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1. PB0707 Neutrophil Extracellular Traps Promote Cancer-Associated Inflammation and Myocardial Stress

Author

Cedervall, J., primary, Herre, M., additional, Vemuri, K., additional, Dragomir, A., additional, Melo, F., additional, Svensson, A., additional, Thålin, C., additional, Rosell, A., additional, Hjalmar, V., additional, Wallén, H., additional, Lindman, H., additional, Pejler, G., additional, Hagström, E., additional, Hultström, M., additional, Larsson, A., additional, and Olsson, A., additional

Published
2023
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4. Associations of Polymorphisms in the Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1 Alpha Gene With Subsequent Coronary Heart Disease: An Individual-Level Meta-Analysis

Author

Schillemans, T., Tragante, V., Maitusong, B., Gigante, B., Cresci, S., Laguzzi, F., Vikström, M., Richards, M., Pilbrow, A., Cameron, V., Foco, L., Doughty, R.N., Kuukasjärvi, P., Allayee, H., Hartiala, J.A., Tang, W.H., Lyytikäinen, L.P., Nikus, K., Laurikka, J.O., Srinivasan, S., Mordi, I.R., Trompet, S., Kraaijeveld, A., Setten, J. van, Gijsberts, C.M., Maitland-van der Zee, A.H., Saely, C.H., Gong, Y., Johnson, J.A., Cooper-DeHoff, R.M., Pepine, C.J., Casu, G., Leiherer, A., Drexel, H., Horne, B.D., Laan, S.W. van der, Marziliano, N., Hazen, S.L., Sinisalo, J., Kähönen, M., Lehtimäki, T., Lang, C.C., Burkhardt, R., Scholz, M., Jukema, J.W., Eriksson, N., Åkerblom, A., James, S., Held, C., Hagström, E., Spertus, J.A., Algra, A., Faire, U. de, Åkesson, A., Asselbergs, F.W., Patel, R.S., Leander, K., Schillemans, T., Tragante, V., Maitusong, B., Gigante, B., Cresci, S., Laguzzi, F., Vikström, M., Richards, M., Pilbrow, A., Cameron, V., Foco, L., Doughty, R.N., Kuukasjärvi, P., Allayee, H., Hartiala, J.A., Tang, W.H., Lyytikäinen, L.P., Nikus, K., Laurikka, J.O., Srinivasan, S., Mordi, I.R., Trompet, S., Kraaijeveld, A., Setten, J. van, Gijsberts, C.M., Maitland-van der Zee, A.H., Saely, C.H., Gong, Y., Johnson, J.A., Cooper-DeHoff, R.M., Pepine, C.J., Casu, G., Leiherer, A., Drexel, H., Horne, B.D., Laan, S.W. van der, Marziliano, N., Hazen, S.L., Sinisalo, J., Kähönen, M., Lehtimäki, T., Lang, C.C., Burkhardt, R., Scholz, M., Jukema, J.W., Eriksson, N., Åkerblom, A., James, S., Held, C., Hagström, E., Spertus, J.A., Algra, A., Faire, U. de, Åkesson, A., Asselbergs, F.W., Patel, R.S., and Leander, K.

Abstract

Contains fulltext : 283506.pdf (Publisher’s version ) (Open Access), Background: The knowledge of factors influencing disease progression in patients with established coronary heart disease (CHD) is still relatively limited. One potential pathway is related to peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PPARGC1A), a transcription factor linked to energy metabolism which may play a role in the heart function. Thus, its associations with subsequent CHD events remain unclear. We aimed to investigate the effect of three different SNPs in the PPARGC1A gene on the risk of subsequent CHD in a population with established CHD. Methods: We employed an individual-level meta-analysis using 23 studies from the GENetIcs of sUbSequent Coronary Heart Disease (GENIUS-CHD) consortium, which included participants (n = 80,900) with either acute coronary syndrome, stable CHD, or a mixture of both at baseline. Three variants in the PPARGC1A gene (rs8192678, G482S; rs7672915, intron 2; and rs3755863, T528T) were tested for their associations with subsequent events during the follow-up using a Cox proportional hazards model adjusted for age and sex. The primary outcome was subsequent CHD death or myocardial infarction (CHD death/myocardial infarction). Stratified analyses of the participant or study characteristics as well as additional analyses for secondary outcomes of specific cardiovascular disease diagnoses and all-cause death were also performed. Results: Meta-analysis revealed no significant association between any of the three variants in the PPARGC1A gene and the primary outcome of CHD death/myocardial infarction among those with established CHD at baseline: rs8192678, hazard ratio (HR): 1.01, 95% confidence interval (CI) 0.98-1.05 and rs7672915, HR: 0.97, 95% CI 0.94-1.00; rs3755863, HR: 1.02, 95% CI 0.99-1.06. Similarly, no significant associations were observed for any of the secondary outcomes. The results from stratified analyses showed null results, except for significant inverse associations between rs7672915 (intro

