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151. 110 Corneal biomechanical properties and vascular compliance in the UK biobank cohort

Author: Woodbridge, Simon, primary, Kang, Swan, additional, Aung, Nay, additional, Biasiolli, Luca, additional, Cooper, Jackie, additional, Sanghvi, Mihir, additional, Fung, Kenneth, additional, Piechnik, Stefan, additional, Neubauer, Stefan, additional, Petersen, Steffen, additional, and Foster, Paul, additional
Published: 2019
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152. ANGPTL4 variants E40K and T266M are associated with lower fasting triglyceride levels in Non-Hispanic White Americans from the Look AHEAD Clinical Trial

Author: Pownall Henry J, Nathan David M, Balasubramanyam Ashok, McCaffrey Jeanne M, Kopin Alan, Cooper Jackie A, Montefusco Maria, Kelley-Hedgepeth Alyson, Smart-Halajko Melissa C, Peter Inga, Talmud Philippa J, and Huggins Gordon S
Subjects: Internal medicine, RC31-1245, Genetics, QH426-470
Abstract: Abstract Background Elevated triglyceride levels are a risk factor for cardiovascular disease. Angiopoietin-like protein 4 (Angptl4) is a metabolic factor that raises plasma triglyceride levels by inhibiting lipoprotein lipase (LPL). In non-diabetic individuals, the ANGPTL4 coding variant E40K has been associated with lower plasma triglyceride levels while the T266M variant has been associated with more modest effects on triglyceride metabolism. The objective of this study was to determine whether ANGPTL4 E40K and T266M are associated with triglyceride levels in the setting of obesity and T2D, and whether modification of triglyceride levels by these genetic variants is altered by a lifestyle intervention designed to treat T2D. Methods The association of ANGPTL4 E40K and T266M with fasting triglyceride levels was investigated in 2,601 participants from the Look AHEAD Clinical Trial, all of whom had T2D and were at least overweight. Further, we tested for an interaction between genotype and treatment effects on triglyceride levels. Results Among non-Hispanic White Look AHEAD participants, ANGPTL4 K40 carriers had mean triglyceride levels of 1.61 ± 0.62 mmol/L, 0.33 mmol/L lower than E40 homozygotes (p = 0.001). Individuals homozygous for the minor M266 allele (MAF 30%) had triglyceride levels of 1.75 ± 0.58 mmol/L, 0.24 mmol/L lower than T266 homozygotes (p = 0.002). The association of the M266 with triglycerides remained significant even after removing K40 carriers from the analysis (p = 0.002). There was no interaction between the weight loss intervention and genotype on triglyceride levels. Conclusions This is the first study to demonstrate that the ANGPTL4 E40K and T266M variants are associated with lower triglyceride levels in the setting of T2D. In addition, our findings demonstrate that ANGPTL4 genotype status does not alter triglyceride response to a lifestyle intervention in the Look AHEAD study.
Published: 2011
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153. Phenome-wide association analysis of LDL-cholesterol lowering genetic variants in PCSK9

Author: Schmidt, Amand F., Holmes, Michael V., Preiss, David, Swerdlow, Daniel I., Denaxas, Spiros, Fatemifar, Ghazaleh, Faraway, Rupert, Finan, Chris, Valentine, Dennis, Fairhurst-Hunter, Zammy, Hartwig, Fernando Pires, Horta, Bernardo Lessa, Hypponen, Elina, Power, Christine, Moldovan, Max, van Iperen, Erik, Hovingh, Kees, Demuth, Ilja, Norman, Kristina, Steinhagen-Thiessen, Elisabeth, Demuth, Juri, Bertram, Lars, Lill, Christina M., Coassin, Stefan, Willeit, Johann, Kiechl, Stefan, Willeit, Karin, Mason, Dan, Wright, John, Morris, Richard, Wanamethee, Goya, Whincup, Peter, Ben-Shlomo, Yoav, McLachlan, Stela, Price, Jackie F., Kivimaki, Mika, Welch, Catherine, Sanchez-Galvez, Adelaida, Marques-Vidal, Pedro, Nicolaides, Andrew, Panayiotou, Andrie G., Onland-Moret, N. Charlotte, van der Schouw, Yvonne T., Matullo, Giuseppe, Fiorito, Giovanni, Guarrera, Simonetta, Sacerdote, Carlotta, Wareham, Nicholas J., Langenberg, Claudia, Scott, Robert A., Luan, Jian'an, Bobak, Martin, Malyutina, Sofia, Pajak, Andrzej, Kubinova, Ruzena, Tamosiunas, Abdonas, Pikhart, Hynek, Grarup, Niels, Pedersen, Oluf, Hansen, Torben, Linneberg, Allan, Jess, Tine, Cooper, Jackie, Humphries, Steve E., Brilliant, Murray, Kitchner, Terrie, Hakonarson, Hakon, Carrell, David S., McCarty, Catherine A., Lester, Kirchner H., Larson, Eric B., Crosslin, David R., de Andrade, Mariza, Roden, Dan M., Denny, Joshua C., Carty, Cara, Hancock, Stephen, Attia, John, Holliday, Elizabeth, Scott, Rodney, Schofield, Peter, O'Donnell, Martin, Yusuf, Salim, Chong, Michael, Pare, Guillaume, van der Harst, Pim, Said, M. Abdullah, Eppinga, Ruben N., Verweij, Niek, Snieder, Harold, Christen, Tim, Mook-Kanamori, D. O., Gustafsson, Stefan, Lind, Lars, Ingelsson, Erik, Pazoki, Raha, Franco, Oscar, Hofman, Albert, Uitterlinden, Andre, Dehghan, Abbas, Teumer, Alexander, Baumeister, Sebastian, Doerr, Marcus, Lerch, Markus M., Voelker, Uwe, Voelzke, Henry, Ward, Joey, Pell, Jill P., Meade, Tom, Christophersen, Ingrid E., Maitland-van der Zee, Anke H., Baranova, Ekaterina V., Young, Robin, Ford, Ian, Campbell, Archie, Padmanabhan, Sandosh, Bots, Michiel L., Grobbee, Diederick E., Froguel, Philippe, Thuillier, Dorothee, Roussel, Ronan, Bonnefond, Amelie, Cariou, Bertrand, Smart, Melissa, Bao, Yanchun, Kumari, Meena, Mahajan, Anubha, Hopewell, Jemma C., Seshadri, Sudha, Dale, Caroline, Costa, Rui Providencia E., Ridker, Paul M., Chasman, Daniel I., Reiner, Alex P., Ritchie, Marylyn D., Lange, Leslie A., Cornish, Alex J., Dobbins, Sara E., Hemminki, Kari, Kinnersley, Ben, Sanson, Marc, Labreche, Karim, Simon, Matthias, Bondy, Melissa, Law, Philip, Speedy, Helen, Allan, James, Li, Ni, Went, Molly, Weinhold, Niels, Morgan, Gareth, Sonneveld, Pieter, Nilsson, Bjorn, Goldschmidt, Hartmut, Sud, Amit, Engert, Andreas, Hansson, Markus, Hemingway, Harry, Asselbergs, Folkert W., Patel, Riyaz S., Keating, Brendan J., Sattar, Naveed, Houlston, Richard, Casas, Juan P., Hingorani, Aroon D., Schmidt, Amand F., Holmes, Michael V., Preiss, David, Swerdlow, Daniel I., Denaxas, Spiros, Fatemifar, Ghazaleh, Faraway, Rupert, Finan, Chris, Valentine, Dennis, Fairhurst-Hunter, Zammy, Hartwig, Fernando Pires, Horta, Bernardo Lessa, Hypponen, Elina, Power, Christine, Moldovan, Max, van Iperen, Erik, Hovingh, Kees, Demuth, Ilja, Norman, Kristina, Steinhagen-Thiessen, Elisabeth, Demuth, Juri, Bertram, Lars, Lill, Christina M., Coassin, Stefan, Willeit, Johann, Kiechl, Stefan, Willeit, Karin, Mason, Dan, Wright, John, Morris, Richard, Wanamethee, Goya, Whincup, Peter, Ben-Shlomo, Yoav, McLachlan, Stela, Price, Jackie F., Kivimaki, Mika, Welch, Catherine, Sanchez-Galvez, Adelaida, Marques-Vidal, Pedro, Nicolaides, Andrew, Panayiotou, Andrie G., Onland-Moret, N. Charlotte, van der Schouw, Yvonne T., Matullo, Giuseppe, Fiorito, Giovanni, Guarrera, Simonetta, Sacerdote, Carlotta, Wareham, Nicholas J., Langenberg, Claudia, Scott, Robert A., Luan, Jian'an, Bobak, Martin, Malyutina, Sofia, Pajak, Andrzej, Kubinova, Ruzena, Tamosiunas, Abdonas, Pikhart, Hynek, Grarup, Niels, Pedersen, Oluf, Hansen, Torben, Linneberg, Allan, Jess, Tine, Cooper, Jackie, Humphries, Steve E., Brilliant, Murray, Kitchner, Terrie, Hakonarson, Hakon, Carrell, David S., McCarty, Catherine A., Lester, Kirchner H., Larson, Eric B., Crosslin, David R., de Andrade, Mariza, Roden, Dan M., Denny, Joshua C., Carty, Cara, Hancock, Stephen, Attia, John, Holliday, Elizabeth, Scott, Rodney, Schofield, Peter, O'Donnell, Martin, Yusuf, Salim, Chong, Michael, Pare, Guillaume, van der Harst, Pim, Said, M. Abdullah, Eppinga, Ruben N., Verweij, Niek, Snieder, Harold, Christen, Tim, Mook-Kanamori, D. O., Gustafsson, Stefan, Lind, Lars, Ingelsson, Erik, Pazoki, Raha, Franco, Oscar, Hofman, Albert, Uitterlinden, Andre, Dehghan, Abbas, Teumer, Alexander, Baumeister, Sebastian, Doerr, Marcus, Lerch, Markus M., Voelker, Uwe, Voelzke, Henry, Ward, Joey, Pell, Jill P., Meade, Tom, Christophersen, Ingrid E., Maitland-van der Zee, Anke H., Baranova, Ekaterina V., Young, Robin, Ford, Ian, Campbell, Archie, Padmanabhan, Sandosh, Bots, Michiel L., Grobbee, Diederick E., Froguel, Philippe, Thuillier, Dorothee, Roussel, Ronan, Bonnefond, Amelie, Cariou, Bertrand, Smart, Melissa, Bao, Yanchun, Kumari, Meena, Mahajan, Anubha, Hopewell, Jemma C., Seshadri, Sudha, Dale, Caroline, Costa, Rui Providencia E., Ridker, Paul M., Chasman, Daniel I., Reiner, Alex P., Ritchie, Marylyn D., Lange, Leslie A., Cornish, Alex J., Dobbins, Sara E., Hemminki, Kari, Kinnersley, Ben, Sanson, Marc, Labreche, Karim, Simon, Matthias, Bondy, Melissa, Law, Philip, Speedy, Helen, Allan, James, Li, Ni, Went, Molly, Weinhold, Niels, Morgan, Gareth, Sonneveld, Pieter, Nilsson, Bjorn, Goldschmidt, Hartmut, Sud, Amit, Engert, Andreas, Hansson, Markus, Hemingway, Harry, Asselbergs, Folkert W., Patel, Riyaz S., Keating, Brendan J., Sattar, Naveed, Houlston, Richard, Casas, Juan P., and Hingorani, Aroon D.
Abstract: Background: We characterised the phenotypic consequence of genetic variation at the PCSK9 locus and compared findings with recent trials of pharmacological inhibitors of PCSK9. Methods: Published and individual participant level data (300,000+ participants) were combined to construct a weighted PCSK9 gene-centric score (GS). Seventeen randomized placebo controlled PCSK9 inhibitor trials were included, providing data on 79,578 participants. Results were scaled to a one mmol/L lower LDL-C concentration. Results: The PCSK9 GS (comprising 4 SNPs) associations with plasma lipid and apolipoprotein levels were consistent in direction with treatment effects. The GS odds ratio (OR) for myocardial infarction (MI) was 0.53 (95% CI 0.42; 0.68), compared to a PCSK9 inhibitor effect of 0.90 (95% CI 0.86; 0.93). For ischemic stroke ORs were 0.84 (95% CI 0.57; 1.22) for the GS, compared to 0.85 (95% CI 0.78; 0.93) in the drug trials. ORs with type 2 diabetes mellitus (T2DM) were 1.29 (95% CI 1.11; 1.50) for the GS, as compared to 1.00 (95% CI 0.96; 1.04) for incident T2DM in PCSK9 inhibitor trials. No genetic associations were observed for cancer, heart failure, atrial fibrillation, chronic obstructive pulmonary disease, or Alzheimer's disease - outcomes for which large-scale trial data were unavailable. Conclusions: Genetic variation at the PCSK9 locus recapitulates the effects of therapeutic inhibition of PCSK9 on major blood lipid fractions and MI. While indicating an increased risk of T2DM, no other possible safety concerns were shown; although precision was moderate.
Published: 2019
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154. Cardiovascular Risk Factors Associated With Venous Thromboembolism

