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1. Assay-related differences in SuPAR levels: implications for measurement and data interpretation

Author: Vasbinder, Alexi, Raffield, Laura Marie, Gao, Yan, Engstrom, Gunnar, Quyyumi, Arshed Ali, Reiner, Alexander Paul, Reiser, Jochen, and Hayek, Salim Salim
Published: 2023
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2. Contribution of Common Genetic Variants to Risk of Early Onset Ischemic Stroke

Author: Jaworek, Thomas, Xu, Huichun, Gaynor, Brady J, Cole, John W., Rannikmae, Kristiina, Stanne, Tara M, Tomppo, Liisa, Abedi, Vida, Amouyel, Philippe, Armstrong, Nicole D, Attia, John, Bell, Steven, Benavente, Oscar R, Boncoraglio, Giorgio B, Butterworth, Adam, Carcel-Marquez, Jara, Chen, Zhengming, Chong, Michael, Cruchaga, Carlos, Cushman, Mary, Danesh, John, Debette, Stephanie, Duggan, David J, Durda, Jon Peter, Engstrom, Gunnar, Enzinger, Chris, Faul, Jessica D, Fecteau, Natalie S, Fernandez-Cadenas, Israel, Gieger, Christian, Giese, Anne-Katrin, Grewal, Raji P, Grittner, Ulrike, Havulinna, Aki S, Heitsch, Laura, Hochberg, Marc C, Holliday, Elizabeth, Hu, Jie, Ilinca, Andreea, Irvin, Marguerite R, Jackson, Rebecca D, Jacob, Mina A., Janssen, Raquel Rabionet, Jimenez-Conde, Jordi, Johnson, Julie A, Kamatani, Yoichiro, Kardia, Sharon L, Koido, Masaru, Kubo, Michiaki, Lange, Leslie, Lee, Jin-Moo, Lemmens, Robin, Levi, Christopher R, Li, Jiang, Li, Liming, Lin, Kuang, Lopez, Haley, Luke, Sothear, Maguire, Jane, McArdle, Patrick F, McDonough, Caitrin W., Meschia, James F, Metso, Tiina, Muller-Nurasyid, Martina, OʼConnor, Timothy D, OʼDonnell, Martin, Peddareddygari, Leema R, Pera, Joanna, Perry, James A, Peters, Annette, Putaala, Jukka, Ray, Debashree, Rexrode, Kathryn, Ribases, Marta, Rosand, Jonathan, Rothwell, Peter M, Rundek, Tatjana, Ryan, Kathleen A, Sacco, Ralph L., Salomaa, Veikko, Sanchez-Mora, Cristina, Schmidt, Reinhold, Sharma, Pankaj, Slowik, Agnieszka, Smith, Jennifer A, Smith, Nicholas L, Wassertheil-Smoller, Sylvia, Soederholm, Martin, Stine, O. C, Strbian, Daniel, Sudlow, Cathie L, Tatlisumak, Turgut, Terao, Chikashi, Thijs, Vincent, Torres-Aguila, Nuria P, Tregouet, David-Alexandre, Tuladhar, Anil M., Veldink, Jan H, Walters, Robin G, Weir, David R, Woo, Daniel, Worrall, Bradford B, Hong, Charles C, Ross, Owen, Zand, Ramin, Leeuw, Frank-Erik de, Lindgren, Arne G, Pare, Guillaume, Anderson, Christopher D., Markus, Hugh S, Jern, Christina, Malik, Rainer, Dichgans, Martin, Mitchell, Braxton D, and Kittner, Steven J
Published: 2022
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3. Factors most strongly associated with breathlessness in a population aged 50-64 years

Author: Olsson, Max, Bjorkelund, Anders J., Sandberg, Jacob, Blomberg, Anders, Borjesson, Mats, Currow, David, Malinovschi, Andrei, Skold, Magnus, Wollmer, Per, Toren, Kjell, Östgren, Carl Johan, Engstrom, Gunnar, Ekstrom, Magnus, Olsson, Max, Bjorkelund, Anders J., Sandberg, Jacob, Blomberg, Anders, Borjesson, Mats, Currow, David, Malinovschi, Andrei, Skold, Magnus, Wollmer, Per, Toren, Kjell, Östgren, Carl Johan, Engstrom, Gunnar, and Ekstrom, Magnus
Abstract: Background Breathlessness is a troublesome and prevalent symptom in the population, but knowledge of related factors is scarce. The aim of this study was to identify the factors most strongly associated with breathlessness in the general population and to describe the shapes of the associations between the main factors and breathlessness. Methods A cross-sectional analysis was carried out of the multicentre population-based Swedish CArdioPulmonary bioImage Study (SCAPIS) of adults aged 50 to 64 years. Breathlessness was defined as a modified Medical Research Council breathlessness rating.2. The machine learning algorithm extreme gradient boosting (XGBoost) was used to classify participants as either breathless or nonbreathless using 449 factors, including physiological measurements, blood samples, computed tomography cardiac and lung measurements, lifestyle, health conditions and socioeconomics. The strength of the associations between the factors and breathlessness were measured by SHapley Additive exPlanations (SHAP), with higher scores reflecting stronger associations. Results A total of 28 730 participants (52% women) were included in the study. The strongest associated factors for breathlessness were (in order of magnitude): body mass index ( SHAP score 0.39), forced expiratory volume in 1 s (0.32), physical activity measured by accelerometery (0.27), sleep apnoea (0.22), diffusing lung capacity for carbon monoxide (0.21), self-reported physical activity (0.17), chest pain when hurrying (0.17), high-sensitivity C-reactive protein (0.17), recent weight change (0.14) and cough (0.13). Conclusion This large population-based study of men and women aged 50-64 years identified the main factors related to breathlessness that may be prevented or amenable to public health interventions., Funding Agencies|Swedish Cardiopulmonary Bioimage Study (SCAPIS); Swedish Heart-Lung Foundation - Knut and Alice Wallenberg Foundation; Swedish Research Council [2019-02081]; VINNOVA (Sweden's innovation agency); University of Gothenburg and Sahlgrenska University Hospital, Karolinska Institutet, Stockholm county council; Skane University Hospital, Umea University
Published: 2024
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4. Long-Term Exposure to Transportation Noise and Ischemic Heart Disease: A Pooled Analysis of Nine Scandinavian Cohorts

Author: Pyko, Andrei, Roswall, Nina, Ogren, Mikael, Oudin, Anna, Rosengren, Annika, Eriksson, Charlotta, Segersson, David, Rizzuto, Debora, Andersson, Eva M., Aasvang, Gunn Marit, Engstrom, Gunnar, Gudjonsdottir, Hrafnhildur, Jorgensen, Jeanette T., Selander, Jenny, Christensen, Jesper H., Brandt, Jorgen, Leander, Karin, Overvad, Kim, Eneroth, Kristina, Mattisson, Kristoffer, Barregard, Lars, Stockfelt, Leo, Albin, Maria, Simonsen, Mette K., Tiittanen, Pekka, Molnar, Peter, Ljungman, Petter, Jensen, Steen Solvang, Gustafsson, Susanna, Lanki, Timo, Lim, Youn-Hee, Andersen, Zorana J., Sorensen, Mette, and Pershagen, Goran
Subjects: Transportation noise -- Health aspects -- Environmental aspects, Noise pollution -- Health aspects, Myocardial ischemia -- Risk factors -- Environmental aspects, Environmental issues, Health
Abstract: Background: Transportation noise may induce cardiovascular disease, but the public health implications are unclear. Objectives: The study aimed to assess exposure-response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes. Methods: Pooled analyses were performed of nine cohorts from Denmark and Sweden, together including 132,801 subjects. Time-weighted longterm exposure to road, railway, and aircraft noise, as well as air pollution, was estimated based on residential histories. Hazard ratios (HRs) were calculated using Cox proportional hazards models following adjustment for lifestyle and socioeconomic risk factors. Results: A total of 22,459 incident cases of IHD were identified during follow-up from national patient and mortality registers, including 7,682 cases of myocardial infarction. The adjusted HR for IHD was 1.03 [95% confidence interval (CI) 1.00, 1.05] per 10 dB [L.sub.den] for both road and railway noise exposure during 5 y prior to the event. Higher risks were indicated for IHD excluding angina pectoris cases, with HRs of 1.06 (95% CI: 1.03, 1.08) and 1.05 (95% CI: 1.01, 1.08) per 10 dB [L.sub.den] for road and railway noise, respectively. Corresponding HRs for myocardial infarction were 1.02 (95% CI: 0.99, 1.05) and 1.04 (95% CI: 0.99, 1.08). Increased risks were observed for aircraft noise but without clear exposure-response relations. A threshold at around 55 dB [L.sub.den] was suggested in the exposure-response relation for road traffic noise and IHD. Discussion: Exposure to road, railway, and aircraft noise in the prior 5 y was associated with an increased risk of IHD, particularly after exclusion of angina pectoris cases, which are less well identified in the registries. https://doi.org/10.1289/EHP10745, Introduction Exposure to traffic noise is increasing because of ongoing urbanization, densification of urban settlements, and growth of the transport sector. In 2017, 113 million Europeans were estimated to be [...]
Published: 2023
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5. Increased soluble urokinase plasminogen activator levels modulate monocyte function to promote atherosclerosis

Author: Hindy, George, Tyrrell, Daniel J., Vasbinder, Alexi, Wei, Changli, Presswalla, Feriel, Wang, Hui, Blakely, Pennelope, Ozel, Ayse Bilge, Graham, Sarah, Holton, Grace H., Dowsett, Joseph, Fahed, Akl C., Amadi, Kingsley-Michael, Erne, Grace K., Tekmulla, Annika, Ismail, Anis, Launius, Christopher, Sotoodehnia, Nona, Pankow, James S., Thorner, Lise Wegner, Erikstrup, Christian, Pedersen, Ole Birger, Banasik, Karina, Brunak, Soren, Ullum, Henrik, Eugen-Olsen, Jesper, Ostrowski, Sisse Rye, Haas, Mary E., Nielsen, Jonas B., Lotta, Luca A., Engstrom, Gunnar, Melander, Olle, Orho-Melander, Marju, Zhao, Lili, Murthy, Venkatesh L., Pinsky, David J., Willer, Cristen J., Heckbert, Susan R., Reiser, Jochen, Goldstein, Daniel R., Desch, Karl C., and Hayek, Salim S.
Subjects: Immune response -- Genetic aspects, Cell receptors -- Health aspects, Atherosclerosis -- Genetic aspects -- Development and progression -- Care and treatment, Health care industry
Abstract: People with kidney disease are disproportionately affected by atherosclerosis for unclear reasons. Soluble urokinase plasminogen activator receptor (suPAR) is an immune-derived mediator of kidney disease, levels of which are strongly associated with cardiovascular outcomes. We assessed suPAR's pathogenic involvement in atherosclerosis using epidemiologic, genetic, and experimental approaches. We found serum suPAR levels to be predictive of coronary artery calcification and cardiovascular events in 5,406 participants without known coronary disease. In a genome-wide association meta-analysis including over 25,000 individuals, we identified a missense variant in the plasminogen activator, urokinase receptor (PLAUR) gene (rs4760), confirmed experimentally to lead to higher suPAR levels. Mendelian randomization analysis in the UK Biobank using rs4760 indicated a causal association between genetically predicted suPAR levels and atherosclerotic phenotypes. In an experimental model of atherosclerosis, proprotein convertase subtilisin/kexin-9 (Pcsk9) transfection in mice overexpressing suPAR ([suPAR.sup.Tg]) led to substantially increased atherosclerotic plaques with necrotic cores and macrophage infiltration compared with those in WT mice, despite similar cholesterol levels. Prior to induction of atherosclerosis, aortas of [suPAR.sup.Tg] mice excreted higher levels of CCL2 and had higher monocyte counts compared with WT aortas. Aortic and circulating [suPAR.sup.Tg] monocytes exhibited a proinflammatory profile and enhanced chemotaxis. These findings characterize suPAR as a pathogenic factor for atherosclerosis acting at least partially through modulation of monocyte function., Introduction People with chronic kidney disease (CKD) are disproportionately affected by cardiovascular disease (CVD), with two-thirds of patients having at least one form of CVD, atherosclerosis being the most common [...]
Published: 2022
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6. Long-Term Exposure to Transportation Noise and Risk of Incident Stroke: A Pooled Study of Nine Scandinavian Cohorts

Author: Roswall, Nina, Pyko, Andrei, Ogren, Mikael, Oudin, Anna, Rosengren, Annika, Lager, Anton, Poulsen, Aslak H., Eriksson, Charlotta, Segersson, David, Rizzuto, Debora, Andersson, Eva M., Aasvang, Gunn Marit, Engstrom, Gunnar, Jorgensen, Jeanette T., Selander, Jenny, Christensen, Jesper H., Thacher, Jesse, Leander, Karin, Overvad, Kim, Eneroth, Kristina, Mattisson, Kristoffer, Barregard, Lars, Stockfelt, Leo, Albin, Maria, Ketzel, Matthias, Simonsen, Mette K., Spanne, Marten, Raaschou-Nielsen, Ole, Magnusson, Patrik K.E., Tiittanen, Pekka, Molnar, Peter, Ljungman, Petter, Lanki, Timo, Lim, Youn-Hee, Andersen, Zorana J., Pershagen, Gor an, and Serensen, Mette
Subjects: Traffic noise -- Health aspects, Stroke (Disease) -- Risk factors -- Environmental aspects, Cardiovascular diseases -- Risk factors -- Development and progression -- Complications and side effects, Environmental issues, Health
Abstract: Background: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse. Objective: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population. Methods: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution. Results: During follow-up (median = 19.5 y), 11,056 stroke cases were identified. Road traffic noise ([L.sub.den]) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual-and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of Discussion: In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise. https://doi.org/10.1289/EHP8949, Introduction Stroke is a leading cause of morbidity and mortality worldwide, and identification of new, modifiable risk factors is a crucial step in prevention (Zhang et al. 2019). Transportation noise [...]
Published: 2021
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7. Cadmium Exposure and Coronary Artery Atherosclerosis: A Cross-Sectional Population-Based Study of Swedish Middle-Aged Adults

Author: Barregard, Lars, Sallsten, Gerd, Harari, Florencia, Andersson, Eva M., Forsgard, Niklas, Hjelmgreti, Ola, Angeras, Oskar, Fagman, Erika, Persson, Margaretha, Lundh, Thomas, Borne, Yan, Fagerberg, Bjorn, Engstrom, Gunnar, and Bergstrom, Goran
Subjects: Coronary heart disease -- Risk factors, Cadmium -- Environmental aspects -- Health aspects, Middle aged persons -- Health aspects, Atherosclerosis -- Risk factors, Environmental issues, Health
Abstract: Background: The general population is ubiquitously exposed to the toxic metal cadmium through the diet and smoking. Cadmium exposure is associated with increased morbidity and mortality in myocardial infarction and stroke. Atherosclerosis is the main underlying mechanism of myocardial infarction. However, associations between cadmium and coronary artery atherosclerosis have not been examined. Objectives: Our study sought to examine the hypothesis that blood cadmium (B-Cd) is positively associated with coronary artery calcification, as a measure of coronary artery atherosclerosis in the population-based Swedish SCAPIS study. Methods: Our analysis included 5,627 individuals (51% women), age 50-64 y, enrolled from 2013 to 2018. The coronary artery calcium score (CACS) was obtained from computed tomography. Blood cadmium was determined by inductively coupled plasma mass spectrometry (ICP-MS). Associations between B-Cd and coronary artery calcium score (CACS Agatston score) were evaluated using prevalence ratios (PRs) in models adjusted for sex, age, smoking, hypertension, diabetes, low-density cholesterol/high-density cholesterol ratio, and family history. Results: The median B-Cd concentration was 0.24 [micro]g/L. The prevalence of positive coronary artery calcium (CACS >0) was 41% and the prevalence of CACS [greater than or equal to]100 was 13%. Relative to the lowest quartile (Q) of B-Cd (0 (PR 1.1; 95% CI: 1.0, 1.3), and a greater relative increase in CACS [greater than or equal to]100 (PR 1.6; 95% CI: 1.3, 2.0). When restricted to 2,446 never-smokers, corresponding PRs were 1.1 (95% CI 0.9, 1.3) for CACS >0 (63 cases in Q4) and 1.7 (95% CI 1.1, 2.7) for CACS [greater than or equal to]100 (17 cases in Q4). Discussion: Blood cadmium in the highest quartile was associated with CACS in a general population sample with low to moderate cadmium exposure. This supports the hypothesis that atherosclerosis is an important mechanism underlying the associations between cadmium and incident cardiovascular disease. The findings suggest that public health measures to reduce cadmium exposure are warranted. https://doi.org/10.1289/EHP8523, Introduction Cadmium (Cd) is a toxic metal with ubiquitous exposure through the diet and smoking as the main sources. Cadmium accumulates mainly in the kidneys and has a half-life of [...]
Published: 2021
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8. Life expectancy associated with different ages at diagnosis of type 2 diabetes in high-income countries : 23 million person-years of observation

Author: Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, Di Angelantonio, Emanuele, Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, and Di Angelantonio, Emanuele
Abstract: Background The prevalence of type 2 diabetes is increasing rapidly, particularly among younger age groups. Estimates suggest that people with diabetes die, on average, 6 years earlier than people without diabetes. We aimed to provide reliable estimates of the associations between age at diagnosis of diabetes and all-cause mortality, cause-specific mortality, and reductions in life expectancy. Methods For this observational study, we conducted a combined analysis of individual-participant data from 19 high income countries using two large-scale data sources: the Emerging Risk Factors Collaboration (96 cohorts, median baseline years 1961-2007, median latest follow-up years 1980-2013) and the UK Biobank (median baseline year 2006, median latest follow-up year 2020). We calculated age-adjusted and sex-adjusted hazard ratios (HRs) for all-cause mortality according to age at diagnosis of diabetes using data from 1 515 718 participants, in whom deaths were recorded during 23 center dot 1 million person-years of follow-up. We estimated cumulative survival by applying age-specific HRs to age-specific death rates from 2015 for the USA and the EU. Findings For participants with diabetes, we observed a linear dose-response association between earlier age at diagnosis and higher risk of all-cause mortality compared with participants without diabetes. HRs were 2 center dot 69 (95% CI 2 center dot 43-2 center dot 97) when diagnosed at 30-39 years, 2 center dot 26 (2 center dot 08-2 center dot 45) at 40-49 years, 1 center dot 84 (1 center dot 72-1 center dot 97) at 50-59 years, 1 center dot 57 (1 center dot 47-1 center dot 67) at 60-69 years, and 1 center dot 39 (1 center dot 29-1 center dot 51) at 70 years and older. HRs per decade of earlier diagnosis were similar for men and women. Using death rates from the USA, a 50-year-old individual with diabetes died on average 14 years earlier when diagnosed aged 30 years, 10 years earlier when diagnosed aged 40 years, or 6 years earlier
Published: 2023
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9. Factors important for health-related quality of life in men and women : The population based SCAPIS study

Author: Olsson, Max, Bjorkelund, Anders J., Sandberg, Jacob, Blomberg, Anders, Borjesson, Mats, Currow, David, Malinovschi, Andrei, Skold, Magnus, Wollmer, Per, Toren, Kjell, Ostgren, Carl-Johan, Engstrom, Gunnar, Ekstrom, Magnus, Olsson, Max, Bjorkelund, Anders J., Sandberg, Jacob, Blomberg, Anders, Borjesson, Mats, Currow, David, Malinovschi, Andrei, Skold, Magnus, Wollmer, Per, Toren, Kjell, Ostgren, Carl-Johan, Engstrom, Gunnar, and Ekstrom, Magnus
Abstract: IntroductionHealth-related quality of life (HRQoL) is essential for human wellbeing, influenced by a complex interplay of factors, and is reported lower in women than men. We aimed to evaluate which factors were the most important for HRQoL in a middle-aged general population.MethodsThis was a cross-sectional, multi-centre study of 29,212 men (48%) and women (52%) aged 50-64 in the general population in Sweden. Physical and mental HRQoL (0-100) was assessed using the Short Form 12 questionnaire, and association was evaluated for 356 variables including demographics, lifestyle, symptoms, physiological measurements, and health conditions. Using machine learning, each variable ' s importance for HRQoL was measured by an importance score, comparable to effect size, and summarised in 54 factors, in men and women separately.ResultsMen and women had similar mean and standard deviation (SD) scores for physical HRQoL (53.4 [SD 8.1] vs 51.4 [9.7]) and mental HRQoL (37.1 [5.0] vs 37.3 [5.4]). The most important factors for physical HRQoL were (importance score) physical activity (40), employment (36), pain (33), sleep (33), and sense of control (26). The most important factors for mental HRQoL were sense of control (18), physical activity (12), depression (12), pain (6), and employment (5).ConclusionsThe factors important for HRQoL identified by this study are likely to be amenable to interventions, and our findings can support prioritising interventions. The identified factors need to be a target even before middle-age to lay the foundation for long and happy lives.
Published: 2023
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10. Prevalence of atherosclerosis in individuals with prediabetes and diabetes compared to normoglycaemic individuals-a Swedish population-based study

