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3. Association of human immunodeficiency virus and hepatitis C virus infection with long-term outcomes post-ST segment elevation myocardial infarction in a disadvantaged urban community

Author

Shitole, Sanyog G, Kuniholm, Mark H, Hanna, David B, Boucher, Thomas, Peng, Angel Y, Berardi, Cecilia, Shah, Tina, Bortnick, Anna E, Christia, Panagiota, Scheuer, James, and Kizer, Jorge R

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Heart Disease, HIV/AIDS, Emerging Infectious Diseases, Infectious Diseases, Chronic Liver Disease and Cirrhosis, Patient Safety, Liver Disease, Prevention, Hepatitis, Heart Disease - Coronary Heart Disease, Digestive Diseases, Cardiovascular, Hepatitis - C, Clinical Research, 2.2 Factors relating to the physical environment, Aetiology, Infection, Good Health and Well Being, Coinfection, HIV, HIV Infections, Hepacivirus, Hepatitis C, Hepatitis C, Chronic, Humans, ST Elevation Myocardial Infarction, Vulnerable Populations, HCV, STEMI, Outcomes, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundHIV and HCV have been linked to an increased risk of cardiovascular disease (CVD). Their impact on long-term outcomes following ST-segment myocardial infarction (STEMI) has not been previously studied.MethodsWe leveraged data from a STEMI registry (n = 1208) at an inner-city health system to assess the influence of HIV and HCV on post-STEMI outcomes. Cox regression was used to compare HIV-monoinfected (n = 22), HCV-monoinfected (n = 26) and HIV-HCV-coinfected patients (n = 8) with the neither-infected group (n = 1152) with regard to death, death or any readmission, and death or CVD readmission.ResultsThe cohort was majority black or Hispanic. Median follow-up was 4.3 years. Compared to the neither-infected group, the HIV-monoinfected group showed near-significantly higher risks of death or any readmission (HR = 1.62, 95% CI = 0.96, 2.74) and death or CVD readmission (HR = 1.82, 95% CI = 0.98, 3.39) after full adjustment. On similar comparison, the HCV-monoinfected group exhibited significantly higher risks of death (HR = 2.09, 95% CI = 1.05, 4.15) and death or any readmission (HR = 1.68, 95% CI = 1.07, 2.65), whereas the HIV-HCV-coinfected group showed higher risk of death (HR = 6.51, 95% CI = 2.28, 18.61).ConclusionsIn this cohort composed mostly of race-ethnic minorities, HIV monoinfection tended to be associated with 1.6-to-1.8-fold higher risk of death or readmission for any cause or CVD over long-term follow-up compared to neither infection, whereas HCV monoinfection was associated with 1.7-to-2.1-fold higher risk of death and death or any readmission, and HIV-HCV coinfection with 6.5-fold higher risk of death. These associations require further study in larger populations, but highlight the importance of identifying and treating HIV and HCV in patients presenting with STEMI.

Published
2020

4. Identifying and visualising multimorbidity and comorbidity patterns in patients in the English National Health Service: a population-based study

Author

Alexander, Daniel C, Asiimwe, Innocent G, Ball, Simon, Bennett, Frances, Borges, Maria Carolina, Butterworth, Adam, Chaturvedi, Nishi, Chopade, Sandesh, Clarkson, Christopher, Cox, Martin, Dale, Caroline, Denaxas, Spiros, Dunca, Diana, Engmann, Jorgen E, Fernandez-Sanles, Alba, Finan, Chris, Fitzpatrick, Natalie, Gallagher, Jean, Gonzalez-Izquierdo, Arturo, Gratton, Jasmine, Gross, Christian, Hemingway, Harry, Henry, Albert, Hidajat, Mira, Hingorani, Aroon, Hukerikar, Nikita, Jorgensen, Andrea, Joshi, Roshni, Katsoulis, Michail, Kuan, Valerie, Kumar, Rashmi, Lai, Alvina G, Langenberg, Claudia, Lawlor, Deborah, Mancini, Mary, Miller, Diane, Ogden, Margaret, Ozyigit, Eda B, Patel, Shilpa, Pirmohamed, Munir, Roberts, Amanda, Ryan, David, Schmidt, Amand F, Shah, Anoop D, Shah, Tina, Sofat, Reecha, Takhar, Rohan, Torralbo, Ana, Ullah, Ayath, Walker, Lauren E, Warwick, Alasdair, Wheeler, Eleanor, Wright, Victoria L, Wu, Honghan, Zwierzyna, Magdalena, Patalay, Praveetha, Nitsch, Dorothea, Mathur, Rohini, Partridge, Linda, Wong, Ian C K, Hingorani, Melanie, and Hingorani, Aroon D

Published
2023
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6. Infective Endocarditis

Author

Shah, Tina, Hamill, Richard J., Ramasubbu, Kumudha, Willerson, James T., Series Editor, and Carabello, Blase A., editor

Published
2020
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9. Validation of lipid-related therapeutic targets for coronary heart disease prevention using human genetics