Author: Gregson, John, Kaptoge, Stephen, Bolton, Thomas, Pennells, Lisa, Willeit, Peter, Burgess, Stephen, Bell, Steven, Sweeting, Michael, Rimm, Eric B., Kabrhel, Christopher, Zoller, Bengt, Assmann, Gerd, Gudnason, Vilmundur, Folsom, Aaron R., Arndt, Volker, Fletcher, Astrid, Norman, Paul E., Nordestgaard, Borge G., Kitamura, Akihiko, Mahmoodi, Bakhtawar K., Whincup, Peter H., Knuiman, Matthew, Salomaa, Veikko, Meisinger, Christa, Koenig, Wolfgang, Kavousi, Maryam, Voelzke, Henry, Cooper, Jackie A., Ninomiya, Toshiharu, Casiglia, Edoardo, Rodriguez, Beatriz, Ben-Shlomo, Yoav, Despres, Jean-Pierre, Simons, Leon, Barrett-Connor, Elizabeth, Bjorkelund, Cecilia, Notdurfter, Marlene, Kromhout, Daan, Price, Jackie, Sutherland, Susan E., Sundstroem, Johan, Kauhanen, Jussi, Gallacher, John, Beulens, Joline W. J., Dankner, Rachel, Cooper, Cyrus, Giampaoli, Simona, Deen, Jason F., Gomez de la Camara, Agustin, Kuller, Lewis H., Rosengren, Annika, Svensson, Peter J., Nagel, Dorothea, Crespo, Carlos J., Brenner, Hermann, Albertorio-Diaz, Juan R., Atkins, Robert, Brunner, Eric J., Shipley, Martin, Njolstad, Inger, Lawlor, Deborah A., van der Schouw, Yvonne T., Selmer, Randi Marie, Trevisan, Maurizio, Verschuren, W. M. Monique, Greenland, Philip, Wassertheil-Smoller, Sylvia, Lowe, Gordon D. O., Wood, Angela M., Butterworth, Adam S., Thompson, Simon G., Danesh, John, Di Angelantonio, Emanuele, Meade, Tom, Rosamond, Wayne, Whitsel, Eric, Cushman, Mary, Barr, Elizabeth L. M., Shaw, Jonathan E., Zimmet, Paul Z., Kiechl, Stefan, Weger, Siegfried, Willeit, Johann, Amuzu, Antoinette, Dale, Caroline, Casas, Juan P., Tikhonoff, Valerie, Nietert, Paul, Tybjaerg-Hansen, Anne, Frikke-Schmidt, Ruth, Jensen, Gorm B., Lora Pablos, David, Cancelas Navia, Pilar, McLachlan, Stela, Schoettker, Ben, Saum, Kai-Uwe, Holleczek, Bernd, Ariansen, Inger, Meyer, Haakon E., Haheim, Lise Lund, Vartiainen, Erkki, Jousilahti, Pekka, Harald, Kennet, Wilhelmsen, Lars, Dennison, Elaine, Syddall, Holly, Westbury, Leo, Flicker, Leon, Hankey, Graeme J., Golledge, Jonathan, Doi, Yasufumi, Kiyohara, Yutaka, Elders, Petra, Stehouwer, Coen, Jensen, Majken, Iso, Hiroyasu, Yamagishi, Kazumasa, Sudhir, Kurl, Tuomainen, Tomi-Pekka, Salonen, Jukka T., Boer, Jolanda M. A., Blokstra, Anneke, Melander, Olle, Nilsson, Peter M., Engstrom, Gunnar, Palmieri, Luigi, Vanuzzo, Diego, Peters, Annette, Thorand, Barbara, Heier, Margit, Hu, Frank B., Manson, JoAnn E., Meijer, Karina, Gansevoort, Ron T., Schulte, Helmut, Sluijs, Ivonne, Cantin, Bernard, Lamarche, Benoit, Dagenais, Gilles R., McEvoy, Linda, Laughlin, Gail, Daniels, Lori B., Aspelund, Thor, Gudmundsson, Elias Freyr, Thorsson, Bolli, Leening, Maarten J. G., Ikram, M. Arfan, Franco, Oscar H., Tunstall-Pedoe, Hugh, Werner, Andre, Devereux, Richard, Jolly, Stacey, Smith, George Davey, Can, Gunay, Yuksel, Husniye, Altay, Servet, Ingelsson, Martin, Giedraitis, Vilmantas, Claessen, Heiner, Rothenbacher, Dietrich, Parikh, Nisha, I, Eaton, Charles, Kivimaki, Mika, Feskens, Edith, Geleijnse, Johanna M., Spackman, Sarah, Walker, Matthew, Gregson, John, Kaptoge, Stephen, Bolton, Thomas, Pennells, Lisa, Willeit, Peter, Burgess, Stephen, Bell, Steven, Sweeting, Michael, Rimm, Eric B., Kabrhel, Christopher, Zoller, Bengt, Assmann, Gerd, Gudnason, Vilmundur, Folsom, Aaron R., Arndt, Volker, Fletcher, Astrid, Norman, Paul E., Nordestgaard, Borge G., Kitamura, Akihiko, Mahmoodi, Bakhtawar K., Whincup, Peter H., Knuiman, Matthew, Salomaa, Veikko, Meisinger, Christa, Koenig, Wolfgang, Kavousi, Maryam, Voelzke, Henry, Cooper, Jackie A., Ninomiya, Toshiharu, Casiglia, Edoardo, Rodriguez, Beatriz, Ben-Shlomo, Yoav, Despres, Jean-Pierre, Simons, Leon, Barrett-Connor, Elizabeth, Bjorkelund, Cecilia, Notdurfter, Marlene, Kromhout, Daan, Price, Jackie, Sutherland, Susan E., Sundstroem, Johan, Kauhanen, Jussi, Gallacher, John, Beulens, Joline W. J., Dankner, Rachel, Cooper, Cyrus, Giampaoli, Simona, Deen, Jason F., Gomez de la Camara, Agustin, Kuller, Lewis H., Rosengren, Annika, Svensson, Peter J., Nagel, Dorothea, Crespo, Carlos J., Brenner, Hermann, Albertorio-Diaz, Juan R., Atkins, Robert, Brunner, Eric J., Shipley, Martin, Njolstad, Inger, Lawlor, Deborah A., van der Schouw, Yvonne T., Selmer, Randi Marie, Trevisan, Maurizio, Verschuren, W. M. Monique, Greenland, Philip, Wassertheil-Smoller, Sylvia, Lowe, Gordon D. O., Wood, Angela M., Butterworth, Adam S., Thompson, Simon G., Danesh, John, Di Angelantonio, Emanuele, Meade, Tom, Rosamond, Wayne, Whitsel, Eric, Cushman, Mary, Barr, Elizabeth L. M., Shaw, Jonathan E., Zimmet, Paul Z., Kiechl, Stefan, Weger, Siegfried, Willeit, Johann, Amuzu, Antoinette, Dale, Caroline, Casas, Juan P., Tikhonoff, Valerie, Nietert, Paul, Tybjaerg-Hansen, Anne, Frikke-Schmidt, Ruth, Jensen, Gorm B., Lora Pablos, David, Cancelas Navia, Pilar, McLachlan, Stela, Schoettker, Ben, Saum, Kai-Uwe, Holleczek, Bernd, Ariansen, Inger, Meyer, Haakon E., Haheim, Lise Lund, Vartiainen, Erkki, Jousilahti, Pekka, Harald, Kennet, Wilhelmsen, Lars, Dennison, Elaine, Syddall, Holly, Westbury, Leo, Flicker, Leon, Hankey, Graeme J., Golledge, Jonathan, Doi, Yasufumi, Kiyohara, Yutaka, Elders, Petra, Stehouwer, Coen, Jensen, Majken, Iso, Hiroyasu, Yamagishi, Kazumasa, Sudhir, Kurl, Tuomainen, Tomi-Pekka, Salonen, Jukka T., Boer, Jolanda M. A., Blokstra, Anneke, Melander, Olle, Nilsson, Peter M., Engstrom, Gunnar, Palmieri, Luigi, Vanuzzo, Diego, Peters, Annette, Thorand, Barbara, Heier, Margit, Hu, Frank B., Manson, JoAnn E., Meijer, Karina, Gansevoort, Ron T., Schulte, Helmut, Sluijs, Ivonne, Cantin, Bernard, Lamarche, Benoit, Dagenais, Gilles R., McEvoy, Linda, Laughlin, Gail, Daniels, Lori B., Aspelund, Thor, Gudmundsson, Elias Freyr, Thorsson, Bolli, Leening, Maarten J. G., Ikram, M. Arfan, Franco, Oscar H., Tunstall-Pedoe, Hugh, Werner, Andre, Devereux, Richard, Jolly, Stacey, Smith, George Davey, Can, Gunay, Yuksel, Husniye, Altay, Servet, Ingelsson, Martin, Giedraitis, Vilmantas, Claessen, Heiner, Rothenbacher, Dietrich, Parikh, Nisha, I, Eaton, Charles, Kivimaki, Mika, Feskens, Edith, Geleijnse, Johanna M., Spackman, Sarah, and Walker, Matthew
Abstract: IMPORTANCE: It is uncertain to what extent established cardiovascular risk factors are associated with venous thromboembolism (VTE). OBJECTIVE To estimate the associations of major cardiovascular risk factors with VTE, ie, deep vein thrombosis and pulmonary embolism. DESIGN, SETTING, AND PARTICIPANTS: This study included individual participant data mostly from essentially population-based cohort studies from the Emerging Risk Factors Collaboration (ERFC; 731728 participants; 75 cohorts; years of baseline surveys, February 1960 to June 2008; latest date of follow-up, December 2015) and the UK Biobank (421537 participants; years of baseline surveys, March 2006 to September 2010; latest date of follow-up, February 2016). Participants without cardiovascular disease at baseline were included. Data were analyzed from June 2017 to September 2018. EXPOSURES: A panel of several established cardiovascular risk factors. MAIN OUTCOMES AND MEASURES: Hazard ratios (HRs) per 1-SD higher usual risk factor levels (or presence/absence). Incident fatal outcomes in ERFC (VTE, 1041; coronary heart disease [CND], 25131) and incident fatal/nonfatal outcomes in UK Biobank (VTE, 2321; CHD, 3385). Hazard ratios were adjusted for age, sex, smoking status, diabetes, and body mass index (BMI). RESULTS: Of the 731728 participants from the ERFC. 403 396 (55.1%) were female, and the mean (SD) age at the time of the survey was 51.9 (9.0) years; of the 421537 participants from the UK Biobank, 233 699 (55.4%) were female, and the mean (SD) age at the time of the survey was 56.4 (8.1) years. Risk factors for VTE included older age (ERFC: HR per decade, 2.67; 95% CI, 2.45-2.91; UK Biobank: HR, 1.81; 95% CI, 1.71-1.92), current smoking (ERFC: HR, 1.38; 95% CI, 1.20-1.58; UK Biobank: HR, 1.23; 95% CI, 1.08-1.40), and BMI (ERFC: HR per 1-SD higher BMI, 1.43; 95% CI, 1.35-1.50; UK Biobank: HR, 1.37; 95% CI, 1.32-1.41). For these factors, there were similar HRs for pulmonary embolism and deep vein thrombosi
Published: 2019
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155. Phenome-wide association analysis of LDL-cholesterol lowering genetic variants in PCSK9