Published
2022

5. Apolipoprotein B, Residual Cardiovascular Risk After Acute Coronary Syndrome, and Effects of Alirocumab

Author

Hagström, E., Steg, P.G., Szarek, M., Bhatt, D.L., Bittner, V.A., Danchin, N., Diaz, R., Goodman, S.G., Harrington, R.A., Jukema, J.W., Liberopoulos, E., Marx, N., McGinniss, J., Manvelian, G., Pordy, R., Scemama, M., White, H.D., Suryapranata, H., Zeiher, A.M., Schwartz, G.G., Hagström, E., Steg, P.G., Szarek, M., Bhatt, D.L., Bittner, V.A., Danchin, N., Diaz, R., Goodman, S.G., Harrington, R.A., Jukema, J.W., Liberopoulos, E., Marx, N., McGinniss, J., Manvelian, G., Pordy, R., Scemama, M., White, H.D., Suryapranata, H., Zeiher, A.M., and Schwartz, G.G.

Abstract

Contains fulltext : 283504.pdf (Publisher’s version ) (Open Access), BACKGROUND: Apolipoprotein B (apoB) provides an integrated measure of atherogenic risk. Whether apoB levels and apoB lowering hold incremental predictive information on residual risk after acute coronary syndrome beyond that provided by low-density lipoprotein cholesterol is uncertain. METHODS: The ODYSSEY OUTCOMES trial (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) compared the proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab with placebo in 18 924 patients with recent acute coronary syndrome and elevated atherogenic lipoproteins despite optimized statin therapy. Primary outcome was major adverse cardiovascular events (MACE; coronary heart disease death, nonfatal myocardial infarction, fatal/nonfatal ischemic stroke, hospitalization for unstable angina). Associations between baseline apoB or apoB at 4 months and MACE were assessed in adjusted Cox proportional hazards and propensity score-matched models. RESULTS: Median follow-up was 2.8 years. In proportional hazards analysis in the placebo group, MACE incidence increased across increasing baseline apoB strata (3.2 [95% CI, 2.9-3.6], 4.0 [95% CI, 3.6-4.5], and 5.5 [95% CI, 5.0-6.1] events per 100 patient-years in strata <75, 75-<90, ≥90 mg/dL, respectively; P(trend)<0.0001) and after adjustment for low-density lipoprotein cholesterol (P(trend)=0.035). Higher baseline apoB stratum was associated with greater relative (P(trend)<0.0001) and absolute reduction in MACE with alirocumab versus placebo. In the alirocumab group, the incidence of MACE after month 4 decreased monotonically across decreasing achieved apoB strata (4.26 [95% CI, 3.78-4.79], 3.09 [95% CI, 2.69-3.54], and 2.41 [95% CI, 2.11-2.76] events per 100 patient-years in strata ≥50, >35-<50, and ≤35 mg/dL, respectively). Compared with propensity score-matched patients from the placebo group, treatment hazard ratios for alirocumab also decreased monotonically across achieved apoB s

Published
2022

6. Neutrophil extracellular traps promote cancer-associated inflammation and myocardial stress

Author

Cedervall, J., primary, Herre, M., additional, Dragomir, A., additional, Rabelo-Melo, F., additional, Svensson, A., additional, Thålin, C., additional, Rosell, A., additional, Hjalmar, V., additional, Wallén, H., additional, Lindman, H., additional, Pejler, G., additional, Hagström, E., additional, Hultström, M., additional, Larsson, A., additional, and Olsson, AK., additional

Published
2022
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12. Association of Factor V Leiden With Subsequent Atherothrombotic Events: A GENIUS-CHD Study of Individual Participant Data