Author

Gordillo-Marañón, María, Zwierzyna, Magdalena, Charoen, Pimphen, Drenos, Fotios, Chopade, Sandesh, Shah, Tina, Engmann, Jorgen, Chaturvedi, Nishi, Papacosta, Olia, Wannamethee, Goya, Wong, Andrew, Sofat, Reecha, Kivimaki, Mika, Price, Jackie F., Hughes, Alun D., Gaunt, Tom R., Lawlor, Deborah A., Gaulton, Anna, Hingorani, Aroon D., Schmidt, Amand F., and Finan, Chris

Published
2021
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11. HMG-coenzyme A reductase inhibition, type 2 diabetes, and bodyweight: evidence from genetic analysis and randomised trials

Author

Swerdlow, Daniel I, Preiss, David, Kuchenbaecker, Karoline B, Holmes, Michael V, Engmann, Jorgen EL, Shah, Tina, Sofat, Reecha, Stender, Stefan, Johnson, Paul CD, Scott, Robert A, Leusink, Maarten, Verweij, Niek, Sharp, Stephen J, Guo, Yiran, Giambartolomei, Claudia, Chung, Christina, Peasey, Anne, Amuzu, Antoinette, Li, KaWah, Palmen, Jutta, Howard, Philip, Cooper, Jackie A, Drenos, Fotios, Li, Yun R, Lowe, Gordon, Gallacher, John, Stewart, Marlene CW, Tzoulaki, Ioanna, Buxbaum, Sarah G, van der A, Daphne L, Forouhi, Nita G, Onland-Moret, N Charlotte, van der Schouw, Yvonne T, Schnabel, Renate B, Hubacek, Jaroslav A, Kubinova, Ruzena, Baceviciene, Migle, Tamosiunas, Abdonas, Pajak, Andrzej, Topor-Madry, Romanvan, Stepaniak, Urszula, Malyutina, Sofia, Baldassarre, Damiano, Sennblad, Bengt, Tremoli, Elena, de Faire, Ulf, Veglia, Fabrizio, Ford, Ian, Jukema, J Wouter, Westendorp, Rudi GJ, de Borst, Gert Jan, de Jong, Pim A, Algra, Ale, Spiering, Wilko, der Zee, Anke H Maitland-van, Klungel, Olaf H, de Boer, Anthonius, Doevendans, Pieter A, Eaton, Charles B, Robinson, Jennifer G, Duggan, David, DIAGRAM Consortium, MAGIC Consortium, Kjekshus, John, Downs, John R, Gotto, Antonio M, Keech, Anthony C, Marchioli, Roberto, Tognoni, Gianni, Sever, Peter S, Poulter, Neil R, Waters, David D, Pedersen, Terje R, Amarenco, Pierre, Nakamura, Haruo, McMurray, John JV, Lewsey, James D, Chasman, Daniel I, Ridker, Paul M, Maggioni, Aldo P, Tavazzi, Luigi, Ray, Kausik K, Seshasai, Sreenivasa Rao Kondapally, Manson, JoAnn E, Price, Jackie F, Whincup, Peter H, Morris, Richard W, Lawlor, Debbie A, Smith, George Davey, Ben-Shlomo, Yoav, Schreiner, Pamela J, Fornage, Myriam, Siscovick, David S, Cushman, Mary, Kumari, Meena, Wareham, Nick J, Verschuren, WM Monique, Redline, Susan, Patel, Sanjay R, Whittaker, John C, and Hamsten, Anders

Subjects
Epidemiology, Biomedical and Clinical Sciences, Health Sciences, Clinical Trials and Supportive Activities, Clinical Research, Genetics, Nutrition, Diabetes, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Metabolic and endocrine, Aged, Body Mass Index, Body Weight, Cholesterol, HDL, Cholesterol, LDL, Diabetes Mellitus, Type 2, Female, Genetic Testing, Humans, Hydroxymethylglutaryl CoA Reductases, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Male, Middle Aged, Polymorphism, Single Nucleotide, Randomized Controlled Trials as Topic, Risk Factors, DIAGRAM Consortium, MAGIC Consortium, InterAct Consortium, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundStatins increase the risk of new-onset type 2 diabetes mellitus. We aimed to assess whether this increase in risk is a consequence of inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the intended drug target.MethodsWe used single nucleotide polymorphisms in the HMGCR gene, rs17238484 (for the main analysis) and rs12916 (for a subsidiary analysis) as proxies for HMGCR inhibition by statins. We examined associations of these variants with plasma lipid, glucose, and insulin concentrations; bodyweight; waist circumference; and prevalent and incident type 2 diabetes. Study-specific effect estimates per copy of each LDL-lowering allele were pooled by meta-analysis. These findings were compared with a meta-analysis of new-onset type 2 diabetes and bodyweight change data from randomised trials of statin drugs. The effects of statins in each randomised trial were assessed using meta-analysis.FindingsData were available for up to 223 463 individuals from 43 genetic studies. Each additional rs17238484-G allele was associated with a mean 0·06 mmol/L (95% CI 0·05-0·07) lower LDL cholesterol and higher body weight (0·30 kg, 0·18-0·43), waist circumference (0·32 cm, 0·16-0·47), plasma insulin concentration (1·62%, 0·53-2·72), and plasma glucose concentration (0·23%, 0·02-0·44). The rs12916 SNP had similar effects on LDL cholesterol, bodyweight, and waist circumference. The rs17238484-G allele seemed to be associated with higher risk of type 2 diabetes (odds ratio [OR] per allele 1·02, 95% CI 1·00-1·05); the rs12916-T allele association was consistent (1·06, 1·03-1·09). In 129 170 individuals in randomised trials, statins lowered LDL cholesterol by 0·92 mmol/L (95% CI 0·18-1·67) at 1-year of follow-up, increased bodyweight by 0·24 kg (95% CI 0·10-0·38 in all trials; 0·33 kg, 95% CI 0·24-0·42 in placebo or standard care controlled trials and -0·15 kg, 95% CI -0·39 to 0·08 in intensive-dose vs moderate-dose trials) at a mean of 4·2 years (range 1·9-6·7) of follow-up, and increased the odds of new-onset type 2 diabetes (OR 1·12, 95% CI 1·06-1·18 in all trials; 1·11, 95% CI 1·03-1·20 in placebo or standard care controlled trials and 1·12, 95% CI 1·04-1·22 in intensive-dose vs moderate dose trials).InterpretationThe increased risk of type 2 diabetes noted with statins is at least partially explained by HMGCR inhibition.FundingThe funding sources are cited at the end of the paper.