Author: Planningssecretariaat HCK, Onderzoek Precision medicine, Cardiovasculaire Epi Team 3, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, JC onderzoeksprogramma Kanker, Brain, Cancer, Cardiovasculaire Epidemiologie, Epi Methoden Team 6, Aios en Stafsecr. Cardiologie, Cardiovasculaire Epi Team 5, Cardiovasculaire Epi Team 9, Team Medisch, Schmidt, Amand F., Holmes, Michael V., Preiss, David, Swerdlow, Daniel I., Denaxas, Spiros, Fatemifar, Ghazaleh, Faraway, Rupert, Finan, Chris, Valentine, Dennis, Fairhurst-Hunter, Zammy, Hartwig, Fernando Pires, Horta, Bernardo Lessa, Hypponen, Elina, Power, Christine, Moldovan, Max, Van Iperen, Erik, Hovingh, Kees, Demuth, Ilja, Norman, Kristina, Steinhagen-Thiessen, Elisabeth, Demuth, Juri, Bertram, Lars, Lill, Christina M., Coassin, Stefan, Willeit, Johann, Kiechl, Stefan, Willeit, Karin, Mason, Dan, Wright, John, Morris, Richard, Wanamethee, Goya, Whincup, Peter, Ben-Shlomo, Yoav, McLachlan, Stela, Price, Jackie F., Kivimaki, Mika, Welch, Catherine, Sanchez-Galvez, Adelaida, Marques-Vidal, Pedro, Nicolaides, Andrew, Panayiotou, Andrie G., Onland-Moret, N. Charlotte, Van Der Schouw, Yvonne T., Matullo, Giuseppe, Fiorito, Giovanni, Guarrera, Simonetta, Sacerdote, Carlotta, Wareham, Nicholas J., Langenberg, Claudia, Scott, Robert A., Luan, Jian'An, Bobak, Martin, Malyutina, Sofia, Pajak, Andrzej, Kubinova, Ruzena, Tamosiunas, Abdonas, Pikhart, Hynek, Grarup, Niels, Pedersen, Oluf, Hansen, Torben, Linneberg, Allan, Jess, Tine, Cooper, Jackie, Humphries, Steve E., Brilliant, Murray, Kitchner, Terrie, Hakonarson, Hakon, Carrell, David S., McCarty, Catherine A., Lester, Kirchner H., Larson, Eric B., Crosslin, David R., De Andrade, Mariza, Roden, Dan M., Denny, Joshua C., Carty, Cara, Hancock, Stephen, Attia, John, Holliday, Elizabeth, Scott, Rodney, Schofield, Peter, O'Donnell, Martin, Yusuf, Salim, Chong, Michael, Pare, Guillaume, Van Der Harst, Pim, Said, M. Abdullah, Eppinga, Ruben N., Verweij, Niek, Snieder, Harold, Christen, Tim, Mook-Kanamori, D. O., Gustafsson, Stefan, Lind, Lars, Ingelsson, Erik, Pazoki, Raha, Franco, Oscar, Hofman, Albert, Uitterlinden, Andre, Dehghan, Abbas, Teumer, Alexander, Baumeister, Sebastian, Dörr, Marcus, Lerch, Markus M., Völker, Uwe, Völzke, Henry, Ward, Joey, Pell, Jill P., Meade, Tom, Christophersen, Ingrid E., Maitland-Van Der Zee, Anke H., Baranova, Ekaterina V., Young, Robin, Ford, Ian, Campbell, Archie, Padmanabhan, Sandosh, Bots, Michiel L., Grobbee, Diederick E., Froguel, Philippe, Thuillier, Dorothée, Roussel, Ronan, Bonnefond, Amélie, Cariou, Bertrand, Smart, Melissa, Bao, Yanchun, Kumari, Meena, Mahajan, Anubha, Hopewell, Jemma C., Seshadri, Sudha, Dale, Caroline, Costa, Rui Providencia E., Ridker, Paul M., Chasman, Daniel I., Reiner, Alex P., Ritchie, Marylyn D., Lange, Leslie A., Cornish, Alex J., Dobbins, Sara E., Hemminki, Kari, Kinnersley, Ben, Sanson, Marc, Labreche, Karim, Simon, Matthias, Bondy, Melissa, Law, Philip, Speedy, Helen, Allan, James, Li, Ni, Went, Molly, Weinhold, Niels, Morgan, Gareth, Sonneveld, Pieter, Nilsson, Björn, Goldschmidt, Hartmut, Sud, Amit, Engert, Andreas, Hansson, Markus, Hemingway, Harry, Asselbergs, Folkert W., Patel, Riyaz S., Keating, Brendan J., Sattar, Naveed, Houlston, Richard, Casas, Juan P., Hingorani, Aroon D., Planningssecretariaat HCK, Onderzoek Precision medicine, Cardiovasculaire Epi Team 3, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, JC onderzoeksprogramma Kanker, Brain, Cancer, Cardiovasculaire Epidemiologie, Epi Methoden Team 6, Aios en Stafsecr. Cardiologie, Cardiovasculaire Epi Team 5, Cardiovasculaire Epi Team 9, Team Medisch, Schmidt, Amand F., Holmes, Michael V., Preiss, David, Swerdlow, Daniel I., Denaxas, Spiros, Fatemifar, Ghazaleh, Faraway, Rupert, Finan, Chris, Valentine, Dennis, Fairhurst-Hunter, Zammy, Hartwig, Fernando Pires, Horta, Bernardo Lessa, Hypponen, Elina, Power, Christine, Moldovan, Max, Van Iperen, Erik, Hovingh, Kees, Demuth, Ilja, Norman, Kristina, Steinhagen-Thiessen, Elisabeth, Demuth, Juri, Bertram, Lars, Lill, Christina M., Coassin, Stefan, Willeit, Johann, Kiechl, Stefan, Willeit, Karin, Mason, Dan, Wright, John, Morris, Richard, Wanamethee, Goya, Whincup, Peter, Ben-Shlomo, Yoav, McLachlan, Stela, Price, Jackie F., Kivimaki, Mika, Welch, Catherine, Sanchez-Galvez, Adelaida, Marques-Vidal, Pedro, Nicolaides, Andrew, Panayiotou, Andrie G., Onland-Moret, N. Charlotte, Van Der Schouw, Yvonne T., Matullo, Giuseppe, Fiorito, Giovanni, Guarrera, Simonetta, Sacerdote, Carlotta, Wareham, Nicholas J., Langenberg, Claudia, Scott, Robert A., Luan, Jian'An, Bobak, Martin, Malyutina, Sofia, Pajak, Andrzej, Kubinova, Ruzena, Tamosiunas, Abdonas, Pikhart, Hynek, Grarup, Niels, Pedersen, Oluf, Hansen, Torben, Linneberg, Allan, Jess, Tine, Cooper, Jackie, Humphries, Steve E., Brilliant, Murray, Kitchner, Terrie, Hakonarson, Hakon, Carrell, David S., McCarty, Catherine A., Lester, Kirchner H., Larson, Eric B., Crosslin, David R., De Andrade, Mariza, Roden, Dan M., Denny, Joshua C., Carty, Cara, Hancock, Stephen, Attia, John, Holliday, Elizabeth, Scott, Rodney, Schofield, Peter, O'Donnell, Martin, Yusuf, Salim, Chong, Michael, Pare, Guillaume, Van Der Harst, Pim, Said, M. Abdullah, Eppinga, Ruben N., Verweij, Niek, Snieder, Harold, Christen, Tim, Mook-Kanamori, D. O., Gustafsson, Stefan, Lind, Lars, Ingelsson, Erik, Pazoki, Raha, Franco, Oscar, Hofman, Albert, Uitterlinden, Andre, Dehghan, Abbas, Teumer, Alexander, Baumeister, Sebastian, Dörr, Marcus, Lerch, Markus M., Völker, Uwe, Völzke, Henry, Ward, Joey, Pell, Jill P., Meade, Tom, Christophersen, Ingrid E., Maitland-Van Der Zee, Anke H., Baranova, Ekaterina V., Young, Robin, Ford, Ian, Campbell, Archie, Padmanabhan, Sandosh, Bots, Michiel L., Grobbee, Diederick E., Froguel, Philippe, Thuillier, Dorothée, Roussel, Ronan, Bonnefond, Amélie, Cariou, Bertrand, Smart, Melissa, Bao, Yanchun, Kumari, Meena, Mahajan, Anubha, Hopewell, Jemma C., Seshadri, Sudha, Dale, Caroline, Costa, Rui Providencia E., Ridker, Paul M., Chasman, Daniel I., Reiner, Alex P., Ritchie, Marylyn D., Lange, Leslie A., Cornish, Alex J., Dobbins, Sara E., Hemminki, Kari, Kinnersley, Ben, Sanson, Marc, Labreche, Karim, Simon, Matthias, Bondy, Melissa, Law, Philip, Speedy, Helen, Allan, James, Li, Ni, Went, Molly, Weinhold, Niels, Morgan, Gareth, Sonneveld, Pieter, Nilsson, Björn, Goldschmidt, Hartmut, Sud, Amit, Engert, Andreas, Hansson, Markus, Hemingway, Harry, Asselbergs, Folkert W., Patel, Riyaz S., Keating, Brendan J., Sattar, Naveed, Houlston, Richard, Casas, Juan P., and Hingorani, Aroon D.
Published: 2019

156. Equalization of four cardiovascular risk algorithms after systematic recalibration:individual-participant meta-analysis of 86 prospective studies

Author: Pennells, Lisa, Kaptoge, Stephen, Wood, Angela, Sweeting, Mike, Zhao, Xiaohui, White, Ian, Burgess, Stephen, Willeit, Peter, Bolton, Thomas, Moons, Karel G. M., van der Schouw, Yvonne T., Selmer, Randi, Khaw, Kay-Tee, Gudnason, Vilmundur, Assmann, Gerd, Amouyel, Philippe, Salomaa, Veikko, Kivimaki, Mika, Nordestgaard, Borge G., Blaha, Michael J., Kuller, Lewis H., Brenner, Hermann, Gillum, Richard F., Meisinger, Christa, Ford, Ian, Knuiman, Matthew W., Rosengren, Annika, Lawlor, Debbie A., Volzke, Henry, Cooper, Cyrus, Ibanez, Alejandro Marin, Casiglia, Edoardo, Kauhanen, Jussi, Cooper, Jackie A., Rodriguez, Beatriz, Sundstrom, Johan, Barrett-Connor, Elizabeth, Dankner, Rachel, Nietert, Paul J., Davidson, Karina W., Wallace, Robert B., Blazer, Dan G., Bjorkelund, Cecilia, Donfrancesco, Chiara, Krumholz, Harlan M., Nissinen, Aulikki, Davis, Barry R., Coady, Sean, Whincup, Peter H., Jørgensen, Torben, Ducimetiere, Pierre, Trevisan, Maurizio, Engstrom, Gunnar, Crespo, Carlos J., Meade, Tomw., Visser, Marjolein, Kromhout, Daan, Kiechl, Stefan, Daimon, Makoto, Price, Jackie F., de la Camara, Agustin Gomez, Jukema, J. Wouter, Lamarche, Benoit, Onat, Altan, Simons, Leon A., Kavousi, Maryam, Ben-Shlomo, Yoav, Gallacher, John, Dekker, Jacqueline M., Arima, Hisatomi, Shara, Nawar, Tipping, RobertW., Roussel, Ronan, Brunner, Eric J., Koenig, Wolfgang, Sakurai, Masaru, Pavlovic, Jelena, Gansevoort, Ron T., Nagel, Dorothea, Goldbourt, Uri, Barr, Elizabeth L. M., Palmieri, Luigi, Njølstad, Inger, Sato, Shinichi, Verschuren, W. M. Monique, Varghese, Cherian V., Graham, Ian, Onuma, Oyere, Greenland, Philip, Woodward, Mark, Ezzati, Majid, Psaty, Bruce M., Sattar, Naveed, Jackson, Rod, Ridker, Paul M., Cook, Nancy, D'Agostino, Ralph B., Sr., Thompson, Simon G., Danesh, John, Di Angelantonio, Emanuele, Tipping, Robert W., Simpson, Lara M., Pressel, Sara L., Couper, David J., Nambi, Vijay, Matsushita, Kunihiro, Folsom, Aaron R., Shaw, Jonathan E., Magliano, Dianna J., Zimmet, Paul Z., Wannamethee, S. Goya, Willeit, Johann, Santer, Peter, Egger, Georg, Casas, Juan Pablo, Amuzu, Antointtte, Tikhonoff, Valerie, Sutherland, Susan E., Cushman, Mary, Sogaard, Anne Johanne, Haheim, Lise Lund, Ariansen, Inger, Tybjærg-Hansen, Anne, Jensen, Gorm B., Schnohr, Peter, Giampaoli, Simona, Vanuzzo, Diego, Panico, Salvatore, Balkau, Beverley, Bonnet, Fabrice, Marre, Michel, Herrera, Miguel Angel Rubio, Friedlander, Yechiel, McCallum, John, McLachlan, Stela, Guralnik, Jack, Phillips, Caroline L., Wareham, Nick, Schottker, Ben, Saum, Kai-Uwe, Holleczek, Bernd, Tolonen, Hanna, Jousilahti, Pekka, Harald, Kennet, Massaro, Joseph M., Pencina, Michael, Vasan, Ramachandran, Kayama, Takamasa, Kato, Takeo, Oizumi, Toshihide, Jespersen, Jorgen, Møller, Lars, Bladbjerg, Else Marie, Chetrit, A., Wilhelmsen, Lars, Lissner, Lauren, Dennison, Elaine, Kiyohara, Yutaka, Ninomiya, Toshiharu, Doi, Yasufumi, Nijpels, Giel, Stehouwer, Coen D. A., Kazumasa, Yamagishi, Iso, Hiroyasu, Vartiainen, Erkki, Kurl, Sudhir, Tuomainen, Tomi-Pekka, Salonen, Jukka T., Deeg, Dorly J. H., Nilsson, Peter M., Hedblad, Bo, Melander, Olle, De Boer, Ian H., DeFilippis, Andrew Paul, Watt, Graham, Verschuren, Monique, Tverdal, Aage, Kirkland, Susan, Shimbo, Daichi, Shaffer, Jonathan, Bakker, Stephan J. L., van der Harst, Pim, Hillege, Hans L., Dallongeville, Jean, Schulte, Helmut, Trompet, Stella, Smit, Roelof A. J., Stott, David J., Despres, Jean-Pierre, Cantin, Bernard, Dagenais, Gilles R., Laughlin, Gail, Wingard, Deborah, Aspelund, Thor, Eiriksdottir, Gudny, Gudmundsson, Elias Freyr, Ikram, Arfan, van Rooij, Frank J. A., Franco, Oscar H., Rueda-Ochoa, Oscar L., Muka, Taulant, Glisic, Marija, Tunstall-Pedoe, Hugh, Howard, Barbara V., Zhang, Ying, Jolly, Stacey, Davey-Smith, George, Can, Gunay, Yuksel, Husniye, Nakagawa, Hideaki, Morikawa, Yuko, Miura, Katsuyuki, Ingelsson, Martin, Giedraitis, Vilmantas, Gaziano, J. Michael, Shipley, Martin, Arndt, Volker, Geleijnse, Johanna M., Pennells, Lisa, Kaptoge, Stephen, Wood, Angela, Sweeting, Mike, Zhao, Xiaohui, White, Ian, Burgess, Stephen, Willeit, Peter, Bolton, Thomas, Moons, Karel G. M., van der Schouw, Yvonne T., Selmer, Randi, Khaw, Kay-Tee, Gudnason, Vilmundur, Assmann, Gerd, Amouyel, Philippe, Salomaa, Veikko, Kivimaki, Mika, Nordestgaard, Borge G., Blaha, Michael J., Kuller, Lewis H., Brenner, Hermann, Gillum, Richard F., Meisinger, Christa, Ford, Ian, Knuiman, Matthew W., Rosengren, Annika, Lawlor, Debbie A., Volzke, Henry, Cooper, Cyrus, Ibanez, Alejandro Marin, Casiglia, Edoardo, Kauhanen, Jussi, Cooper, Jackie A., Rodriguez, Beatriz, Sundstrom, Johan, Barrett-Connor, Elizabeth, Dankner, Rachel, Nietert, Paul J., Davidson, Karina W., Wallace, Robert B., Blazer, Dan G., Bjorkelund, Cecilia, Donfrancesco, Chiara, Krumholz, Harlan M., Nissinen, Aulikki, Davis, Barry R., Coady, Sean, Whincup, Peter H., Jørgensen, Torben, Ducimetiere, Pierre, Trevisan, Maurizio, Engstrom, Gunnar, Crespo, Carlos J., Meade, Tomw., Visser, Marjolein, Kromhout, Daan, Kiechl, Stefan, Daimon, Makoto, Price, Jackie F., de la Camara, Agustin Gomez, Jukema, J. Wouter, Lamarche, Benoit, Onat, Altan, Simons, Leon A., Kavousi, Maryam, Ben-Shlomo, Yoav, Gallacher, John, Dekker, Jacqueline M., Arima, Hisatomi, Shara, Nawar, Tipping, RobertW., Roussel, Ronan, Brunner, Eric J., Koenig, Wolfgang, Sakurai, Masaru, Pavlovic, Jelena, Gansevoort, Ron T., Nagel, Dorothea, Goldbourt, Uri, Barr, Elizabeth L. M., Palmieri, Luigi, Njølstad, Inger, Sato, Shinichi, Verschuren, W. M. Monique, Varghese, Cherian V., Graham, Ian, Onuma, Oyere, Greenland, Philip, Woodward, Mark, Ezzati, Majid, Psaty, Bruce M., Sattar, Naveed, Jackson, Rod, Ridker, Paul M., Cook, Nancy, D'Agostino, Ralph B., Sr., Thompson, Simon G., Danesh, John, Di Angelantonio, Emanuele, Tipping, Robert W., Simpson, Lara M., Pressel, Sara L., Couper, David J., Nambi, Vijay, Matsushita, Kunihiro, Folsom, Aaron R., Shaw, Jonathan E., Magliano, Dianna J., Zimmet, Paul Z., Wannamethee, S. Goya, Willeit, Johann, Santer, Peter, Egger, Georg, Casas, Juan Pablo, Amuzu, Antointtte, Tikhonoff, Valerie, Sutherland, Susan E., Cushman, Mary, Sogaard, Anne Johanne, Haheim, Lise Lund, Ariansen, Inger, Tybjærg-Hansen, Anne, Jensen, Gorm B., Schnohr, Peter, Giampaoli, Simona, Vanuzzo, Diego, Panico, Salvatore, Balkau, Beverley, Bonnet, Fabrice, Marre, Michel, Herrera, Miguel Angel Rubio, Friedlander, Yechiel, McCallum, John, McLachlan, Stela, Guralnik, Jack, Phillips, Caroline L., Wareham, Nick, Schottker, Ben, Saum, Kai-Uwe, Holleczek, Bernd, Tolonen, Hanna, Jousilahti, Pekka, Harald, Kennet, Massaro, Joseph M., Pencina, Michael, Vasan, Ramachandran, Kayama, Takamasa, Kato, Takeo, Oizumi, Toshihide, Jespersen, Jorgen, Møller, Lars, Bladbjerg, Else Marie, Chetrit, A., Wilhelmsen, Lars, Lissner, Lauren, Dennison, Elaine, Kiyohara, Yutaka, Ninomiya, Toshiharu, Doi, Yasufumi, Nijpels, Giel, Stehouwer, Coen D. A., Kazumasa, Yamagishi, Iso, Hiroyasu, Vartiainen, Erkki, Kurl, Sudhir, Tuomainen, Tomi-Pekka, Salonen, Jukka T., Deeg, Dorly J. H., Nilsson, Peter M., Hedblad, Bo, Melander, Olle, De Boer, Ian H., DeFilippis, Andrew Paul, Watt, Graham, Verschuren, Monique, Tverdal, Aage, Kirkland, Susan, Shimbo, Daichi, Shaffer, Jonathan, Bakker, Stephan J. L., van der Harst, Pim, Hillege, Hans L., Dallongeville, Jean, Schulte, Helmut, Trompet, Stella, Smit, Roelof A. J., Stott, David J., Despres, Jean-Pierre, Cantin, Bernard, Dagenais, Gilles R., Laughlin, Gail, Wingard, Deborah, Aspelund, Thor, Eiriksdottir, Gudny, Gudmundsson, Elias Freyr, Ikram, Arfan, van Rooij, Frank J. A., Franco, Oscar H., Rueda-Ochoa, Oscar L., Muka, Taulant, Glisic, Marija, Tunstall-Pedoe, Hugh, Howard, Barbara V., Zhang, Ying, Jolly, Stacey, Davey-Smith, George, Can, Gunay, Yuksel, Husniye, Nakagawa, Hideaki, Morikawa, Yuko, Miura, Katsuyuki, Ingelsson, Martin, Giedraitis, Vilmantas, Gaziano, J. Michael, Shipley, Martin, Arndt, Volker, and Geleijnse, Johanna M.
Published: 2019