Author

Mahmoodi, B.K., Tragante, V., Kleber, M.E., Holmes, M.V., Schmidt, A.F., McCubrey, R.O., Howe, L.J., Direk, K., Allayee, H., Baranova, E.V., Braund, P.S., Delgado, G.E., Eriksson, N., Gijsberts, C.M., Gong, Y., Hartiala, J., Heydarpour, M., Pasterkamp, G., Kotti, S., Kuukasjärvi, P., Lenzini, P.A., Levin, D., Lyytikäinen, L.P., Muehlschlegel, J.D., Nelson, C.P., Nikus, K., Pilbrow, A.P., Tang, W.H., Laan, S.W. van der, Setten, J. van, Vilmundarson, R.O., Deanfield, J., Deloukas, P., Dudbridge, F., James, S., Mordi, I.R., Teren, A., Bergmeijer, T.O., Body, S.C., Bots, M., Burkhardt, R., Cooper-DeHoff, R.M., Cresci, S., Danchin, N., Doughty, R.N., Grobbee, D.E., Hagström, E., Hazen, S.L., Held, C., Hoefer, I.E., Hovingh, G.K., Johnson, J.A., Kaczor, M.P., Kähönen, M., Klungel, O.H., Laurikka, J.O., Lehtimäki, T., Maitland-van der Zee, A.H., McPherson, R., Palmer, C.N., Kraaijeveld, A.O., Pepine, C.J., Sanak, M., Sattar, N., Scholz, M., Simon, T., Spertus, J.A., Stewart, A.F., Szczeklik, W., Thiery, J., Visseren, F.L., Waltenberger, J., Richards, A.M.S., Lang, C.C., Cameron, V.A., Åkerblom, A., Pare, G., März, W., Samani, N.J., Hingorani, A.D., Berg, J.M. ten, Wallentin, L., Asselbergs, F.W., Patel, R.S., Mahmoodi, B.K., Tragante, V., Kleber, M.E., Holmes, M.V., Schmidt, A.F., McCubrey, R.O., Howe, L.J., Direk, K., Allayee, H., Baranova, E.V., Braund, P.S., Delgado, G.E., Eriksson, N., Gijsberts, C.M., Gong, Y., Hartiala, J., Heydarpour, M., Pasterkamp, G., Kotti, S., Kuukasjärvi, P., Lenzini, P.A., Levin, D., Lyytikäinen, L.P., Muehlschlegel, J.D., Nelson, C.P., Nikus, K., Pilbrow, A.P., Tang, W.H., Laan, S.W. van der, Setten, J. van, Vilmundarson, R.O., Deanfield, J., Deloukas, P., Dudbridge, F., James, S., Mordi, I.R., Teren, A., Bergmeijer, T.O., Body, S.C., Bots, M., Burkhardt, R., Cooper-DeHoff, R.M., Cresci, S., Danchin, N., Doughty, R.N., Grobbee, D.E., Hagström, E., Hazen, S.L., Held, C., Hoefer, I.E., Hovingh, G.K., Johnson, J.A., Kaczor, M.P., Kähönen, M., Klungel, O.H., Laurikka, J.O., Lehtimäki, T., Maitland-van der Zee, A.H., McPherson, R., Palmer, C.N., Kraaijeveld, A.O., Pepine, C.J., Sanak, M., Sattar, N., Scholz, M., Simon, T., Spertus, J.A., Stewart, A.F., Szczeklik, W., Thiery, J., Visseren, F.L., Waltenberger, J., Richards, A.M.S., Lang, C.C., Cameron, V.A., Åkerblom, A., Pare, G., März, W., Samani, N.J., Hingorani, A.D., Berg, J.M. ten, Wallentin, L., Asselbergs, F.W., and Patel, R.S.

Abstract

Contains fulltext : 235380.pdf (Publisher’s version ) (Closed access), BACKGROUND: Studies examining the role of factor V Leiden among patients at higher risk of atherothrombotic events, such as those with established coronary heart disease (CHD), are lacking. Given that coagulation is involved in the thrombus formation stage on atherosclerotic plaque rupture, we hypothesized that factor V Leiden may be a stronger risk factor for atherothrombotic events in patients with established CHD. METHODS: We performed an individual-level meta-analysis including 25 prospective studies (18 cohorts, 3 case-cohorts, 4 randomized trials) from the GENIUS-CHD (Genetics of Subsequent Coronary Heart Disease) consortium involving patients with established CHD at baseline. Participating studies genotyped factor V Leiden status and shared risk estimates for the outcomes of interest using a centrally developed statistical code with harmonized definitions across studies. Cox proportional hazards regression models were used to obtain age- and sex-adjusted estimates. The obtained estimates were pooled using fixed-effect meta-analysis. The primary outcome was composite of myocardial infarction and CHD death. Secondary outcomes included any stroke, ischemic stroke, coronary revascularization, cardiovascular mortality, and all-cause mortality. RESULTS: The studies included 69 681 individuals of whom 3190 (4.6%) were either heterozygous or homozygous (n=47) carriers of factor V Leiden. Median follow-up per study ranged from 1.0 to 10.6 years. A total of 20 studies with 61 147 participants and 6849 events contributed to analyses of the primary outcome. Factor V Leiden was not associated with the combined outcome of myocardial infarction and CHD death (hazard ratio, 1.03 [95% CI, 0.92-1.16]; I(2)=28%; P-heterogeneity=0.12). Subgroup analysis according to baseline characteristics or strata of traditional cardiovascular risk factors did not show relevant differences. Similarly, risk estimates for the secondary outcomes including stroke, coronary revascularization, card