Published
2015

12. Understanding by General Providers of the Echocardiogram Report

Author

Trang, Amanda, Kampangkaew, June, Fernandes, Robin, Tiwana, Jasleen, Misra, Arunima, Hamzeh, Ihab, Blaustein, Alvin, Aguilar, David, Shah, Tina, Ballantyne, Christie, Quinones, Miguel, Nagueh, Sherif F., Dokanish, Hisham, Virani, Salim S., Deswal, Anita, Kirkpatrick, James N., and Nambi, Vijay

Published
2019
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13. Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data.

Author

Holmes, Michael V, Dale, Caroline E, Zuccolo, Luisa, Silverwood, Richard J, Guo, Yiran, Ye, Zheng, Prieto-Merino, David, Dehghan, Abbas, Trompet, Stella, Wong, Andrew, Cavadino, Alana, Drogan, Dagmar, Padmanabhan, Sandosh, Li, Shanshan, Yesupriya, Ajay, Leusink, Maarten, Sundstrom, Johan, Hubacek, Jaroslav A, Pikhart, Hynek, Swerdlow, Daniel I, Panayiotou, Andrie G, Borinskaya, Svetlana A, Finan, Chris, Shah, Sonia, Kuchenbaecker, Karoline B, Shah, Tina, Engmann, Jorgen, Folkersen, Lasse, Eriksson, Per, Ricceri, Fulvio, Melander, Olle, Sacerdote, Carlotta, Gamble, Dale M, Rayaprolu, Sruti, Ross, Owen A, McLachlan, Stela, Vikhireva, Olga, Sluijs, Ivonne, Scott, Robert A, Adamkova, Vera, Flicker, Leon, Bockxmeer, Frank M van, Power, Christine, Marques-Vidal, Pedro, Meade, Tom, Marmot, Michael G, Ferro, Jose M, Paulos-Pinheiro, Sofia, Humphries, Steve E, Talmud, Philippa J, Mateo Leach, Irene, Verweij, Niek, Linneberg, Allan, Skaaby, Tea, Doevendans, Pieter A, Cramer, Maarten J, van der Harst, Pim, Klungel, Olaf H, Dowling, Nicole F, Dominiczak, Anna F, Kumari, Meena, Nicolaides, Andrew N, Weikert, Cornelia, Boeing, Heiner, Ebrahim, Shah, Gaunt, Tom R, Price, Jackie F, Lannfelt, Lars, Peasey, Anne, Kubinova, Ruzena, Pajak, Andrzej, Malyutina, Sofia, Voevoda, Mikhail I, Tamosiunas, Abdonas, Maitland-van der Zee, Anke H, Norman, Paul E, Hankey, Graeme J, Bergmann, Manuela M, Hofman, Albert, Franco, Oscar H, Cooper, Jackie, Palmen, Jutta, Spiering, Wilko, de Jong, Pim A, Kuh, Diana, Hardy, Rebecca, Uitterlinden, Andre G, Ikram, M Arfan, Ford, Ian, Hyppönen, Elina, Almeida, Osvaldo P, Wareham, Nicholas J, Khaw, Kay-Tee, Hamsten, Anders, Husemoen, Lise Lotte N, Tjønneland, Anne, Tolstrup, Janne S, Rimm, Eric, Beulens, Joline WJ, and Verschuren, WM Monique

Subjects
InterAct Consortium, Humans, Coronary Disease, Alcohol Dehydrogenase, Genetic Markers, Models, Statistical, Alcohol Drinking, Genotype, Polymorphism, Single Nucleotide, Adult, Aged, Middle Aged, Female, Male, Stroke, Mendelian Randomization Analysis, Biomarkers, General & Internal Medicine, Clinical Sciences, Public Health and Health Services
Abstract

