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  • 1
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    Online Resource
    Predictive Accuracy of a Polygenic Risk Score–Enhanced Prediction Model vs a Clinical Risk Score for Coronary Artery Disease
    American Medical Association (AMA) ; 2020
    In:  JAMA Vol. 323, No. 7 ( 2020-02-18), p. 636-
    Details
    In: JAMA, American Medical Association (AMA), Vol. 323, No. 7 ( 2020-02-18), p. 636-
    Type of Medium: Online Resource
    ISSN: 0098-7484
    URL: Article
    DOI: 10.1001/jama.2019.22241
    RVK:
    XA 10000
    Language: English
    Publisher: American Medical Association (AMA)
    Publication Date: 2020
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    SSG: 5,21
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  • 2
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    Estimated 24-Hour Urinary Sodium Excretion and Incident Cardiovascular Disease and Mortality Among 398 628 Individuals in UK Biobank
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Hypertension Vol. 76, No. 3 ( 2020-09), p. 683-691
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 76, No. 3 ( 2020-09), p. 683-691
    Abstract: We report on an analysis to explore the association between estimated 24-hour urinary sodium excretion (surrogate for sodium intake) and incident cardiovascular disease (CVD) and mortality. Data were obtained from 398 628 UK Biobank prospective cohort study participants (40–69 years) recruited between 2006 and 2010, with no history of CVD, renal disease, diabetes mellitus or cancer, and cardiovascular events and mortality recorded during follow-up. Hazard ratios between 24-hour sodium excretion were estimated from spot urinary sodium concentrations across incident CVD and its components and all-cause and cause-specific mortality. In restricted cubic splines analyses, there was little evidence for an association between estimated 24-hour sodium excretion and CVD, coronary heart disease, or stroke; hazard ratios for CVD (95% CIs) for the 15th and 85th percentiles (2.5 and 4.2 g/day, respectively) compared with the 50th percentile of estimated sodium excretion (3.2 g/day) were 1.05 (1.01–1.10) and 0.96 (0.92–1.00), respectively. An inverse association was observed with heart failure, but that was no longer apparent in sensitivity analysis. A J-shaped association was observed between estimated sodium excretion and mortality. Our findings do not support a J-shaped association of estimated sodium excretion with CVD, although such an association was apparent for all-cause and cause-specific mortality across a wide range of diseases. Reasons for these differences are unclear; methodological limitations, including the use of estimating equations based on spot urinary data, need to be considered in interpreting our findings.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.119.14302
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2094210-2
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  • 3
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    DataSheet2.DOCX
    Frontiers Media SA ; 2023
    In:  Frontiers in Genetics Vol. 14 ( 2023-2-17)
    Details
    In: Frontiers in Genetics, Frontiers Media SA, Vol. 14 ( 2023-2-17)
    Abstract: Background and objectives: Mechanistic research suggests synergistic effects of cardiovascular disease (CVD) and dementia pathologies on cognitive decline. Interventions targeting proteins relevant to shared mechanisms underlying CVD and dementia could also be used for the prevention of cognitive impairment. Methods: We applied Mendelian randomisation (MR) and colocalization analysis to investigate the causal relationships of 90 CVD-related proteins measured by the Olink CVD I panel with cognitive traits. Genetic instruments for circulatory protein concentrations were obtained using a meta-analysis of genome-wide association studies (GWAS) from the SCALLOP consortium (N = 17,747) based on three sets of criteria: 1) protein quantitative trait loci (pQTL); 2) cis -pQTL (pQTL within ±500 kb from the coding gene); and 3) brain-specific cis -expression QTL ( cis -eQTL) which accounts for coding gene expression based on GTEx8. Genetic associations of cognitive performance were obtained from GWAS for either: 1) general cognitive function constructed using Principal Component Analysis (N = 300,486); or, 2) g Factor constructed using genomic structural equation modelling (N = 11,263–331,679). Findings for candidate causal proteins were replicated using a separate protein GWAS in Icelanders (N = 35,559). Results: A higher concentration of genetically predicted circulatory myeloperoxidase (MPO) was nominally associated with better cognitive performance ( p & lt; 0.05) using different selection criteria for genetic instruments. Particularly, brain-specific cis -eQTL predicted MPO, which accounts for protein-coding gene expression in brain tissues, was associated with general cognitive function (β Wald = 0.22, P Wald = 2.4 × 10 −4 ). The posterior probability for colocalization (PP.H4) of MPO pQTL with the g Factor was 0.577. Findings for MPO were replicated using the Icelandic GWAS. Although we did not find evidence for colocalization, we found that higher genetically predicted concentrations of cathepsin D and CD40 were associated with better cognitive performance and a higher genetically predicted concentration of CSF-1 was associated with poorer cognitive performance. Conclusion: We conclude that these proteins are involved in shared pathways between CVD and those for cognitive reserve or affecting cognitive decline, suggesting therapeutic targets able to reduce genetic risks conferred by cardiovascular disease.
