident diabetes and cancer, of individuals' survival. The cumulative incidence of the key endpoints predicted by the CTT-UKB model corresponded well to their observed incidence in the UK Biobank cohort, overall (Figure 1) and in categories of participants by age, sex, prior CVD and CVD risk. Predicted remaining life expectancy across UK Biobank participants without history of CVD ranged between 22 and 43 years in men and between 24 and 46 years in women, depending on their age and CVD risk (Figure 2). Among UK Biobank participants with history of CVD, depending on their age, predicted remaining life expectancy ranged from 20 to 32 years in men and from 26 to 38 years in women. Conclusion This new lifetime CVD model accurately predicts morbidity and mortality in a large UK population cohort. It will be made available to provide individualised projections of expected lifetime health outcomes and benefits of treatments. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): UK National Institute for Health Research (NIHR) Health Technology Assessment (HTA) Programme, UK Medical Research Council (MRC), British Heart Foundation Figure 1. Predicted (in black) versus observed (95% CI; in red) incidence of major clinical outcomes in the UK Biobank. Figure 2. Predicted remaining life expectancy of participants in UK Biobank cohort, by age and CVD risk or previous CVD at entry. QRISK, a 10-year CVD risk scoring algorithm for people without previous CVD, recommended for use in the UK National Health Service.

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Fitness, Physical Activity, and Cardiovascular Disease: Longitudinal and Genetic Analyses in the UK Biobank Study

10.1101/136192 ◽

2017 ◽

Cited By ~ 1

Author(s):

Emmi Tikkanen ◽

Stefan Gustafsson ◽

Erik Ingelsson

Keyword(s):

Physical Activity ◽

Cardiovascular Disease ◽

Grip Strength ◽

Cardiorespiratory Fitness ◽

Genetic Risk ◽

Cardiovascular Events ◽

Large Scale ◽

Mendelian Randomization ◽

Uk Biobank ◽

The Uk

AbstractBackgroundExercise is inversely related with cardiovascular disease (CVD), but large-scale studies of incident CVD events are lacking. Moreover, little is known about genetic determinants of fitness and physical activity, and modifiable effects of exercise in individuals with elevated genetic risk of CVD. Finally, causal analyses of exercise traits are limited.MethodsWe estimated associations of grip strength, physical activity, and cardiorespiratory fitness with CVD and all-cause death in up to 502,635 individuals from the UK Biobank. We also examined these associations in individuals with different genetic burden on coronary heart disease (CHD) and atrial fibrillation (AF). Finally, we performed genome-wide association study (GWAS) of grip strength and physical activity, as well as Mendelian randomization analysis to assess the causal role of grip strength in CHD.FindingsGrip strength, physical activity, and cardiorespiratory fitness showed strong inverse associations with incident cardiovascular events and all-cause death (for composite CVD; HR, 0.78, 95% CI, 0.77-0.80; HR, 0.94, 95% CI, 0.93-0.95, and HR, 0.67, 95% CI, 0.63-0.71, per SD change, respectively). We observed stronger associations of grip strength with CHD and AF for individuals in the lowest tertile of genetic risk (Pinteraction = 0.006, Pinteraction = 0.03, respectively), but the inverse associations were present in each category of genetic risk. We report 27 novel genetic loci associated with grip strength and 2 loci with physical activity, with the strongest associations in FTO (rs56094641, P=3.8×10-24) and SMIM2 (rs9316077, P=1.4×10-8), respectively. By use of Mendelian randomization, we provide evidence that grip strength is causally related to CHD.InterpretationMaintaining physical strength is likely to prevent future cardiovascular events, also in individuals with elevated genetic risk for CVD.FundingNational Institutes of Health (1 R01 HL135313-01), Knut and Alice Wallenberg Foundation (2013.0126), and the Finnish Cultural Foundation.

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