157. Influence of a stearic acid–rich structured triacylglycerol on postprandial lipemia, factor VII concentrations, and fibrinolytic activity in healthy subjects

Author: Sanders, Thomas AB, Oakley, Francesca R, Cooper, Jackie A, and Miller, George J
Published: 2001
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158. Variation in left ventricular cardiac magnetic resonance normal reference ranges: systematic review and meta-analysis.

Author: Raisi-Estabragh, Zahra, Kenawy, Asmaa A M, Aung, Nay, Cooper, Jackie, Munroe, Patricia B, Harvey, Nicholas C, Petersen, Steffen E, and Khanji, Mohammed Y
Subjects: REFERENCE values, LEFT heart ventricle, META-analysis, SYSTEMATIC reviews, AGE distribution, MAGNETIC resonance imaging, SEX distribution, HEART physiology, ETHNIC groups
Abstract: Aims To determine population-related and technical sources of variation in cardiac magnetic resonance (CMR) reference ranges for left ventricular (LV) quantification through a formal systematic review and meta-analysis. Methods and results This study is registered with the International Prospective Register of Systematic Reviews (CRD42019147161). Relevant studies were identified through electronic searches and assessed by two independent reviewers based on predefined criteria. Fifteen studies comprising 2132 women and 1890 men aged 20–91 years are included in the analysis. Pooled LV reference ranges calculated using random effects meta-analysis with inverse variance weighting revealed significant differences by age, sex, and ethnicity. Men had larger LV volumes and higher LV mass than women [LV end-diastolic volume (mean difference = 6.1 mL/m2, P -value = 0.014), LV end-systolic volume (MD = 4 mL/m2, P -value = 0.033), LV mass (mean difference = 12 g/m2, P -value = 7.8 × 10−9)]. Younger individuals had larger LV end-diastolic volumes than older ages (20–40 years vs. ≥65 years: women MD = 14.0 mL/m2, men MD = 14.7 mL/m2). East Asians (Chinese, Korean, Singaporean-Chinese, n = 514) had lower LV mass than Caucasians (women: MD = 6.4 g/m2, P -value = 0.016; men: MD = 9.8 g/m2, P -value = 6.7 × 10−5). Between-study heterogeneity was high for all LV parameters despite stratification by population-related factors. Sensitivity analyses identified differences in contouring methodology, magnet strength, and post-processing software as potential sources of heterogeneity. Conclusion There is significant variation between CMR normal reference ranges due to multiple population-related and technical factors. Whilst there is need for population-stratified reference ranges, limited sample sizes and technical heterogeneity precludes derivation of meaningful unified ranges from existing reports. Wider representation of different populations and standardization of image analysis is urgently needed to establish such reference distributions. [ABSTRACT FROM AUTHOR]
Published: 2021
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159. 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
Subjects: Science & Technology, GOUT, UCLEB (University College London-London School of Hygiene & Tropical Medicine-Edinburgh-Bristol Consortium, Smoking, ENDOTHELIAL FUNCTION, Coronary Disease, BLOOD-PRESSURE, Articles, URIC-ACID, ASSOCIATION, Mendelian Randomization Analysis, INSTRUMENTS, Uric Acid, Observational Studies as Topic, Endocrinology & Metabolism, Meta-Analysis as Topic, Risk Factors, CARDIOVASCULAR-DISEASE, REGRESSION, Humans, Life Sciences & Biomedicine, International Consortium for Blood Pressure (ICBP), ALLOPURINOL
Abstract: BACKGROUND: Increased circulating plasma urate concentration is associated with an increased risk of coronary heart disease, but the extent of any causative effect of urate on risk of coronary heart disease is still unclear. In this study, we aimed to clarify any causal role of urate on coronary heart disease risk using Mendelian randomisation analysis.METHODS: We first did a fixed-effects meta-analysis of the observational association of plasma urate and risk of coronary heart disease. We then used a conventional Mendelian randomisation approach to investigate the causal relevance using a genetic instrument based on 31 urate-associated single nucleotide polymorphisms (SNPs). To account for potential pleiotropic associations of certain SNPs with risk factors other than urate, we additionally did both a multivariable Mendelian randomisation analysis, in which the genetic associations of SNPs with systolic and diastolic blood pressure, HDL cholesterol, and triglycerides were included as covariates, and an Egger Mendelian randomisation (MR-Egger) analysis to estimate a causal effect accounting for unmeasured pleiotropy.FINDINGS: In the meta-analysis of 17 prospective observational studies (166 486 individuals; 9784 coronary heart disease events) a 1 SD higher urate concentration was associated with an odds ratio (OR) for coronary heart disease of 1·07 (95% CI 1·04-1·10). The corresponding OR estimates from the conventional, multivariable adjusted, and Egger Mendelian randomisation analysis (58 studies; 198 598 individuals; 65 877 events) were 1·18 (95% CI 1·08-1·29), 1·10 (1·00-1·22), and 1·05 (0·92-1·20), respectively, per 1 SD increment in plasma urate.INTERPRETATION: Conventional and multivariate Mendelian randomisation analysis implicates a causal role for urate in the development of coronary heart disease, but these estimates might be inflated by hidden pleiotropy. Egger Mendelian randomisation analysis, which accounts for pleiotropy but has less statistical power, suggests there might be no causal effect. These results might help investigators to determine the priority of trials of urate lowering for the prevention of coronary heart disease compared with other potential interventions.FUNDING: UK National Institute for Health Research, British Heart Foundation, and UK Medical Research Council.
Published: 2018
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160. Persistent Postsurgical Pain Following Thoracotomy: A Comparison of Thoracic Epidural and Paravertebral Blockade as Preventive Analgesia

Author: Wong, Jonathon, primary, Cooper, Jackie, additional, Thomas, Rik, additional, Langford, Richard, additional, and Anwar, Sibtain, additional
Published: 2019
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161. Poor Bone Quality is Associated With Greater Arterial Stiffness: Insights From the UK Biobank.

Author: Raisi‐Estabragh, Zahra, Biasiolli, Luca, Cooper, Jackie, Aung, Nay, Fung, Kenneth, Paiva, José M, Sanghvi, Mihir M, Thomson, Ross J, Curtis, Elizabeth, Paccou, Julien, Rayner, Jennifer J, Werys, Konrad, Puchta, Henrike, Thomas, Katharine E, Lee, Aaron M, Piechnik, Stefan K, Neubauer, Stefan, Munroe, Patricia B, Cooper, Cyrus, and Petersen, Steffen E
Abstract: Osteoporosis and ischemic heart disease (IHD) represent important public health problems. Existing research suggests an association between the two conditions beyond that attributable to shared risk factors, with a potentially causal relationship. In this study, we tested the association of bone speed of sound (SOS) from quantitative heel ultrasound with (i) measures of arterial compliance from cardiovascular magnetic resonance (aortic distensibility [AD]); (ii) finger photoplethysmography (arterial stiffness index [ASI]); and (iii) incident myocardial infarction and IHD mortality in the UK Biobank cohort. We considered the potential mediating effect of a range of blood biomarkers and cardiometabolic morbidities and evaluated differential relationships by sex, menopause status, smoking, diabetes, and obesity. Furthermore, we considered whether associations with arterial compliance explained association of SOS with ischemic cardiovascular outcomes. Higher SOS was associated with lower arterial compliance by both ASI and AD for both men and women. The relationship was most consistent with ASI, likely relating to larger sample size available for this variable (n = 159,542 versus n = 18,229). There was no clear evidence of differential relationship by menopause, smoking, diabetes, or body mass index (BMI). Blood biomarkers appeared important in mediating the association for both men and women, but with different directions of effect and did not fully explain the observed effects. In fully adjusted models, higher SOS was associated with significantly lower IHD mortality in men, but less robustly in women. The association of SOS with ASI did not explain this observation. In conclusion, our findings support a positive association between bone and vascular health with consistent patterns of association in men and women. The underlying mechanisms are complex and appear to vary by sex. © 2020 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR). [ABSTRACT FROM AUTHOR]
Published: 2021
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162. Association Between Ambient Air Pollution and Cardiac Morpho-Functional Phenotypes

Author: Aung, Nay, primary, Sanghvi, Mihir M., additional, Zemrak, Filip, additional, Lee, Aaron M., additional, Cooper, Jackie A., additional, Paiva, Jose M., additional, Thomson, Ross J., additional, Fung, Kenneth, additional, Khanji, Mohammed Y., additional, Lukaschuk, Elena, additional, Carapella, Valentina, additional, Kim, Young Jin, additional, Munroe, Patricia B., additional, Piechnik, Stefan K., additional, Neubauer, Stefan, additional, and Petersen, Steffen E., additional
Published: 2018
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163. Phenome-wide association analysis of LDL-cholesterol lowering genetic variants in PCSK9

Author: Schmidt, Amand F, primary, Holmes, Michael V, additional, Preiss, David, additional, Swerdlow, Daniel, additional, Denaxas, Spiros, additional, Fatemifar, Ghazaleh, additional, Faraway, Rupert, additional, Finan, Chris, additional, Lumbers, Tom, additional, Henry, Albert, additional, Valentine, Dennis, additional, Fairhurst-Hunter, Zammy, additional, Hartwig, Fernando Pires, additional, Horta, Bernardo Lessa, additional, Hypponen, Elina, additional, Power, Christine, additional, Moldovan, Max, additional, van Iperen, Erik, additional, Hovingh, Kees, additional, Demuth, Ilja, additional, Norman, Kristina, additional, Steinhagen-Thiessen, Elisabeth, additional, Demuth, Juri, additional, Bertram, Lars, additional, Lill, Christina M, additional, Coassin, Stefan, additional, Willeit, Johann, additional, Kiechl, Stefan, additional, Willeit, Karin, additional, Mason, Dan, additional, Wright, John, additional, Morris, Richard, additional, Wanamethee, Goya, additional, Whincup, Peter, additional, Ben-Shlomo, Yoav, additional, McLachlan, Stela, additional, Price, Jackie F., additional, Kivimaki, Mika, additional, Welch, Catherine, additional, Sanchez-Galvez, Adelaida, additional, Marques-Vidal, Pedro, additional, Nicolaides, Andrew, additional, Panayiotou, Andrie G., additional, Onland-Moret, N. Charlotte, additional, van der Schouw, Yvonne T., additional, Matullo, Giuseppe, additional, Fiorito, Giovanni, additional, Guarrera, Simonetta, additional, Sacerdote, Carlotta, additional, Wareham, Nicholas J, additional, Langenberg, Claudia, additional, Scott, Robert A, additional, Luan, Jian’an, additional, Bobak, Martin, additional, Malyutina, Sofia, additional, Pajak, Andrzej, additional, Kubinova, Ruzena, additional, Tamosiunas, Abdonas, additional, Pikhart, Hynek, additional, Grarup, Niels, additional, Pedersen, Oluf, additional, Hansen, Torben, additional, Linneberg, Allan, additional, Jess, Tine, additional, Cooper, Jackie, additional, Humphries, Steve E, additional, Brilliant, Murray, additional, Kitchner, Terrie, additional, Hakonarson, Hakon, additional, Carrell, David S., additional, McCarty, Catherine A., additional, Lester, Kirchner H, additional, Larson, Eric B., additional, Crosslin, David R., additional, Andrade, Mariza de, additional, Roden, Dan M, additional, Denny, Joshua C, additional, Carty, Cara, additional, Hancock, Stephen, additional, Attia, John, additional, Holliday, Elizabeth, additional, Scott, Rodney, additional, Schofield, Peter, additional, O’Donnell, Martin, additional, Yusuf, Salim, additional, Chong, Michael, additional, Pare, Guillaume, additional, van der Harst, Pim, additional, Said, M. Abdullah, additional, Eppinga, Ruben N., additional, Verweij, Niek, additional, Snieder, Harold, additional, Christen, Tim, additional, Mook-Kanamori, D.O., additional, Gustafsson, Stefan, additional, Lind, Lars, additional, Ingelsson, Erik, additional, Pazoki, Raha, additional, Franco, Oscar, additional, Hofman, Albert, additional, Uitterlinden, Andre, additional, Dehghan, Abbas, additional, Teumer, Alexander, additional, Baumeister, Sebastian, additional, Dörr, Marcus, additional, Lerch, Markus M., additional, Völker, Uwe, additional, Völzke, Henry, additional, Ward, Joey, additional, Pell, Jill P, additional, Meade, Tom, additional, Christophersen, Ingrid E., additional, Maitland-van der Zee, Anke H., additional, Baranova, Ekaterina V., additional, Young, Robin, additional, Ford, Ian, additional, Campbell, Archie, additional, Padmanabhan, Sandosh, additional, Bots, Michiel L, additional, Grobbee, Diederick E., additional, Froguel, Philippe, additional, Thuillier, Dorothée, additional, Roussel, Ronan, additional, Bonnefond, Amelie, additional, Cariou, Bertrand, additional, Smart, Melissa, additional, Bao, Yanchun, additional, Kumari, Meena, additional, Mahajan, Anubha, additional, Hopewell, Jemma C., additional, Seshadri, Sudha, additional, Dale, Caroline, additional, Costa, Rui Providencia E, additional, Ridker, Paul M, additional, Chasman, Daniel I., additional, Reiner, Alex P., additional, Ritchie, Marylyn D, additional, Lange, Leslie A, additional, Cornish, Alex J., additional, Dobbins, Sara E., additional, Hemminki, Kari, additional, Kinnersley, Ben, additional, Sanson, Marc, additional, Labreche, Karim, additional, Simon, Matthias, additional, Bondy, Melissa, additional, Law, Philip, additional, Speedy, Helen, additional, Allan, James, additional, Li, Ni, additional, Went, Molly, additional, Weinhold, Niels, additional, Morgan, Gareth, additional, Sonneveld, Pieter, additional, Nilsson, Björn, additional, Goldschmidt, Hartmut, additional, Sud, Amit, additional, Engert, Andreas, additional, Hansson, Markus, additional, Hemingway, Harry, additional, Asselbergs, Folkert W, additional, Patel, Riyaz S, additional, Keating, Brendan J, additional, Sattar, Naveed, additional, Houlston, Richard, additional, Casas, Juan P, additional, and Hingorani, Aroon D, additional
Published: 2018
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164. Prospective association between handgrip strength and cardiac structure and function in UK adults