    Type of Medium: Online Resource
    ISSN: 1664-8021
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fgene.2023.1124431
    DOI: 10.3389/fgene.2023.1124431.s001
    DOI: 10.3389/fgene.2023.1124431.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606823-0
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  • 4
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    Metabolome-wide association study on physical activity
    Springer Science and Business Media LLC ; 2023
    In:  Scientific Reports Vol. 13, No. 1 ( 2023-02-09)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2023-02-09)
    Abstract: The underlying mechanisms linking physical activity to better health are not fully understood. Here we examined the associations between physical activity and small circulatory molecules, the metabolome, to highlight relevant biological pathways. We examined plasma metabolites associated with self-reported physical activity among 2217 participants from the Airwave Health Monitoring Study. Metabolic profiling was conducted using the mass spectrometry-based Metabolon platform (LC/GC–MS), measuring 828 known metabolites. We replicated our findings in an independent subset of the study (n = 2971) using untargeted LC–MS. Mendelian randomisation was carried out to investigate potential causal associations between physical activity, body mass index, and metabolites. Higher vigorous physical activity was associated (P  〈  0.05/828 = 6.03 × 10 –5 ) with circulatory levels of 28 metabolites adjusted for age, sex and body mass index. The association was inverse for glutamate and diacylglycerol lipids, and direct for 3–4-hydroxyphenyllactate, phenyl lactate (PLA), alpha-hydroxy isovalerate, tiglylcarnitine, alpha-hydroxyisocaproate, 2-hydroxy-3-methylvalerate, isobutyrylcarnitine, imidazole lactate, methionine sulfone, indole lactate, plasmalogen lipids, pristanate and fumarate. In the replication panel, we found 23 untargeted LC–MS features annotated to the identified metabolites, for which we found nominal associations with the same direction of effect for three features annotated to 1-(1-enyl-palmitoyl)-2-oleoyl-GPC (P-16:0/18:1), 1-(1-enyl-palmitoyl)-2-linoleoyl-GPC (P-16:0/18:2), 1-stearoyl-2-dihomo-linolenoyl-GPC (18:0/20:3n3 or 6). Using Mendelian randomisation, we showed a potential causal relationship between body mass index and three identified metabolites. Circulatory metabolites are associated with physical activity and may play a role in mediating its health effects.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-022-26377-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2615211-3
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  • 5
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    Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of the American Heart Association Vol. 6, No. 6 ( 2017-11-06)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 6 ( 2017-11-06)
    Abstract: Plasminogen activator inhibitor type 1 ( PAI ‐1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI ‐1 levels are associated with increased risk of coronary heart disease ( CHD ). However, it is unclear whether the association reflects a causal influence of PAI ‐1 on CHD risk. Methods and Results To evaluate the association between PAI ‐1 and CHD , we applied a 3‐step strategy. First, we investigated the observational association between PAI ‐1 and CHD incidence using a systematic review based on a literature search for PAI ‐1 and CHD studies. Second, we explored the causal association between PAI ‐1 and CHD using a Mendelian randomization approach using summary statistics from large genome‐wide association studies. Finally, we explored the causal effect of PAI ‐1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta‐analysis, the highest quantile of blood PAI ‐1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age‐ and sex‐adjusted model. The effect size was reduced in studies using a multivariable‐adjusted model (odds ratio=1.46; 95% CI : 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI ‐1 level on CHD risk (odds ratio=1.22 per unit increase of log‐transformed PAI ‐1; 95% CI : 1.01, 1.47). In addition, we also detected a causal effect of PAI ‐1 on elevating blood glucose and high‐density lipoprotein cholesterol. Conclusions Our study indicates a causal effect of elevated PAI ‐1 level on CHD risk, which may be mediated by glucose dysfunction.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.116.004918
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2653953-6
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  • 6
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    Direct and indirect effect of the COVID-19 pandemic on patients with cardiomyopathy
    BMJ ; 2022
    In:  Open Heart Vol. 9, No. 1 ( 2022-01), p. e001918-
    Details
    In: Open Heart, BMJ, Vol. 9, No. 1 ( 2022-01), p. e001918-