Author: Ostgren, Carl Johan, Otten, Julia, Festin, Karin, Angeras, Oskar, Bergstrom, Goran, Cederlund, Kerstin, Engstrom, Gunnar, Eriksson, Maria J., Eriksson, Mats, Fall, Tove, Gummesson, Anders, Hagström, Emil, Hellman, Urban, James, Stefan, Jernberg, Tomas, Kihlberg, Johan, Kylhammar, David, Markstad, Hanna, Nilsson, Peter, Persson, Anders, Persson, Margaretha, Pirazzi, Carlo, Renklint, Rebecka, Rosengren, Annika, Soderberg, Stefan, Sundström, Johan, Ostgren, Carl Johan, Otten, Julia, Festin, Karin, Angeras, Oskar, Bergstrom, Goran, Cederlund, Kerstin, Engstrom, Gunnar, Eriksson, Maria J., Eriksson, Mats, Fall, Tove, Gummesson, Anders, Hagström, Emil, Hellman, Urban, James, Stefan, Jernberg, Tomas, Kihlberg, Johan, Kylhammar, David, Markstad, Hanna, Nilsson, Peter, Persson, Anders, Persson, Margaretha, Pirazzi, Carlo, Renklint, Rebecka, Rosengren, Annika, Soderberg, Stefan, and Sundström, Johan
Abstract: Background: Patients with type 2 diabetes have an increased risk of death and cardiovascular events and people with diabetes or prediabetes have been found to have increased atherosclerotic burden in the coronary and carotid arteries. This study will estimate the cross-sectional prevalence of atherosclerosis in the coronary and carotid arteries in individuals with prediabetes and diabetes, compared with normoglycaemic individuals in a large population-based cohort. Methods: The 30,154 study participants, 50-64 years, were categorized according to their fasting glycaemic status or self-reported data as normoglycaemic, prediabetes, and previously undetected or known diabetes. Prevalence of affected coronary artery segments, severity of stenosis and coronary artery calcium score (CACS) were determined by coronary computed tomography angiography. Total atherosclerotic burden was assessed in the 11 clinically most relevant segments using the Segment Involvement Score and as the presence of any coronary atherosclerosis. The presence of atherosclerotic plaque in the carotid arteries was determined by ultrasound examination. Results: Study participants with prediabetes (n = 4804, 16.0%) or diabetes (n = 2282, 7.6%) had greater coronary artery plaque burden, more coronary stenosis and higher CACS than normoglycaemic participants (all, p < 0.01). Among male participants with diabetes 35.3% had CACS >= 100 compared to 16.1% among normoglycaemic participants. For women, the corresponding figures were 8.9% vs 6.1%. The prevalence of atherosclerosis in the coronary arteries was higher in participants with previously undetected diabetes than prediabetes, but lower than in patients with known diabetes. The prevalence of any plaque in the carotid arteries was higher in participants with prediabetes or diabetes than in normoglycaemic participants. Conclusions: In this large population-based cohort of currently asymptomatic people, the atherosclerotic burden in the coronary and
Published: 2023
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11. Short-term association between outdoor temperature and the hydration-marker copeptin : a pooled analysis in five cohorts

Author: Timpka, Simon, Melander, Olle, Engstrom, Gunnar, Elmstahl, Solve, Nilsson, Peter M., Lind, Lars, Pihlsgard, Mats, Enhorning, Sofia, Timpka, Simon, Melander, Olle, Engstrom, Gunnar, Elmstahl, Solve, Nilsson, Peter M., Lind, Lars, Pihlsgard, Mats, and Enhorning, Sofia
Abstract: Background: Whereas outdoor temperature is linked to both mortality and hydration status, the hormone vasopressin, measured through the surrogate copeptin, is a marker of cardiometabolic risk and hydration. We recently showed that copeptin has a seasonal pattern with higher plasma concentration in winter. Here, we aimed to investigate the as-sociation between outdoor temperature and copeptin. Methods: Copeptin was analysed in fasting plasma from five cohorts in Malm & ouml;, Sweden (n = 26,753, 49.7% men, age 18-86 years). We utilized a multivariable adjusted non-linear spline model with four knots to investigate the association between short-term temperature (24 h mean apparent) and log copeptin z-score. Findings: We found a distinct non-linear association between temperature and log copeptin z-score, with both moderately low and high temperatures linked to higher copeptin concentration (p < 0.0001). Between 0( ?)C and nadir at the 75th temperature percentile (corresponding to 14.3 ?C), log copeptin decreased 0.13 z-scores (95% CI 0.096; 0.16), which also inversely corresponded to the increase in z-score log copeptin between the nadir and 21.3 C-?. Interpretation: The J-shaped association between short-term temperature and copeptin resembles the J-shaped association between temperature and mortality. Whereas the untangling of temperature from other seasonal effects on hydration warrants further study, moderately increased water intake constitutes a feasible intervention to lower vasopressin and might mitigate adverse health effects of both moderately cold and hot outdoor temperatures. Fundin:g Swedish Research Council, & Aring; Wiberg, M Stephen, A P & aring;hlsson, Crafoord and Swedish Heart-Lung Foun-dations, Swedish Society for Medical Research and Swedish Society of Medicine.
Published: 2023
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12. Polygenic risk of type 2 diabetes is associated with incident vascular dementia: a prospective cohort study

Author: Dybjer, Elin, Kumar, Atul, Nägga, Katarina, Engstrom, Gunnar, Mattsson-Carlgren, Niklas, Nilsson, Peter M., Melander, Olle, Hansson, Oskar, Dybjer, Elin, Kumar, Atul, Nägga, Katarina, Engstrom, Gunnar, Mattsson-Carlgren, Niklas, Nilsson, Peter M., Melander, Olle, and Hansson, Oskar
Abstract: Dybjer et al. report that polygenic risk of type 2 diabetes is associated with dementia risk, in particular vascular dementia. Associations were strongest for non-carriers of the gene APOE epsilon 4. However, two-sample Mendelian randomization analyses did not support a causal relationship between type 2 diabetes and vascular dementia. Type 2 diabetes and dementia are associated, but it is unclear whether the two diseases have common genetic risk markers that could partly explain their association. It is also unclear whether the association between the two diseases is of a causal nature. Furthermore, few studies on diabetes and dementia have validated dementia end-points with high diagnostic precision. We tested associations between polygenic risk scores for type 2 diabetes, fasting glucose, fasting insulin and haemoglobin A(1c) as exposure variables and dementia as outcome variables in 29 139 adults (mean age 55) followed for 20-23 years. Dementia diagnoses were validated by physicians through data from medical records, neuroimaging and biomarkers in cerebrospinal fluid. The dementia end-points included all-cause dementia, mixed dementia, Alzheimers disease and vascular dementia. We also tested causal associations between type 2 diabetes and dementia through two-sample Mendelian randomization analyses. Seven different polygenic risk scores including single-nucleotide polymorphisms with different significance thresholds for type 2 diabetes were tested. A polygenic risk score including 4891 single-nucleotide polymorphisms with a P-value of <5e-04 showed the strongest association with different outcomes, including all-cause dementia (hazard ratio 1.11; Bonferroni corrected P = 3.6e-03), mixed dementia (hazard ratio 1.18; Bonferroni corrected P = 3.3e-04) and vascular dementia cases (hazard ratio 1.28; Bonferroni corrected P = 9.6e-05). The associations were stronger for non-carriers of the Alzheimers disease risk gene APOE epsilon 4. There was, however, no sign
Published: 2023
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13. Markers of Atrial Myopathy in the General Population Prevalence, Predictors, and Inter-Relations

Author: Johnson, Linda S., Platonov, Pyotr G., Conen, David, Kennback, Cecilia, Jujic, Amra, Healey, Jeffrey S., Holm, Hannes, Sundström, Johan, Engstrom, Gunnar, Johnson, Linda S., Platonov, Pyotr G., Conen, David, Kennback, Cecilia, Jujic, Amra, Healey, Jeffrey S., Holm, Hannes, Sundström, Johan, and Engstrom, Gunnar
Abstract: Background Atrial myopathy refers to structural and functional cardiac abnormalities associated with atrial fibrillation and stroke, but appropriate diagnostic criteria are lacking.Objectives This study aimed to assess prevalence, clinical correlates, and overlap between potential atrial myopathy markers.Methods The population-based SCAPIS (Swedish CArdioPulmonary bioImage Study) prospectively included 6,013 subjects without atrial fibrillation with 24-hour electrocardiograms. Resting electrocardiograms measuring P-wave indices were collected at 1 screening site (n = 1,201), and a random sample (n = 385) had echocardiographic left atrial volume index (LAVi). Atrial myopathy markers were defined as >= 500 premature atrial complexes/24 h, LAVi >= 34 mL/m(2), P-wave duration >120 milliseconds, or P-wave terminal force in V-1 >4,000 mss. Clinical correlates included age, sex, body mass index, height, smoking, physical activity, coronary artery disease, diabetes, systolic blood pressure, antihypertensive medication, and low education.Results Atrial myopathy was common; 42% of the sample with all diagnostic modalities available had >= 1 atrial myopathy marker, but only 9% had 2 and 0.3% had >= 3. Only P-wave duration and LAVi were correlated (rho = 0.10; P = 0.04). Clinical correlates of premature atrial complexes, P-wave indices, and LAVi differed; current smoking (34% increase; P < 0.001), systolic blood pressure (4%/mm Hg increase; P = 0.01), diabetes (35% increase; P = 0.001), and coronary artery disease (71% increase; P = 0.003) were associated with premature atrial complexes, physical activity >= 2 h/wk was associated with increased LAVi (beta-coefficient = 3.1; P < 0.0001) and body mass index was associated with P-wave duration (beta-coefficient = 0.4/kg/m(2); P < 0.0001).Conclusions In the general population, indirect markers of atrial myopathy are common but only weakly correlated, and their risk factor patterns are
Published: 2023
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14. Causal analysis of plasma IL-8 on carotid intima media thickness, a measure of subclinical atherosclerosis

Author: Velasquez, Ilais Moreno, Malarstig, Anders, Baldassarre, Damiano, Borne, Yan, de Faire, Ulf, Engstrom, Gunnar, Eriksson, Per, Giral, Philippe, Humphries, Steve E., Kurl, Sudhir, Leander, Karin, Lind, Lars, Linden, Anders, Orsini, Nicola, Pirro, Matteo, Silveira, Angela, Smit, Andries J., Tremoli, Elena, Veglia, Fabrizio, Strawbridge, Rona J., Gigante, Bruna, Velasquez, Ilais Moreno, Malarstig, Anders, Baldassarre, Damiano, Borne, Yan, de Faire, Ulf, Engstrom, Gunnar, Eriksson, Per, Giral, Philippe, Humphries, Steve E., Kurl, Sudhir, Leander, Karin, Lind, Lars, Linden, Anders, Orsini, Nicola, Pirro, Matteo, Silveira, Angela, Smit, Andries J., Tremoli, Elena, Veglia, Fabrizio, Strawbridge, Rona J., and Gigante, Bruna
Abstract: Background: We investigated the causality of IL-8 on carotid intima-media thickness (c-IMT), a measure of sub-clinical atherosclerosis. Methods: The IMPROVE is a multicenter European study (n = 3,711). The association of plasma IL-8 with c-IMT (mm) was estimated by quantile regression. Genotyping was performed using the Illumina CardioMetabo and Immuno chips. Replication was attempted in three independent studies and a meta-analysis was performed using a random model. Results: In IMPROVE, each unit increase in plasma IL-8 was associated with an increase in median c-IMT measures (all p<0.03) in multivariable analyses. Linear regression identified rs117518778 and rs8057084 as associated with IL-8 levels and with measures of c-IMT. The two SNPs were combined in an IL-8-increasing genetic risk that showed causality of IL-8 on c-IMT in IMPROVE and in the UK Biobank (n = 22,179). The effect of IL-8 on c-IMT measures was confirmed in PIVUS (n = 1,016) and MDC-CC (n = 6,103). The association of rs8057084 with c-IMT was confirmed in PIVUS and UK Biobank with a pooled estimate effect (beta) of -0.006 with 95%CI (-0.008- -0.003). Conclusion: Our results indicate that genetic variants associated with plasma IL-8 also associate with c-IMT. However, we cannot infer causality of this association, as these variants lie outside of the IL8 locus. (c) 2022 The Author(s). Published by Elsevier Masson SAS. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)
Published: 2023
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15. Body weight at age 20 and in midlife is more important than weight gain for coronary atherosclerosis : Results from SCAPIS

Author: Bergstrom, Goran, Rosengren, Annika, Brolin, Elin Bacsovics, Brandberg, John, Cederlund, Kerstin, Engstrom, Gunnar, Engvall, Jan E., Eriksson, Maria J., Goncalves, Isabel, Hagström, Emil, James, Stefan, Jernberg, Tomas, Lilja, Mikael, Magnusson, Martin, Persson, Anders, Persson, Margaretha, Sandstrom, Anette, Schmidt, Caroline, Larsson, Linn Skoglund, Sundström, Johan, Swahn, Eva, Soderberg, Stefan, Toren, Kjell, Ostgren, Carl Johan, Lampa, Erik, Lind, Lars, Bergstrom, Goran, Rosengren, Annika, Brolin, Elin Bacsovics, Brandberg, John, Cederlund, Kerstin, Engstrom, Gunnar, Engvall, Jan E., Eriksson, Maria J., Goncalves, Isabel, Hagström, Emil, James, Stefan, Jernberg, Tomas, Lilja, Mikael, Magnusson, Martin, Persson, Anders, Persson, Margaretha, Sandstrom, Anette, Schmidt, Caroline, Larsson, Linn Skoglund, Sundström, Johan, Swahn, Eva, Soderberg, Stefan, Toren, Kjell, Ostgren, Carl Johan, Lampa, Erik, and Lind, Lars
Abstract: Background and aims: Elevated body weight in adolescence is associated with early cardiovascular disease, but whether this association is traceable to weight in early adulthood, weight in midlife or to weight gain is not known. The aim of this study is to assess the risk of midlife coronary atherosclerosis being associated with body weight at age 20, body weight in midlife and body weight change. Methods: We used data from 25,181 participants with no previous myocardial infarction or cardiac procedure in the Swedish CArdioPulmonary bioImage Study (SCAPIS, mean age 57 years, 51% women). Data on coronary atherosclerosis, self-reported body weight at age 20 and measured midlife weight were recorded together with potential confounders and mediators. Coronary atherosclerosis was assessed using coronary computed tomog-raphy angiography (CCTA) and expressed as segment involvement score (SIS). Results: The probability of having coronary atherosclerosis was markedly higher with increasing weight at age 20 and with mid-life weight (p < 0.001 for both sexes). However, weight increase from age 20 until mid-life was only modestly associated with coronary atherosclerosis. The association between weight gain and coronary atherosclerosis was mainly seen in men. However, no significant sex difference could be detected when adjusting for the 10-year delay in disease development in women. Conclusions: Similar in men and women, weight at age 20 and weight in midlife are strongly related to coronary atherosclerosis while weight increase from age 20 until midlife is only modestly related to coronary atherosclerosis.
Published: 2023
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16. Arterial stiffness and subclinical atherosclerosis in the coronary arteries at different stages of dysglycaemia

Author: Cederqvist, John, Rådholm, Karin, Muhammad, Iram Faqir, Engstrom, Gunnar, Engvall, Jan, Östgren, Carl Johan, Cederqvist, John, Rådholm, Karin, Muhammad, Iram Faqir, Engstrom, Gunnar, Engvall, Jan, and Östgren, Carl Johan
Abstract: Aim: Our aim was to investigate in a large population -based cohort study whether increased arterial stiffness and subclinical atherosclerosis in the coronary arteries differ at different stages of dysglycaemia.Methods: Data were obtained from SCAPIS, a population -based cohort of participants 50- 64 years. The study population of 9379 participants was categorised according to glycaemic status: normoglycaemic, pre-diabetes (fasting glucose: 6.1- 6.9 mmol/L and/or HbA1c 6%- 6.4%) and diabetes. Pulse wave velocity (PWV) was measured by the SphygmoCor XCEL system and arterial stiffness was defined by PWV =10 m/s. Coronary artery calcium score (CACS) was assessed by coronary computed tomography and coronary artery calcification was defined by CACS =100.Results: We identified 1964 (21%) participants with dysglycaemia, out of which 742 (7.9%) had diabetes mellitus. PWV =10 m/s was present in 808 (11%), 191 (16%), 200 (27%) and CACS =100 in 801 (11%), 190 (16%), 191 (28%) participants with normoglycaemia, pre-diabetes and diabetes, respectively, all, p < 0.001. The overlap between PWV =10 m/s and CACS =100 within each glycaemic category was 188 (2.5%), 44 (3.6%) and 77 (10) respectively. There was an association between glycaemic status and increased PWV in the fully adjusted models, but not for glycaemic status and CACS =100, where there was no difference for pre-diabetes compared to normoglycaemia, OR 1.2 (95% CI 0.98- 1.4). In the total study population, there was an association between HbA1c and PWV after adjustment, p <0.001.Conclusions: Our results show that increased arterial stiffness and subclinical coronary artery atherosclerosis are present in the early stages of dysglycaemia, but the overlap between markers of major subclinical vascular damage was small in all glycaemic categories. This could be explained by different pathways in the pathogenesis of arterial stiffness or atherosclerosis in the coronary arteries., Funding Agencies|Swedish Heart and Lung Foundation [2016- 0315]; Knut and Alice Wallenberg Foundation [2014- 0047]; Swedish Research Council [822- 2013- 2000]; VINNOVA [2012- 04476]; University of Gothenburg and Sahlgrenska University Hospital; Stockholm County Council; Linkoeping University; Lund University; Skane University Hospital; Umea University; Uppsala University; Swedish Heart and Lung Foundation
Published: 2023
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17. Orthostatic blood pressure adaptations, aortic stiffness, and central hemodynamics in the general population: insights from the Malmo Offspring Study (MOS)

Author: Johansson, Madeleine, Fedorowski, Artur, Jordan, Jens, Engstrom, Gunnar, Nilsson, Peter M., Hamrefors, Viktor, Johansson, Madeleine, Fedorowski, Artur, Jordan, Jens, Engstrom, Gunnar, Nilsson, Peter M., and Hamrefors, Viktor
Abstract: PurposeArterial stiffness is independently associated with orthostatic hypotension in older individuals. The relationship between orthostatic blood pressure adaptation and aortic stiffness has not been thoroughly examined in a younger population. We investigated the relationship between orthostatic blood pressure adaptations, central aortic hemodynamics, and aortic stiffness in a cohort of predominantly younger and middle-aged adults. MethodsWe analyzed an observational, population-based study of 5259 individuals living in Malmo, Sweden. We related aortic stiffness and central hemodynamics assessed by carotid-femoral pulse wave velocity and pulse wave analysis at the arteria radialis using Sphygmocor to orthostatic blood pressure adaptation after 3 min standing. ResultsThe mean age of the population was 41.9 & PLUSMN; 14.5 years, and 52.1% were women. We observed the highest aortic stiffness and central aortic blood pressure measurements in the lowest and highest quartiles of orthostatic systolic blood pressure differences (p < 0.001). Aortic stiffness and central aortic blood pressure gradually decreased across increasing quartiles of orthostatic diastolic blood pressure difference (p < 0.001). After full adjustment, orthostatic diastolic blood pressure remained significantly associated with aortic stiffness (p = 0.001) and central aortic blood pressure (p < 0.001), whereas orthostatic systolic blood pressure was significantly associated only with central aortic systolic blood pressure (p = 0.009). No significant associations were found between subclinical orthostatic hypotension, aortic stiffness, and central hemodynamics. ConclusionsOur findings demonstrate that altered blood pressure responses to orthostatic challenges, both blood pressure reductions and blood pressure increases, are independently and inversely associated with markers of aortic stiffness (vascular aging) in a predominantly young to middle-aged population.
Published: 2023