Author: Beyer, Sebastian E., primary, Sanghvi, Mihir M., additional, Aung, Nay, additional, Hosking, Alice, additional, Cooper, Jackie A., additional, Paiva, José Miguel, additional, Lee, Aaron M., additional, Fung, Kenneth, additional, Lukaschuk, Elena, additional, Carapella, Valentina, additional, Mittleman, Murray A., additional, Brage, Soren, additional, Piechnik, Stefan K., additional, Neubauer, Stefan, additional, and Petersen, Steffen E., additional
Published: 2018
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165. The impact of menopausal hormone therapy (MHT) on cardiac structure and function: Insights from the UK Biobank imaging enhancement study

Author: Sanghvi, Mihir M., primary, Aung, Nay, additional, Cooper, Jackie A., additional, Paiva, José Miguel, additional, Lee, Aaron M., additional, Zemrak, Filip, additional, Fung, Kenneth, additional, Thomson, Ross J., additional, Lukaschuk, Elena, additional, Carapella, Valentina, additional, Kim, Young Jin, additional, Harvey, Nicholas C., additional, Piechnik, Stefan K., additional, Neubauer, Stefan, additional, and Petersen, Steffen E., additional
Published: 2018
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166. Risk thresholds for alcohol consumption : combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies

Author: Wood, Angela M., Kaptoge, Stephen, Butterworth, Adam S., Willeit, Peter, Warnakula, Samantha, Bolton, Thomas, Paige, Ellie, Paul, Dirk S., Sweeting, Michael, Burgess, Stephen, Bell, Steven, Astle, William, Stevens, David, Koulman, Albert, Selmer, Randi M., Verschuren, W. M. Monique, Sato, Shinichi, Njolstad, Inger, Woodward, Mark, Salomaa, Veikko, Nordestgaard, Borge G., Yeap, Bu B., Fletcher, Astrid, Melander, Olle, Kuller, Lewis H., Balkau, Beverley, Marmot, Michael, Koenig, Wolfgang, Casiglia, Edoardo, Cooper, Cyrus, Arndt, Volker, Franco, Oscar H., Wennberg, Patrik, Gallacher, John, de la Camara, Agustin Gomez, Volzke, Henry, Dahm, Christina C., Dale, Caroline E., Bergmann, Manuela M., Crespo, Carlos J., van der Schouw, Yvonne T., Kaaks, Rudolf, Simons, Leon A., Lagiou, Pagona, Schoufour, Josje D., Boer, Jolanda M. A., Key, Timothy J., Rodriguez, Beatriz, Moreno-Iribas, Conchi, Davidson, Karina W., Taylor, James O., Sacerdote, Carlotta, Wallace, Robert B., Quiros, J. Ramon, Tumino, Rosario, Blazer, Dan G., II, Linneberg, Allan, Daimon, Makoto, Panico, Salvatore, Howard, Barbara, Skeie, Guri, Strandberg, Timo, Weiderpass, Elisabete, Nietert, Paul J., Psaty, Bruce M., Kromhout, Daan, Salamanca-Fernandez, Elena, Kiechl, Stefan, Krumholz, Harlan M., Grioni, Sara, Palli, Domenico, Huerta, Jose M., Price, Jackie, Sundström, Johan, Arriola, Larraitz, Arima, Hisatomi, Travis, Ruth C., Panagiotakos, Demosthenes B., Karakatsani, Anna, Trichopoulou, Antonia, Kuhn, Tilman, Grobbee, Diederick E., Barrett-Connor, Elizabeth, van Schoor, Natasja, Boeing, Heiner, Overvad, Kim, Kauhanen, Jussi, Wareham, Nick, Langenberg, Claudia, Forouhi, Nita, Wennberg, Maria, Despres, Jean-Pierre, Cushman, Mary, Cooper, Jackie A., Rodriguez, Carlos J., Sakurai, Masaru, Shaw, Jonathan E., Knuiman, Matthew, Voortman, Trudy, Meisinger, Christa, Tjonneland, Anne, Brenner, Hermann, Palmieri, Luigi, Dallongeville, Jean, Brunner, Eric J., Assmann, Gerd, Trevisan, Maurizio, Gillum, Richard F., Ford, Ian, Sattar, Naveed, Lazo, Mariana, Thompson, Simon G., Ferrari, Pietro, Leon, David A., Smith, George Davey, Peto, Richard, Jackson, Rod, Banks, Emily, Di Angelantonio, Emanuele, Danesh, John, Wood, Angela M., Kaptoge, Stephen, Butterworth, Adam S., Willeit, Peter, Warnakula, Samantha, Bolton, Thomas, Paige, Ellie, Paul, Dirk S., Sweeting, Michael, Burgess, Stephen, Bell, Steven, Astle, William, Stevens, David, Koulman, Albert, Selmer, Randi M., Verschuren, W. M. Monique, Sato, Shinichi, Njolstad, Inger, Woodward, Mark, Salomaa, Veikko, Nordestgaard, Borge G., Yeap, Bu B., Fletcher, Astrid, Melander, Olle, Kuller, Lewis H., Balkau, Beverley, Marmot, Michael, Koenig, Wolfgang, Casiglia, Edoardo, Cooper, Cyrus, Arndt, Volker, Franco, Oscar H., Wennberg, Patrik, Gallacher, John, de la Camara, Agustin Gomez, Volzke, Henry, Dahm, Christina C., Dale, Caroline E., Bergmann, Manuela M., Crespo, Carlos J., van der Schouw, Yvonne T., Kaaks, Rudolf, Simons, Leon A., Lagiou, Pagona, Schoufour, Josje D., Boer, Jolanda M. A., Key, Timothy J., Rodriguez, Beatriz, Moreno-Iribas, Conchi, Davidson, Karina W., Taylor, James O., Sacerdote, Carlotta, Wallace, Robert B., Quiros, J. Ramon, Tumino, Rosario, Blazer, Dan G., II, Linneberg, Allan, Daimon, Makoto, Panico, Salvatore, Howard, Barbara, Skeie, Guri, Strandberg, Timo, Weiderpass, Elisabete, Nietert, Paul J., Psaty, Bruce M., Kromhout, Daan, Salamanca-Fernandez, Elena, Kiechl, Stefan, Krumholz, Harlan M., Grioni, Sara, Palli, Domenico, Huerta, Jose M., Price, Jackie, Sundström, Johan, Arriola, Larraitz, Arima, Hisatomi, Travis, Ruth C., Panagiotakos, Demosthenes B., Karakatsani, Anna, Trichopoulou, Antonia, Kuhn, Tilman, Grobbee, Diederick E., Barrett-Connor, Elizabeth, van Schoor, Natasja, Boeing, Heiner, Overvad, Kim, Kauhanen, Jussi, Wareham, Nick, Langenberg, Claudia, Forouhi, Nita, Wennberg, Maria, Despres, Jean-Pierre, Cushman, Mary, Cooper, Jackie A., Rodriguez, Carlos J., Sakurai, Masaru, Shaw, Jonathan E., Knuiman, Matthew, Voortman, Trudy, Meisinger, Christa, Tjonneland, Anne, Brenner, Hermann, Palmieri, Luigi, Dallongeville, Jean, Brunner, Eric J., Assmann, Gerd, Trevisan, Maurizio, Gillum, Richard F., Ford, Ian, Sattar, Naveed, Lazo, Mariana, Thompson, Simon G., Ferrari, Pietro, Leon, David A., Smith, George Davey, Peto, Richard, Jackson, Rod, Banks, Emily, Di Angelantonio, Emanuele, and Danesh, John
Abstract: Background: Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease. Methods: We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose-response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12.5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5.6 years [5th-95th percentile 1.04-13.5]) from 71 011 participants from 37 studies. Findings: In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5.4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around
Published: 2018
Full Text: View/download PDF

167. Risk thresholds for alcohol consumption: combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies

Author: Wood, Angela M, Kaptoge, Stephen, Butterworth, Adam S, Willeit, Peter, Warnakula, Samantha, Bolton, Thomas, Paige, Ellie, Paul, Dirk S, Sweeting, Michael, Burgess, Stephen, Bell, Steven, Tjønneland, Anne, Brenner, Hermann, Palmieri, Luigi, Dallongeville, Jean, Brunner, Eric J, Assmann, Gerd, Trevisan, Maurizio, Gillum, Richard F, Ford, Ian, Sattar, Naveed, Astle, William, Lazo, Mariana, Thompson, Simon G, Ferrari, Pietro, Leon, David A, Smith, George Davey, Peto, Richard, Jackson, Rod, Banks, Emily, Di Angelantonio, Emanuele, Danesh, John, Stevens, David, Butterworth, Adam, Koulman, Albert, Selmer, Randi M, Verschuren, Monique, Sato, Shinichi, Njølstad, Inger, Woodward, Mark, Veikko, Salomaa, Nordestgaard, Børge G, Yeap, Bu B, Flecther, Astrid, Melander, Olle, Kuller, Lewis H, Balkau, Beverley, Marmot, Michael, Koenig, Wolfgang, Casiglia, Edoardo, Cooper, Cyrus, Verschuren, W M Monique, Arndt, Volker, Franco, Oscar H, Wennberg, Patrik, Gallacher, John, Gómez de la Cámara, Agustín, Völzke, Henry, Dahm, Christina C, Dale, Caroline E, Bergmann, Manuela, Crespo, Carlos, van der Schouw, Yvonne T, Kaaks, Rudolf, Simons, Leon A, Lagiou, Pagona, Schoufour, Josje D, Boer, Jolanda M.A, Key, Timothy J, Rodriguez, Beatriz, Moreno-Iribas, Conchi, Davidson, Karina W, Taylor, James O, Sacerdote, Carlotta, Wallace, Robert B, Quiros, J. Ramon, Rimm, Eric B, Tumino, Rosario, Blazer III, Dan G, Linneberg, Allan, Daimon, Makoto, Panico, Salvatore, Howard, Barbara, Skeie, Guri, Salomaa, Veikko, Strandberg, Timo, Weiderpass, Elisabete, Nietert, Paul J, Psaty, Bruce M, Kromhout, Daan, Salamanca-Fernandez, Elena, Kiechl, Stefan, Krumholz, Harlan M, Grioni, Sara, Palli, Domenico, Huerta, José M, Price, Jackie, Sundström, Johan, Arriola, Larraitz, Arima, Hisatomi, Travis, Ruth C, Panagiotakos, Demosthenes B, Karakatsani, Anna, Trichopoulou, Antonia, Kühn, Tilman, Grobbee, Diederick E, Barrett-Connor, Elizabeth, van Schoor, Natasja, Boeing, Heiner, Overvad, Kim, Kauhanen, Jussi, Wareham, Nick, Langenberg, Claudia, Forouhi, Nita, Wennberg, Maria, Després, Jean-Pierre, Cushman, Mary, Cooper, Jackie A, Rodriguez, Carlos J, Sakurai, Masaru, Shaw, Jonathan E, Knuiman, Matthew, Fletcher, Astrid, Voortman, Trudy, Meisinger, Christa, Dallongeville, Jean-Pierre, Gillumn, Richard F, Ford, Ian Ford, Thompson, Simon, Davey Smith, George, de la Cámara, Agustín Gómez, Bergmann, Manuela M, Crespo, Carlos J, Boer, Jolanda M A, Quiros, J Ramon, Blazer, Dan G, Wood, Angela M, Kaptoge, Stephen, Butterworth, Adam S, Willeit, Peter, Warnakula, Samantha, Bolton, Thomas, Paige, Ellie, Paul, Dirk S, Sweeting, Michael, Burgess, Stephen, Bell, Steven, Tjønneland, Anne, Brenner, Hermann, Palmieri, Luigi, Dallongeville, Jean, Brunner, Eric J, Assmann, Gerd, Trevisan, Maurizio, Gillum, Richard F, Ford, Ian, Sattar, Naveed, Astle, William, Lazo, Mariana, Thompson, Simon G, Ferrari, Pietro, Leon, David A, Smith, George Davey, Peto, Richard, Jackson, Rod, Banks, Emily, Di Angelantonio, Emanuele, Danesh, John, Stevens, David, Butterworth, Adam, Koulman, Albert, Selmer, Randi M, Verschuren, Monique, Sato, Shinichi, Njølstad, Inger, Woodward, Mark, Veikko, Salomaa, Nordestgaard, Børge G, Yeap, Bu B, Flecther, Astrid, Melander, Olle, Kuller, Lewis H, Balkau, Beverley, Marmot, Michael, Koenig, Wolfgang, Casiglia, Edoardo, Cooper, Cyrus, Verschuren, W M Monique, Arndt, Volker, Franco, Oscar H, Wennberg, Patrik, Gallacher, John, Gómez de la Cámara, Agustín, Völzke, Henry, Dahm, Christina C, Dale, Caroline E, Bergmann, Manuela, Crespo, Carlos, van der Schouw, Yvonne T, Kaaks, Rudolf, Simons, Leon A, Lagiou, Pagona, Schoufour, Josje D, Boer, Jolanda M.A, Key, Timothy J, Rodriguez, Beatriz, Moreno-Iribas, Conchi, Davidson, Karina W, Taylor, James O, Sacerdote, Carlotta, Wallace, Robert B, Quiros, J. Ramon, Rimm, Eric B, Tumino, Rosario, Blazer III, Dan G, Linneberg, Allan, Daimon, Makoto, Panico, Salvatore, Howard, Barbara, Skeie, Guri, Salomaa, Veikko, Strandberg, Timo, Weiderpass, Elisabete, Nietert, Paul J, Psaty, Bruce M, Kromhout, Daan, Salamanca-Fernandez, Elena, Kiechl, Stefan, Krumholz, Harlan M, Grioni, Sara, Palli, Domenico, Huerta, José M, Price, Jackie, Sundström, Johan, Arriola, Larraitz, Arima, Hisatomi, Travis, Ruth C, Panagiotakos, Demosthenes B, Karakatsani, Anna, Trichopoulou, Antonia, Kühn, Tilman, Grobbee, Diederick E, Barrett-Connor, Elizabeth, van Schoor, Natasja, Boeing, Heiner, Overvad, Kim, Kauhanen, Jussi, Wareham, Nick, Langenberg, Claudia, Forouhi, Nita, Wennberg, Maria, Després, Jean-Pierre, Cushman, Mary, Cooper, Jackie A, Rodriguez, Carlos J, Sakurai, Masaru, Shaw, Jonathan E, Knuiman, Matthew, Fletcher, Astrid, Voortman, Trudy, Meisinger, Christa, Dallongeville, Jean-Pierre, Gillumn, Richard F, Ford, Ian Ford, Thompson, Simon, Davey Smith, George, de la Cámara, Agustín Gómez, Bergmann, Manuela M, Crespo, Carlos J, Boer, Jolanda M A, Quiros, J Ramon, and Blazer, Dan G
Abstract: BACKGROUND: Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease. METHODS:We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose–response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12·5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5·6 years [5th–95th percentile 1·04–13·5]) from 71 011 participants from 37 studies. FINDINGS: In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5·4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around o
Published: 2018