    Abstract: (1) To evaluate the prevalence and hospitalisation rate of COVID-19 infections among patients with dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM) in the Royal Brompton and Harefield Hospital Cardiovascular Research Centre (RBHH CRC) Biobank. (2) To evaluate the indirect impact of the pandemic on patients with cardiomyopathy through the Heart Hive COVID-19 study. (3) To assess the impact of the pandemic on national cardiomyopathy-related hospital admissions. Methods (1) 1236 patients (703 DCM, 533 HCM) in the RBHH CRC Biobank were assessed for COVID-19 infections and hospitalisations; (2) 207 subjects (131 cardiomyopathy, 76 without heart disease) in the Heart Hive COVID-19 study completed online surveys evaluating physical health, psychological well-being, and behavioural adaptations during the pandemic and (3) 11 447 cardiomyopathy-related hospital admissions across National Health Service (NHS) England were studied from NHS Digital Hospital Episode Statistics over 2019–2020. Results A comparable proportion of patients with cardiomyopathy in the RBHH CRC Biobank had tested positive for COVID-19 compared with the UK population (1.1% vs 1.6%, p=0.14), but a higher proportion of those infected were hospitalised (53.8% vs 16.5%, p=0.002). In the Heart Hive COVID-19 study, more patients with cardiomyopathy felt their physical health had deteriorated due to the pandemic than subjects without heart disease (32.3% vs 13.2%, p=0.004) despite only 4.6% of the cardiomyopathy cohort reporting COVID-19 symptoms. A 17.9% year-on-year reduction in national cardiomyopathy-related hospital admissions was observed in 2020. Conclusion Patients with cardiomyopathy had similar reported rates of testing positive for COVID-19 to the background population, but those with test-proven infection were hospitalised more frequently. Deterioration in physical health amongst patients could not be explained by COVID-19 symptoms, inferring a significant contribution of the indirect consequences of the pandemic. Trial registration number NCT04468256
    Type of Medium: Online Resource
    ISSN: 2053-3624
    URL: Article
    DOI: 10.1136/openhrt-2021-001918
    Language: English
    Publisher: BMJ
    Publication Date: 2022
    detail.hit.zdb_id: 2747269-3
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  • 7
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    Abstract P389: Sex-Specific Genetic Interrogation of Cardiovascular Disease Drug Targets
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Circulation Vol. 147, No. Suppl_1 ( 2023-02-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 147, No. Suppl_1 ( 2023-02-28)
    Abstract: Investigating sex-specific effects of genetically-proxied drug target inhibition on cardiovascular disease (CVD) liability may improve the understanding of CVD pathophysiology and therapeutic intervention, to enhance the formulation of sex-specific treatment in clinical practice. We aimed to investigate sex-specific associations between genetic variation at CVD drug targets and CVD risk factors in the UK Biobank for anti-hypertensive, lipid-lowering and anti-inflammatory drug targets. Firstly, we conducted genome-wide association studies (GWAS) for systolic blood pressure (SBP), C-reactive protein (CRP), low density lipoprotein (LDL)-cholesterol for 488,226 women and men in the UK Biobank. We then performed genetic colocalization analyses to identify shared or differential genetic loci for CVD risk factors in males and females. Our findings highlight that females and males share potentially causal variants for SBP at the ADRB1, CACNA1D, CACNB2, CACNB3 and SLC12A3 drug targets, for LDL-cholesterol at PCSK9, HMGCR, and for CRP at IL6R . Notably, we highlight heterogeneous effects of SBP in men and women at ACE, CACNA1S, CACNA1C . This is the first comprehensive genetic interrogation of sex-specific effects on drug targets, suggesting physiological differences in hypertension-mediated CVD between men and women and potential differential response to anti-hypertensive medication. Whether this has viable clinical implications is yet to be formally tested in further sex-specific analyses in genetic association studies and clinical trials.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.147.suppl_1.P389
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 1466401-X
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  • 8
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    Pleiotropic genetic architecture and novel loci for C-reactive protein levels
    Springer Science and Business Media LLC ; 2022
    In:  Nature Communications Vol. 13, No. 1 ( 2022-11-14)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2022-11-14)
    Abstract: C-reactive protein is involved in a plethora of pathophysiological conditions. Many genetic loci associated with C-reactive protein are annotated to lipid and glucose metabolism genes supporting common biological pathways between inflammation and metabolic traits. To identify novel pleiotropic loci, we perform multi-trait analysis of genome-wide association studies on C-reactive protein levels along with cardiometabolic traits, followed by a series of in silico analyses including colocalization, phenome-wide association studies and Mendelian randomization. We find 41 novel loci and 19 gene sets associated with C-reactive protein with various pleiotropic effects. Additionally, 41 variants colocalize between C-reactive protein and cardiometabolic risk factors and 12 of them display unexpected discordant effects between the shared traits which are translated into discordant associations with clinical outcomes in subsequent phenome-wide association studies. Our findings provide insights into shared mechanisms underlying inflammation and lipid metabolism, representing potential preventive and therapeutic targets.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-022-34688-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2553671-0