18. The cost-effectiveness of a uniform versus age-based threshold for one-off screening for prevention of cardiovascular disease

Author: Spacirova, Zuzana, Kaptoge, Stephen, Garcia-Mochon, Leticia, Rodriguez Barranco, Miguel, Sanchez Perez, Maria Jose, Bondonno, Nicola P., Tjønneland, Anne, Weiderpass, Elisabete, Grioni, Sara, Espin, Jaime, Sacerdote, Carlotta, Schiborn, Catarina, Masala, Giovanna, Colorado-Yohar, Sandra M., Kim, Lois, Moons, Karel G. M., Engstrom, Gunnar, Schulze, Matthias B., Bresson, Lea, Moreno-Iribas, Concepcion, Epstein, David, Spacirova, Zuzana, Kaptoge, Stephen, Garcia-Mochon, Leticia, Rodriguez Barranco, Miguel, Sanchez Perez, Maria Jose, Bondonno, Nicola P., Tjønneland, Anne, Weiderpass, Elisabete, Grioni, Sara, Espin, Jaime, Sacerdote, Carlotta, Schiborn, Catarina, Masala, Giovanna, Colorado-Yohar, Sandra M., Kim, Lois, Moons, Karel G. M., Engstrom, Gunnar, Schulze, Matthias B., Bresson, Lea, Moreno-Iribas, Concepcion, and Epstein, David
Abstract: The objective of this article was to assess the cost-effectiveness of screening strategies for cardiovascular diseases (CVD). A decision analytic model was constructed to estimate the costs and benefits of one-off screening strategies differentiated by screening age, sex and the threshold for initiating statin therapy ("uniform" or "age-adjusted") from the Spanish NHS perspective. The age-adjusted thresholds were configured so that the same number of people at high risk would be treated as under the uniform threshold. Health benefit was measured in quality-adjusted life years (QALY). Transition rates were estimated from the European Prospective Investigation into Cancer and Nutrition (EPIC-CVD), a large multicentre nested case-cohort study with 12 years of follow-up. Unit costs of primary care, hospitalizations and CVD care were taken from the Spanish health system. Univariate and probabilistic sensitivity analyses were employed. The comparator was no systematic screening program. The base case model showed that the most efficient one-off strategy is to screen both men and women at 40 years old using a uniform risk threshold for initiating statin treatment (Incremental Cost-Effectiveness Ratio of euro3,274/QALY and euro6,085/QALY for men and women, respectively). Re-allocating statin treatment towards younger individuals at high risk for their age and sex would not offset the benefit obtained using those same resources to treat older individuals. Results are sensitive to assumptions about CVD incidence rates. To conclude, one-off screening for CVD using a uniform risk threshold appears cost-effective compared with no systematic screening. These results should be evaluated in clinical studies.
Published: 2023

19. Random Indexing for Finding Similar Nodes within Large RDF Graphs

Author: Damljanovic, Danica, Petrak, Johann, Lupu, Mihai, Cunningham, Hamish, Carlsson, Mats, Engstrom, Gunnar, Andersson, Bo, Hutchison, David, Series editor, Kanade, Takeo, Series editor, Kittler, Josef, Series editor, Kleinberg, Jon M., Series editor, Mattern, Friedemann, Series editor, Mitchell, John C., Series editor, Naor, Moni, Series editor, Nierstrasz, Oscar, Series editor, Pandu Rangan, C., Series editor, Steffen, Bernhard, Series editor, Sudan, Madhu, Series editor, Terzopoulos, Demetri, Series editor, Tygar, Doug, Series editor, Vardi, Moshe Y., Series editor, Weikum, Gerhard, Series editor, García-Castro, Raúl, editor, Fensel, Dieter, editor, and Antoniou, Grigoris, editor
Published: 2012
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20. Blood Lead Levels and Risk of Atherosclerosis in the Carotid Artery: Results from a Swedish Cohort

Author: Harari, Florencia, Barregard, Lars, Ostling, Gerd, Sallsten, Gerd, Hedblad, Bo, Forsgard, Niklas, Borne, Yan, Fagerberg, Bjorn, and Engstrom, Gunnar
Subjects: Atherosclerosis -- Risk factors -- Research, Cancer research, Postmenopausal women, Mass spectrometry, Spectroscopy, Atherosclerotic plaque, Ultrasound imaging, Elderly men, Menopause, Women's associations, Environmental issues, Health, European Union. European Food Safety Authority
Abstract: Background: Lead exposure has been associated with increased incidence of adverse clinical cardiovascular outcomes. Atherosclerosis has been suggested as one of the underlying mechanisms, and findings from experimental studies support this, but human data are scarce. Objectives: Our objective was to determine the association between environmental lead exposure based on blood lead (B- Pb) concentrations and the prevalence of atherosclerotic plaque in the carotid artery. Methods: We used cross-sectional data from the Malmo Diet and Cancer Study cardiovascular cohort (MDCS-CC; recruitment in 1991-1994) covering 4,172 middle-aged men and women. B-Pb at baseline, measured by inductively coupled plasma mass spectrometry, was used as the exposure biomarker. The presence of atherosclerotic plaque in the carotid artery was determined by B-mode ultrasonography. We used logistic regression to estimate odds ratios (ORs) for prevalence of plaque in the carotid artery according to B-Pb quartiles. Results: The median B-Pb was 25 [micro]g/L (range: 1.5-258), and 36% of the cohort had any atherosclerotic plaque. After controlling for confounders and known cardiovascular risk factors, the OR for prevalence of plaque in the highest quartile (Q4) of B-Pb compared with the lowest quartile (Q1) was 1.35 (95% CI: 1.09, 1.66) in the total group, 1.58 (95% CI: 1.20, 2.08) among women, and 1.18 (95% CI: 0.83, 1.69) among men. Among women, associations were limited to those who were postmenopausal [OR for Q4 vs. Q1 = 1.72 (95% CI: 1.26, 2.34) vs. OR = 0.96 (95% CI: 0.49, 1.89 in premenopausal women)]. Associations were weak and nonsignificant in never-smokers [OR for Q4 vs. Q1 = 1.14 (95% CI: 0.81, 1.61)]. Discussion: Our study shows an association between B-Pb concentrations and occurrence of atherosclerotic plaque in the carotid artery, adding evidence for an underlying pro-atherogenic role of lead in cardiovascular disease. Associations appeared to be limited to postmenopausal (vs. premenopausal) women. https://doi.org/10.1289/EHP5057, Introduction Environmental exposure to the toxic metal lead (Pb) remains a public health problem. Despite a considerable decrease in lead exposure in the last two decades, there are still reports [...]
Published: 2019
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21. 1.3 Prediction of Cardiovascular Mortality and Morbidity in the Malmö Diet-Cancer Cohort for the Identification of Healthy Vascular Ageing, using Markers of Vascular Status

Author: Wadström, Benjamin Nilsson, Nilsson, Peter, Fatehali, Abd Al-Hakim, and Engstrom, Gunnar
Published: 2018
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22. An online atlas of human plasma metabolite signatures of gut microbiome composition

Author: Dekkers, Koen, Sayols-Baixeras, Sergi, Baldanzi, Gabriel, Nowak, Christoph, Hammar, Ulf, Nguyen, Diem, Varotsis, Georgios, Brunkwall, Louise, Nielsen, Nynne, Eklund, Aron C., Holm, Jacob Bak, Nielsen, H. Bjorn, Ottosson, Filip, Yi-Ting, Lin, Ahmad, Shafqat, Lind, Lars, Sundström, Johan, Engstrom, Gunnar, Smith, J. Gustav, Arnlov, Johan, Orho-Melander, Marju, Fall, Tove, Dekkers, Koen, Sayols-Baixeras, Sergi, Baldanzi, Gabriel, Nowak, Christoph, Hammar, Ulf, Nguyen, Diem, Varotsis, Georgios, Brunkwall, Louise, Nielsen, Nynne, Eklund, Aron C., Holm, Jacob Bak, Nielsen, H. Bjorn, Ottosson, Filip, Yi-Ting, Lin, Ahmad, Shafqat, Lind, Lars, Sundström, Johan, Engstrom, Gunnar, Smith, J. Gustav, Arnlov, Johan, Orho-Melander, Marju, and Fall, Tove
Abstract: Human gut microbiota produce a variety of molecules, some of which enter the bloodstream and impact health. Conversely, dietary or pharmacological compounds may affect the microbiota before entering the circulation. Characterization of these interactions is an important step towards understanding the effects of the gut microbiota on health. In this cross-sectional study, we used deep metagenomic sequencing and ultra-high-performance liquid chromatography linked to mass spectrometry for a detailed characterization of the gut microbiota and plasma metabolome, respectively, of 8583 participants invited at age 50 to 64 from the population-based Swedish CArdioPulmonary bioImage Study. Here, we find that the gut microbiota explain up to 58% of the variance of individual plasma metabolites and we present 997 associations between alpha diversity and plasma metabolites and 546,819 associations between specific gut metagenomic species and plasma metabolites in an online atlas (https://gutsyatlas.serve.scilifelab.se/). We exemplify the potential of this resource by presenting novel associations between dietary factors and oral medication with the gut microbiome, and microbial species strongly associated with the uremic toxin p-cresol sulfate. This resource can be used as the basis for targeted studies of perturbation of specific metabolites and for identification of candidate plasma biomarkers of gut microbiota composition.
Published: 2022
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23. Seasonal variation of vasopressin and its relevance for the winter peak of cardiometabolic disease : A pooled analysis of five cohorts

Author: Enhorning, Sofia, Melander, Olle, Engstrom, Gunnar, Elmstahl, Solve, Lind, Lars, Nilsson, Peter M., Pihlsgard, Mats, Timpka, Simon, Enhorning, Sofia, Melander, Olle, Engstrom, Gunnar, Elmstahl, Solve, Lind, Lars, Nilsson, Peter M., Pihlsgard, Mats, and Timpka, Simon
Abstract: Background Vasopressin concentration is typically higher at night, during stress, and in males, but readily lowered by water intake. Vasopressin is also a causal candidate for cardiometabolic disease, which shows seasonal variation. Objective To study whether vasopressin concentration varies by season in a temperate climate. Methods The vasopressin surrogate marker copeptin was analyzed in fasting plasma samples from five population-based cohorts in Malmo, Sweden (n = 25,907, 50.4% women, age 18-86 years). We investigated seasonal variation of copeptin concentration and adjusted for confounders in sinusoidal models. Results The predicted median copeptin level was 5.81 pmol/L (7.18 pmol/L for men and 4.44 pmol/L for women). Copeptin exhibited a distinct seasonal pattern with a peak in winter (mid-February to mid-March) and nadir in late summer (mid-August to mid-September). The adjusted absolute seasonal variation in median copeptin was 0.62 pmol/L (95% confidence interval [CI] 0.50; 0.74, 0.98 pmol/L [95% CI 0.73; 1.23] for men and 0.46 pmol/L [95% CI 0.33; 0.59] for women). The adjusted relative seasonal variation in mean log copeptin z-score was 0.20 (95% CI 0.17; 0.24, 0.18 [95% CI 0.14; 0.23] in men and 0.24 [95% CI 0.19; 0.29] in women). The observed seasonal variation of copeptin corresponded to a risk increase of 4% for incident diabetes mellitus and 2% for incident coronary artery disease. Conclusion The seasonal variation of the vasopressin marker copeptin corresponds to increased disease risk and mirrors the known variation in cardiometabolic status across the year. Moderately increased water intake might mitigate the winter peak of cardiometabolic disease.
Published: 2022
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24. Stroke genetics informs drug discovery and risk prediction across ancestries