168. Let's focus on burdens of family caregivers

Author: Cooper, Jackie
Subjects: Caregivers, General interest, News, opinion and commentary
Abstract: Byline: Jackie Cooper For the past several years, AARP has made finding ways to lighten the responsibilities of our family caregivers a top priority. Here in New Mexico, we worked [...]
Published: 2017

169. PCSK9 genetic variants and risk of type 2 diabetes: a mendelian randomisation study

Author: Schmidt, Amand F., Swerdlow, Daniel I., Holmes, Michael V., Patel, Riyaz S., Fairhurst-Hunter, Zammy, Lyall, Donald M., Hartwig, Fernando Pires, Horta, Bernardo Lessa, Hyppönen, Elina, Power, Christine, Moldovan, Max, van Iperen, Erik, Hovingh, G. Kees, Demuth, Ilja, Norman, Kristina, Steinhagen-Thiessen, Elisabeth, Demuth, Juri, Bertram, Lars, Liu, Tian, Coassin, Stefan, Willeit, Johann, Kiechl, Stefan, Willeit, Karin, Mason, Dan, Wright, John, Morris, Richard, Wanamethee, Goya, Whincup, Peter, Ben-Shlomo, Yoav, McLachlan, Stela, Price, Jackie F., Kivimaki, Mika, Welch, Catherine, Sanchez-Galvez, Adelaida, Marques-Vidal, Pedro, Nicolaides, Andrew, Panayiotou, Andrie G., Onland-Moret, N. Charlotte, van der Schouw, Yvonne T., Matullo, Giuseppe, Fiorito, Giovanni, Guarrera, Simonetta, Sacerdote, Carlotta, Wareham, Nicholas J., Langenberg, Claudia, Scott, Robert, Luan, Jian'an, Bobak, Martin, Malyutina, Sofia, Pająk, Andrzej, Kubinova, Ruzena, Tamosiunas, Abdonas, Pikhart, Hynek, Husemoen, Lise Lotte Nystrup, Garup, Niels, Pedersen, Oluf, Hansen, Torben, Linneberg, Allan, Simonsen, Kenneth Starup, Cooper, Jackie, Humphries, Steve E., Brilliant, Murray, Kitchner, Terrie, Hakonarson, Hakon, Carrell, David S., McCarty, Catherine A., Kirchner, H. Lester, Larson, Eric B., Crosslin, David R., de Andrade, Mariza, Roden, Dan M., Denny, Joshua C., Carty, Cara, Hancock, Stephen, Attia, John, Holliday, Elizabeth, O'Donnell, Martin, Yusuf, Salim, Chong, Michael, Pare, Guillaume, van der Harst, Pim, Said, M. Abdullah, Eppinga, Ruben N., Verweij, Niek, Snieder, Harold, Christen, Tim, Mook-Kanamori, Dennis O., Gustafsson, Stefan, Lind, Lars, Ingelsson, Erik, Pazoki, Raha, Franco, Oscar, Hofman, Albert, Uitterlinden, Andre, Dehghan, Abbas, Teumer, Alexander, Baumeister, Sebastian, Dörr, Marcus, Lerch, Markus M., Völker, Uwe, Völzke, Henry, Ward, Joey, Pell, Jill P., Smith, Daniel J., Meade, Tom, Maitland-van der Zee, Anke H., Baranova, Ekaterina V., Young, Robin, Ford, Ian, Campbell, Archie, Padmanabhan, Sandosh, Bots, Michiel L., Grobbee, Diederick E., Froguel, Philippe, Thuillier, Dorothée, Balkau, Beverley, Bonnefond, Amélie, Cariou, Bertrand, Smart, Melissa, Bao, Yanchun, Kumari, Meena, Mahajan, Anubha, Ridker, Paul M., Chasman, Daniel I., Reiner, Alex P., Lange, Leslie A., Ritchie, Marylyn D., Asselbergs, Folkert, Casas, Juan-Pablo, Keating, Brendan J., Preiss, David, Hingorani, Aroon D., Sattar, Naveed, LifeLines Cohort study group, UCLEB consortium, Epidemiology, and Internal Medicine
Subjects: Blood Glucose, STATIN THERAPY, Endocrinology, Diabetes and Metabolism, HEART-DISEASE, Endocrinology and Diabetes, Heart disease, Internal Medicine, Endocrinology, Medical and Health Sciences, HYPERCHOLESTEROLEMIA, Cohort Studies, Endocrinology & Metabolism, SDG 3 - Good Health and Well-being, Health Sciences, Journal Article, Diabetes Mellitus, Humans, LDL-cholesterol, Genetic Predisposition to Disease, Mendelian randomisation, COMMON, METAANALYSIS, Genetic Association Studies, Randomized Controlled Trials as Topic, ARCHITECTURE, Science & Technology, CHOLESTEROL, Diabetes, Genetic Variation, PATHWAYS, nutritional and metabolic diseases, Cholesterol, LDL, ASSOCIATION, Mendelian Randomization Analysis, UCLEB consortium, PCSK9 inhibition, Diabetes and Metabolism, INSIGHTS, Diabetes Mellitus, Type 2, Case-Control Studies, Endokrinologi och diabetes, LDL cholesterol, Proprotein Convertase 9, Blood Glucose/metabolism, Cholesterol, LDL/blood, Cholesterol, LDL/genetics, Diabetes Mellitus, Type 2/blood, Diabetes Mellitus, Type 2/diagnosis, Diabetes Mellitus, Type 2/genetics, Genetic Predisposition to Disease/genetics, Genetic Variation/genetics, Mendelian Randomization Analysis/methods, Proprotein Convertase 9/genetics, Randomized Controlled Trials as Topic/methods, Life Sciences & Biomedicine, LifeLines Cohort study group
Abstract: Background: Statin treatment and variants in the gene encoding HMG-CoA reductase are associated with reductions\ud in both the concentration of LDL cholesterol and the risk of coronary heart disease, but also with modest\ud hyperglycaemia, increased bodyweight, and modestly increased risk of type 2 diabetes, which in no way offsets their\ud substantial benefits. We sought to investigate the associations of LDL cholesterol-lowering PCSK9 variants with type 2\ud diabetes and related biomarkers to gauge the likely effects of PCSK9 inhibitors on diabetes risk.\ud Methods: In this mendelian randomisation study, we used data from cohort studies, randomised controlled trials,\ud case control studies, and genetic consortia to estimate associations of PCSK9 genetic variants with LDL cholesterol,\ud fasting blood glucose, HbA1c, fasting insulin, bodyweight, waist-to-hip ratio, BMI, and risk of type 2 diabetes, using\ud a standardised analysis plan, meta-analyses, and weighted gene-centric scores.\ud Findings: Data were available for more than 550 000 individuals and 51 623 cases of type 2 diabetes. Combined analyses\ud of four independent PCSK9 variants (rs11583680, rs11591147, rs2479409, and rs11206510) scaled to 1 mmol/L lower\ud LDL cholesterol showed associations with increased fasting glucose (0·09 mmol/L, 95% CI 0·02 to 0·15), bodyweight\ud (1·03 kg, 0·24 to 1·82), waist-to-hip ratio (0·006, 0·003 to 0·010), and an odds ratio for type diabetes of 1·29 (1·11 to 1·50).\ud Based on the collected data, we did not identify associations with HbA1c (0·03%, –0·01 to 0·08), fasting insulin (0·00%,\ud –0·06 to 0·07), and BMI (0·11 kg/m², –0·09 to 0·30).\ud Interpretation: PCSK9 variants associated with lower LDL cholesterol were also associated with circulating higher\ud fasting glucose concentration, bodyweight, and waist-to-hip ratio, and an increased risk of type 2 diabetes. In trials of\ud PCSK9 inhibitor drugs, investigators should carefully assess these safety outcomes and quantify the risks and benefits\ud of PCSK9 inhibitor treatment, as was previously done for statins.\ud Funding: British Heart Foundation, and University College London Hospitals NHS Foundation Trust (UCLH) National\ud Institute for Health Research (NIHR) Biomedical Research Centre.
Published: 2017
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170. Predictors of total morbidity burden on days 3, 5 and 8 after cardiac surgery

Author: Sanders, Julie, Cooper, Jackie, Mythen, Michael G., and Montgomery, Hugh E.
Subjects: C-POMS, Research, Morbidity outcome, Risk factor, Cardiac surgery
Abstract: Background Post-operative morbidity affects up to 36% of cardiac surgical patients. However, few countries reliably record morbidity outcome data, despite patients wanting to be informed of all the risks associated with surgery. The Cardiac Post-Operative Morbidity Score (C-POMS) is a new tool for describing and scoring (0–13) total morbidity burden after cardiac surgery, derived by noting the presence/absence of 13 morbidity domains on days 3, 5, 8 and 15. Identifying modifiable C-POMS risk factors may suggest targets for intervention to reduce morbidity and healthcare costs. Thus, we explored the association of C-POMS with previously identified predictors of post-operative morbidity. Methods A systematic literature review of pre-operative risk assessment models for post-operative morbidity was conducted to identify variables associated with post-operative morbidity. The association of those variables with C-POMS was explored in patients drawn from the original C-POMS study (n = 444). Results Seventy risk factors were identified, of which 56 were available in the study and 49 were suitable for analysis. Numbers were too few to analyse associations on D15. Thirty-three (67.3%) and 20 (40.8%) variables were associated with C-POMS on at least 1 or 2 days, respectively. Pre-operative albumin concentration, left ventricular ejection fraction and New York Heart Association functional class were associated with C-POMS on all days. Of the 16 independent risk factors, pre-operative albumin and haemoglobin concentrations and weight are potentially modifiable. Conclusions Different risk factors are associated with total morbidity burden on different post-operative days. Pre-operative albumin and haemoglobin concentrations and weight were independently predictive of post-operative total morbidity burden suggesting therapeutic interventions aimed at these might reduce both post-operative morbidity risk and health-care costs in patients undergoing cardiac surgery. Electronic supplementary material The online version of this article (doi:10.1186/s13741-017-0060-9) contains supplementary material, which is available to authorized users.
Published: 2017

171. Additional file 1: Table S1. of Common variants in the genes of triglyceride and HDL-C metabolism lack association with coronary artery disease in the Pakistani subjects

Author: Shahid, Saleem, N.A. Shabana, Cooper, Jackie, Rehman, Abdul, and Humphries, Steve
Abstract: List of primers and probes used in KASPar assay. (DOCX 11Â kb)
Published: 2017
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172. Additional file 2: Table S2. of Common variants in the genes of triglyceride and HDL-C metabolism lack association with coronary artery disease in the Pakistani subjects

Author: Shahid, Saleem, N.A. Shabana, Cooper, Jackie, Rehman, Abdul, and Humphries, Steve
Abstract: Sequence of primers used in PCR. (DOCX 11Â kb)
Published: 2017
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173. Additional file 3: Table S3. of Common variants in the genes of triglyceride and HDL-C metabolism lack association with coronary artery disease in the Pakistani subjects