Published
2020

18. Association of Chromosome 9p21 With Subsequent Coronary Heart Disease Events

Author

Patel, RS, Schmidt, AF, Tragante, V, McCubrey, RO, Holmes, MV, Howe, LJ, Direk, K, Åkerblom, A, Leander, K, Virani, SS, Kaminski, KA, Muehlschlegel, JD, Dubé, M-P, Allayee, H, Almgren, P, Alver, M, Baranova, EV, Behlouli, H, Boeckx, B, Braund, PS, Breitling, LP, Delgado, G, Duarte, NE, Dufresne, L, Eriksson, N, Foco, L, Gijsberts, CM, Gong, Y, Hartiala, J, Heydarpour, M, Hubacek, JA, Kleber, M, Kofink, D, Kuukasjärvi, P, Lee, V-V, Leiherer, A, Lenzini, PA, Levin, D, Lyytikäinen, L-P, Martinelli, N, Mons, U, Nelson, CP, Nikus, K, Pilbrow, AP, Ploski, R, Sun, YV, Tanck, MWT, Tang, WHW, Trompet, S, Van Der Laan, SW, Van Setten, J, Vilmundarson, RO, Anselmi, C, Vlachopoulou, E, Boerwinkle, E, Briguori, C, Carlquist, JF, Carruthers, KF, Casu, G, Deanfield, J, Deloukas, P, Dudbridge, F, Fitzpatrick, N, Gigante, B, James, S, Lokki, M-L, Lotufo, PA, Marziliano, N, Mordi, IR, Muhlestein, JB, Newton-Cheh, C, Pitha, J, Saely, CH, Samman-Tahhan, A, Sandesara, PB, Teren, A, Timmis, A, Van De Werf, F, Wauters, E, Wilde, AAM, Ford, I, Stott, DJ, Algra, A, Andreassi, MG, Ardissino, D, Arsenault, BJ, Ballantyne, CM, Bergmeijer, TO, Bezzina, CR, Body, SC, Bogaty, P, De Borst, GJ, Brenner, H, Burkhardt, R, Carpeggiani, C, Condorelli, G, Cooper-Dehoff, RM, Cresci, S, De Faire, U, Doughty, RN, Drexel, H, Engert, JC, Fox, KAA, Girelli, D, Hagström, E, Hazen, SL, Held, C, Hemingway, H, Hoefer, IE, Hovingh, GK, Johnson, JA, De Jong, PA, Jukema, JW, Kaczor, MP, Kähönen, M, Kettner, J, Kiliszek, M, Klungel, OH, Lagerqvist, B, Lambrechts, D, Laurikka, JO, Lehtimäki, T, Lindholm, D, Mahmoodi, BK, Der Zee, AH, McPherson, R, Melander, O, Metspalu, A, Pepinski, W, Olivieri, O, Opolski, G, Palmer, CN, Pasterkamp, G, Pepine, CJ, Pereira, AC, Pilote, L, Quyyumi, AA, Richards, AM, Sanak, M, Scholz, M, Siegbahn, A, Sinisalo, J, Smith, JG, Spertus, JA, Stewart, AFR, Szczeklik, W, Szpakowicz, A, Berg, JM, Thanassoulis, G, Thiery, J, Van Der Graaf, Y, Visseren, FLJ, Waltenberger, J, Van Der Harst, P, Tardif, J-C, Sattar, N, Lang, CC, Paré, G, Brophy, JM, Anderson, JL, März, W, Wallentin, L, Cameron, VA, Horne, BD, Samani, NJ, Hingorani, AD, and Asselbergs, FW

Subjects
Male, Myocardial Infarction, genetic risk factor, Coronary Artery Disease, Middle Aged, Article, chromosome 9p21, Gene Frequency, Risk Factors, Case-Control Studies, Odds Ratio, Humans, Female, Genetic Predisposition to Disease, cardiovascular diseases, Chromosomes, Human, Pair 9, secondary prevention
Abstract