Author: Mishra, Aniket, Malik, Rainer, Hachiya, Tsuyoshi, Jurgenson, Tuuli, Namba, Shinichi, Posner, Daniel C, Kamanu, Frederick K, Koido, Masaru, Le Grand, Quentin, Shi, Mingyang, He, Yunye, Georgakis, Marios K, Caro, Ilana, Krebs, Kristi, Liaw, Yi-Ching, Vaura, Felix C, Lin, Kuang, Winsvold, Bendik Slagsvold, Srinivasasainagendra, Vinodh, Parodi, Livia, Bae, Hee-Joon, Chauhan, Ganesh, Chong, Michael R, Tomppo, Liisa, Akinyemi, Rufus, Roshchupkin, Gennady V, Habib, Naomi, Jee, Yon Ho, Thomassen, Jesper Qvist, Abedi, Vida, Carcel-Marquez, Jara, Nygaard, Marianne, Leonard, Hampton L, Yang, Chaojie, Yonova-Doing, Ekaterina, Knol, Maria J, Lewis, Adam J, Judy, Renae L, Ago, Tetsuro, Amouyel, Philippe, Armstrong, Nicole D, Bakker, Mark K, Bartz, Traci M, Bennett, David A, Bis, Joshua C, Bordes, Constance, Borte, Sigrid, Cain, Anael, Ridker, Paul M, Cho, Kelly, Chen, Zhengming, Cruchaga, Carlos, Cole, John W, de Jager, Phil L, de Cid, Rafael, Endres, Matthias, Ferreira, Leslie E, Geerlings, Mirjam I, Gasca, Natalie C, Gudnason, Vilmundur, Hata, Jun, He, Jing, Heath, Alicia K, Ho, Yuk-Lam, Havulinna, Aki S, Hopewell, Jemma C, Hyacinth, Hyacinth I, Inouye, Michael, Jacob, Mina A, Jeon, Christina E, Jern, Christina, Kamouchi, Masahiro, Keene, Keith L, Kitazono, Takanari, Kittner, Steven J, Konuma, Takahiro, Kumar, Amit, Lacaze, Paul, Launer, Lenore J, Lee, Keon-Joo, Lepik, Kaido, Li, Jiang, Li, Liming, Manichaikul, Ani, Markus, Hugh S, Marston, Nicholas A, Meitinger, Thomas, Mitchell, Braxton D, Montellano, Felipe A, Morisaki, Takayuki, Mosley, Thomas H, Nalls, Mike A, Nordestgaard, Borge G, O'Donnell, Martin J, Okada, Yukinori, Onland-Moret, N Charlotte, Ovbiagele, Bruce, Peters, Annette, Psaty, Bruce M, Rich, Stephen S, Rosand, Jonathan, Sabatine, Marc S, Sacco, Ralph L, Saleheen, Danish, Sandset, Else Charlotte, Salomaa, Veikko, Sargurupremraj, Muralidharan, Sasaki, Makoto, Satizabal, Claudia L, Schmidt, Carsten O, Shimizu, Atsushi, Smith, Nicholas L, Sloane, Kelly L, Sutoh, Yoichi, Sun, Yan V, Tanno, Kozo, Tiedt, Steffen, Tatlisumak, Turgut, Torres-Aguila, Nuria P, Tiwari, Hemant K, Tregouet, David-Alexandre, Trompet, Stella, Tuladhar, Anil Man, Tybjaerg-Hansen, Anne, van Vugt, Marion, Vibo, Riina, Verma, Shefali S, Wiggins, Kerri L, Wennberg, Patrik, Woo, Daniel, Wilson, Peter WF, Xu, Huichun, Yang, Qiong, Yoon, Kyungheon, Lee, Jin-Moo, Cheng, Yu-Ching, Meschia, James F, Chen, Wei Min, Sale, Michele M, Zonderman, Alan B, Evans, Michele K, Wilson, James G, Correa, Adolfo, Traylor, Matthew, Lewis, Cathryn M, Carty, Cara L, Reiner, Alexander, Haessler, Jeffrey, Langefeld, Carl D, Gottesman, Rebecca F, Yaffe, Kristine, Liu, Yong Mei, Kooperberg, Charles, Lange, Leslie A, Furie, Karen L, Arnett, Donna K, Benavente, Oscar R, Grewal, Raji P, Peddareddygari, Leema Reddy, Hveem, Kristian, Lindstrom, Sara, Wang, Lu, Smith, Erin N, Gordon, William, van Hylckama Vlieg, Astrid, de Andrade, Mariza, Brody, Jennifer A, Pattee, Jack W, Brumpton, Ben M, Suchon, Pierre, Chen, Ming-Huei, Frazer, Kelly A, Turman, Constance, Germain, Marine, MacDonald, James, Braekkan, Sigrid K, Armasu, Sebastian M, Pankratz, Nathan, Jackson, Rebecca D, Nielsen, Jonas B, Giulianini, Franco, Puurunen, Marja K, Ibrahim, Manal, Heckbert, Susan R, Bammler, Theo K, McCauley, Bryan M, Taylor, Kent D, Pankow, James S, Reiner, Alexander P, Gabrielsen, Maiken E, Deleuze, Jean-Francois, O'Donnell, Chris J, Kim, Jihye, McKnight, Barbara, Kraft, Peter, Hansen, John-Bjarne, Rosendaal, Frits R, Heit, John A, Tang, Weihong, Morange, Pierre-Emmanuel, Johnson, Andrew D, Kabrhel, Christopher, van Dijk, Ewoud J, Koudstaal, Peter J, Luijckx, Gert-Jan, Nederkoorn, Paul J, van Oostenbrugge, Robert J, Visser, Marieke C, Wermer, Marieke JH, Kappelle, L Jaap, Esko, Tonu, Metspalu, Andres, Magi, Reedik, Nelis, Mari, Irvin, Marguerite R, de Leeuw, Frank-Erik, Levi, Christopher R, Maguire, Jane, Jimenez-Conde, Jordi, Sharma, Pankaj, Sudlow, Cathie LM, Rannikmae, Kristiina, Schmidt, Reinhold, Slowik, Agnieszka, Pera, Joanna, Thijs, Vincent NS, Lindgren, Arne G, Ilinca, Andreea, Melander, Olle, Engstrom, Gunnar, Rexrode, Kathryn M, Rothwell, Peter M, Stanne, Tara M, Johnson, Julie A, Danesh, John, Butterworth, Adam S, Heitsch, Laura, Boncoraglio, Giorgio B, Kubo, Michiaki, Pezzini, Alessandro, Rolfs, Arndt, Giese, Anne-Katrin, Weir, David, Ross, Owen A, Lemmons, Robin, Soderholm, Martin, Cushman, Mary, Jood, Katarina, McDonough, Caitrin W, Bell, Steven, Linkohr, Birgit, Lee, Tsong-Hai, Putaala, Jukka, Anderson, Christopher D, Lopez, Oscar L, Jian, Xueqiu, Schminke, Ulf, Cullell, Natalia, Delgado, Pilar, Ibanez, Laura, Krupinski, Jerzy, Lioutas, Vasileios, Matsuda, Koichi, Montaner, Joan, Muino, Elena, Roquer, Jaume, Sarnowski, Chloe, Sattar, Naveed, Sibolt, Gerli, Teumer, Alexander, Rutten-Jacobs, Loes, Kanai, Masahiro, Gretarsdottir, Solveig, Rost, Natalia S, Yusuf, Salim, Almgren, Peter, Ay, Hakan, Bevan, Steve, Brown, Robert D, Carrera, Caty, Buring, Julie E, Chen, Wei-Min, Cotlarciuc, Ioana, de Bakker, Paul IW, DeStefano, Anita L, den Hoed, Marcel, Duan, Qing, Engelter, Stefan T, Falcone, Guido J, Gustafsson, Stefan, Hassan, Ahamad, Holliday, Elizabeth G, Howard, George, Hsu, Fang-Chi, Ingelsson, Erik, Harris, Tamara B, Kissela, Brett M, Kleindorfer, Dawn O, Langenberg, Claudia, Lemmens, Robin, Leys, Didier, Lin, Wei-Yu, Lorentzen, Erik, Magnusson, Patrik K, McArdle, Patrick F, Pulit, Sara L, Rice, Kenneth, Sakaue, Saori, Sapkota, Bishwa R, Tanislav, Christian, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tzourio, Christophe, van Duijn, Cornelia M, Walters, Matthew, Wareham, Nicholas J, Amin, Najaf, Aparicio, Hugo J, Attia, John, Beiser, Alexa S, Berr, Claudine, Bustamante, Mariana, Caso, Valeria, Choi, Seung Hoan, Chowhan, Ayesha, Dartigues, Jean-Francois, Delavaran, Hossein, Dorr, Marcus, Ford, Ian, Gurpreet, Wander S, Hamsten, Anders, Hozawa, Atsushi, Ingelsson, Martin, Iwasaki, Motoki, Kaffashian, Sara, Kalra, Lalit, Kjartansson, Olafur, Kloss, Manja, Labovitz, Daniel L, Laurie, Cathy C, Li, Linxin, Lind, Lars, Lindgren, Cecilia M, Makoto, Hirata, Minegishi, Naoko, Morris, Andrew P, Muller-Nurasyid, Martina, Norrving, Bo, Ogishima, Soichi, Parati, Eugenio A, Pedersen, Nancy L, Perola, Markus, Jousilahti, Pekka, Pileggi, Silvana, Rabionet, Raquel, Riba-Llena, Iolanda, Ribases, Marta, Romero, Jose R, Rudd, Anthony G, Sarin, Antti-Pekka, Sarju, Ralhan, Satoh, Mamoru, Sawada, Norie, Sigurdsson, Asgeir, Smith, Albert, Stine, O Colin, Stott, David J, Strauch, Konstantin, Takai, Takako, Tanaka, Hideo, Touze, Emmanuel, Tsugane, Shoichiro, Uitterlinden, Andre G, Valdimarsson, Einar M, van der Lee, Sven J, Wakai, Kenji, Williams, Stephen R, Wolfe, Charles DA, Wong, Quenna, Yamaji, Taiki, Sanghera, Dharambir K, Stefansson, Kari, Martinez-Majander, Nicolas, Sobue, Kenji, Soriano-Tarraga, Carolina, Volzke, Henry, Akpa, Onoja, Sarfo, Fred S, Akpalu, Albert, Obiako, Reginald, Wahab, Kolawole, Osaigbovo, Godwin, Owolabi, Lukman, Komolafe, Morenikeji, Jenkins, Carolyn, Arulogun, Oyedunni, Ogbole, Godwin, Adeoye, Abiodun M, Akinyemi, Joshua, Agunloye, Atinuke, Fakunle, Adekunle G, Uvere, Ezinne, Olalere, Abimbola, Adebajo, Olayinka J, Chen, Junshi, Clarke, Robert, Collins, Rory, Guo, Yu, Wang, Chen, Lv, Jun, Peto, Richard, Chen, Yiping, Fairhurst-Hunter, Zammy, Hill, Michael, Pozarickij, Alfred, Schmidt, Dan, Stevens, Becky, Turnbull, Iain, Yu, Canqing, Nagai, Akiko, Murakami, Yoishinori, Shiroma, Eric J, Sigurdsson, Sigurdur, Ghanbari, Mohsen, Boerwinkle, Eric, Fongang, Bernard, Wang, Ruiqi, Ikram, Mohammad K, Volker, Uwe, de Laat, Karlijn F, van Norden, Anouk GW, de Kort, Paul L, Vermeer, Sarah E, Brouwers, Paul JAM, Gons, Rob AR, den Heijer, Tom, van Dijk, Gert W, van Rooij, Frank GW, Aamodt, Anne H, Skogholt, Anne H, Willer, Cristen J, Heuch, Ingrid, Hagen, Knut, Fritsche, Lars G, Pedersen, Linda M, Ellekjaer, Hanne, Zhou, Wei, Martinsen, Amy E, Kristoffersen, Espen S, Thomas, Laurent F, Kleinschnitz, Christoph, Frantz, Stefan, Ungethum, Kathrin, Gallego-Fabrega, Cristina, Lledos, Miquel, Llucia-Carol, Laia, Sobrino, Tomas, Campos, Francisco, Castillo, Jose, Freijo, Marimar, Arenillas, Juan Francisco, Obach, Victor, Alvarez-Sabin, Jose, Molina, Carlos A, Ribo, Marc, Munoz-Narbona, Lucia, Lopez-Cancio, Elena, Millan, Monica, Diaz-Navarro, Rosa, Vives-Bauza, Cristofol, Serrano-Heras, Gemma, Segura, Tomas, Dhar, Rajat, Delgado-Mederos, Raquel, Prats-Sanchez, Luis, Camps-Renom, Pol, Blay, Natalia, Sumoy, Lauro, Marti-Fabregas, Joan, Schnohr, Peter, Jensen, Gorm B, Benn, Marianne, Afzal, Shoaib, Kamstrup, Pia R, van Setten, Jessica, van der Laan, Sander W, Vonk, Jet MJ, Kim, Bong-Jo, Curtze, Sami, Tiainen, Marjaana, Kinnunen, Janne, Menon, Vilas, Sung, Yun Ju, Yang, Chengran, Saillour-Glenisson, Florence, Gravel, Simon, Millwood, Iona Y, Gieger, Christian, Ninomiya, Toshiharu, Grabe, Hans J, Jukema, J Wouter, Rissanen, Ina L, Strbian, Daniel, Kim, Young Jin, Chen, Pei-Hsin, Mayerhofer, Ernst, Howson, Joanna MM, Adams, Hieab, Wassertheil-Smoller, Sylvia, Christensen, Kaare, Ikram, Mohammad A, Rundek, Tatjana, Worrall, Bradford B, Lathrop, G Mark, Riaz, Moeen, Simonsick, Eleanor M, Korv, Janika, Franca, Paulo HC, Zand, Ramin, Prasad, Kameshwar, Frikke-Schmidt, Ruth, Liman, Thomas, Haeusler, Karl Georg, Ruigrok, Ynte M, Heuschmann, Peter Ulrich, Longstreth, WT, Jung, Keum Ji, Bastarache, Lisa, Pare, Guillaume, Damrauer, Scott M, Chasman, Daniel I, Rotter, Jerome I, Zwart, John-Anker, Niiranen, Teemu J, Fornage, Myriam, Liaw, Yung-Po, Seshadri, Sudha, Fernandez-Cadenas, Israel, Walters, Robin G, Ruff, Christian T, Owolabi, Mayowa O, Huffman, Jennifer E, Milani, Lili, Kamatani, Yoichiro, Dichgans, Martin, Debette, Stephanie, Mishra, Aniket, Malik, Rainer, Hachiya, Tsuyoshi, Jurgenson, Tuuli, Namba, Shinichi, Posner, Daniel C, Kamanu, Frederick K, Koido, Masaru, Le Grand, Quentin, Shi, Mingyang, He, Yunye, Georgakis, Marios K, Caro, Ilana, Krebs, Kristi, Liaw, Yi-Ching, Vaura, Felix C, Lin, Kuang, Winsvold, Bendik Slagsvold, Srinivasasainagendra, Vinodh, Parodi, Livia, Bae, Hee-Joon, Chauhan, Ganesh, Chong, Michael R, Tomppo, Liisa, Akinyemi, Rufus, Roshchupkin, Gennady V, Habib, Naomi, Jee, Yon Ho, Thomassen, Jesper Qvist, Abedi, Vida, Carcel-Marquez, Jara, Nygaard, Marianne, Leonard, Hampton L, Yang, Chaojie, Yonova-Doing, Ekaterina, Knol, Maria J, Lewis, Adam J, Judy, Renae L, Ago, Tetsuro, Amouyel, Philippe, Armstrong, Nicole D, Bakker, Mark K, Bartz, Traci M, Bennett, David A, Bis, Joshua C, Bordes, Constance, Borte, Sigrid, Cain, Anael, Ridker, Paul M, Cho, Kelly, Chen, Zhengming, Cruchaga, Carlos, Cole, John W, de Jager, Phil L, de Cid, Rafael, Endres, Matthias, Ferreira, Leslie E, Geerlings, Mirjam I, Gasca, Natalie C, Gudnason, Vilmundur, Hata, Jun, He, Jing, Heath, Alicia K, Ho, Yuk-Lam, Havulinna, Aki S, Hopewell, Jemma C, Hyacinth, Hyacinth I, Inouye, Michael, Jacob, Mina A, Jeon, Christina E, Jern, Christina, Kamouchi, Masahiro, Keene, Keith L, Kitazono, Takanari, Kittner, Steven J, Konuma, Takahiro, Kumar, Amit, Lacaze, Paul, Launer, Lenore J, Lee, Keon-Joo, Lepik, Kaido, Li, Jiang, Li, Liming, Manichaikul, Ani, Markus, Hugh S, Marston, Nicholas A, Meitinger, Thomas, Mitchell, Braxton D, Montellano, Felipe A, Morisaki, Takayuki, Mosley, Thomas H, Nalls, Mike A, Nordestgaard, Borge G, O'Donnell, Martin J, Okada, Yukinori, Onland-Moret, N Charlotte, Ovbiagele, Bruce, Peters, Annette, Psaty, Bruce M, Rich, Stephen S, Rosand, Jonathan, Sabatine, Marc S, Sacco, Ralph L, Saleheen, Danish, Sandset, Else Charlotte, Salomaa, Veikko, Sargurupremraj, Muralidharan, Sasaki, Makoto, Satizabal, Claudia L, Schmidt, Carsten O, Shimizu, Atsushi, Smith, Nicholas L, Sloane, Kelly L, Sutoh, Yoichi, Sun, Yan V, Tanno, Kozo, Tiedt, Steffen, Tatlisumak, Turgut, Torres-Aguila, Nuria P, Tiwari, Hemant K, Tregouet, David-Alexandre, Trompet, Stella, Tuladhar, Anil Man, Tybjaerg-Hansen, Anne, van Vugt, Marion, Vibo, Riina, Verma, Shefali S, Wiggins, Kerri L, Wennberg, Patrik, Woo, Daniel, Wilson, Peter WF, Xu, Huichun, Yang, Qiong, Yoon, Kyungheon, Lee, Jin-Moo, Cheng, Yu-Ching, Meschia, James F, Chen, Wei Min, Sale, Michele M, Zonderman, Alan B, Evans, Michele K, Wilson, James G, Correa, Adolfo, Traylor, Matthew, Lewis, Cathryn M, Carty, Cara L, Reiner, Alexander, Haessler, Jeffrey, Langefeld, Carl D, Gottesman, Rebecca F, Yaffe, Kristine, Liu, Yong Mei, Kooperberg, Charles, Lange, Leslie A, Furie, Karen L, Arnett, Donna K, Benavente, Oscar R, Grewal, Raji P, Peddareddygari, Leema Reddy, Hveem, Kristian, Lindstrom, Sara, Wang, Lu, Smith, Erin N, Gordon, William, van Hylckama Vlieg, Astrid, de Andrade, Mariza, Brody, Jennifer A, Pattee, Jack W, Brumpton, Ben M, Suchon, Pierre, Chen, Ming-Huei, Frazer, Kelly A, Turman, Constance, Germain, Marine, MacDonald, James, Braekkan, Sigrid K, Armasu, Sebastian M, Pankratz, Nathan, Jackson, Rebecca D, Nielsen, Jonas B, Giulianini, Franco, Puurunen, Marja K, Ibrahim, Manal, Heckbert, Susan R, Bammler, Theo K, McCauley, Bryan M, Taylor, Kent D, Pankow, James S, Reiner, Alexander P, Gabrielsen, Maiken E, Deleuze, Jean-Francois, O'Donnell, Chris J, Kim, Jihye, McKnight, Barbara, Kraft, Peter, Hansen, John-Bjarne, Rosendaal, Frits R, Heit, John A, Tang, Weihong, Morange, Pierre-Emmanuel, Johnson, Andrew D, Kabrhel, Christopher, van Dijk, Ewoud J, Koudstaal, Peter J, Luijckx, Gert-Jan, Nederkoorn, Paul J, van Oostenbrugge, Robert J, Visser, Marieke C, Wermer, Marieke JH, Kappelle, L Jaap, Esko, Tonu, Metspalu, Andres, Magi, Reedik, Nelis, Mari, Irvin, Marguerite R, de Leeuw, Frank-Erik, Levi, Christopher R, Maguire, Jane, Jimenez-Conde, Jordi, Sharma, Pankaj, Sudlow, Cathie LM, Rannikmae, Kristiina, Schmidt, Reinhold, Slowik, Agnieszka, Pera, Joanna, Thijs, Vincent NS, Lindgren, Arne G, Ilinca, Andreea, Melander, Olle, Engstrom, Gunnar, Rexrode, Kathryn M, Rothwell, Peter M, Stanne, Tara M, Johnson, Julie A, Danesh, John, Butterworth, Adam S, Heitsch, Laura, Boncoraglio, Giorgio B, Kubo, Michiaki, Pezzini, Alessandro, Rolfs, Arndt, Giese, Anne-Katrin, Weir, David, Ross, Owen A, Lemmons, Robin, Soderholm, Martin, Cushman, Mary, Jood, Katarina, McDonough, Caitrin W, Bell, Steven, Linkohr, Birgit, Lee, Tsong-Hai, Putaala, Jukka, Anderson, Christopher D, Lopez, Oscar L, Jian, Xueqiu, Schminke, Ulf, Cullell, Natalia, Delgado, Pilar, Ibanez, Laura, Krupinski, Jerzy, Lioutas, Vasileios, Matsuda, Koichi, Montaner, Joan, Muino, Elena, Roquer, Jaume, Sarnowski, Chloe, Sattar, Naveed, Sibolt, Gerli, Teumer, Alexander, Rutten-Jacobs, Loes, Kanai, Masahiro, Gretarsdottir, Solveig, Rost, Natalia S, Yusuf, Salim, Almgren, Peter, Ay, Hakan, Bevan, Steve, Brown, Robert D, Carrera, Caty, Buring, Julie E, Chen, Wei-Min, Cotlarciuc, Ioana, de Bakker, Paul IW, DeStefano, Anita L, den Hoed, Marcel, Duan, Qing, Engelter, Stefan T, Falcone, Guido J, Gustafsson, Stefan, Hassan, Ahamad, Holliday, Elizabeth G, Howard, George, Hsu, Fang-Chi, Ingelsson, Erik, Harris, Tamara B, Kissela, Brett M, Kleindorfer, Dawn O, Langenberg, Claudia, Lemmens, Robin, Leys, Didier, Lin, Wei-Yu, Lorentzen, Erik, Magnusson, Patrik K, McArdle, Patrick F, Pulit, Sara L, Rice, Kenneth, Sakaue, Saori, Sapkota, Bishwa R, Tanislav, Christian, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tzourio, Christophe, van Duijn, Cornelia M, Walters, Matthew, Wareham, Nicholas J, Amin, Najaf, Aparicio, Hugo J, Attia, John, Beiser, Alexa S, Berr, Claudine, Bustamante, Mariana, Caso, Valeria, Choi, Seung Hoan, Chowhan, Ayesha, Dartigues, Jean-Francois, Delavaran, Hossein, Dorr, Marcus, Ford, Ian, Gurpreet, Wander S, Hamsten, Anders, Hozawa, Atsushi, Ingelsson, Martin, Iwasaki, Motoki, Kaffashian, Sara, Kalra, Lalit, Kjartansson, Olafur, Kloss, Manja, Labovitz, Daniel L, Laurie, Cathy C, Li, Linxin, Lind, Lars, Lindgren, Cecilia M, Makoto, Hirata, Minegishi, Naoko, Morris, Andrew P, Muller-Nurasyid, Martina, Norrving, Bo, Ogishima, Soichi, Parati, Eugenio A, Pedersen, Nancy L, Perola, Markus, Jousilahti, Pekka, Pileggi, Silvana, Rabionet, Raquel, Riba-Llena, Iolanda, Ribases, Marta, Romero, Jose R, Rudd, Anthony G, Sarin, Antti-Pekka, Sarju, Ralhan, Satoh, Mamoru, Sawada, Norie, Sigurdsson, Asgeir, Smith, Albert, Stine, O Colin, Stott, David J, Strauch, Konstantin, Takai, Takako, Tanaka, Hideo, Touze, Emmanuel, Tsugane, Shoichiro, Uitterlinden, Andre G, Valdimarsson, Einar M, van der Lee, Sven J, Wakai, Kenji, Williams, Stephen R, Wolfe, Charles DA, Wong, Quenna, Yamaji, Taiki, Sanghera, Dharambir K, Stefansson, Kari, Martinez-Majander, Nicolas, Sobue, Kenji, Soriano-Tarraga, Carolina, Volzke, Henry, Akpa, Onoja, Sarfo, Fred S, Akpalu, Albert, Obiako, Reginald, Wahab, Kolawole, Osaigbovo, Godwin, Owolabi, Lukman, Komolafe, Morenikeji, Jenkins, Carolyn, Arulogun, Oyedunni, Ogbole, Godwin, Adeoye, Abiodun M, Akinyemi, Joshua, Agunloye, Atinuke, Fakunle, Adekunle G, Uvere, Ezinne, Olalere, Abimbola, Adebajo, Olayinka J, Chen, Junshi, Clarke, Robert, Collins, Rory, Guo, Yu, Wang, Chen, Lv, Jun, Peto, Richard, Chen, Yiping, Fairhurst-Hunter, Zammy, Hill, Michael, Pozarickij, Alfred, Schmidt, Dan, Stevens, Becky, Turnbull, Iain, Yu, Canqing, Nagai, Akiko, Murakami, Yoishinori, Shiroma, Eric J, Sigurdsson, Sigurdur, Ghanbari, Mohsen, Boerwinkle, Eric, Fongang, Bernard, Wang, Ruiqi, Ikram, Mohammad K, Volker, Uwe, de Laat, Karlijn F, van Norden, Anouk GW, de Kort, Paul L, Vermeer, Sarah E, Brouwers, Paul JAM, Gons, Rob AR, den Heijer, Tom, van Dijk, Gert W, van Rooij, Frank GW, Aamodt, Anne H, Skogholt, Anne H, Willer, Cristen J, Heuch, Ingrid, Hagen, Knut, Fritsche, Lars G, Pedersen, Linda M, Ellekjaer, Hanne, Zhou, Wei, Martinsen, Amy E, Kristoffersen, Espen S, Thomas, Laurent F, Kleinschnitz, Christoph, Frantz, Stefan, Ungethum, Kathrin, Gallego-Fabrega, Cristina, Lledos, Miquel, Llucia-Carol, Laia, Sobrino, Tomas, Campos, Francisco, Castillo, Jose, Freijo, Marimar, Arenillas, Juan Francisco, Obach, Victor, Alvarez-Sabin, Jose, Molina, Carlos A, Ribo, Marc, Munoz-Narbona, Lucia, Lopez-Cancio, Elena, Millan, Monica, Diaz-Navarro, Rosa, Vives-Bauza, Cristofol, Serrano-Heras, Gemma, Segura, Tomas, Dhar, Rajat, Delgado-Mederos, Raquel, Prats-Sanchez, Luis, Camps-Renom, Pol, Blay, Natalia, Sumoy, Lauro, Marti-Fabregas, Joan, Schnohr, Peter, Jensen, Gorm B, Benn, Marianne, Afzal, Shoaib, Kamstrup, Pia R, van Setten, Jessica, van der Laan, Sander W, Vonk, Jet MJ, Kim, Bong-Jo, Curtze, Sami, Tiainen, Marjaana, Kinnunen, Janne, Menon, Vilas, Sung, Yun Ju, Yang, Chengran, Saillour-Glenisson, Florence, Gravel, Simon, Millwood, Iona Y, Gieger, Christian, Ninomiya, Toshiharu, Grabe, Hans J, Jukema, J Wouter, Rissanen, Ina L, Strbian, Daniel, Kim, Young Jin, Chen, Pei-Hsin, Mayerhofer, Ernst, Howson, Joanna MM, Adams, Hieab, Wassertheil-Smoller, Sylvia, Christensen, Kaare, Ikram, Mohammad A, Rundek, Tatjana, Worrall, Bradford B, Lathrop, G Mark, Riaz, Moeen, Simonsick, Eleanor M, Korv, Janika, Franca, Paulo HC, Zand, Ramin, Prasad, Kameshwar, Frikke-Schmidt, Ruth, Liman, Thomas, Haeusler, Karl Georg, Ruigrok, Ynte M, Heuschmann, Peter Ulrich, Longstreth, WT, Jung, Keum Ji, Bastarache, Lisa, Pare, Guillaume, Damrauer, Scott M, Chasman, Daniel I, Rotter, Jerome I, Zwart, John-Anker, Niiranen, Teemu J, Fornage, Myriam, Liaw, Yung-Po, Seshadri, Sudha, Fernandez-Cadenas, Israel, Walters, Robin G, Ruff, Christian T, Owolabi, Mayowa O, Huffman, Jennifer E, Milani, Lili, Kamatani, Yoichiro, Dichgans, Martin, and Debette, Stephanie
Abstract: Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.
Published: 2022