Author: Shahid, Saleem, N.A. Shabana, Cooper, Jackie, Rehman, Abdul, and Humphries, Steve
Abstract: Basic features of SNPs under study. (DOCX 13Â kb)
Published: 2017
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174. Additional file 2: of Predictors of total morbidity burden on days 3, 5 and 8 after cardiac surgery

Author: Sanders, Julie, Cooper, Jackie, Mythen, Michael, and Montgomery, Hugh
Abstract: Univariate analysis: tier 1 and 2 not predictive of C-POMS summary score on D3, D5 and D8. (DOCX 20Â kb)
Published: 2017
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175. Bezafibrate in men with lower extremity arterial disease: randomised controlled trial. (Papers)

Author: Meade, Tom, Zuhrie, Riaz, Cook, Claire, and Cooper, Jackie
Subjects: Diseases, Evaluation, Complications and side effects, Risk factors, Coronary heart disease -- Risk factors -- Complications and side effects, Arterial occlusive diseases -- Complications and side effects -- Risk factors, Leg -- Diseases, Stroke -- Risk factors -- Complications and side effects, Drug therapy -- Evaluation, Stroke (Disease) -- Risk factors -- Complications and side effects, Arterial occlusions -- Complications and side effects -- Risk factors, Extremities, Lower -- Diseases
Abstract: Objective To assess the effect of bezafibrate on the risk of coronary heart disease and stroke in men with lower extremity arterial disease. Design Double blind placebo controlled randomised trial. [...]
Published: 2002

176. Variant rs10911021 that associates with coronary heart disease in type 2 diabetes, is associated with lower concentrations of circulating HDL cholesterol and large HDL particles but not with amino acids

Author: Beaney, Katherine E, Cooper, Jackie A, McLachlan, Stela, Wannamethee, S Goya, Jefferis, Barbara J, Whincup, Peter, Ben-Shlomo, Yoav, Price, Jacqueline F, Kumari, Meena, Wong, Andrew, Ong, Ken, Hardy, Rebecca, Kuh, Diana, Kivimaki, Mika, Kangas, Antti J, Soininen, Pasi, Ala-Korpela, Mika, Drenos, Fotios, Humphries, Steve E, UCLEB consortium, Ong, Kenneth [0000-0003-4689-7530], and Apollo - University of Cambridge Repository
Subjects: Male, Magnetic Resonance Spectroscopy, endocrine system diseases, Down-Regulation, Coronary Disease, Polymorphism, Single Nucleotide, Risk Assessment, Gene Frequency, Risk Factors, Metabolomics, Humans, Genetic Predisposition to Disease, cardiovascular diseases, Amino Acids, Particle Size, Genetic Association Studies, Aged, Genetic risk, Cholesterol, HDL, nutritional and metabolic diseases, Middle Aged, Protective Factors, HDL-cholesterol, High-Throughput Screening Assays, Coronary heart disease, Phenotype, Diabetes Mellitus, Type 2, Chromosomes, Human, Pair 1, DNA, Intergenic, Female, Biomarkers
Abstract: AIMS: An intergenic locus on chromosome 1 (lead SNP rs10911021) was previously associated with coronary heart disease (CHD) in type 2 diabetes (T2D). Using data from the UCLEB consortium we investigated the relationship between rs10911021 and CHD in T2D, whether rs10911021 was associated with levels of amino acids involved in the γ-glutamyl cycle or any conventional risk factors (CRFs) for CHD in the T2D participants. METHODS: Four UCLEB studies (n = 6531) had rs10911021 imputation, CHD in T2D, CRF and metabolomics data determined using a nuclear magnetic resonance based platform. RESULTS: The expected direction of effect between rs10911021 and CHD in T2D was observed (1377 no CHD/160 CHD; minor allele OR 0.80, 95 % CI 0.60-1.06) although this was not statistically significant (p = 0.13). No association between rs10911021 and CHD was seen in non-T2D participants (11218 no CHD/1274 CHD; minor allele OR 1.00 95 % CIs 0.92-1.10). In T2D participants, while no associations were observed between rs10911021 and the nine amino acids measured, rs10911021 was associated with HDL-cholesterol (p = 0.0005) but the minor "protective" allele was associated with lower levels (-0.034 mmol/l per allele). Focusing more closely on the HDL-cholesterol subclasses measured, we observed that rs10911021 was associated with six large HDL particle measures in T2D (all p < 0.001). No significant associations were seen in non-T2D subjects. CONCLUSIONS: Our findings are consistent with a true association between rs10911021 and CHD in T2D. The protective minor allele was associated with lower HDL-cholesterol and reductions in HDL particle traits. Our results indicate a complex relationship between rs10911021 and CHD in T2D.
Published: 2016
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177. Marginal role for 53 common genetic variants in cardiovascular disease prediction

Author: Morris, Richard W, Cooper, Jackie A, Shah, Tina, Wong, Andrew, Drenos, Fotios, Engmann, Jorgen, McLachlan, Stela, Jefferis, Barbara, Dale, Caroline, Hardy, Rebecca, Kuh, Diana, Ben-Shlomo, Yoav, Wannamethee, S Goya, Whincup, Peter H, Casas, Juan-Pablo, Kivimaki, Mika, Kumari, Meena, Talmud, Philippa J, Price, Jacqueline F, Dudbridge, Frank, Hingorani, Aroon D, Humphries, Steve E, and UCLEB Consortium
Abstract: OBJECTIVE: We investigated discrimination and calibration of cardiovascular disease (CVD) risk scores when genotypic was added to phenotypic information. The potential of genetic information for those at intermediate risk by a phenotype-based risk score was assessed. METHODS: Data were from seven prospective studies including 11 851 individuals initially free of CVD or diabetes, with 1444 incident CVD events over 10 years' follow-up. We calculated a score from 53 CVD-related single nucleotide polymorphisms and an established CVD risk equation 'QRISK-2' comprising phenotypic measures. The area under the receiver operating characteristic curve (AUROC), detection rate for given false-positive rate (FPR) and net reclassification improvement (NRI) index were estimated for gene scores alone and in addition to the QRISK-2 CVD risk score. We also evaluated use of genetic information only for those at intermediate risk according to QRISK-2. RESULTS: The AUROC was 0.635 for QRISK-2 alone and 0.623 with addition of the gene score. The detection rate for 5% FPR improved from 11.9% to 12.0% when the gene score was added. For a 10-year CVD risk cut-off point of 10%, the NRI was 0.25% when the gene score was added to QRISK-2. Applying the genetic risk score only to those with QRISK-2 risk of 10%
Published: 2016

178. Diarrhoea in the critically ill is common, associated with poor outcome, and rarely due to Clostridium difficile

Author: Tirlapur, Nikhil, Puthucheary, Zudin A., Cooper, Jackie A., Sanders, Julie, Coen, Pietro G., Moonesinghe, S. Ramani, Wilson, A. Peter, Mythen, Michael G., and Montgomery, Hugh E.
Subjects: Adult, Diarrhea, Male, Clostridioides difficile, Critical Illness, Kaplan-Meier Estimate, Middle Aged, Prognosis, Severity of Illness Index, Article, Intensive Care Units, Outcome Assessment, Health Care, Prevalence, Humans, Female, Enterocolitis, Pseudomembranous, Aged
Abstract: Diarrhoea is common in Intensive Care Unit (ICU) patients, with a reported prevalence of 15–38%. Many factors may cause diarrhoea, including Clostridium difficile, drugs (e.g. laxatives, antibiotics) and enteral feeds. Diarrhoea impacts on patient dignity, increases nursing workload and healthcare costs, and exacerbates morbidity through dermal injury, impaired enteral uptake and subsequent fluid imbalance. We analysed a cohort of 9331 consecutive patients admitted to a mixed general intensive care unit to establish the prevalence of diarrhoea in intensive care unit patients, and its relationship with infective aetiology and clinical outcomes. We provide evidence that diarrhoea is common (12.9% (1207/9331) prevalence) in critically ill patients, independently associated with increased intensive care unit length of stay (mean (standard error) 14.8 (0.26) vs 3.2 (0.09) days, p
Published: 2016
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179. 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, and Holmes, Michael V
Abstract: BACKGROUND: Increased circulating plasma urate concentration is associated with an increased risk of coronary heart disease, but the extent of any causative effect of urate on risk of coronary heart disease is still unclear. In this study, we aimed to clarify any causal role of urate on coronary heart disease risk using Mendelian randomisation analysis.METHODS: We first did a fixed-effects meta-analysis of the observational association of plasma urate and risk of coronary heart disease. We then used a conventional Mendelian randomisation approach to investigate the causal relevance using a genetic instrument based on 31 urate-associated single nucleotide polymorphisms (SNPs). To account for potential pleiotropic associations of certain SNPs with risk factors other than urate, we additionally did both a multivariable Mendelian randomisation analysis, in which the genetic associations of SNPs with systolic and diastolic blood pressure, HDL cholesterol, and triglycerides were included as covariates, and an Egger Mendelian randomisation (MR-Egger) analysis to estimate a causal effect accounting for unmeasured pleiotropy.FINDINGS: In the meta-analysis of 17 prospective observational studies (166 486 individuals; 9784 coronary heart disease events) a 1 SD higher urate concentration was associated with an odds ratio (OR) for coronary heart disease of 1·07 (95% CI 1·04-1·10). The corresponding OR estimates from the conventional, multivariable adjusted, and Egger Mendelian randomisation analysis (58 studies; 198 598 individuals; 65 877 events) were 1·18 (95% CI 1·08-1·29), 1·10 (1·00-1·22), and 1·05 (0·92-1·20), respectively, per 1 SD increment in plasma urate.INTERPRETATION: Conventional and multivariate Mendelian randomisation analysis implicates a causal role for urate in the development of coronary heart disease, but these estimates might be inflated by hidden pleiotropy. Egger Mendelian randomisation analysis, which accounts for pleiotropy but has less statistical power, suggests there might be no causal effect. These results might help investigators to determine the priority of trials of urate lowering for the prevention of coronary heart disease compared with other potential interventions.FUNDING: UK National Institute for Health Research, British Heart Foundation, and UK Medical Research Council.
Published: 2016
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180. Broken Hill

Author: Beck, Haig and Cooper, Jackie
Subjects: Museum architecture -- Innovations, Mineral industry
Published: 1992

181. Adverse cardiovascular magnetic resonance phenotypes are associated with greater likelihood of incident coronavirus disease 2019: findings from the UK Biobank

Author: Raisi-Estabragh, Zahra, McCracken, Celeste, Cooper, Jackie, Fung, Kenneth, Paiva, José M., Khanji, Mohammed Y., Rauseo, Elisa, Biasiolli, Luca, Raman, Betty, Piechnik, Stefan K., Neubauer, Stefan, Munroe, Patricia B., Harvey, Nicholas C., and Petersen, Steffen E.
Abstract: Background: Coronavirus disease 2019 (COVID-19) disproportionately affects older people. Observational studies suggest indolent cardiovascular involvement after recovery from acute COVID-19. However, these findings may reflect pre-existing cardiac phenotypes. Aims: We tested the association of baseline cardiovascular magnetic resonance (CMR) phenotypes with incident COVID-19. Methods: We studied UK Biobank participants with CMR imaging and COVID-19 testing. We considered left and right ventricular (LV, RV) volumes, ejection fractions, and stroke volumes, LV mass, LV strain, native T1, aortic distensibility, and arterial stiffness index. COVID-19 test results were obtained from Public Health England. Co-morbidities were ascertained from self-report and hospital episode statistics (HES). Critical care admission and death were from HES and death register records. We investigated the association of each cardiovascular measure with COVID-19 test result in multivariable logistic regression models adjusting for age, sex, ethnicity, deprivation, body mass index, smoking, diabetes, hypertension, high cholesterol, and prior myocardial infarction. Results: We studied 310 participants (n= 70 positive). Median age was 63.8 [57.5, 72.1] years; 51.0% (n= 158) were male. 78.7% (n= 244) were tested in hospital, 3.5% (n= 11) required critical care admission, and 6.1% (n= 19) died. In fully adjusted models, smaller LV/RV end-diastolic volumes, smaller LV stroke volume, and poorer global longitudinal strain were associated with significantly higher odds of COVID-19 positivity. Discussion: We demonstrate association of pre-existing adverse CMR phenotypes with greater odds of COVID-19 positivity independent of classical cardiovascular risk factors. Conclusions: Observational reports of cardiovascular involvement after COVID-19 may, at least partly, reflect pre-existing cardiac status rather than COVID-19 induced alterations.
Published: 2021
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182. The UK Paediatric Familial Hypercholesterolaemia Register: Statin-related safety and 1-year growth data

Author: Humphries, Steve E., primary, Cooper, Jackie, additional, Dale, Peter, additional, and Ramaswami, Uma, additional
Published: 2018
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183. Telomere length, antioxidant status and incidence of ischaemic heart disease in type 2 diabetes

Author: Masi, Stefano, D’Aiuto, Francesco, Cooper, Jackie, Salpea, Klelia, Stephens, Jeffrey W., Hurel, Steven J., Deanfield, John E., and Humphries, Steve E.
Subjects: Adult, Male, Myocardial Ischemia, Antioxidants, Article, Plasma, Risk Factors, 80 and over, Diabetes Mellitus, Humans, cardiovascular diseases, Cardiovascular risk, Diabetes, Oxidative stress, Telomeres, Aged, Aged, 80 and over, Cell Aging, Diabetes Mellitus, Type 2, Female, Incidence, Middle Aged, Oxidative Stress, Telomere, Telomere Homeostasis, Medicine (all), Cardiology and Cardiovascular Medicine, Cellular Senescence, Type 2
Abstract: Background Type 2 diabetes (T2D) is associated with an increased risk of ischaemic heart disease (IHD). An accelerated process of vascular ageing induced by an increased oxidative stress exposure is suggested as potential pathway accounting for this association. However, no studies have explored the relationship between markers of vascular ageing, measures of oxidative stress and risk of IHD in T2D. Objectives To explore the association between plasma antioxidant status, marker of cellular ageing (leukocyte telomere length, LTL) and 10 years risk of IHD in patients with T2D. Methods Between 2001 and 2002, 489 Caucasians subjects with T2D were enrolled at the diabetic clinic, University College London Hospital. Plasma total anti-oxidant status (TAOS) and LTL were measured by photometric microassay and RT-PCR, respectively. The incidence of IHD over 10 years was determined through linkage with the national clinical audit of acute coronary syndrome in UK. Results At baseline, TAOS was associated with LTL (age adjusted: r = 0.106, p = 0.024). After 10 years, 61 patients developed IHD. Lower TAOS and shorter LTL at baseline predicted an increased IHD risk at follow-up (age adjusted: p = 0.033 and p = 0.040, respectively). These associations were independent of age, gender, cardiovascular risk factors, circulating levels of CRP and medication differences. Conclusions Reduced TAOS and short LTL are interrelated pathways which predict risk of IHD in patients with T2D. Our findings suggest that antioxidant defences are important to maintain telomere integrity, potentially reducing the progression of vascular ageing in patients with T2D.
Published: 2016