ObjectiveTo use the rs1229984 variant in the alcohol dehydrogenase 1B gene (ADH1B) as an instrument to investigate the causal role of alcohol in cardiovascular disease.DesignMendelian randomisation meta-analysis of 56 epidemiological studies.Participants261 991 individuals of European descent, including 20 259 coronary heart disease cases and 10 164 stroke events. Data were available on ADH1B rs1229984 variant, alcohol phenotypes, and cardiovascular biomarkers.Main outcome measuresOdds ratio for coronary heart disease and stroke associated with the ADH1B variant in all individuals and by categories of alcohol consumption.ResultsCarriers of the A-allele of ADH1B rs1229984 consumed 17.2% fewer units of alcohol per week (95% confidence interval 15.6% to 18.9%), had a lower prevalence of binge drinking (odds ratio 0.78 (95% CI 0.73 to 0.84)), and had higher abstention (odds ratio 1.27 (1.21 to 1.34)) than non-carriers. Rs1229984 A-allele carriers had lower systolic blood pressure (-0.88 (-1.19 to -0.56) mm Hg), interleukin-6 levels (-5.2% (-7.8 to -2.4%)), waist circumference (-0.3 (-0.6 to -0.1) cm), and body mass index (-0.17 (-0.24 to -0.10) kg/m(2)). Rs1229984 A-allele carriers had lower odds of coronary heart disease (odds ratio 0.90 (0.84 to 0.96)). The protective association of the ADH1B rs1229984 A-allele variant remained the same across all categories of alcohol consumption (P=0.83 for heterogeneity). Although no association of rs1229984 was identified with the combined subtypes of stroke, carriers of the A-allele had lower odds of ischaemic stroke (odds ratio 0.83 (0.72 to 0.95)).ConclusionsIndividuals with a genetic variant associated with non-drinking and lower alcohol consumption had a more favourable cardiovascular profile and a reduced risk of coronary heart disease than those without the genetic variant. This suggests that reduction of alcohol consumption, even for light to moderate drinkers, is beneficial for cardiovascular health.

Published
2014

16. Large-Scale Gene-Centric Meta-analysis across 32 Studies Identifies Multiple Lipid Loci

Author

Asselbergs, Folkert W, Guo, Yiran, van Iperen, Erik PA, Sivapalaratnam, Suthesh, Tragante, Vinicius, Lanktree, Matthew B, Lange, Leslie A, Almoguera, Berta, Appelman, Yolande E, Barnard, John, Baumert, Jens, Beitelshees, Amber L, Bhangale, Tushar R, Chen, Yii-Der Ida, Gaunt, Tom R, Gong, Yan, Hopewell, Jemma C, Johnson, Toby, Kleber, Marcus E, Langaee, Taimour Y, Li, Mingyao, Li, Yun R, Liu, Kiang, McDonough, Caitrin W, Meijs, Matthijs FL, Middelberg, Rita PS, Musunuru, Kiran, Nelson, Christopher P, O’Connell, Jeffery R, Padmanabhan, Sandosh, Pankow, James S, Pankratz, Nathan, Rafelt, Suzanne, Rajagopalan, Ramakrishnan, Romaine, Simon PR, Schork, Nicholas J, Shaffer, Jonathan, Shen, Haiqing, Smith, Erin N, Tischfield, Sam E, van der Most, Peter J, van Vliet-Ostaptchouk, Jana V, Verweij, Niek, Volcik, Kelly A, Zhang, Li, Bailey, Kent R, Bailey, Kristian M, Bauer, Florianne, Boer, Jolanda MA, Braund, Peter S, Burt, Amber, Burton, Paul R, Buxbaum, Sarah G, Chen, Wei, Cooper-DeHoff, Rhonda M, Cupples, L Adrienne, deJong, Jonas S, Delles, Christian, Duggan, David, Fornage, Myriam, Furlong, Clement E, Glazer, Nicole, Gums, John G, Hastie, Claire, Holmes, Michael V, Illig, Thomas, Kirkland, Susan A, Kivimaki, Mika, Klein, Ronald, Klein, Barbara E, Kooperberg, Charles, Kottke-Marchant, Kandice, Kumari, Meena, LaCroix, Andrea Z, Mallela, Laya, Murugesan, Gurunathan, Ordovas, Jose, Ouwehand, Willem H, Post, Wendy S, Saxena, Richa, Scharnagl, Hubert, Schreiner, Pamela J, Shah, Tina, Shields, Denis C, Shimbo, Daichi, Srinivasan, Sathanur R, Stolk, Ronald P, Swerdlow, Daniel I, Taylor, Herman A, Topol, Eric J, Toskala, Elina, van Pelt, Joost L, van Setten, Jessica, Yusuf, Salim, Whittaker, John C, Zwinderman, AH, Study, LifeLines Cohort, Anand, Sonia S, Balmforth, Anthony J, and Berenson, Gerald S