25. The value of combining individual and small area sociodemographic data for assessing and handling selective participation in cohort studies: Evidence from the Swedish CardioPulmonary bioImage Study

Author: Bonander, Carl, Nilsson, Anton, Bjork, Jonas, Blomberg, Anders, Engstrom, Gunnar, Jernberg, Tomas, Sundstrom, Johan, Östgren, Carl Johan, Bergstrom, Goran, Stromberg, Ulf, Bonander, Carl, Nilsson, Anton, Bjork, Jonas, Blomberg, Anders, Engstrom, Gunnar, Jernberg, Tomas, Sundstrom, Johan, Östgren, Carl Johan, Bergstrom, Goran, and Stromberg, Ulf
Abstract: Objectives To study the value of combining individual- and neighborhood-level sociodemographic data to predict study participation and assess the effects of baseline selection on the distribution of metabolic risk factors and lifestyle factors in the Swedish CardioPulmonary bioImage Study (SCAPIS). Methods We linked sociodemographic register data to SCAPIS participants (n = 30,154, ages: 50-64 years) and a random sample of the studys target population (n = 59,909). We assessed the classification ability of participation models based on individual-level data, neighborhood-level data, and combinations of both. Standardized mean differences (SMD) were used to examine how reweighting the sample to match the population affected the averages of 32 cardiopulmonary risk factors at baseline. Absolute SMDs > 0.10 were considered meaningful. Results Combining both individual-level and neighborhood-level data gave rise to a model with better classification ability (AUC: 71.3%) than models with only individual-level (AUC: 66.9%) or neighborhood-level data (AUC: 65.5%). We observed a greater change in the distribution of risk factors when we reweighted the participants using both individual and area data. The only meaningful change was related to the (self-reported) frequency of alcohol consumption, which appears to be higher in the SCAPIS sample than in the population. The remaining risk factors did not change meaningfully. Conclusions Both individual- and neighborhood-level characteristics are informative in assessing study selection effects. Future analyses of cardiopulmonary outcomes in the SCAPIS cohort can benefit from our study, though the average impact of selection on risk factor distributions at baseline appears small., Funding Agencies|Swedish Research Council for Health, Working life and Welfare (Forte) [2017-00414, 2020-00962]; Swedish Research Council (VR) [2019-00198]; Swedish Heart-Lung Foundation; Knut and Alice Wallenberg Foundation [2014-0047]; VINNOVA (Swedens Innovation agency) [2012-04476]; Swedish Research Council [822-2013-2000]; Uppsala University and University Hospital; Umea University and University Hospital; Skane University Hospital; Lund University; Linkoping University and University Hospital; Stockholm county council; University of Gothenburg; Sahlgrenska University Hospital; Karolinska Institutet
Published: 2022
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26. Assay-related differences in SuPAR levels: implications for measurement and data interpretation

Author: Vasbinder, Alexi, primary, Raffield, Laura Marie, additional, Gao, Yan, additional, Engstrom, Gunnar, additional, Quyyumi, Arshed Ali, additional, Reiner, Alexander Paul, additional, Reiser, Jochen, additional, and Hayek, Salim Salim, additional
Published: 2022
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27. Abstract 12137: Common Metabolic Determinants of Cardiac and Pulmonary Function in the General Population

Author: Ghosh, Nilanjana, primary, Wibom, Sandra, additional, Czuba, Tomasz, additional, Landenhed Smith, Maya l, additional, Engstrom, Gunnar, additional, and Smith, Gustav, additional
Published: 2021
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28. Assay-related Differences in SuPAR Levels: Implications for Measurement and Data Interpretation

Author: Hayek, Salim S., primary, Raffield, Laura M., additional, Gao, Yan, additional, Engstrom, Gunnar, additional, Quyyumi, Arshed A., additional, Reiner, Alexander P., additional, and Reiser, Jochen, additional
Published: 2021
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29. Systematic Coronary Risk Evaluation estimated risk and prevalent subclinical atherosclerosis in coronary and carotid arteries : A population-based cohort analysis from the Swedish Cardiopulmonary Bioimage Study

Author: Ostgren, Carl J., Söderberg, Stefan, Festin, Karin, Angeras, Oskar, Bergstrom, Goran, Blomberg, Anders, Brandberg, John, Cederlund, Kerstin, Eliasson, Mats, Engstrom, Gunnar, Erlinge, David, Fagman, Erika, Hagstrom, Emil, Lind, Lars, Mannila, Maria, Nilsson, Ulf, Oldgren, Jonas, Ostenfeld, Ellen, Persson, Anders, Persson, Jonas, Persson, Margaretha, Rosengren, Annika, Sundstrom, Johan, Swahn, Eva, Engvall, Jan E., Jernberg, Tomas, Ostgren, Carl J., Söderberg, Stefan, Festin, Karin, Angeras, Oskar, Bergstrom, Goran, Blomberg, Anders, Brandberg, John, Cederlund, Kerstin, Eliasson, Mats, Engstrom, Gunnar, Erlinge, David, Fagman, Erika, Hagstrom, Emil, Lind, Lars, Mannila, Maria, Nilsson, Ulf, Oldgren, Jonas, Ostenfeld, Ellen, Persson, Anders, Persson, Jonas, Persson, Margaretha, Rosengren, Annika, Sundstrom, Johan, Swahn, Eva, Engvall, Jan E., and Jernberg, Tomas
Abstract: Background: It is not clear if the European Systematic Coronary Risk Evaluation algorithm is useful for identifying prevalent subclinical atherosclerosis in a population of apparently healthy individuals. Our aim was to explore the association between the risk estimates from Systematic Coronary Risk Evaluation and prevalent subclinical atherosclerosis. Design: The design of this study was as a cross-sectional analysis from a population-based study cohort. Methods: From the general population, the Swedish Cardiopulmonary Bioimage Study randomly invited individuals aged 50–64 years and enrolled 13,411 participants mean age 57 (standard deviation 4.3) years; 46% males between November 2013–December 2016. Associations between Systematic Coronary Risk Evaluation risk estimates and coronary artery calcification and plaques in the carotid arteries by using imaging data from a computed tomography of the heart and ultrasonography of the carotid arteries were examined. Results: Coronary calcification was present in 39.5% and carotid plaque in 56.0%. In men, coronary artery calcium score >0 ranged from 40.7–65.9% and presence of carotid plaques from 54.5% to 72.8% in the age group 50–54 and 60–65 years, respectively. In women, the corresponding difference was from 17.1–38.9% and from 41.0–58.4%. A doubling of Systematic Coronary Risk Evaluation was associated with an increased probability to have coronary artery calcium score >0 (odds ratio: 2.18 (95% confidence interval 2.07–2.30)) and to have >1 carotid plaques (1.67 (1.61–1.74)). Conclusion: Systematic Coronary Risk Evaluation estimated risk is associated with prevalent subclinical atherosclerosis in two major vascular beds in a general population sample without established cardiovascular disease or diabetes mellitus. Thus, the Systematic Coronary Risk Evaluation risk chart may be of use for estimating the risk of subclinical atherosclerosis.
Published: 2021
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30. Prevalence of Subclinical Coronary Artery Atherosclerosis in the General Population

Author: Bergstrom, Goran, Persson, Margaretha, Adiels, Martin, Bjornson, Elias, Bonander, Carl, Ahlström, Håkan, Alfredsson, Joakim, Angeras, Oskar, Berglund, Goran, Blomberg, Anders, Brandberg, John, Borjesson, Mats, Cederlund, Kerstin, de Faire, Ulf, Duvernoy, Olov, Ekblom, Orjan, Engstrom, Gunnar, Engvall, Jan E., Fagman, Erika, Eriksson, Mats, Erlinge, David, Fagerberg, Bjorn, Flinck, Agneta, Goncalves, Isabel, Hagström, Emil, Hjelmgren, Ola, Lind, Lars, Lindberg, Eva, Lindqvist, Per, Ljungberg, Johan, Magnusson, Martin, Mannila, Maria, Markstad, Hanna, Mohammad, Moman A., Nystrom, Fredrik H., Ostenfeld, Ellen, Persson, Anders, Rosengren, Annika, Sandstrom, Anette, Sjalander, Anders, Skold, Magnus C., Sundström, Johan, Swahn, Eva, Soderberg, Stefan, Toren, Kjell, Ostgren, Carl Johan, Jernberg, Tomas, Bergstrom, Goran, Persson, Margaretha, Adiels, Martin, Bjornson, Elias, Bonander, Carl, Ahlström, Håkan, Alfredsson, Joakim, Angeras, Oskar, Berglund, Goran, Blomberg, Anders, Brandberg, John, Borjesson, Mats, Cederlund, Kerstin, de Faire, Ulf, Duvernoy, Olov, Ekblom, Orjan, Engstrom, Gunnar, Engvall, Jan E., Fagman, Erika, Eriksson, Mats, Erlinge, David, Fagerberg, Bjorn, Flinck, Agneta, Goncalves, Isabel, Hagström, Emil, Hjelmgren, Ola, Lind, Lars, Lindberg, Eva, Lindqvist, Per, Ljungberg, Johan, Magnusson, Martin, Mannila, Maria, Markstad, Hanna, Mohammad, Moman A., Nystrom, Fredrik H., Ostenfeld, Ellen, Persson, Anders, Rosengren, Annika, Sandstrom, Anette, Sjalander, Anders, Skold, Magnus C., Sundström, Johan, Swahn, Eva, Soderberg, Stefan, Toren, Kjell, Ostgren, Carl Johan, and Jernberg, Tomas
Abstract: Background: Early detection of coronary atherosclerosis using coronary computed tomography angiography (CCTA), in addition to coronary artery calcification (CAC) scoring, may help inform prevention strategies. We used CCTA to determine the prevalence, severity, and characteristics of coronary atherosclerosis and its association with CAC scores in a general population. Methods: We recruited 30 154 randomly invited individuals age 50 to 64 years to SCAPIS (the Swedish Cardiopulmonary Bioimage Study). The study includes individuals without known coronary heart disease (ie, no previous myocardial infarctions or cardiac procedures) and with high-quality results from CCTA and CAC imaging performed using dedicated dual-source CT scanners. Noncontrast images were scored for CAC. CCTA images were visually read and scored for coronary atherosclerosis per segment (defined as no atherosclerosis, 1% to 49% stenosis, or >= 50% stenosis). External validity of prevalence estimates was evaluated using inverse probability for participation weighting and Swedish register data. Results: In total, 25 182 individuals without known coronary heart disease were included (50.6% women). Any CCTA-detected atherosclerosis was found in 42.1%; any significant stenosis (>= 50%) in 5.2%; left main, proximal left anterior descending artery, or 3-vessel disease in 1.9%; and any noncalcified plaques in 8.3% of this population. Onset of atherosclerosis was delayed on average by 10 years in women. Atherosclerosis was more prevalent in older individuals and predominantly found in the proximal left anterior descending artery. Prevalence of CCTA-detected atherosclerosis increased with increasing CAC scores. Among those with a CAC score >400, all had atherosclerosis and 45.7% had significant stenosis. In those with 0 CAC, 5.5% had atherosclerosis and 0.4% had significant stenosis. In participants with 0 CAC and intermediate 10-year risk of atherosclerotic cardiovascular disease according to the poo
Published: 2021
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31. Plasma Protein Profile of Carotid Artery Atherosclerosis and Atherosclerotic Outcomes Meta-Analyses and Mendelian Randomization Analyses

Author: Lind, Lars, Gigante, Bruna, Borne, Yan, Feldreich, Tobias, Leppert, Jerzy, Hedberg, Par, Östgren, Carl Johan, Nyström, Fredrik H, Sundstrom, Johan, Arnlov, Johan, Baldassarre, Damiano, Tremoli, Elena, Veglia, Fabrizio, Hamsten, Anders, ODonnell, Christopher J., Franceschini, Nora, Orho-Melander, Marju, Nilsson, Jan, Melander, Olle, Engstrom, Gunnar, Malarstig, Anders, Lind, Lars, Gigante, Bruna, Borne, Yan, Feldreich, Tobias, Leppert, Jerzy, Hedberg, Par, Östgren, Carl Johan, Nyström, Fredrik H, Sundstrom, Johan, Arnlov, Johan, Baldassarre, Damiano, Tremoli, Elena, Veglia, Fabrizio, Hamsten, Anders, ODonnell, Christopher J., Franceschini, Nora, Orho-Melander, Marju, Nilsson, Jan, Melander, Olle, Engstrom, Gunnar, and Malarstig, Anders
Abstract: OBJECTIVE: To identify causal pathophysiological mechanisms for atherosclerosis and incident cardiovascular events using protein measurements. APPROACH AND RESULTS: Carotid artery atherosclerosis was assessed by ultrasound, and 86 cardiovascular-related proteins were measured using the Olink CVD-I panel in 7 Swedish prospective studies (11 754 individuals). The proteins were analyzed in relation to intima-media thickness in the common carotid artery (IMT-CCA), plaque occurrence, and incident cardiovascular events (composite end point of myocardial infarction or ischemic stroke) using a discovery/replication approach in different studies. After adjustments for traditional cardiovascular risk factors, 11 proteins remained significantly associated with IMT-CCA in the replication stage, whereas 9 proteins were replicated for plaque occurrence and 17 proteins for incident cardiovascular events. NT-proBNP (N-terminal pro-B-type natriuretic peptide) and MMP (matrix metalloproteinase)-12 were associated with both IMT-CCA and incident events, but the overlap was considerably larger between plaque occurrence and incident events, including MMP-12, TIM-1 (T-cell immunoglobulin and mucin domain 1), GDF (growth/differentiation factor)-15, IL (interleukin)-6, U-PAR (urokinase plasminogen activator surface receptor), LOX-1 (lectin-like oxidized LDL [low-density lipoprotein] receptor 1), and TRAIL-R2 (TNF [tumor necrosis factor]-related apoptosis-inducing ligand receptor 2). Only MMP-12 was associated with IMT-CCA, plaque, and incident events with a positive and concordant direction of effect. However, a 2-sample Mendelian randomization analysis suggested that increased MMP-12 may be protective against ischemic stroke (P=5.5x10(-7)), which is in the opposite direction of the observational analyses. CONCLUSIONS: The present meta-analysis discovered several proteins related to carotid atherosclerosis that partly differed in their association with IMT-CCA, plaque, and incident atherosc, Funding Agencies|Uppsala University Hospital; Swedish Heart and Lung foundationSwedish Heart-Lung Foundation; Swedish research councilSwedish Research CouncilEuropean Commission; Stockholm County Council (ALF)Stockholm County Council; EU grantEuropean Commission
Published: 2021
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32. Novel and conventional biomarkers for prediction of incident cardiovascular events in the community

Author: Melander, Olle, Newton-Cheh, Christopher, Almgren, Peter, Hedblad, Bo, Berglund, Goran, Engstrom, Gunnar, Persson, Margaretha, Smith, J. Gustav, Magnusson, Martin, Christensson, Anders, Struck, Joachim, Morgenthaler, Nils G., Bergmann, Andreas, Pencina, Michael J., and Wang, Thomas J.
Subjects: Risk factors (Health) -- Comparative analysis, Cardiovascular diseases -- Risk factors, Biological markers -- Usage
Abstract: The study aims to investigate the benefits of novel and conventional biomarkers, as against conventional risk factors in predicting the risk of cardiovascular events. The results indicate that even though some biomarkers are useful in predicting cardiovascular events as compared with conventional risk factors, benefits of both are the same.
Published: 2009

33. Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Author: Shah, Sonia, Henry, Albert, Roselli, Carolina, Lin, Honghuang, Sveinbjornsson, Gardar, Fatemifar, Ghazaleh, Hedman, Asa K, Wilk, Jemma B, Morley, Michael P, Chaffin, Mark D, Helgadottir, Anna, Verweij, Niek, Dehghan, Abbas, Almgren, Peter, Andersson, Charlotte, Aragam, Krishna G, Arnlov, Johan, Backman, Joshua D, Biggs, Mary L, Bloom, Heather L, Brandimarto, Jeffrey, Brown, Michael R, Buckbinder, Leonard, Carey, David J, Chasman, Daniel I, Chen, Xing, Chen, Xu, Chung, Jonathan, Chutkow, William, Cook, James P, Delgado, Graciela E, Denaxas, Spiros, Doney, Alexander S, Doerr, Marcus, Dudley, Samuel C, Dunn, Michael E, Engstrom, Gunnar, Esko, Tonu, Felix, Stephan B, Finan, Chris, Ford, Ian, Ghanbari, Mohsen, Ghasemi, Sahar, Giedraitis, Vilmantas, Giulianini, Franco, Gottdiener, John S, Gross, Stefan, Gudbjartsson, Daniel F, Gutmann, Rebecca, Haggerty, Christopher M, van der Harst, Pim, Hyde, Craig L, Ingelsson, Erik, Jukema, J Wouter, Kavousi, Maryam, Khaw, Kay-Tee, Kleber, Marcus E, Kober, Lars, Koekemoer, Andrea, Langenberg, Claudia, Lind, Lars, Lindgren, Cecilia M, London, Barry, Lotta, Luca A, Lovering, Ruth C, Luan, Jian'an, Magnusson, Patrik, Mahajan, Anubha, Margulies, Kenneth B, Maerz, Winfried, Melander, Olle, Mordi, Ify R, Morgan, Thomas, Morris, Andrew D, Morris, Andrew P, Morrison, Alanna C, Nagle, Michael W, Nelson, Christopher P, Niessner, Alexander, Niiranen, Teemu, O'Donoghue, Michelle L, Owens, Anjali T, Palmer, Colin NA, Parry, Helen M, Perola, Markus, Portilla-Fernandez, Eliana, Psaty, Bruce M, Rice, Kenneth M, Ridker, Paul M, Romaine, Simon PR, Rotter, Jerome I, Salo, Perttu, Salomaa, Veikko, van Setten, Jessica, Shalaby, Alaa A, Smelser, Diane T, Smith, Nicholas L, Stender, Steen, Stott, David J, Svensson, Per, Tammesoo, Mari-Liis, Taylor, Kent D, Teder-Laving, Maris, Teumer, Alexander, Thorgeirsson, Gudmundur, Thorsteinsdottir, Unnur, Torp-Pedersen, Christian, Trompet, Stella, Tyl, Benoit, Uitterlinden, Andre G, Veluchamy, Abirami, Voelker, Uwe, Voors, Adriaan A, Wang, Xiaosong, Wareham, Nicholas J, Waterworth, Dawn, Weeke, Peter E, Weiss, Raul, Wiggins, Kerri L, Xing, Heming, Yerges-Armstrong, Laura M, Yu, Bing, Zannad, Faiez, Zhao, Jing Hua, Hemingway, Harry, Samani, Nilesh J, McMurray, John JV, Yang, Jian, Visscher, Peter M, Newton-Cheh, Christopher, Malarstig, Anders, Holm, Hilma, Lubitz, Steven A, Sattar, Naveed, Holmes, Michael V, Cappola, Thomas P, Asselbergs, Folkert W, Hingorani, Aroon D, Kuchenbaecker, Karoline, Ellinor, Patrick T, Lang, Chim C, Stefansson, Kari, Smith, J Gustav, Vasan, Ramachandran S, Swerdlow, Daniel I, Lumbers, R Thomas, Abecasis, Goncalo, Backman, Joshua, Bai, Xiaodong, Balasubramanian, Suganthi, Banerjee, Nilanjana, Baras, Aris, Barnard, Leland, Beechert, Christina, Blumenfeld, Andrew, Cantor, Michael, Chai, Yating, Coppola, Giovanni, Damask, Amy, Dewey, Frederick, Economides, Aris, Eom, Gisu, Forsythe, Caitlin, Fuller, Erin D, Gu, Zhenhua, Gurski, Lauren, Guzzardo, Paloma M, Habegger, Lukas, Hahn, Young, Hawes, Alicia, van Hout, Cristopher, Jones, Marcus B, Khalid, Shareef, Lattari, Michael, Li, Alexander, Lin, Nan, Liu, Daren, Lopez, Alexander, Manoochehri, Kia, Marchini, Jonathan, Marcketta, Anthony, Maxwell, Evan K, McCarthy, Shane, Mitnaul, Lyndon J, O'Dushlaine, Colm, Overton, John D, Padilla, Maria Sotiropoulos, Paulding, Charles, Penn, John, Pradhan, Manasi, Reid, Jeffrey G, Schleicher, Thomas D, Schurmann, Claudia, Shuldiner, Alan, Staples, Jeffrey C, Sun, Dylan, Toledo, Karina, Ulloa, Ricardo H, Widom, Louis, Wolf, Sarah E, Yadav, Ashish, Ye, Bin, Ctr, Regeneron Genetics, Shah, Sonia [0000-0001-5860-4526], Henry, Albert [0000-0001-7422-2288], Roselli, Carolina [0000-0001-5267-6756], Lin, Honghuang [0000-0003-3043-3942], Chaffin, Mark D. [0000-0002-1234-5562], Helgadottir, Anna [0000-0002-1806-2467], Verweij, Niek [0000-0002-4303-7685], Almgren, Peter [0000-0002-0473-0241], Chen, Xu [0000-0002-7299-3238], Ghanbari, Mohsen [0000-0002-9476-7143], Giedraitis, Vilmantas [0000-0003-3423-2021], Gross, Stefan [0000-0003-4121-7161], Guðbjartsson, Daníel F. [0000-0002-5222-9857], Hyde, Craig L. [0000-0002-6939-287X], Ingelsson, Erik [0000-0003-2256-6972], Jukema, J. Wouter [0000-0002-3246-8359], Kleber, Marcus E. [0000-0003-0663-7275], Koekemoer, Andrea [0000-0001-8222-3547], Langenberg, Claudia [0000-0002-5017-7344], Lindgren, Cecilia M. [0000-0002-4903-9374], Lovering, Ruth C. [0000-0002-9791-0064], Luan, Jian’an [0000-0003-3137-6337], Magnusson, Patrik [0000-0002-7315-7899], Mahajan, Anubha [0000-0001-5585-3420], Mordi, Ify R. [0000-0002-2686-729X], Morris, Andrew D. [0000-0002-1766-0473], Nagle, Michael W. [0000-0002-4677-7582], Nelson, Christopher P. [0000-0001-8025-2897], Palmer, Colin N. A. [0000-0002-6415-6560], Rice, Kenneth M. [0000-0002-3071-7278], Rotter, Jerome I. [0000-0001-7191-1723], Salomaa, Veikko [0000-0001-7563-5324], van Setten, Jessica [0000-0002-4934-7510], Svensson, Per [0000-0003-0372-6272], Taylor, Kent D. [0000-0002-2756-4370], Teder-Laving, Maris [0000-0002-5872-1850], Teumer, Alexander [0000-0002-8309-094X], Tyl, Benoit [0000-0001-5297-8412], Uitterlinden, Andre G. [0000-0002-7276-3387], Völker, Uwe [0000-0002-5689-3448], Wiggins, Kerri L. [0000-0003-2749-1279], Hemingway, Harry [0000-0003-2279-0624], Yang, Jian [0000-0003-2001-2474], Visscher, Peter M. [0000-0002-2143-8760], Lubitz, Steven A. [0000-0002-9599-4866], Sattar, Naveed [0000-0002-1604-2593], Cappola, Thomas P. [0000-0002-9630-7204], Asselbergs, Folkert W. [0000-0002-1692-8669], Kuchenbaecker, Karoline [0000-0001-9726-603X], Ellinor, Patrick T. [0000-0002-2067-0533], Vasan, Ramachandran S. [0000-0001-7357-5970], Lumbers, R. Thomas [0000-0002-9077-4741], Apollo - University of Cambridge Repository, Chaffin, Mark D [0000-0002-1234-5562], Guðbjartsson, Daníel F [0000-0002-5222-9857], Hyde, Craig L [0000-0002-6939-287X], Jukema, J Wouter [0000-0002-3246-8359], Kleber, Marcus E [0000-0003-0663-7275], Lindgren, Cecilia M [0000-0002-4903-9374], Lovering, Ruth C [0000-0002-9791-0064], Luan, Jian'an [0000-0003-3137-6337], Mordi, Ify R [0000-0002-2686-729X], Morris, Andrew D [0000-0002-1766-0473], Nagle, Michael W [0000-0002-4677-7582], Nelson, Christopher P [0000-0001-8025-2897], Palmer, Colin NA [0000-0002-6415-6560], Rice, Kenneth M [0000-0002-3071-7278], Rotter, Jerome I [0000-0001-7191-1723], Taylor, Kent D [0000-0002-2756-4370], Uitterlinden, Andre G [0000-0002-7276-3387], Wiggins, Kerri L [0000-0003-2749-1279], Visscher, Peter M [0000-0002-2143-8760], Lubitz, Steven A [0000-0002-9599-4866], Cappola, Thomas P [0000-0002-9630-7204], Asselbergs, Folkert W [0000-0002-1692-8669], Ellinor, Patrick T [0000-0002-2067-0533], Vasan, Ramachandran S [0000-0001-7357-5970], Lumbers, R Thomas [0000-0002-9077-4741], Palmer, Colin N A [0000-0002-6415-6560], Cardiovascular Centre (CVC), University of Queensland [Brisbane], University College of London [London] (UCL), Broad Institute of MIT and Harvard (BROAD INSTITUTE), Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], University Medical Center Groningen [Groningen] (UMCG), Boston University School of Medicine (BUSM), Boston University [Boston] (BU), Framingham Heart Study, National Heart, Lung, and Blood Institute [Bethesda] (NHLBI)-Boston University [Boston] (BU), deCODE genetics [Reykjavik], Karolinska Institutet [Stockholm], Pfizer, University of Pennsylvania [Philadelphia], University of Groningen [Groningen], Imperial College London, Lund University [Lund], Herlev and Gentofte Hospital, Massachusetts General Hospital [Boston], Department of Neurobiology, Care Sciences and Society [Stockholm, Sweden] (Division of Family Medicine), Dalarna University, Regeneron Genetics Center, 777 Old Saw Mill River Road, Tarrytown, Department of Biostatistics, University of Washington [Seattle], Emory University School of Medicine, Emory University [Atlanta, GA], The University of Texas Medical School at Houston, Department of Molecular and Functional Genomics, Geisinger, Danville, PA, Brigham and Women's Hospital [Boston], Harvard Medical School [Boston] (HMS), Regeneron Genetics Center, 777 Old Saw Mill River Road, Tarrytown, NY, Novartis Institutes for BioMedical Research (NIBR), University of Liverpool, Universität Heidelberg [Heidelberg], Medizinische Fakultät Mannheim, The Alan Turing Institute, Ninewells Hospital and Medical School [Dundee], Universität Greifswald - University of Greifswald, German Center for Cardiovascular Research (DZHK), Berlin Institute of Health (BIH), University of Minnesota System, Regeneron Pharmaceuticals [Tarrytown], Department of Clinical Sciences, Cardiovascular Epidemiology, Skane University Hospital [Lund], Institute of Genomics [Tartu, Estonia], University of Tartu, Robertson Centre for Biostatistics, University of Glasgow, Department of Epidemiology, Erasmus University Medical Center, Rotterdam, Erasmus University Medical Center [Rotterdam] (Erasmus MC), Uppsala University, Brigham & Women’s Hospital [Boston] (BWH), University of Maryland School of Medicine, University of Maryland System, School of Science and Engineering (Reykjavik University), Carver College of Medicine, University of Iowa, Geisinger Health System [Danville, PA, USA], Durrer Center for Cardiogenetic Research, ICIN-Netherlands Heart Institute, Utrecht, Stanford School of Medicine [Stanford], Stanford Medicine, Stanford University-Stanford University, Stanford Cardiovascular Institute, Uppsala Universitet [Uppsala], Leiden University Medical Center (LUMC), Einthoven Laboratory for Experimental Vascular Medicine (ELEVM - LEIDEN), Department of Public Health and Primary Care, University of Cambridge [UK] (CAM), Rigshospitalet [Copenhagen], Copenhagen University Hospital, Glenfield Hospital, University Hospitals Leicester, MRC Epidemiology Unit, University of Cambridge [UK] (CAM)-Institute of Metabolic Science, Big Data Institute, University of Oxford [Oxford], University of Iowa [Iowa City], The Wellcome Trust Centre for Human Genetics [Oxford], Synlab Academy, Synlab Holding Deutschland GmbH, Mannheim, Medical University Graz, Skane University Hospital [Malmo], Vanderbilt University School of Medicine [Nashville], University of Edinburgh, Université médicale de Vienne, Autriche, National Institute for Health and Welfare [Helsinki], University of Turku, Birmingham Women's and Children's NHS Foundation Trust, Kaiser Permanente, Harbor UCLA Medical Center [Torrance, Ca.], Los Angeles Biomedical Research Institute (LA BioMed), University Medical Center [Utrecht], University of Pittsburgh (PITT), Pennsylvania Commonwealth System of Higher Education (PCSHE), Seattle Epidemiologic Research and Information Center [Seattle], Institute of Cardiovascular and Medical Sciences [Glasgow], University of Glasgow, Department of Cardiology, Södersjukhuset, Stockholm, Estonian Genome and Medicine, Landspitali National University Hospital of Iceland, University of Iceland [Reykjavik], Aalborg University [Denmark] (AAU), Institut de Recherches SERVIER (IRS), Interfaculty Institute for Genetics and Functional Genomics, Ernst-Moritz-Arndt-Universität Greifswald, GlaxoSmithKline, Glaxo Smith Kline, Northeastern Ohio Medical University (NEOMED), Centre d'investigation clinique plurithématique Pierre Drouin [Nancy] (CIC-P), Centre d'investigation clinique [Nancy] (CIC), Université de Lorraine (UL)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM), Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Cardiovascular and Renal Clinical Trialists [Vandoeuvre-les-Nancy] (INI-CRCT), Institut Lorrain du Coeur et des Vaisseaux Louis Mathieu [Nancy], French-Clinical Research Infrastructure Network - F-CRIN [Paris] (Cardiovascular & Renal Clinical Trialists - CRCT ), MRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, British Heart Foundation Glasgow Cardiovascular Research Centre (BHF GCRC), University of Glasgow-NHS Greater Glasgow and Clyde, Department of Cardiovascular Sciences [Leicester], University of Leicester, Queensland Brain Institute, Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA, University of Dundee, National Heart and Lung Institute [London] (NHLI), Imperial College London-Royal Brompton and Harefield NHS Foundation Trust, Atherosclerosis Risk in Communities Study (ARIC)The Atherosclerosis Risk in Communities Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts N01-HC-55015, N01-HC- 55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC55021, N01-HC-55022, R01HL087641, R01HL59367, R01HL086694 and RC2 HL102419, National Human Genome Research Institute contract U01HG004402, and National Institutes of Health contract HHSN268200625226C. The authors thank the staff and participants of the ARIC study for their important contributions. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. A systems BIOlogy Study to TAilored Treatment in Chronic Heart Failure (BIOSTAT- CHF)This project was funded by a grant from the European Commission (FP7‐242209‐ BIOSTAT‐CHF, EudraCT 2010–020808–29). Cardiovascular Health Study (CHS) This CHS research was supported by NHLBI contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, HHSN268200960009C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086, and NHLBI grants U01HL080295, R01HL087652, R01HL105756, R01HL103612, R01HL120393, and U01HL130114 with additional contribution from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided through R01AG023629 from the National Institute on Aging (NIA). A full list of principal CHS investigators and institutions can be found at CHS-NHLBI.org. The provision of genotyping data was supported in part by the National Center for Advancing Translational Sciences, CTSI grant UL1TR001881, and the National Institute of Diabetes and Digestive and Kidney Disease Diabetes Research Center (DRC) grant DK063491 to the Southern California Diabetes Endocrinology Research Center. deCODE Heart Failure Study (deCODE) We at deCODE thank the women and men of Iceland that have participated in our studies and our colleagues that contributed to data collection and processing. DiscovEHR We acknowledge and thank all participants in Geisinger’s MyCode Community Health Initiative for their support and permission to use their health and genomic information in the DiscovEHR collaboration. This work was supported by the Regeneron Genetics Center and Geisinger. Estonian Genome Center at the University of Tartu (EGCUT) This study was supported by Estonian Research Council Grant IUT20-60, EU, H2020 grant 692145, European Union through the European Regional Development Fund (Project No. 2014-2020.4.01.15-0012) GENTRANSMED. Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) The EPHESUS was supported by Pfizer, Inc. The European Prospective Investigation of Cancer, Norfolk study (EPIC-Norfolk) The EPIC-Norfolk Study is supported by programme grants from the Medical Research Council UK (G1000143) and Cancer Research UK (C864/A14136) and with additional support from the European Union, Stroke Association, British Heart Foundation, Research into Ageing, Department of Health, The Wellcome Trust and the Food Standards Agency. NJW and CL also acknowledge support from the Medical Research Council, UK (MC_UU_12015/1, MC_PC_13048). We thank all EPIC participants and staff for their contribution to the study, and thank staff from the Technical, Field Epidemiology and Data Functional Group Teams of the Medical Research Council Epidemiology Unit in Cambridge, UK, for carrying out sample preparation, DNA provision and quality control, genotyping and data handling work. Framingham Heart Study (FHS) This work was conducted using data and resources from the Framingham Heart Study (FHS) of the National Heart Lung and Blood Institute and Boston University School of Medicine. The study was supported by the National Heart, Lung and Blood Institute’s Framingham Heart Study (Contract No. N01-HC-25195 and HHSN268201500001I) and its contract with Affymetrix, Inc for genotyping services (Contract No.N02-HL-6-4278). The work was also supported by R01 HL093328, R01 HL105993, and R01 HL71039 (PI: Ramachandran). FINRISK V.S. has been supported by the Finnish Foundation for Cardiovascular Research. Genetics of Diabetes Audit and Research Tayside Scotland GoDARTS) The Wellcome Trust United Kingdom Type 2 Diabetes Case Control Collection (supporting GoDARTS) was funded by the Wellcome Trust (072960/Z/03/Z, 084726/Z/08/Z, 084727/Z/08/Z, 085475/Z/08/Z, 085475/B/08/Z) and as part of the EU IMI-SUMMIT programme. We acknowledge the support of the Health Informatics Centre, University of Dundee, for managing and supplying the anonymized data and NHS Tayside, the original data owner. The Genetic Risk Assessment of Defibrillator Events (GRADE) NIH-NHLBI R01 HL77398 (Genetic Modulators of Sudden Death). S.L. is supported by NIH grant 1R01HL139731 and American Heart Association 18SFRN34250007. The LUdwigshafen RIsk and Cardiovascular Health (LURIC) study We extend our appreciation to the participants of the LURIC study, without their collaboration, this article would not have been written. We thank the LURIC study team who were either temporarily or permanently involved in patient recruitment as well as sample and data handling, in addition to the laboratory staff at the Ludwigshafen General Hospital and the Universities of Freiburg and Ulm, Germany. LURIC has received funding from the 7th Framework Program (RiskyCAD, grant agreement number 305739 and Atheroremo, grant agreement number 201668) of the European Union. Malmö Diet and Cancer Study (MDCS) J. Gustav Smith was supported by grants from the Swedish Heart-Lung Foundation (2016- 0134 and 2016-0315), the Swedish Research Council (2017-02554), the European Research Council (ERC-STG-2015-679242), the Crafoord Foundation, Skåne University Hospital, the Scania county, governmental funding of clinical research within the Swedish National Health Service, a generous donation from the Knut and Alice Wallenberg foundation to the Wallenberg Center for Molecular Medicine in Lund, and funding from the Swedish Research Council (Linnaeus grant Dnr 349-2006-237, Strategic Research Area Exodiab Dnr 2009-1039) and Swedish Foundation for Strategic Research (Dnr IRC15- 0067) to the Lund University Diabetes Center. The Malmo Diet and Cancer Study was made possible by grants from the Swedish Cancer Society, the Swedish Medical Research Council, the Swedish Dairy Association, and the Malmo city council. Penn Heart Failure Study (PHFS) The study was supported by NIH grants (NIH R01L088577 and NIH R01H105993). Prevention of REnal and Vascular ENd-stage Disease (PREVEND) The Prevention of Renal and Vascular Endstage Disease Study (PREVEND) genetics is supported by the Dutch Kidney Foundation (Grant E033), the EU project grant GENECURE (FP-6 LSHM CT 2006 037697), the National Institutes of Health (grant LM010098), the Netherlands organisation for health research and development (NWO VENI grant 916.761.70), and the Dutch Inter University Cardiology Institute Netherlands (ICIN). Niek Verweij was supported by NWO VENI grant 016.186.125. PROspective Study of Pravastatin in the Elderly at Risk for vascular disease (PROSPER)The PROSPER study was supported by an investigator-initiated grant obtained from Bristol- Myers Squibb. Support for genotyping was provided by the seventh framework program of the European commission (grant 223004) and by the Netherlands Genomics Initiative (Netherlands Consortium for Healthy Aging grant 050-060-810). J.W.J. is an Established Clinical Investigator of the Netherlands Heart Foundation (grant 2001 D 032). Study of Health in Pomerania (SHIP) SHIP is part of the Community Medicine Research net of the University of Greifswald, Germany, which is funded by the Federal Ministry of Education and Research (grants no. 01ZZ9603, 01ZZ0103, and 01ZZ0403), the Ministry of Cultural Affairs as well as the Social Ministry of the Federal State of Mecklenburg-West Pomerania, and the network ‘Greifswald Approach to Individualized Medicine (GANI_MED)’ funded by the Federal Ministry of Education and Research (grant 03IS2061A). Genome-wide data have been supported by the Federal Ministry of Education and Research (grant no. 03ZIK012) and a joint grant from Siemens Healthineers, Erlangen, Germany and the Federal State of Mecklenburg- West Pomerania. The University of Greifswald is a member of the Caché Campus program of the InterSystems GmbH. Stabilization of Plaque using Darapladib-Thrombolysis in Myocardial Infarction 52 (SOLID)SOLID-TIMI 52 was funded by GlaxoSmithKline. TwinGene (TwinGene) TwinGene received funding from the Swedish Research Council (M-2005-1112), GenomEUtwin (EU/QLRT-2001-01254, QLG2-CT-2002-01254), NIH DK U01-066134, The Swedish Foundation for Strategic Research (SSF) and the Heart and Lung foundation no. 20070481. TwinGene is part of the Swedish Twin Registry which is managed by Karolinska Institutet and receives funding through the Swedish Research Council (2017–00641). UK Biobank (UKBiobank) This research has been conducted using the UK Biobank Resource under Application Number 15422. This work was supported in part by grants to R.T.L. from the EU/EFPIA Innovative Medicines Initiative 2 Joint Undertaking BigData@Heart grant no. 116074, MRC Proximity to Discovery Award Scheme, the American Heart Association Institute for Precision Mecidine, Pfizer Ltd, the University College London British Heart Foundation Research Accelerator (AA/18/6/34223), and was supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. A. H. is supported by the British Heart Foundation Cardiovascular Biomedicine PhD studentship. R.T.L is supported by a UK Research and Innovation Rutherford Fellowship and was previously supported by a National Institutes of Health Research Clinical Lectureship. Uppsala Longitudinal Study of Adult Men (ULSAM) J.Ä. is supported by the Swedish Research Council and the Swedish Heart Lung foundation. C.M.L is supported by the Li Ka Shing Foundation, WT-SSI/John Fell funds and by the NIHR Biomedical Research Centre, Oxford, by Widenlife and NIH (5P50HD028138- 27). Women’s Genome Health Study (WGHS) The WGHS is supported by the National Heart, Lung, and Blood Institute (HL043851 and HL080467, HL099355) and the National Cancer Institute (CA047988 and UM1CA182913), with collaborative scientific support and funding for genotyping provided by Amgen., Epidemiology, Internal Medicine, Læknadeild (HÍ), Faculty of Medicine (UI), Verkfræði- og náttúruvísindasvið (HÍ), School of Engineering and Natural Sciences (UI), Heilbrigðisvísindasvið (HÍ), School of Health Sciences (UI), Háskóli Íslands, and University of Iceland
Subjects: 0301 basic medicine, Dánartíðni, Epidemiology, LOCI, 45/43, General Physics and Astronomy, Muscle Proteins, Genome-wide association study, Disease, Coronary Artery Disease, 030204 cardiovascular system & hematology, Bioinformatics, Genome-wide association studies, DISEASE, Ventricular Function, Left, Coronary artery disease, 0302 clinical medicine, Risk Factors, Atrial Fibrillation, IMPUTATION, Medicine, Blóðrásarsjúkdómar, 692/308/174, lcsh:Science, 2. Zero hunger, RISK, Multidisciplinary, Microfilament Proteins, article, Atrial fibrillation, Mendelian Randomization Analysis, CATALOG, 3. Good health, OBESITY, Erfðarannsóknir, Cardiomyopathies, Medical Genetics, Cyclin-Dependent Kinase Inhibitor p21, Science, 631/208/205/2138, Heart failure, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, 631/443/592/2727, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, RESOURCE, Humans, Mortality, METAANALYSIS, Genetic association, Medicinsk genetik, Adaptor Proteins, Signal Transducing, Heart Failure, HYPERTENSION, business.industry, Case-control study, Klinisk medicin, 692/699/75/230, General Chemistry, Cardiovascular genetics, medicine.disease, R1, 030104 developmental biology, Case-Control Studies, lcsh:Q, Morbidity, Clinical Medicine, business, Apoptosis Regulatory Proteins, Carrier Proteins, Genome-Wide Association Study
Abstract: Publisher's version (útgefin grein), Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies., We acknowledge the contribution from the EchoGen Consortium.
Published: 2020