Genetic variation at chromosome 9p21 is a recognized risk factor for coronary heart disease (CHD). However, its effect on disease progression and subsequent events is unclear, raising questions about its value for stratification of residual risk.A variant at chromosome 9p21 (rs1333049) was tested for association with subsequent events during follow-up in 103 357 Europeans with established CHD at baseline from the GENIUS-CHD (Genetics of Subsequent Coronary Heart Disease) Consortium (73.1% male, mean age 62.9 years). The primary outcome, subsequent CHD death or myocardial infarction (CHD death/myocardial infarction), occurred in 13 040 of the 93 115 participants with available outcome data. Effect estimates were compared with case/control risk obtained from the CARDIoGRAMplusC4D consortium (Coronary Artery Disease Genome-wide Replication and Meta-analysis [CARDIoGRAM] plus The Coronary Artery Disease [C4D] Genetics) including 47 222 CHD cases and 122 264 controls free of CHD.Meta-analyses revealed no significant association between chromosome 9p21 and the primary outcome of CHD death/myocardial infarction among those with established CHD at baseline (GENIUS-CHD odds ratio, 1.02; 95% CI, 0.99-1.05). This contrasted with a strong association in CARDIoGRAMPlusC4D odds ratio 1.20; 95% CI, 1.18-1.22; P for interaction0.001 compared with the GENIUS-CHD estimate. Similarly, no clear associations were identified for additional subsequent outcomes, including all-cause death, although we found a modest positive association between chromosome 9p21 and subsequent revascularization (odds ratio, 1.07; 95% CI, 1.04-1.09).In contrast to studies comparing individuals with CHD to disease-free controls, we found no clear association between genetic variation at chromosome 9p21 and risk of subsequent acute CHD events when all individuals had CHD at baseline. However, the association with subsequent revascularization may support the postulated mechanism of chromosome 9p21 for promoting atheroma development.