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Epidemiology, Health Sciences, Human Genome, Cardiovascular, Atherosclerosis, Aetiology, 2.1 Biological and endogenous factors, Cholesterol, HDL, Cholesterol, LDL, Female, Genome-Wide Association Study, Genotype, Humans, Lipids, Male, Phenotype, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Sex Factors, Triglycerides, White People, LifeLines Cohort Study, Medical and Health Sciences, Genetics & Heredity, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Genome-wide association studies (GWASs) have identified many SNPs underlying variations in plasma-lipid levels. We explore whether additional loci associated with plasma-lipid phenotypes, such as high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TGs), can be identified by a dense gene-centric approach. Our meta-analysis of 32 studies in 66,240 individuals of European ancestry was based on the custom ∼50,000 SNP genotyping array (the ITMAT-Broad-CARe array) covering ∼2,000 candidate genes. SNP-lipid associations were replicated either in a cohort comprising an additional 24,736 samples or within the Global Lipid Genetic Consortium. We identified four, six, ten, and four unreported SNPs in established lipid genes for HDL-C, LDL-C, TC, and TGs, respectively. We also identified several lipid-related SNPs in previously unreported genes: DGAT2, HCAR2, GPIHBP1, PPARG, and FTO for HDL-C; SOCS3, APOH, SPTY2D1, BRCA2, and VLDLR for LDL-C; SOCS3, UGT1A1, BRCA2, UBE3B, FCGR2A, CHUK, and INSIG2 for TC; and SERPINF2, C4B, GCK, GATA4, INSR, and LPAL2 for TGs. The proportion of explained phenotypic variance in the subset of studies providing individual-level data was 9.9% for HDL-C, 9.5% for LDL-C, 10.3% for TC, and 8.0% for TGs. This large meta-analysis of lipid phenotypes with the use of a dense gene-centric approach identified multiple SNPs not previously described in established lipid genes and several previously unknown loci. The explained phenotypic variance from this approach was comparable to that from a meta-analysis of GWAS data, suggesting that a focused genotyping approach can further increase the understanding of heritability of plasma lipids.

Published
2012

17. Linking observational and genetic approaches to determine the role of C-reactive protein in coronary disease risk

Author

Shah, Tina

Subjects
616.1
Abstract

Inflammation may contribute to atherogenesis. C-reactive protein (CRP) is an acute phase protein whose circulating concentrations provide an index of infection or inflammation. Prospective studies have consistently shown associations of CRP among apparently healthy individuals with risk of future hypertension, diabetes and coronary heart disease (CHD) events, leading to the proposal that CRP may play a causal role in atherogenesis, and its measurement could help predict CHD events. However, CRP is associated with a range of risk factors and biomarkers linked to atherosclerosis, so its predictive utility could be limited once these are accounted for. Its causal relevance is also uncertain because of the potential for confounding and reverse causation in observational studies. Experimental data have not resolved controversy on causation, as recent studies have indicated that apparently pro-atherogenic actions of CRP may have been mediated by preservatives or contaminants in commercial CRP preparations. Studies were therefore undertaken to evaluate the role of CRP in the prediction and pathogenesis of atherosclerotic events, by linking observational with genetic approaches. Appropriate analytical tools were used to evaluate the performance of CRP as a screening test for CHD. Single nucleotide polymorphisms (SNPs) in the CRP gene were identified using a bioinformatic approach and linkage disequilibrium was assessed to identify 'tagging SNPs" from which haplotypes could be inferred. A literature-based systematic review was undertaken to obtain precise estimates of the effect of SNPs on CRP concentration and to confirm the expected balanced distribution of potential confounders. In new studies, associations between haplotype (or genotype for a potentially functional promoter variant), and CRP concentration were tested. The effect of SNPs and haplotypes on CRP following an acute inflammatory stimulus was also assessed. The frequency of CRP SNPs and their effect on CRP were also examined in different ethnic groups. Having confirmed that SNPs and haplotypes of the CRP gene provide an unbiased proxy for CRP itself, associations with pro-atherogenic phenotypes, incident hypertension, diabetes and CHD were tested. Despite showing association with CHD, CRP performed poorly as a predictive test. Reasons for the poor performance were explored and comparisons were made with established risk factors and emerging biomarkers. SNPs and haplotypes were associated robustly with CRP, but not with other risk factors for CHD. A Mendelian randomisation approach linking genetic and non-genetic information provided no positive evidence that CRP induces a proatherogenic phenotype, nor increases risk of hypertension, diabetes or CHD. However, larger sample sizes will be required to exclude a small but potentially important causal influence of CRP on cardiovascular risk. In the absence of a selective CRP-lowering drug, this approach provides the only currently practical method for obtaining randomised evidence on the causal relevance of CRP in atherogenesis.

Published
2007

21. Heart Failure, Introduction

Author

Shah, Tina, Palaskas, Nicolas, Bozkurt, Biykem, Jagadeesh, Gowraganahalli, editor, Balakumar, Pitchai, editor, and Maung-U, Khin, editor

Published
2015
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24. Plasma urate concentration and risk of coronary heart disease: a Mendelian randomisation analysis

Author

White, Jon, Sofat, Reecha, Hemani, Gibran, Shah, Tina, Engmann, Jorgen, Dale, Caroline, Shah, Sonia, Kruger, Felix A, Giambartolomei, Claudia, Swerdlow, Daniel I, Palmer, Tom, McLachlan, Stela, Langenberg, Claudia, Zabaneh, Delilah, Lovering, Ruth, Cavadino, Alana, Jefferis, Barbara, Finan, Chris, Wong, Andrew, Amuzu, Antoinette, Ong, Ken, Gaunt, Tom R, Warren, Helen, Davies, Teri-Louise, Drenos, Fotios, Cooper, Jackie, Ebrahim, Shah, Lawlor, Debbie A, Talmud, Philippa J, Humphries, Steve E, Power, Christine, Hypponen, Elina, Richards, Marcus, Hardy, Rebecca, Kuh, Diana, Wareham, Nicholas, Ben-Shlomo, Yoav, Day, Ian N, Whincup, Peter, Morris, Richard, Strachan, Mark W J, Price, Jacqueline, Kumari, Meena, Kivimaki, Mika, Plagnol, Vincent, Whittaker, John C, Smith, George Davey, Dudbridge, Frank, Casas, Juan P, Holmes, Michael V, and Hingorani, Aroon D