184. Additional file 2: Table S2. of Effect of SORT1, APOB and APOE polymorphisms on LDL-C and coronary heart disease in Pakistani subjects and their comparison with Northwick Park Heart Study II

Author: Shahid, Saleem, Shabana á , Cooper, Jackie, Beaney, Katherine, Kawah Li, Rehman, Abdul, and Humphries, Stephen
Abstract: Comparison of RAFs between Pakistani and NPHSII study groups. (DOC 31 kb)
Published: 2016
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185. MOESM1 of Variant rs10911021 that associates with coronary heart disease in type 2 diabetes, is associated with lower concentrations of circulating HDL cholesterol and large HDL particles but not with amino acids

Author: Beaney, Katherine, Cooper, Jackie, McLachlan, Stela, S. Wannamethee, Jefferis, Barbara, Whincup, Peter, Ben-Shlomo, Yoav, Price, Jacqueline, Kumari, Meena, Wong, Andrew, Ong, Ken, Hardy, Rebecca, Kuh, Diana, Kivimaki, Mika, Kangas, Antti, Soininen, Pasi, Ala-Korpela, Mika, Drenos, Fotios, and Humphries, Steve
Subjects: endocrine system diseases, nutritional and metabolic diseases
Abstract: Additional file 1: Table S1. Sensitivity analysis for fixed-effects meta-analysis of association between rs10911021 and CHD in T2D. Table S2. Sensitivity analysis for random-effects meta-analysis of association between rs10911021 and CHD in T2D. Table S3. HDL traits with a suggestive association with rs10911021 in diabetic participants. Table S4. HDL traits which did not show an association with rs10911021 in those with or without T2D. Figure S1. Flow-chart showing number of UCLEB participants with and without prevalent T2D used in the different analyses.
Published: 2016
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186. Additional file 3: Figure S1. of Effect of SORT1, APOB and APOE polymorphisms on LDL-C and coronary heart disease in Pakistani subjects and their comparison with Northwick Park Heart Study II

Author: Shahid, Saleem, Shabana á , Cooper, Jackie, Beaney, Katherine, Kawah Li, Rehman, Abdul, and Humphries, Stephen
Subjects: cardiovascular diseases
Abstract: Box plot showing the distribution of gene score in non CHD and CHD subjects and its association with LDL-C in Pakistani people. The figure shows the distribution of gene score in Pakistani CHD and non CHD. It is clear that the gene score is high in CHD than non CHD and LDL-C levels are also high along high gene score. (DOCX 32 kb)
Published: 2016
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187. Additional file 1: Table S1. of Effect of SORT1, APOB and APOE polymorphisms on LDL-C and coronary heart disease in Pakistani subjects and their comparison with Northwick Park Heart Study II

Author: Shahid, Saleem, Shabana á , Cooper, Jackie, Beaney, Katherine, Kawah Li, Rehman, Abdul, and Humphries, Stephen
Abstract: Basic features of SNPs under study. (DOC 33 kb)
Published: 2016
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188. Additional file 4: Table S3. of Effect of SORT1, APOB and APOE polymorphisms on LDL-C and coronary heart disease in Pakistani subjects and their comparison with Northwick Park Heart Study II

Author: Shahid, Saleem, Shabana á , Cooper, Jackie, Beaney, Katherine, Kawah Li, Rehman, Abdul, and Humphries, Stephen
Subjects: lipids (amino acids, peptides, and proteins)
Abstract: Mean LDL-C by number of LDL-C raising SNPs for the unweighted gene score. (DOC 37 kb)
Published: 2016
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189. The impact of cardiovascular risk factors on cardiac structure and function: Insights from the UK Biobank imaging enhancement study

Author: Petersen, Steffen E., primary, Sanghvi, Mihir M., additional, Aung, Nay, additional, Cooper, Jackie A., additional, Paiva, José Miguel, additional, Zemrak, Filip, additional, Fung, Kenneth, additional, Lukaschuk, Elena, additional, Lee, Aaron M., additional, Carapella, Valentina, additional, Kim, Young Jin, additional, Piechnik, Stefan K., additional, and Neubauer, Stefan, additional
Published: 2017
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190. Plasma Concentrations of Afamin Are Associated With Prevalent and Incident Type 2 Diabetes: A Pooled Analysis in More Than 20,000 Individuals

Author: Kollerits, Barbara, primary, Lamina, Claudia, additional, Huth, Cornelia, additional, Marques-Vidal, Pedro, additional, Kiechl, Stefan, additional, Seppälä, Ilkka, additional, Cooper, Jackie, additional, Hunt, Steven C., additional, Meisinger, Christa, additional, Herder, Christian, additional, Kedenko, Ludmilla, additional, Willeit, Johann, additional, Thorand, Barbara, additional, Dähnhardt, Doreen, additional, Stöckl, Doris, additional, Willeit, Karin, additional, Roden, Michael, additional, Rathmann, Wolfgang, additional, Paulweber, Bernhard, additional, Peters, Annette, additional, Kähönen, Mika, additional, Lehtimäki, Terho, additional, Raitakari, Olli T., additional, Humphries, Steve E., additional, Vollenweider, Peter, additional, Dieplinger, Hans, additional, and Kronenberg, Florian, additional
Published: 2017
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191. Assessing the effects of mitofusin 2 deficiency in the adult heart using 3D electron tomography

Author: Beikoghli Kalkhoran, Siavash, primary, Hall, Andrew R., additional, White, Ian J., additional, Cooper, Jackie, additional, Fan, Qiao, additional, Ong, Sang-Bing, additional, Hernández-Reséndiz, Sauri, additional, Cabrera-Fuentes, Hector, additional, Chinda, Kroekkiat, additional, Chakraborty, Bibhas, additional, Dorn, Gerald W., additional, Yellon, Derek M., additional, and Hausenloy, Derek J., additional
Published: 2017
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192. Greater preclinical atherosclerosis in treated monogenic familial hypercholesterolemia vs. polygenic hypercholesterolemia

Author: Sharifi, Mahtab, primary, Higginson, Elizabeth, additional, Bos, Sven, additional, Gallivan, Angela, additional, Harvey, Darren, additional, Li, Ka Wah, additional, Abeysekera, Amali, additional, Haddon, Angela, additional, Ashby, Helen, additional, Shipman, Kate E., additional, Cooper, Jackie A., additional, Futema, Marta, additional, Roeters van Lennep, Jeanine E., additional, Sijbrands, Eric J.G., additional, Labib, Mourad, additional, Nair, Devaki, additional, and Humphries, Steve E., additional
Published: 2017
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193. Lipoprotein(a) level is higher inpatients with familial hypercholesterolaemia than in normal healthy subjects, contribution of variants in the LPA gene

Author: Seed, Mary, primary, Sharifi, Mahtab, additional, Nair, Devaki, additional, Jain, Anijly, additional, Persuad, Jahm, additional, Futema, Marta, additional, Cooper, Jackie, additional, Neil, Andrew, additional, and H, Steve, additional
Published: 2017
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194. Identifying LDL-C associated variants in the Annexin a2 (ANXA2) gene

Author: Fairoozy, Roaa Hani, primary, White, Jon, additional, Cooper, Jackie, additional, Folkersen, Lasse, additional, Giambartolomei, Claudia, additional, Kalea, Anastasia, additional, Grewal, Thomas, additional, and Humphries, Steve, additional
Published: 2017
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195. SEnsitivity and specificity of biochemical screening for familial hypercholesterolaemia in childhood: avon longitudinal study of parents and children (ALSPAC)

Author: Humphries, Steve, primary, Futema, Marta, additional, Cooper, Jackie, additional, Charakida, Marietta, additional, Boustred, Chris, additional, Sattar, Naveed, additional, Deanfield, John, additional, Lawlor, Debbie, additional, Timpson, Nick, additional, and Hingorani, Aroon, additional
Published: 2017
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196. Identifying low density lipoprotein cholesterol associated variants in the Annexin A2 ( ANXA2 ) gene

Author: Fairoozy, Roaa Hani, primary, Cooper, Jackie, additional, White, Jon, additional, Giambartolomei, Claudia, additional, Folkersen, Lasse, additional, Wannamethee, S. Goya, additional, Jefferis, Barbara J., additional, Whincup, Peter, additional, Ben-Shlomo, Yoav, additional, Kumari, Meena, additional, Kivimaki, Mika, additional, Wong, Andrew, additional, Hardy, Rebecca, additional, Kuh, Diana, additional, Gaunt, Tom R., additional, Casas, J.P., additional, McLachlan, Stela, additional, Price, Jackie F., additional, Hingorani, Aroon, additional, Franco-Cereceda, Anders, additional, Grewal, Thomas, additional, Kalea, Anastasia Z., additional, and Humphries, Steve E., additional
Published: 2017
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197. Screening for familial hypercholesterolaemia in childhood: Avon Longitudinal Study of Parents and Children (ALSPAC)

Author: Futema, Marta, primary, Cooper, Jackie A., additional, Charakida, Marietta, additional, Boustred, Christopher, additional, Sattar, Naveed, additional, Deanfield, John, additional, Lawlor, Debbie A., additional, Timpson, Nicholas J., additional, Humphries, Steve E., additional, and Hingorani, Aroon D., additional
Published: 2017
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198. Mendelian Randomisation study of the influence of eGFR on coronary heart disease

Author: Charoen, Pimphen, Nitsch, Dorothea, Engmann, Jorgen, Shah, Tina, White, Jonathan, Zabaneh, Delilah, Jefferis, Barbara, Wannamethee, Goya, Whincup, Peter, Mulick Cassidy, Amy, Gaunt, Tom, Day, Ian, Mclachlan, Stela, Price, Jacqueline, Kumari, Meena, Kivimaki, Mika, Brunner, Eric, Langenberg, Claudia, Ben-shlomo, Yoav, Hingorani, Aroon, Whittaker, John, Pablo Casas, Juan, Dudbridge, Frank, Dale, Caroline, Finan, Chris, Wong, Andrew, Ong, Ken, Drenos, Fotios, Cooper, Jackie, Sofat, Reecha, Schmidt, Floriaan, Lawlor, Debbie A., Talmud, Philippa J., Humphries, Steve E., Hardy, Rebecca, Kuh, Diana, Wareham, Nicholas, Morris, Richard, Plagno, Vincent, Langenberg, Claudia [0000-0002-5017-7344], and Apollo - University of Cambridge Repository
Subjects: 0301 basic medicine, Oncology, medicine.medical_specialty, Cardiology, Renal function, Genome-wide association study, Coronary Disease, Bioinformatics, Kidney, Polymorphism, Single Nucleotide, Article, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Internal medicine, medicine, Genetics, Odds Ratio, Humans, 030212 general & internal medicine, Multidisciplinary, business.industry, Confounding, Kidney metabolism, Mendelian Randomization Analysis, Odds ratio, medicine.disease, 030104 developmental biology, Observational study, business, Genome-Wide Association Study, Glomerular Filtration Rate
Abstract: Impaired kidney function, as measured by reduced estimated glomerular filtration rate (eGFR), has been associated with increased risk of coronary heart disease (CHD) in observational studies, but it is unclear whether this association is causal or the result of confounding or reverse causation. In this study we applied Mendelian randomisation analysis using 17 genetic variants previously associated with eGFR to investigate the causal role of kidney function on CHD. We used 13,145 participants from the UCL-LSHTM-Edinburgh-Bristol (UCLEB) Consortium and 194,427 participants from the Coronary ARtery DIsease Genome-wide Replication and Meta-analysis plus Coronary Artery Disease (CARDIoGRAMplusC4D) consortium. We observed significant association of an unweighted gene score with CHD risk (odds ratio = 0.983 per additional eGFR-increasing allele, 95% CI = 0.970–0.996, p = 0.008). However, using weights calculated from UCLEB, the gene score was not associated with disease risk (p = 0.11). These conflicting results could be explained by a single SNP, rs653178, which was not associated with eGFR in the UCLEB sample, but has known pleiotropic effects that prevent us from drawing a causal conclusion. The observational association between low eGFR and increased CHD risk was not explained by potential confounders and there was no evidence of reverse causation, therefore leaving the remaining unexplained association as an open question.
Published: 2015
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199. Effect of Intermittent or Continuous Feed on Muscle Wasting in Critical Illness

Author: McNelly, Angela S., Bear, Danielle E., Connolly, Bronwen A., Arbane, Gill, Allum, Laura, Tarbhai, Azhar, Cooper, Jackie A., Hopkins, Philip A., Wise, Matthew P., Brealey, David, Rooney, Kieron, Cupitt, Jason, Carr, Bryan, Koelfat, Kiran, Damink, Steven Olde, Atherton, Philip J., Hart, Nicholas, Montgomery, Hugh E., and Puthucheary, Zudin A.
Abstract: Acute skeletal muscle wasting in critical illness is associated with excess morbidity and mortality. Continuous feeding may suppress muscle protein synthesis as a result of the muscle-full effect, unlike intermittent feeding, which may ameliorate it.
Published: 2020
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200. The Prognostic Significance of Quantitative Myocardial Perfusion

Author: Knott, Kristopher D., Seraphim, Andreas, Augusto, Joao B., Xue, Hui, Chacko, Liza, Aung, Nay, Petersen, Steffen E., Cooper, Jackie A., Manisty, Charlotte, Bhuva, Anish N., Kotecha, Tushar, Bourantas, Christos V., Davies, Rhodri H., Brown, Louise A.E., Plein, Sven, Fontana, Marianna, Kellman, Peter, and Moon, James C.
Abstract: Supplemental Digital Content is available in the text.
Published: 2020
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