Published
2019

21. Subsequent Event Risk in Individuals With Established Coronary Heart Disease

Author

Patel, R.S. (Riyaz), Tragante, V. (Vinicius), Schmidt, A.F. (Amand), McCubrey, R.O. (Raymond O.), Holmes, M.V. (Michael), Howe, L.J. (Laurence J.), Direk, K. (Kenan), Åkerblom, A. (Axel), Leander, K. (Karin), Virani, S.S. (Salim), Kaminski, K.A. (Karol A.), Muehlschlegel, J.D. (Jochen), Allayee, H. (Hooman), Almgren, P. (Peter), Alver, M. (Maris), Baranova, E.V. (Ekaterina V.), Behloui, H. (Hassan), Boeckx, B. (Bram), Braund, P.S. (Peter), Breitling, L.P. (Lutz), Delgado, G., Duarte, N.E. (Nubia E.), Dubé, G.P. (Gregory), Dufresne, L. (Line), Eriksson, N. (Niclas), Foco, L. (Luisa), Scholz, M. (Markus), Gijsberts, C.M. (Crystel M.), Glinge, C. (Charlotte), Gong, Y. (Yan), Hartiala, J. (Jaana), Heydarpour, M. (Mahyar), Hubacek, J.A. (Jaroslav A.), Kleber, M.E. (Marcus), Kofink, D. (Daniel), Kotti, S. (Salma), Kuukasjärvi, P. (Pekka), Lee, V.-V. (Vei-Vei), Leiherer, A. (Andreas), Lenzini, P.A. (Petra A.), Levin, D. (Daniel), Lyytikäinen, L.-P. (Leo-Pekka), Martinelli, N. (Nicola), Mons, U. (Ute), Nelson, C.P. (Christopher P.), Nikus, K. (Kjell), Pilbrow, A.P. (Anna P.), Ploski, R. (Rafal), Sun, Y.V. (Yan V.), Tanck, M.W.T. (Michael), Tang, W. (W.), Trompet, S. (Stella), van der Laan, S.W. (Sander W.), Setten, J. (Jessica) van, Vilmundarson, R.O. (Ragnar O.), Viviani Anselmi, C. (Chiara), Vlachopoulou, E. (Efthymia), Al Ali, L. (Lawien), Boerwinkle, E.A. (Eric), Briguori, C. (Carlo), Carlquist, J.F. (John), Carruthers, K.F. (Kathryn), Casu, G. (Gavino), Deanfield, J. (John), Deloukas, P. (Panos), Dudbridge, F. (Frank), Engstrøm, T. (Thomas), Fitzpatrick, N. (Natalie), Fox, K.M. (Kim), Gigante, B. (Bruna), James, S.K. (Stefan), Lokki, M.-L. (Marja-Liisa), Lotufo, P.A. (Paulo A.), Marziliano, N. (Nicola), Mordi, I.R. (Ify R.), Muhlestein, J.B. (Joseph), Newton-Cheh, C. (Christopher), Pitha, J. (Jan), Saely, C.H. (Christoph H.), Samman-Tahhan, A. (Ayman), Sandesara, P.B. (Pratik B.), Teren, A. (Andrej), Timmis, A. (Adam), Van de Werf, F. (Frans), Wilde, A.A.M. (Arthur), Ford, I. (Ian), Stott, D.J. (David. J.), Algra, A. (Ale), Andreassi, M.G. (Maria G.), Ardissino, D. (Diego), Arsenault, B.J. (Benoit J.), Ballantyne, C. (Christie), Bergmeijer, T.O. (Thomas O.), Bezzina, C.R. (Connie R.), Body, S.C. (Simon C.), Boersma, E.H. (Eric H.), Bogaty, P. (Peter), Bots, M.L. (Michiel), Brenner, H. (Hermann), Brugts, J.J. (Jasper), Burkhardt, R. (Ralph), Carpeggiani, C. (Clara), Condorelli, G. (Gianluigi), Cooper-Dehoff, R.M. (Rhonda), Cresci, S. (Sharon), Danchin, N. (Nicolas), Faire, U. (Ulf) de, Doughty, R.N. (Robert N.), Drexel, H. (Heinz), Engert, J.C. (James C.), Fox, K.A.A. (Keith), Girelli, D. (Domenico), Grobbee, D.E. (Diederick E.), Hagström, E. (Emil), Hazen, S.L. (Stanley), Held, C. (Claes), Hemingway, H., Hoefer, I.E. (Imo), Hovingh, G.K. (G Kees), Jabbari, R. (Reza), Johnson, J.A. (Jennifer ), Jukema, J.W. (Jan Wouter), Kaczor, M.P. (Marcin P.), Kähönen, M. (Mika), Kettner, J. (Jiri), Kiliszek, M. (Marek), Klungel, O.H. (Olaf), Lagerqvist, B. (Bo), Lambrechts, D. (Diether), Laurikka, J.O. (Jari O.), Lehtimäki, T. (Terho), Lindholm, D. (Daniel), Mahmoodi, B.K. (Bakhtawar K.), Maitland-van der Zee, A-H. (Anke-Hilse), McPherson, R. (Ruth), Melander, O. (Olle), Metspalu, A. (Andres), Niemcunowicz-Janica, A. (Anna), Olivieri, O. (Oliviero), Opolski, G. (Grzegorz), Palmer, C.N.A. (Colin), Pasterkamp, G. (Gerard), Pepine, C.J. (Carl), Pereira, A. (A.), Pilote, L. (Louise), Erdmann, J. (Jeanette), Richards, A.M. (A Mark), Sanak, M. (Marek), Siegbahn, A. (Agneta), Simon, T. (Tabassome), Sinisalo, J. (Juha), Smith, J.G. (J Gustav), Schwartz, S.M. (Stephen), Stender, S. (Steen), Stewart, A.F. (Alexandre F.), Szczeklik, W. (Wojciech), Szpakowicz, A. (Anna), Tardif, J.