Published
2016
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26. Contributors

Author

Abbara, Suhny, primary, Aguilar, David, additional, Awtry, Eric H., additional, Baez-Escudero, Jose L., additional, Bakaeen, Faisal, additional, Balady, Gary J., additional, Beauchesne, Luc M., additional, Bernard, Sheilah A., additional, Bilen, Ozlem, additional, Birnbaum, Itamar, additional, Birnbaum, Yochai, additional, Boccalandro, Fernando, additional, Bozkurt, Biykem, additional, Carabello, Blase, additional, Chandrasekhar, Jaya, additional, Cooper, Leslie T., additional, Cunningham, Luke, additional, Denktas, Ali E., additional, Deswal, Anita, additional, Elgharably, Haytham, additional, Faber, Lothar, additional, Farkouh, Michael E., additional, Faza, Nadeen N., additional, Fedson, Savitri, additional, Felker, G. Michael, additional, Fenton, James J., additional, Field, Michael E., additional, Flamm, Scott D., additional, Fleisher, Lee A., additional, Flink, Laura Epstein, additional, French, Amy, additional, Fudim, Marat, additional, Gannon, Stephen A., additional, Governatori, Nicholas, additional, Grines, Cindy, additional, Habib, Gabriel B., additional, Hamzeh, Ihab, additional, Hinohara, Tomoya Timothy, additional, Hoang, Vu, additional, Hoit, Brian D., additional, Jneid, Hani, additional, Joglar, Jose A., additional, Johnston, Douglas R., additional, Joseph, Lee, additional, Kayani, Waleed T., additional, Kent, Thomas A., additional, Kerrigan, Jimmy L., additional, Kfoury, Elias, additional, Khalaf, Shaden, additional, Khalid, Mirza Umair, additional, Kim, Esther S.H., additional, Kougias, Panos, additional, Krishnaswamy, Amar, additional, Kroll, Michael H., additional, Kulkarni, Nitin, additional, Lange, Richard A., additional, Mangione, Salvatore, additional, Martini, Sharyl R., additional, McCord, James, additional, Mehran, Roxana, additional, Merli, Geno J., additional, Mick, Stephanie L., additional, Moore, Curtiss, additional, Nair, Ajith, additional, Nambi, Vijay, additional, Nicewarner, Heidi, additional, Ohman, E. Magnus, additional, Palaskas, Nicolas, additional, Pandit, Lavannya M., additional, Patel, Niraj R., additional, Phillips, Lawrence, additional, Pipe, Andrew, additional, Pollack, Charles V., additional, Pollet, Mark, additional, Prenner, Stuart B., additional, Rajiah, Prabhakar, additional, Rodriguez-Manero, Moises, additional, Roselli, Eric E., additional, Safdar, Zeenat, additional, Sanchez-Alvarez, Catalina, additional, Schurmann, Paul, additional, Shah, Nishant R., additional, Shah, Sanjiv J., additional, Shah, Tina, additional, Shaib, Fidaa, additional, Sidhu, Mandeep S., additional, Soltesz, Edward G., additional, Spinler, Sarah A., additional, Sun, Yamin, additional, Tamara, Luis A., additional, Tapson, Victor, additional, Thamwiwat, Alisa, additional, Thavendiranathan, Paaladinesh, additional, Thomas, Rahul, additional, Thompson, Kara A., additional, Titas, Megan, additional, Zhen-Yu Tong, Michael, additional, Valderrábano, Miguel, additional, Vekstein, Andrew, additional, Virani, Salim, additional, Virk, Fawad, additional, Von Schoettler, Hercilia, additional, Weinberg, Aaron S., additional, and Zeeshan, Ahmad, additional

Published
2018
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28. Identifying and visualising multimorbidity and comorbidity patterns in patients in the English National Health Service: a population-based study

Author

Kuan, Valerie, primary, Denaxas, Spiros, additional, Patalay, Praveetha, additional, Nitsch, Dorothea, additional, Mathur, Rohini, additional, Gonzalez-Izquierdo, Arturo, additional, Sofat, Reecha, additional, Partridge, Linda, additional, Roberts, Amanda, additional, Wong, Ian C K, additional, Hingorani, Melanie, additional, Chaturvedi, Nishi, additional, Hemingway, Harry, additional, Hingorani, Aroon D, additional, Alexander, Daniel C, additional, Asiimwe, Innocent G, additional, Ball, Simon, additional, Bennett, Frances, additional, Borges, Maria Carolina, additional, Butterworth, Adam, additional, Chopade, Sandesh, additional, Clarkson, Christopher, additional, Cox, Martin, additional, Dale, Caroline, additional, Dunca, Diana, additional, Engmann, Jorgen E, additional, Fernandez-Sanles, Alba, additional, Finan, Chris, additional, Fitzpatrick, Natalie, additional, Gallagher, Jean, additional, Gratton, Jasmine, additional, Gross, Christian, additional, Henry, Albert, additional, Hidajat, Mira, additional, Hingorani, Aroon, additional, Hukerikar, Nikita, additional, Jorgensen, Andrea, additional, Joshi, Roshni, additional, Katsoulis, Michail, additional, Kuan, Valerie, additional, Kumar, Rashmi, additional, Lai, Alvina G, additional, Langenberg, Claudia, additional, Lawlor, Deborah, additional, Mancini, Mary, additional, Miller, Diane, additional, Ogden, Margaret, additional, Ozyigit, Eda B, additional, Patel, Shilpa, additional, Pirmohamed, Munir, additional, Ryan, David, additional, Schmidt, Amand F, additional, Shah, Anoop D, additional, Shah, Tina, additional, Takhar, Rohan, additional, Torralbo, Ana, additional, Ullah, Ayath, additional, Walker, Lauren E, additional, Warwick, Alasdair, additional, Wheeler, Eleanor, additional, Wright, Victoria L, additional, Wu, Honghan, additional, and Zwierzyna, Magdalena, additional