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  • 9
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    Early exposure to social disadvantages and later life body mass index beyond genetic predisposition in three generations of Finnish birth cohorts
    Springer Science and Business Media LLC ; 2020
    In:  BMC Public Health Vol. 20, No. 1 ( 2020-12)
    Details
    In: BMC Public Health, Springer Science and Business Media LLC, Vol. 20, No. 1 ( 2020-12)
    Abstract: The study aimed to explore the association between early life and life-course exposure to social disadvantage and later life body mass index (BMI) accounting for genetic predisposition and maternal BMI. Methods We studied participants of Helsinki Birth Cohort Study born in 1934–1944 (HBCS1934–1944, n  = 1277) and Northern Finland Birth Cohorts born in 1966 and 1986 (NFBC1966, n  = 5807, NFBC1986, n  = 6717). Factor analysis produced scores of social disadvantage based on social and economic elements in early life and adulthood/over the life course, and was categorized as high, intermediate and low. BMI was measured at 62 years in HBCS1934–1944, at 46 years in NFBC1966 and at 16 years in NFBC1986. Multivariable linear regression analysis was used to explore associations between social disadvantages and BMI after adjustments for polygenic risk score for BMI (PRS BMI), maternal BMI and sex. Results The association between exposure to high early social disadvantage and increased later life BMI persisted after adjustments (β = 0.79, 95% CI, 0.33, 1.25, p   〈  0.001) in NFBC1966. In NFBC1986 this association was attenuated by PRS BMI ( p  = 0.181), and in HBCS1934–1944 there was no association between high early social disadvantage and increased later life BMI (β 0.22, 95% CI –0.91,1.35, p  = 0.700). In HBCS1934–1944 and NFBC1966, participants who had reduced their exposure to social disadvantage during the life-course had lower later life BMI than those who had increased their exposure (β − 1.34, [− 2.37,-0.31], p  = 0.011; β − 0.46, [− 0.89,-0.03], p  = 0.038, respectively). Conclusions High social disadvantage in early life appears to be associated with higher BMI in later life. Reducing exposure to social disadvantage during the life-course may be a potential pathway for obesity reduction.
    Type of Medium: Online Resource
    ISSN: 1471-2458
    URL: Article
    DOI: 10.1186/s12889-020-08763-w
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2041338-5
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  • 10
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    Abstract 11185: Impact of Covid-19 on Acute Myocarditis Hospital Admissions in the National Health Service of England, Uk (2019-2020)
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Abstract: Introduction: Acute myocarditis has been reported in patients infected with COVID-19 in case series and imaging-based studies. We sought to assess this link by evaluating trends in hospital admissions due to acute myocarditis and COVID-19 on a national level during the pandemic. Methods: Data on all NHS England hospital admissions with a primary or secondary diagnosis of acute myocarditis were acquired and curated from the NHS Digital hospital episode statistics dataset from 2019-2020. COVID-19 data was obtained from the UK government daily statistics. Rolling averages over 28-day periods are presented. Results: Across all ages, there were 1,894 hospital admissions due to myocarditis in 2019 compared with 1,610 in 2020 (15% reduction). During the first national lockdown (23 rd Mar-19 th Jun 2020), myocarditis admissions were 32% lower than the same period in 2019. During the second lockdown (5 th Nov-2 nd Dec), myocarditis admissions were 9% greater than in 2019, although this increase was not sustained throughout December despite the subsequent surge in COVID-19 admissions. In general, patients admitted in 2020, compared to 2019, were older (median age 46 years, interquartile range 28-61 vs 41 years, IQR 26-58; p 〈 0.001), but sex (66% men), ethnicity (39% non-Caucasian, 9% unknown) and duration of hospital admission (median 2 days; IQR 1-4) were similar for both years. Discussion: As COVID-19 admissions peaked in early 2020, there was a sharp decline in myocarditis admissions, probably attributed to profound disruptions in healthcare provision, but possibly due to reduced transmission of other viruses during lockdown. Whilst myocarditis admissions increased during the second lockdown, there was no clear association between COVID-19 and myocarditis admission numbers. Further research may identify delayed presentations or sequelae of myocarditis, particularly following the larger COVID-19 peak in January 2021, as well as the impact of the vaccination programme.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.11185
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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