-C. (Jean-Claude), Berg, J.M. (Jurrien) ten, Tfelt-Hansen, J. (Jacob), Thanassoulis, G. (George), Thiery, J.P. (Joachim), Torp-Pedersen, C. (Christian Tobias), Graaf, Y. (Yolanda) van der, Visseren, F.L.J. (Frank), Waltenberger, J. (Johannes), Weeke, P.E. (Peter E.), Harst, P. (Pim) van der, Lang, C.C. (Chim C.), Sattar, N. (Naveed), Cameron, V.A. (Vicky A.), Anderson, J.L. (Jeffrey), Brophy, J.M. (James M.), Pare, G. (Guillame), Horne, B.D. (Benjamin), Ye, S. (Shu), Wallentin, L. (Lars), Wauters, E. (Els), Samani, N.J. (Nilesh), Hingorani, A. (Aroon), Asselbergs, F.W. (Folkert), Patel, R.S. (Riyaz), Tragante, V. (Vinicius), Schmidt, A.F. (Amand), McCubrey, R.O. (Raymond O.), Holmes, M.V. (Michael), Howe, L.J. (Laurence J.), Direk, K. (Kenan), Åkerblom, A. (Axel), Leander, K. (Karin), Virani, S.S. (Salim), Kaminski, K.A. (Karol A.), Muehlschlegel, J.D. (Jochen), Allayee, H. (Hooman), Almgren, P. (Peter), Alver, M. (Maris), Baranova, E.V. (Ekaterina V.), Behloui, H. (Hassan), Boeckx, B. (Bram), Braund, P.S. (Peter), Breitling, L.P. (Lutz), Delgado, G., Duarte, N.E. (Nubia E.), Dubé, G.P. (Gregory), Dufresne, L. (Line), Eriksson, N. (Niclas), Foco, L. (Luisa), Scholz, M. (Markus), Gijsberts, C.M. (Crystel M.), Glinge, C. (Charlotte), Gong, Y. (Yan), Hartiala, J. (Jaana), Heydarpour, M. (Mahyar), Hubacek, J.A. (Jaroslav A.), Kleber, M.E. (Marcus), Kofink, D. (Daniel), Kotti, S. (Salma), Kuukasjärvi, P. (Pekka), Lee, V.-V. (Vei-Vei), Leiherer, A. (Andreas), Lenzini, P.A. (Petra A.), Levin, D. (Daniel), Lyytikäinen, L.-P. (Leo-Pekka), Martinelli, N. (Nicola), Mons, U. (Ute), Nelson, C.P. (Christopher P.), Nikus, K. (Kjell), Pilbrow, A.P. (Anna P.), Ploski, R. (Rafal), Sun, Y.V. (Yan V.), Tanck, M.W.T. (Michael), Tang, W. (W.), Trompet, S. (Stella), van der Laan, S.W. (Sander W.), Setten, J. (Jessica) van, Vilmundarson, R.O. (Ragnar O.), Viviani Anselmi, C. (Chiara), Vlachopoulou, E. (Efthymia), Al Ali, L. (Lawien), Boerwinkle, E.A. (Eric), Briguori, C. (Carlo), Carlquist, J.F. (John), Carruthers, K.F. (Kathryn), Casu, G. (Gavino), Deanfield, J. (John), Deloukas, P. (Panos), Dudbridge, F. (Frank), Engstrøm, T. (Thomas), Fitzpatrick, N. (Natalie), Fox, K.M. (Kim), Gigante, B. (Bruna), James, S.K. (Stefan), Lokki, M.-L. (Marja-Liisa), Lotufo, P.A. (Paulo A.), Marziliano, N. (Nicola), Mordi, I.R. (Ify R.), Muhlestein, J.B. (Joseph), Newton-Cheh, C. (Christopher), Pitha, J. (Jan), Saely, C.H. (Christoph H.), Samman-Tahhan, A. (Ayman), Sandesara, P.B. (Pratik B.), Teren, A. (Andrej), Timmis, A. (Adam), Van de Werf, F. (Frans), Wilde, A.A.M. (Arthur), Ford, I. (Ian), Stott, D.J. (David. J.), Algra, A. (Ale), Andreassi, M.G. (Maria G.), Ardissino, D. (Diego), Arsenault, B.J. (Benoit J.), Ballantyne, C. (Christie), Bergmeijer, T.O. (Thomas O.), Bezzina, C.R. (Connie R.), Body, S.C. (Simon C.), Boersma, E.H. (Eric H.), Bogaty, P. (Peter), Bots, M.L. (Michiel), Brenner, H. (Hermann), Brugts, J.J. (Jasper), Burkhardt, R. (Ralph), Carpeggiani, C. (Clara), Condorelli, G. (Gianluigi), Cooper-Dehoff, R.M. (Rhonda), Cresci, S. (Sharon), Danchin, N. (Nicolas), Faire, U. (Ulf) de, Doughty, R.N. (Robert N.), Drexel, H. (Heinz), Engert, J.C. (James C.), Fox, K.A.A. (Keith), Girelli, D. (Domenico), Grobbee, D.E. (Diederick E.), Hagström, E. (Emil), Hazen, S.L. (Stanley), Held, C. (Claes), Hemingway, H., Hoefer, I.E. (Imo), Hovingh, G.K. (G Kees), Jabbari, R. (Reza), Johnson, J.A. (Jennifer ), Jukema, J.W. (Jan Wouter), Kaczor, M.P. (Marcin P.), Kähönen, M. (Mika), Kettner, J. (Jiri), Kiliszek, M. (Marek), Klungel, O.H. (Olaf), Lagerqvist, B. (Bo), Lambrechts, D. (Diether), Laurikka, J.O. (Jari O.), Lehtimäki, T. (Terho), Lindholm, D. (Daniel), Mahmoodi, B.K. (Bakhtawar K.), Maitland-van der Zee, A-H. (Anke-Hilse), McPherson, R. (Ruth), Melander, O. (Olle), Metspalu, A. (Andres), Niemcunowicz-Janica, A. (Anna), Olivieri, O. (Oliviero), Opolski, G. (Grzegorz), Palmer, C.N.A. (Colin), Pasterkamp, G. (Gerard), Pepine, C.J. (Carl), Pereira, A. (A.), Pilote, L. (Louise), Erdmann, J. (Jeanette), Richards, A.M. (A Mark), Sanak, M. (Marek), Siegbahn, A. (Agneta), Simon, T. (Tabassome), Sinisalo, J. (Juha), Smith, J.G. (J Gustav), Schwartz, S.M. (Stephen), Stender, S. (Steen), Stewart, A.F. (Alexandre F.), Szczeklik, W. (Wojciech), Szpakowicz, A. (Anna), Tardif, J.-C. (Jean-Claude), Berg, J.M. (Jurrien) ten, Tfelt-Hansen, J. (Jacob), Thanassoulis, G. (George), Thiery, J.P. (Joachim), Torp-Pedersen, C. (Christian Tobias), Graaf, Y. (Yolanda) van der, Visseren, F.L.J. (Frank), Waltenberger, J. (Johannes), Weeke, P.E. (Peter E.), Harst, P. (Pim) van der, Lang, C.C. (Chim C.), Sattar, N. (Naveed), Cameron, V.A. (Vicky A.), Anderson, J.L. (Jeffrey), Brophy, J.M. (James M.), Pare, G. (Guillame), Horne, B.D. (Benjamin), Ye, S. (Shu), Wallentin, L. (Lars), Wauters, E. (Els), Samani, N.J. (Nilesh), Hingorani, A. (Aroon), and Asselbergs, F.W. (Folkert)