Published
2023
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29. GWAS and colocalization analyses implicate carotid intima-media thickness and carotid plaque loci in cardiovascular outcomes

Author

Franceschini, Nora, Giambartolomei, Claudia, de Vries, Paul S., Finan, Chris, Bis, Joshua C., Huntley, Rachael P., Lovering, Ruth C., Tajuddin, Salman M., Winkler, Thomas W., Graff, Misa, Kavousi, Maryam, Dale, Caroline, Smith, Albert V., Hofer, Edith, van Leeuwen, Elisabeth M., Nolte, Ilja M., Lu, Lingyi, Scholz, Markus, Sargurupremraj, Muralidharan, Pitkänen, Niina, Franzén, Oscar, Joshi, Peter K., Noordam, Raymond, Marioni, Riccardo E., Hwang, Shih-Jen, Musani, Solomon K., Schminke, Ulf, Palmas, Walter, Isaacs, Aaron, Correa, Adolfo, Zonderman, Alan B., Hofman, Albert, Teumer, Alexander, Cox, Amanda J., Uitterlinden, André G., Wong, Andrew, Smit, Andries J., Newman, Anne B., Britton, Annie, Ruusalepp, Arno, Sennblad, Bengt, Hedblad, Bo, Pasaniuc, Bogdan, Penninx, Brenda W., Langefeld, Carl D., Wassel, Christina L., Tzourio, Christophe, Fava, Cristiano, Baldassarre, Damiano, O’Leary, Daniel H., Teupser, Daniel, Kuh, Diana, Tremoli, Elena, Mannarino, Elmo, Grossi, Enzo, Boerwinkle, Eric, Schadt, Eric E., Ingelsson, Erik, Veglia, Fabrizio, Rivadeneira, Fernando, Beutner, Frank, Chauhan, Ganesh, Heiss, Gerardo, Snieder, Harold, Campbell, Harry, Völzke, Henry, Markus, Hugh S., Deary, Ian J., Jukema, J. Wouter, de Graaf, Jacqueline, Price, Jacqueline, Pott, Janne, Hopewell, Jemma C., Liang, Jingjing, Thiery, Joachim, Engmann, Jorgen, Gertow, Karl, Rice, Kenneth, Taylor, Kent D., Dhana, Klodian, Kiemeney, Lambertus A. L. M., Lind, Lars, Raffield, Laura M., Launer, Lenore J., Holdt, Lesca M., Dörr, Marcus, Dichgans, Martin, Traylor, Matthew, Sitzer, Matthias, Kumari, Meena, Kivimaki, Mika, Nalls, Mike A., Melander, Olle, Raitakari, Olli, Franco, Oscar H., Rueda-Ochoa, Oscar L., Roussos, Panos, Whincup, Peter H., Amouyel, Philippe, Giral, Philippe, Anugu, Pramod, Wong, Quenna, Malik, Rainer, Rauramaa, Rainer, Burkhardt, Ralph, Hardy, Rebecca, Schmidt, Reinhold, de Mutsert, Renée, Morris, Richard W., Strawbridge, Rona J., Wannamethee, S. Goya, Hägg, Sara, Shah, Sonia, McLachlan, Stela, Trompet, Stella, Seshadri, Sudha, Kurl, Sudhir, Heckbert, Susan R., Ring, Susan, Harris, Tamara B., Lehtimäki, Terho, Galesloot, Tessel E., Shah, Tina, de Faire, Ulf, Plagnol, Vincent, Rosamond, Wayne D., Post, Wendy, Zhu, Xiaofeng, Zhang, Xiaoling, Guo, Xiuqing, Saba, Yasaman, MEGASTROKE Consortium, Dehghan, Abbas, Seldenrijk, Adrie, Morrison, Alanna C., Hamsten, Anders, Psaty, Bruce M., van Duijn, Cornelia M., Lawlor, Deborah A., Mook-Kanamori, Dennis O., Bowden, Donald W., Schmidt, Helena, Wilson, James F., Wilson, James G., Rotter, Jerome I., Wardlaw, Joanna M., Deanfield, John, Halcox, Julian, Lyytikäinen, Leo-Pekka, Loeffler, Markus, Evans, Michele K., Debette, Stéphanie, Humphries, Steve E., Völker, Uwe, Gudnason, Vilmundur, Hingorani, Aroon D., Björkegren, Johan L. M., Casas, Juan P., and O’Donnell, Christopher J.