34. Social support at work and the risk of myocardial infarction and stroke in women and men

Author: Andre-Petersson, Lena, Engstrom, Gunnar, Hedblad, Bo, Janzon, Lars, and Rosvall, Maria
Subjects: Heart attack -- Causes of, Job stress -- Health aspects, Social networks -- Influence, Stroke (Disease) -- Causes of, Health, Social sciences
Abstract: It has been proposed that lack of social support in a work place characterized by high levels of stress, may increase the likelihood of future cardiovascular disease. The aim of this study was to analyze the prospective impact of social support at work in combination with self-reported work stress on incidence of myocardial infarction (MI) and stroke in a cohort of 4707 women (mean age: 54.2 years) and 3063 men (mean age: 55.5 years) in Maim6, Sweden. The results are based on selfreports of work-related stress and social support collected at baseline examinations between the years 1992 and 1996. Work-stress was operationalized according to the Karasek job strain model. Data on incidence of MI and stroke were obtained from national and regional registers. At the end of follow-up, December 3 I, 2001, 38 women had experienced an MI and 53 had had a stroke. Corresponding figures for men were 114 Mls and 81 strokes. The first finding was that social support at work was an independent predictor of an MI and stroke among women. The second finding was that there was no evidence to support the iso-strain model. The third finding was that low levels of social support at work together with a passive work situation indicated an increased risk of a future cardiovascular outcome (MI or stroke) during follow-up in the female group. In men, no association was found between any psychosocial work conditions and incidence of MI or stroke during the same follow-up period. Keywords: Myocardial infarction; Stroke; Social support at work: Job strain; Psychological demands; Decision latitude; Sweden
Published: 2007

35. Measures of lung function and their relationship with advanced glycation end-products

Author: Zaigham, Suneela, Persson, Margaretha, Jujic, Amra, Frantz, Sophia, Borne, Yan, Malinovschi, Andrei, Wollmer, Per, Engstrom, Gunnar, Zaigham, Suneela, Persson, Margaretha, Jujic, Amra, Frantz, Sophia, Borne, Yan, Malinovschi, Andrei, Wollmer, Per, and Engstrom, Gunnar
Abstract: Background: Advanced glycation end-products (AGEs) have been implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). However, the association between AGE accumulation in the skin measured by skin autofluorescence (SAF) and lung function in healthy subjects has not been explored in detail. We use a population-based study of 50-64-year-olds to assess spirometry, diffusing capacity of the lung for carbon monoxide (D-LCO) and impulse oscillometry (IOS) in relation to SAF. Methods: Participants with information on SAF, lung function and potential confounding variables were included from the Swedish Cardiopulmonary Bioimage Study (SCAPIS) cohort (spirometry, n=4111; D-LCO, n=3889; IOS, n=3970). Linear regression was used to assess changes in lung function (as measured by spirometry (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC), D-LCO and IOS (resistance measured at 5 (R-5) and 20 Hz (R-20), R-5-R-20, area of reactance, reactance measured at 5 Hz (X-5), and resonant frequency)) by a 1-SD increase in SAF. Results: FEV1, FVC and D-LCO were significantly and inversely associated with SAF after adjustment for potential confounding factors (per 1-SD increase in SAF: FEV1 -0.03 L (95% CI -0.04 - -0.02 L), p<0.001; FVC -0.03 L (95% CI -0.05 - -0.02 L), p<0.001; D-LCO -0.07 mmol.min(-1).kPa(-1) (95% CI -0.11 -0.03 mmol.min(-1).kPa(-1)), p<0.001). This association was also found in nonsmokers and in non-COPD subjects. Pulmonary reactance (X5) but not pulmonary resistance (R-5, R-20 and R-5-R-20) was significantly associated with SAF (per 1-SD increase in SAF: X-5 -0.001 kPa.L-1.s (95% CI -0.003-0.00 kPa.L-1.s), p=0.042), which was mirrored in non-COPD patients but not in current nonsmokers. Conclusions: AGE accumulation, as measured by SAF, is significantly associated with lung function decrements indicative of changes in the lung parenchyma
Published: 2020
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36. The associations of major foods and fibre with risks of ischaemic and haemorrhagic stroke : a prospective study of 418 329 participants in the EPIC cohort across nine European countries

Author: Tong, Tammy Y. N., Appleby, Paul N., Key, Timothy J., Dahm, Christina C., Overvad, Kim, Olsen, Anja, Tjonneland, Anne, Katzke, Verena, Kuhn, Tilman, Boeing, Heiner, Karakatsani, Anna, Peppa, Eleni, Trichopoulou, Antonia, Weiderpass, Elisabete, Masala, Giovanna, Grioni, Sara, Panico, Salvatore, Tumino, Rosario, Boer, Jolanda M. A., Verschuren, W. M. Monique, Quiros, J. Ramon, Agudo, Antonio, Rodriguez-Barranco, Miguel, Imaz, Liher, Chirlaque, Maria-Dolores, Moreno-Iribas, Conchi, Engstrom, Gunnar, Sonestedt, Emily, Lind, Marcus, Otten, Julia, Khaw, Kay-Tee, Aune, Dagfinn, Riboli, Elio, Wareham, Nicholas J., Imamura, Fumiaki, Forouhi, Nita G., di Angelantonio, Emanuele, Wood, Angela M., Butterworth, Adam S., Perez-Cornago, Aurora, Tong, Tammy Y. N., Appleby, Paul N., Key, Timothy J., Dahm, Christina C., Overvad, Kim, Olsen, Anja, Tjonneland, Anne, Katzke, Verena, Kuhn, Tilman, Boeing, Heiner, Karakatsani, Anna, Peppa, Eleni, Trichopoulou, Antonia, Weiderpass, Elisabete, Masala, Giovanna, Grioni, Sara, Panico, Salvatore, Tumino, Rosario, Boer, Jolanda M. A., Verschuren, W. M. Monique, Quiros, J. Ramon, Agudo, Antonio, Rodriguez-Barranco, Miguel, Imaz, Liher, Chirlaque, Maria-Dolores, Moreno-Iribas, Conchi, Engstrom, Gunnar, Sonestedt, Emily, Lind, Marcus, Otten, Julia, Khaw, Kay-Tee, Aune, Dagfinn, Riboli, Elio, Wareham, Nicholas J., Imamura, Fumiaki, Forouhi, Nita G., di Angelantonio, Emanuele, Wood, Angela M., Butterworth, Adam S., and Perez-Cornago, Aurora
Abstract: Aim: To investigate the associations between major foods and dietary fibre with subtypes of stroke in a large prospective cohort. Methods and results: We analysed data on 418 329 men and women from nine European countries, with an average of 12.7 years of follow-up. Diet was assessed using validated country-specific questionnaires which asked about habitual intake over the past year, calibrated using 24-h recalls. Multivariable-adjusted Cox regressions were used to estimate hazard ratios (HRs) for ischaemic and haemorrhagic stroke associated with consumption of red and processed meat, poultry, fish, dairy foods, eggs, cereals, fruit and vegetables, legumes, nuts and seeds, and dietary fibre. For ischaemic stroke (4281 cases), lower risks were observed with higher consumption of fruit and vegetables combined (HR; 95% CI per 200 g/day higher intake, 0.87; 0.82–0.93, P-trend < 0.001), dietary fibre (per 10 g/day, 0.77; 0.69–0.86, P-trend < 0.001), milk (per 200 g/day, 0.95; 0.91–0.99, P-trend = 0.02), yogurt (per 100 g/day, 0.91; 0.85–0.97, P-trend = 0.004), and cheese (per 30 g/day, 0.88; 0.81–0.97, P-trend = 0.008), while higher risk was observed with higher red meat consumption which attenuated when adjusted for the other statistically significant foods (per 50 g/day, 1.07; 0.96–1.20, P-trend = 0.20). For haemorrhagic stroke (1430 cases), higher risk was associated with higher egg consumption (per 20 g/day, 1.25; 1.09–1.43, P-trend = 0.002). Conclusion: Risk of ischaemic stroke was inversely associated with consumption of fruit and vegetables, dietary fibre, and dairy foods, while risk of haemorrhagic stroke was positively associated with egg consumption. The apparent differences in the associations highlight the importance of examining ischaemic and haemorrhagic stroke subtypes separately.
Published: 2020
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37. Assessment of Global Lung Function Initiative (GLI) reference equations for diffusing capacity in relation to respiratory burden in the Swedish CArdioPulmonary bioImage Study (SCAPIS)

Author: Malinovschi, Andrei, Zhou, Xingwu, Bake, Bjorn, Bergstrom, Goran, Blomberg, Anders, Brisman, Jonas, Caidahl, Kenneth, Engstrom, Gunnar, Eriksson, Maria J., Frølich, Andreas, Janson, Christer, Jansson, Kjell, Vikgren, Jenny, Lindberg, Anne, Linder, Robert, Mannila, Maria, Persson, Hans L., Skold, C. Magnus, Toren, Kjell, Ostgren, Carl J., Wollmer, Per, Engvall, Jan E., Malinovschi, Andrei, Zhou, Xingwu, Bake, Bjorn, Bergstrom, Goran, Blomberg, Anders, Brisman, Jonas, Caidahl, Kenneth, Engstrom, Gunnar, Eriksson, Maria J., Frølich, Andreas, Janson, Christer, Jansson, Kjell, Vikgren, Jenny, Lindberg, Anne, Linder, Robert, Mannila, Maria, Persson, Hans L., Skold, C. Magnus, Toren, Kjell, Ostgren, Carl J., Wollmer, Per, and Engvall, Jan E.
Abstract: The Global Lung Function Initiative (GLI) has recently published international reference values for diffusing capacity of the lung for carbon monoxide (DLCO). Lower limit of normal (LLN), i.e. the 5th percentile, usually defines impaired D-LCO. We examined if the GLI LLN for D-LCO differs from the LLN in a Swedish population of healthy, never-smoking individuals and how any such differences affect identification of subjects with respiratory burden. Spirometry, D-LCO, chest high-resolution computed tomography (HRCT) and questionnaires were obtained from the first 15 040 participants, aged 50-64 years, of the Swedish CArdioPulmonary bioImage Study (SCAPIS). Both GLI reference values and the lambda-mu-sigma (LMS) method were used to define the LLN in asymptomatic never-smokers without respiratory disease (n=4903, of which 2329 were women). Both the median and LLN for D-LCO from SCAPIS were above the median and LLN from the GLI (p<0.05). The prevalence of D-LCO GLI LLN but GLI LLN but GLI LLN and >SCAPIS LLN). No differences were found with regard to physician-diagnosed asthma. The GLI LLN for D-LCO is lower than the estimated LLN in healthy, never-smoking, middle-aged Swedish adults. Individuals with D-LCO above the GLI LLN but below the SCAPIS LLN had, to a larger extent, an increased respiratory burden. This suggests clinical implications for choosing an adequate LLN for studied populations.
Published: 2020
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38. The associations of major foods and fibre with risks of ischaemic and haemorrhagic stroke:a prospective study of 418 329 participants in the EPIC cohort across nine European countries

Author: Tong, Tammy Y. N., Appleby, Paul N., Key, Timothy J., Dahm, Christina C., Overvad, Kim, Olsen, Anja, Tjønneland, Anne, Katzke, Verena, Kuhn, Tilman, Boeing, Heiner, Karakatsani, Anna, Peppa, Eleni, Trichopoulou, Antonia, Weiderpass, Elisabete, Masala, Giovanna, Grioni, Sara, Panico, Salvatore, Tumino, Rosario, Boer, Jolanda M. A., Verschuren, W. M. Monique, Quiros, J. Ramon, Agudo, Antonio, Rodriguez-Barranco, Miguel, Imaz, Liher, Chirlaque, Maria-Dolores, Moreno-Iribas, Conchi, Engstrom, Gunnar, Sonestedt, Emily, Lind, Marcus, Otten, Julia, Khaw, Kay-Tee, Aune, Dagfinn, Riboli, Elio, Wareham, Nicholas J., Imamura, Fumiaki, Forouhi, Nita G., di Angelantonio, Emanuele, Wood, Angela M., Butterworth, Adam S., Perez-Cornago, Aurora, Tong, Tammy Y. N., Appleby, Paul N., Key, Timothy J., Dahm, Christina C., Overvad, Kim, Olsen, Anja, Tjønneland, Anne, Katzke, Verena, Kuhn, Tilman, Boeing, Heiner, Karakatsani, Anna, Peppa, Eleni, Trichopoulou, Antonia, Weiderpass, Elisabete, Masala, Giovanna, Grioni, Sara, Panico, Salvatore, Tumino, Rosario, Boer, Jolanda M. A., Verschuren, W. M. Monique, Quiros, J. Ramon, Agudo, Antonio, Rodriguez-Barranco, Miguel, Imaz, Liher, Chirlaque, Maria-Dolores, Moreno-Iribas, Conchi, Engstrom, Gunnar, Sonestedt, Emily, Lind, Marcus, Otten, Julia, Khaw, Kay-Tee, Aune, Dagfinn, Riboli, Elio, Wareham, Nicholas J., Imamura, Fumiaki, Forouhi, Nita G., di Angelantonio, Emanuele, Wood, Angela M., Butterworth, Adam S., and Perez-Cornago, Aurora
Abstract: Aim To investigate the associations between major foods and dietary fibre with subtypes of stroke in a large prospective cohort.Methods and results We analysed data on 418 329 men and women from nine European countries, with an average of 12.7years of follow-up. Diet was assessed using validated country-specific questionnaires which asked about habitual intake over the past year, calibrated using 24-h recalls. Multivariable-adjusted Cox regressions were used to estimate hazard ratios (HRs) for ischaemic and haemorrhagic stroke associated with consumption of red and processed meat, poultry, fish, dairy foods, eggs, cereals, fruit and vegetables, legumes, nuts and seeds, and dietary fibre. For ischaemic stroke (4281 cases), lower risks were observed with higher consumption of fruit and vegetables combined (HR; 95% CI per 200g/day higher intake, 0.87; 0.82-0.93, P-trendConclusion Risk of ischaemic stroke was inversely associated with consumption of fruit and vegetables, dietary fibre, and dairy foods, while risk of haemorrhagic stroke was positively associated with egg consumption. The apparent differences in the associations highlight the importance of examining ischaemic and haemorrhagic stroke subtypes separately.
Published: 2020

39. Weight gain and blood pressure

Author: Sundstrom, Johan, Lind, Lars, Lampa, Erik, Angeras, Oskar, Bachus, Erasmus, Bergstrom, Goran, Carlberg, Bo, Engstrom, Gunnar, Engvall, Jan, Eriksson, Mats, Gigante, Bruna, Hagstrom, Emil, Hjelmgren, Ola, Jansson, Jan-Hakan, Jernberg, Tomas, Mannila, Maria, Nyström, Fredrik H, Oldgren, Jonas, Persson, Margaretha, Sandstrom, Anette, Swahn, Eva, Soderberg, Stefan, Toren, Kjell, Östgren, Carl Johan, Rosengren, Annika, Sundstrom, Johan, Lind, Lars, Lampa, Erik, Angeras, Oskar, Bachus, Erasmus, Bergstrom, Goran, Carlberg, Bo, Engstrom, Gunnar, Engvall, Jan, Eriksson, Mats, Gigante, Bruna, Hagstrom, Emil, Hjelmgren, Ola, Jansson, Jan-Hakan, Jernberg, Tomas, Mannila, Maria, Nyström, Fredrik H, Oldgren, Jonas, Persson, Margaretha, Sandstrom, Anette, Swahn, Eva, Soderberg, Stefan, Toren, Kjell, Östgren, Carl Johan, and Rosengren, Annika
Abstract: Objective: Although the causality of the obesity--hypertension association is established, the potential for prevention is not. We hypothesized that weight gain between early adulthood and mid-life is associated with higher mid-life blood pressure. Methods: We investigated the hypothesis using a large contemporaneous population-based mid-life cohort of men and women aged 50-64 years. Recalled body weight at age 20 years was self-reported, and mid-life body weight and office blood pressures were measured in accordance with a detailed protocol. Results: On average, men had gained 14.9 (95% CI 14.6-15.2) kg of weight, and women 14.6 (95% CI 14.4-14.9) kg, between age 20 years and the mid-life examination, corresponding to 0.40 (95% CI 0.39-0.41) kg/year for men and women. Both weight at age 20 years and weight at the mid-life examination were associated with mid-life blood pressures. On average, a 10 kg weight increase between age 20 years and mid-life was associated with 2.2 (95% CI 0.9-3.5) mmHg higher systolic and 1.7 (95% CI 0.9-2.5) mmHg higher diastolic mid-life blood pressure in men, and 3.2 (2.5-4.0) mmHg higher systolic and 2.4 (1.9-2.9) mmHg higher diastolic mid-life blood pressure in women. Mid-life weight was more closely associated than weight at age 20 years with mid-life blood pressure. For a given mid-life weight, blood pressure was higher in persons with higher weight gain from age 20 years. Conclusion: In sum, weight gain between early adulthood and mid-life was associated with higher mid-life blood pressure. The magnitude of the association indicates a potentially great public health impact of strategies to prevent weight gain throughout adulthood., Funding Agencies|Swedish Heart-Lung FoundationSwedish Heart-Lung Foundation [2019-0012]; Knut and Alice Wallenberg FoundationKnut & Alice Wallenberg Foundation [2014-0047]; Swedish Research CouncilSwedish Research Council [822-2013-2000]; VINNOVA (Swedens Innovation agency)Vinnova [2012-04476]; University of Gothenburg; Sahlgrenska University Hospital; Karolinska Institutet and Karolinska University Hospital; Linkoping University and University Hospital; Lund University; Ska ne University Hospital; Umea University and University Hospital; Uppsala University and University Hospital; AFA Insurance [160334]; Swedish government [ALF-GBG-718851, ALF-VLL-548791, ALFLIO-700841]
Published: 2020
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40. Meta-analysis of genome-wide association studies confirms a susceptibility locus for knee osteoarthritis on chromosome 7q22