Published
2018
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36. Association between alcohol and cardiovascular disease : Mendelian randomisation analysis based on individual participant data

Author

IMPROVE study group, The InterAct Consortium, Holmes, Michael V, Dale, Caroline E, Zuccolo, Luisa, Silverwood, Richard J, Guo, Yiran, Ye, Zheng, Prieto-Merino, David, Dehghan, Abbas, Trompet, Stella, Wong, Andrew, Cavadino, Alana, Drogan, Dagmar, Padmanabhan, Sandosh, Li, Shanshan, Yesupriya, Ajay, Leusink, Maarten, Sundstrom, Johan, Hubacek, Jaroslav A, Pikhart, Hynek, Swerdlow, Daniel I, Panayiotou, Andrie G, Borinskaya, Svetlana A, Finan, Chris, Shah, Sonia, Kuchenbaecker, Karoline B, Shah, Tina, Engmann, Jorgen, Folkersen, Lasse, Eriksson, Per, Ricceri, Fulvio, Melander, Olle, Sacerdote, Carlotta, Gamble, Dale M, Rayaprolu, Sruti, Ross, Owen A, McLachlan, Stela, Vikhireva, Olga, Sluijs, Ivonne, Scott, Robert A, Adamkova, Vera, Flicker, Leon, van Bockxmeer, Frank M, Power, Christine, Marques-Vidal, Pedro, Meade, Tom, Marmot, Michael G, Ferro, Jose M, Paulos-Pinheiro, Sofia, Humphries, Steve E, Talmud, Philippa J, Leach, Irene Mateo, Verweij, Niek, Linneberg, Allan, Skaaby, Tea, Doevendans, Pieter A, Cramer, Maarten J, van der Harst, Pim, Klungel, Olaf H, Dowling, Nicole F, Dominiczak, Anna F, Kumari, Meena, Nicolaides, Andrew N, Weikert, Cornelia, Boeing, Heiner, Ebrahim, Shah, Gaunt, Tom R, Price, Jackie F, Lannfelt, Lars, Peasey, Anne, Kubinova, Ruzena, Pajak, Andrzej, Malyutina, Sofia, Voevoda, Mikhail I, Tamosiunas, Abdonas, Maitland-vanderZee, Anke H, Norman, Paul E, Hankey, Graeme J, Bergmann, Manuela M, Hofman, Albert, Franco, Oscar H, Cooper, Jackie, Palmen, Jutta, Spiering, Wilko, de Jong, Pim A, Kuh, Diana, Hardy, Rebecca, Uitterlinden, Andre G, Ikram, M Arfan, Ford, Ian, Hyppönen, Elina, Almeida, Osvaldo P, Wareham, Nicholas J, Khaw, Kay-Tee, Hamsten, Anders, Husemoen, Lise Lotte N, Tjønneland, Anne, Tolstrup, Janne S, Rimm, Eric, Beulens, Joline W J, Verschuren, W M Monique, Onland-Moret, N Charlotte, Hofker, Marten H, Wannamethee, S Goya, Whincup, Peter H, Morris, Richard, Vicente, Astrid M, Watkins, Hugh, Farrall, Martin, Jukema, J Wouter, Meschia, James, Cupples, L Adrienne, Sharp, Stephen J, Fornage, Myriam, Kooperberg, Charles, LaCroix, Andrea Z, Dai, James Y, Lanktree, Matthew B, Siscovick, David S, Jorgenson, Eric, Spring, Bonnie, Coresh, Josef, Li, Yun R, Buxbaum, Sarah G, Schreiner, Pamela J, Curtis, R, Y Tsai, Michael, Patel, Sanjay R, Redline, Susan, Johnson, Andrew D, Hoogeveen, Ron C, Hakonarson, Hakon, Rotter, Jerome I, Boerwinkle, Eric, de Bakker, Paul I W, Kivimaki, Mika, Asselbergs, Folkert W, Sattar, Naveed, Lawlor, Debbie A, Whittaker, John, Smith, George Davey, Mukamal, Kenneth, Psaty, Bruce M, Wilson, James G, Lange, Leslie A, Hamidovic, Ajna, Hingorani, Aroon D, Nordestgaard, Børge G, Bobak, Martin, Leon, David A, Langenberg, Claudia, Palmer, Tom M, Reiner, Alex P, Keating, Brendan J, Dudbridge, Frank, and Casas, Juan P

Published
2014

44. Potential Impact of the 2019 ACC/AHA Guidelines on the Primary Prevention of Cardiovascular Disease Recommendations on the Inappropriate Routine Use of Aspirin and Aspirin Use Without a Recommended Indication for Primary Prevention of Cardiovascular Disease in Cardiology Practices: Insights From the NCDR PINNACLE Registry

Author

Hira, Ravi S., primary, Gosch, Kensey L., additional, Kazi, Dhruv S., additional, Yeh, Robert W., additional, Kataruka, Akash, additional, Maddox, Thomas M., additional, Shah, Tina, additional, Jneid, Hani, additional, Bhatt, Deepak L., additional, and Virani, Salim S., additional

Published
2022
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