Author: Evangelou, Evangelos, Valdes, Ana M, Kerkhof, Hanneke J M, Styrkarsdottir, Unnur, Zhu, YanYan, Meulenbelt, Ingrid, Lories, Rik J, Karassa, Fotini B, Tylzanowski, Przemko, Bos, Steffan D, Akune, Toru, Arden, Nigel K, Carr, Andrew, Chapman, Kay, Cupples, L Adrienne, Dai, Jin, Deloukas, Panos, Doherty, Michael, Doherty, Sally, Engstrom, Gunnar, Gonzalez, Antonio, Halldorsson, Bjarni V, Hammond, Christina L, Hart, Deborah J, Helgadottir, Hafdis, Hofman, Albert, Ikegawa, Shiro, Ingvarsson, Thorvaldur, Jiang, Qing, Jonsson, Helgi, Kaprio, Jaakko, Kawaguchi, Hiroshi, Kisand, Kalle, Kloppenburg, Margreet, Kujala, Urho M, Lohmander, L Stefan, Loughlin, John, Luyten, Frank P, Mabuchi, Akihiko, McCaskie, Andrew, Nakajima, Masahiro, Nilsson, Peter M, Nishida, Nao, Ollier, William E R, Panoutsopoulou, Kalliope, van de Putte, Tom, Ralston, Stuart H, Rivadeneira, Fernado, Saarela, Janna, Schulte-Merker, Stefan, Shi, Dongquan, Slagboom, P Eline, Sudo, Akihiro, Tamm, Agu, Tamm, Ann, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tsezou, Aspasia, Wallis, Gillian A, Wilkinson, J Mark, Yoshimura, Noriko, Zeggini, Eleftheria, Zhai, Guangju, Zhang, Feng, Jonsdottir, Ingileif, Uitterlinden, Andre G, Felson, David T, van Meurs, Joyce B, Stefansson, Kari, Ioannidis, John P A, and Spector, Timothy D
Published: 2011
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41. Population-based study of lung function and incidence of heart failure hospitalisations

Author: Engstrom, Gunnar, Melander, Olle, and Hedblad, Bo
Subjects: Pulmonary function tests -- Demographic aspects, Pulmonary function tests -- Research, Heart failure -- Distribution, Heart failure -- Demographic aspects, Heart failure -- Risk factors, Heart failure -- Research, Company distribution practices, Health
Published: 2010

42. BP variability and cardiovascular autonomic function in relation to forced expiratory volume: a population-based study

Author: Engstrom, Gunnar, de Verdier, Maria Gerhardsson, Dahlback, Magnus, Janson, Christer, and Lind, Lars
Subjects: Forced expiratory volume -- Research, Forced expiratory volume -- Physiological aspects, Blood pressure -- Research, Blood pressure -- Physiological aspects, Cardiovascular diseases -- Risk factors, Lung diseases, Obstructive -- Research, Lung diseases, Obstructive -- Physiological aspects, Health
Published: 2009

43. Blood cadmium levels and incident cardiovascular events during follow-up in a population-based cohort of Swedish adults: the Malmo Diet and Cancer Study

Author: Barregard, Lars, Sallsten, Gerd, Fagerberg, Bjorn, Borne, Yan, Persson, Margaretha, Hedblad, Bo, and Engstrom, Gunnar
Subjects: Cadmium -- Research -- Influence, Cardiovascular diseases -- Research -- Risk factors -- Causes of, Adults -- Research -- Health aspects, Environmental issues, Health
Abstract: BACKGROUND: Cadmium exposure may increase the risk of cardiovascular disease. The only published longitudinal study on cadmium and incident cardiovascular disease was performed in American Indians with relatively high cadmium exposure. OBJECTIVES: Our aim was to examine the association between blood cadmium at baseline and incident cardiovascular events in a population-based study of Swedish men and women with cadmium levels similar to those of most European and U.S. populations. METHODS: A Swedish population-based cohort (n = 6,103, age 46-67 years) was recruited between 1991 and 1994. After we excluded those with missing data on smoking, 4,819 participants remained. Acute coronary events, other major cardiac events, stroke, and cardiovascular mortality were followed until 2010. Associations with blood cadmium (estimated from cadmium in erythrocytes) were analyzed using Cox proportional hazards regression including potential confounders and important cardiovascular risk factors. RESULTS: Hazard ratios for all cardiovascular end points were consistently increased for participants in the 4th blood cadmium quartile (median, 0.99 [micro]g/L). In models that also included sex, smoking, waist circumference, education, physical activity, alcohol intake, serum triglycerides, HbA1c, and C-reactive protein, the hazard ratios comparing the highest and lowest quartiles of exposure were 1.8 (95% CI: 1.2, 2.7) for acute coronary events, and 1.9 (1.3, 2.9) for stroke. Hazard ratios in never-smokers were consistent with these estimates. CONCLUSIONS: Blood cadmium in the highest quartile was associated with incident cardiovascular disease and mortality in our population-based samples of Swedish adults. The consistent results among never-smokers are important because smoking is a strong confounder. Our findings suggest that measures to reduce cadmium exposures are warranted, even in populations without unusual sources of exposure. http://dx.doi.org/10.1289/ehp.1509735, Introduction Exposure to the toxic metal cadmium (Cd) has adverse health effects at occupational or high-level environmental exposure. The most well-known toxic effects are kidney damage and osteoporosis/osteomalacia (Akesson et [...]
Published: 2016
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44. Cardiovascular risk factors are 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, Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), Kaptoge, Stephen [0000-0002-1155-4872], Pennells, Lisa [0000-0002-8594-3061], Burgess, Stephen [0000-0001-5365-8760], Bell, Steven [0000-0001-6774-3149], Sweeting, Michael [0000-0003-0980-8965], Wood, Angela [0000-0002-7937-304X], Butterworth, Adam [0000-0002-6915-9015], Danesh, John [0000-0003-1158-6791], Di Angelantonio, Emanuele [0000-0001-8776-6719], Apollo - University of Cambridge Repository, Epidemiology, ACS - Diabetes & metabolism, APH - Health Behaviors & Chronic Diseases, Epidemiology and Data Science, and ACS - Heart failure & arrhythmias
Subjects: Male, Outcome Assessment, ALCOHOL-CONSUMPTION, Coronary Disease, 030204 cardiovascular system & hematology, Body Mass Index, 0302 clinical medicine, Risk Factors, Outcome Assessment, Health Care, Cardiac and Cardiovascular Systems, 030212 general & internal medicine, Prospective Studies, DEEP-VEIN THROMBOSIS, Prospective cohort study, Original Investigation, Venous Thrombosis, education.field_of_study, Kardiologi, Hazard ratio, INDIVIDUAL-PARTICIPANT DATA, Venous Thromboembolism, Middle Aged, Biobank, 3. Good health, Pulmonary embolism, ddc, Cardiovascular Diseases, OBESITY, Female, SMOKING, Cardiology and Cardiovascular Medicine, Cohort study, Adult, medicine.medical_specialty, PULMONARY-EMBOLISM, Population, 03 medical and health sciences, Internal medicine, medicine, Journal Article, Diabetes Mellitus, Online First, Life Science, Humans, CORONARY-HEART-DISEASE, ddc:610, Obesity, Pulmonary Embolism, Smoking, United Kingdom, Risk factor, education, METAANALYSIS, VLAG, Global Nutrition, Wereldvoeding, business.industry, Research, DIABETES-MELLITUS, medicine.disease, Health Care, LIPOPROTEIN, business, Body mass index
Abstract: Key Points Question To what extent are established cardiovascular risk factors associated with risk of venous thromboembolism (VTE)? Findings In this analysis of individual participant data from the Emerging Risk Factors Collaboration and the UK Biobank including 1.1 million participants, among a panel of several established cardiovascular risk factors, older age, smoking, and greater adiposity were consistently associated with higher VTE risk. Meaning There is overlap in at least some of the major population determinants of important venous and arterial thrombotic diseases., This analysis of data from the Emerging Risk Factors Collaboration and the UK Biobank estimates the associations of major cardiovascular risk factors with venous thromboembolism., 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; 731 728 participants; 75 cohorts; years of baseline surveys, February 1960 to June 2008; latest date of follow-up, December 2015) and the UK Biobank (421 537 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 [CHD], 25 131) 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 731 728 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 421 537 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 thrombosis in UK Biobank (except adiposity was more strongly associated with pulmonary embolism) and similar HRs for unprovoked vs provoked VTE. Apart from adiposity, these risk factors were less strongly associated with VTE than CHD. There were inconsistent associations of VTEs with diabetes and blood pressure across ERFC and UK Biobank, and there was limited ability to study lipid and inflammation markers. Conclusions and Relevance Older age, smoking, and adiposity were consistently associated with higher VTE risk.
Published: 2019

45. The association of body mass index, weight gain and central obesity with activity-related breathlessness : the Swedish Cardiopulmonary Bioimage Study

Author: Ekström, Magnus Par, Blomberg, Anders, Bergstrom, Goran, Brandberg, John, Caidahl, Kenneth, Engstrom, Gunnar, Engvall, Jan, Eriksson, Maria, Gransbo, Klas, Hansen, Tomas, Jernberg, Tomas, Nilsson, Lars, Nilsson, Ulf, Olin, Anna-Carin, Persson, Lennart, Rosengren, Annika, Sandelin, Martin, Skold, Magnus, Sundstrom, Johan, Swahn, Eva, Soderberg, Stefan, Tanash, Hanan A., Toren, Kjell, Ostgren, Carl Johan, Lindberg, Eva, Ekström, Magnus Par, Blomberg, Anders, Bergstrom, Goran, Brandberg, John, Caidahl, Kenneth, Engstrom, Gunnar, Engvall, Jan, Eriksson, Maria, Gransbo, Klas, Hansen, Tomas, Jernberg, Tomas, Nilsson, Lars, Nilsson, Ulf, Olin, Anna-Carin, Persson, Lennart, Rosengren, Annika, Sandelin, Martin, Skold, Magnus, Sundstrom, Johan, Swahn, Eva, Soderberg, Stefan, Tanash, Hanan A., Toren, Kjell, Ostgren, Carl Johan, and Lindberg, Eva
Abstract: Introduction Breathlessness is common in the population, especially in women and associated with adverse health outcomes. Obesity (body mass index (BMI) >30 kg/m2) is rapidly increasing globally and its impact on breathlessness is unclear. Methods This population-based study aimed primarily to evaluate the association of current BMI and self-reported change in BMI since age 20 with breathlessness (modified Research Council score ≥1) in the middle-aged population. Secondary aims were to evaluate factors that contribute to breathlessness in obesity, including the interaction with spirometric lung volume and sex. Results We included 13 437 individuals; mean age 57.5 years; 52.5% women; mean BMI 26.8 (SD 4.3); mean BMI increase since age 20 was 5.0 kg/m2; and 1283 (9.6%) reported breathlessness. Obesity was strongly associated with increased breathlessness, OR 3.54 (95% CI, 3.03 to 4.13) independent of age, sex, smoking, airflow obstruction, exercise level and the presence of comorbidities. The association between BMI and breathlessness was modified by lung volume; the increase in breathlessness prevalence with higher BMI was steeper for individuals with lower forced vital capacity (FVC). The higher breathlessness prevalence in obese women than men (27.4% vs 12.5%; p<0.001) was related to their lower FVC. Irrespective of current BMI and confounders, individuals who had increased in BMI since age 20 had more breathlessness. Conclusion Breathlessness is independently associated with obesity and with weight gain in adult life, and the association is stronger for individuals with lower lung volumes.
Published: 2019
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46. 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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47. 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, Sundström, 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., Jorgensen, 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, Njolstad, 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 R., 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, Tybjaerg-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, Moller, 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, Cook, Nancy, 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, Sundström, 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., Jorgensen, 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, Njolstad, 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 R., 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, Tybjaerg-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, Moller, 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, Cook, Nancy, and Geleijnse, Johanna M.
Abstract: Aims: There is debate about the optimum algorithm for cardiovascular disease (CVD) risk estimation. We conducted head-to-head comparisons of four algorithms recommended by primary prevention guidelines, before and after ‘recalibration’, a method that adapts risk algorithms to take account of differences in the risk characteristics of the populations being studied. Methods and results: Using individual-participant data on 360 737 participants without CVD at baseline in 86 prospective studies from 22 countries, we compared the Framingham risk score (FRS), Systematic COronary Risk Evaluation (SCORE), pooled cohort equations (PCE), and Reynolds risk score (RRS). We calculated measures of risk discrimination and calibration, and modelled clinical implications of initiating statin therapy in people judged to be at ‘high’ 10 year CVD risk. Original risk algorithms were recalibrated using the risk factor profile and CVD incidence of target populations. The four algorithms had similar risk discrimination. Before recalibration, FRS, SCORE, and PCE over-predicted CVD risk on average by 10%, 52%, and 41%, respectively, whereas RRS under-predicted by 10%. Original versions of algorithms classified 29–39% of individuals aged ≥40 years as high risk. By contrast, recalibration reduced this proportion to 22–24% for every algorithm. We estimated that to prevent one CVD event, it would be necessary to initiate statin therapy in 44–51 such individuals using original algorithms, in contrast to 37–39 individuals with recalibrated algorithms. Conclusion: Before recalibration, the clinical performance of four widely used CVD risk algorithms varied substantially. By contrast, simple recalibration nearly equalized their performance and improved modelled targeting of preventive action to clinical need.
Published: 2019
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48. Circulating high sensitivity C reactive protein concentrations and risk of lung cancer : nested case-control study within Lung Cancer Cohort Consortium

Author: Muller, David C., Larose, Tricia L., Hodge, Allison, Guida, Florence, Langhammer, Arnulf, Grankvist, Kjell, Meyer, Klaus, Cai, Qiuyin, Arslan, Alan A., Zeleniuch-Jacquotte, Anne, Albanes, Demetrius, Giles, Graham G., Sesso, Howard D., Lee, I-Min, Gaziano, J. Michael, Yuan, Jian-Min, Bolton, Judith Hoffman, Buring, Julie E., Visvanathan, Kala, Le Marchand, Loic, Purdue, Mark P., Caporaso, Neil E., Midttun, Oivind, Ueland, Per M., Prentice, Ross L., Weinstein, Stephanie J., Stevens, Victoria L., Zheng, Wei, Blot, William J., Shu, Xiao-Ou, Zhang, Xuehong, Xiang, Yong-Bing, Koh, Woon-Puay, Hveem, Kristian, Thomson, Cynthia A., Pettinger, Mary, Engstrom, Gunnar, Brunnstrom, Hans, Milne, Roger L., Stampfer, Meir J., Han, Jiali, Johansson, Mikael, Brennan, Paul, Severi, Gianluca, Johansson, Mattias, Muller, David C., Larose, Tricia L., Hodge, Allison, Guida, Florence, Langhammer, Arnulf, Grankvist, Kjell, Meyer, Klaus, Cai, Qiuyin, Arslan, Alan A., Zeleniuch-Jacquotte, Anne, Albanes, Demetrius, Giles, Graham G., Sesso, Howard D., Lee, I-Min, Gaziano, J. Michael, Yuan, Jian-Min, Bolton, Judith Hoffman, Buring, Julie E., Visvanathan, Kala, Le Marchand, Loic, Purdue, Mark P., Caporaso, Neil E., Midttun, Oivind, Ueland, Per M., Prentice, Ross L., Weinstein, Stephanie J., Stevens, Victoria L., Zheng, Wei, Blot, William J., Shu, Xiao-Ou, Zhang, Xuehong, Xiang, Yong-Bing, Koh, Woon-Puay, Hveem, Kristian, Thomson, Cynthia A., Pettinger, Mary, Engstrom, Gunnar, Brunnstrom, Hans, Milne, Roger L., Stampfer, Meir J., Han, Jiali, Johansson, Mikael, Brennan, Paul, Severi, Gianluca, and Johansson, Mattias
Abstract: Objectives To conduct a comprehensive analysis of prospectively measured circulating high sensitivity C reactive protein (hsCRP) concentration and risk of lung cancer overall, by smoking status (never, former, and current smokers), and histological sub-type. Design Nested case-control study. Setting 20 population based cohort studies in Asia, Europe, Australia, and the United States. Participants 5299 patients with incident lung cancer, with individually incidence density matched controls. Exposure Circulating hsCRP concentrations in prediagnostic serum or plasma samples. Main outcome measure Incident lung cancer diagnosis. Results A positive association between circulating hsCRP concentration and the risk of lung cancer for current (odds ratio associated with a doubling in hsCRP concentration 1.09, 95% confidence interval 1.05 to 1.13) and former smokers (1.09, 1.04 to 1.14) was observed, but not for never smokers (P<0.01 for interaction). This association was strong and consistent across all histological subtypes, except for adenocarcinoma, which was not strongly associated with hsCRP concentration regardless of smoking status (odds ratio for adenocarcinoma overall 0.97, 95% confidence interval 0.94 to 1.01). The association between circulating hsCRP concentration and the risk of lung cancer was strongest in the first two years of follow-up for former and current smokers. Including hsCRP concentration in a risk model, in addition to smoking based variables, did not improve risk discrimination overall, but slightly improved discrimination for cancers diagnosed in the first two years of follow-up. Conclusions Former and current smokers with higher circulating hsCRP concentrations had a higher risk of lung cancer overall. Circulating hsCRP concentration was not associated with the risk of lung adenocarcinoma. Circulating hsCRP concentration could be a prediagnostic marker of lung cancer rather than a causal risk factor.
Published: 2019
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49. Body mass index, weight gain and activity-related breathlessness : the Swedish CArdioPulmonary bioImage Study

Author: Ekstrom, Magnus, Blomberg, Anders, Bergstrom, Goran, Brandberg, John, Caidahl, Kenneth, Engstrom, Gunnar, Engvall, Jan, Eriksson, Maria, Gransbo, Klas, Hansen, Tomas, Jernberg, Tomas, Nilsson, Lars, Nilsson, Ulf, Olin, Anna-Carin, Persson, Lennart, Rosengren, Annika, Sandelin, Martin, Sköld, Magnus, Sundström, Johan, Swahn, Eva, Söderberg, Stefan, Tanash, Hanan, Torén, Kjell, Östgren, Carl-Johan, Lindberg, Eva, Ekstrom, Magnus, Blomberg, Anders, Bergstrom, Goran, Brandberg, John, Caidahl, Kenneth, Engstrom, Gunnar, Engvall, Jan, Eriksson, Maria, Gransbo, Klas, Hansen, Tomas, Jernberg, Tomas, Nilsson, Lars, Nilsson, Ulf, Olin, Anna-Carin, Persson, Lennart, Rosengren, Annika, Sandelin, Martin, Sköld, Magnus, Sundström, Johan, Swahn, Eva, Söderberg, Stefan, Tanash, Hanan, Torén, Kjell, Östgren, Carl-Johan, and Lindberg, Eva
Abstract: Supplement: 63. Meeting Abstract: OA1584.
Published: 2019
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50. Factors associated with health-related quality of life among adults with tetralogy of Fallot

Author: Sandstrom, Anette, Sandberg, Camilla, Rinnstrom, Daniel, Engstrom, Gunnar, Dellborg, Mikael, Thilen, Ulf, Sorensson, Peder, Nielsen, Niels Erik, Christersson, Christina, Johansson, Bengt, Sandstrom, Anette, Sandberg, Camilla, Rinnstrom, Daniel, Engstrom, Gunnar, Dellborg, Mikael, Thilen, Ulf, Sorensson, Peder, Nielsen, Niels Erik, Christersson, Christina, and Johansson, Bengt
Abstract: Background Due to improved care, the numbers of patients with tetralogy of Fallot (ToF) are increasing. However, long-term morbidity and need for reinterventions are concerns and also address issues of quality of life (QoL). Methods Patients with ToF and valid EuroQol-5 dimensions questionnaire (EQ-5D) were identified in the national Swedish register on congenital heart disease. EQ5D index was calculated and dichotomised into best possible health-related QoL (EQ-5D index = 1) or differed from 1. Results 288 patients met the criteria and were analysed. Univariate logistic regression showed a positive association between New York Heart Association (NYHA) class I (OR 8.32, 95% CI 3.80 to 18.21), physical activity amp;gt; 3 h/ week (OR 3.34, 95% CI 1.67 to 6.66) and a better right ventricular function (OR 2.56, 95% CI 1.09 to 6.02). A negative association between symptoms (OR 0.23, 95% CI 0.13 to 0.42), cardiovascular medication (OR 0.31, 95% CI 0.18 to 0.53), age (OR 0.97, 95% CI 0.96 to 0.99) and EQ-5D index was observed. In multivariate logistic regression, NYHA I (OR 7.28, 95% CI 3.29 to 16.12) and physical activity amp;gt; 3 h/ week (OR 2.27, 95% CI 1.07 to 4.84) remained associated with best possible health-related QoL. Replacing NYHA with symptoms in the model yielded similar results. Conclusion In this registry study, self-reported physical activity, staff-reported NYHA class and absence of symptoms were strongly associated with best possible health-related QoL measured by EQ-5D. Physical activity level is a potential target for intervention to improve QoL in this population but randomised trials are needed to test such a hypothesis., Funding Agencies|Vasterbotten Lans Landsting, Norrlandska Hjartfonden; Hjart-Lungfonden
Published: 2019
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