Abstract

BACKGROUND: The Genetics of Subsequent Coronary Heart Disease (GENIUS-CHD) consortium was established to facilitate discovery and validation of genetic variants a

Published
2019
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22. Excessive daytime sleepiness, morning tiredness and major adverse cardiovascular events in patients with chronic coronary syndrome.

Author

Olszowka, M., Held, C., Hadziosmanovic, N., Denchev, S., Manolis, A., Wallentin, L., White, H. D., Stewart, R. A. H., and Hagström, E.

Subjects
CARDIOVASCULAR diseases, SLEEP apnea syndromes, MYOCARDIAL infarction, DROWSINESS, SYMPTOMS, MAJOR adverse cardiovascular events
Abstract

Background: Sleep‐related breathing disorders (SRBDs), particularly obstructive sleep apnoea, are associated with increased cardiovascular (CV) risk. However, it is not known whether individual questions used for SRBD screening are associated with major adverse CV events (MACE) and death specifically in patients with chronic coronary syndrome (CCS). Methods: Symptoms associated with SRBD were assessed by a baseline questionnaire in 15,640 patients with CCS on optimal secondary preventive therapy in the STABILITY trial. The patients reported the frequency (never/rarely, sometimes, often and always) of: 1) loud snoring; 2) more than one awakening/night; 3) morning tiredness (MT); 4) excessive daytime sleepiness (EDS); or 5) gasping, choking or apnoea when asleep. In adjusted Cox regression models, associations between the frequency of SRBD symptoms and CV outcomes were assessed with never/rarely as reference. Results: During a median follow‐up time of 3.7 years, 1,588 MACE events (541 CV deaths, 749 nonfatal myocardial infarctions [MI] and 298 nonfatal strokes) occurred. EDS was associated (hazard ratio [HR], 95% confidence interval [CI]) with increased risk of MACE (sometimes 1.14 [1.01–1.29], often 1.19 [1.01–1.40] and always 1.43 [1.15–1.78]), MI (always 1.61 [1.17–2.20]) and all‐cause death (often 1.26 [1.05–1.52] and always 1.71 [1.35–2.15]). MT was associated with higher risk of MACE (often 1.23 [1.04–1.45] and always 1.46 [1.18–1.81]), MI (always 1.61 [1.22–2.14]) and all‐cause death (always 1.54 [1.20–1.98]). The other SRBD‐related questions were not consistently associated with worse outcomes. Conclusions: In patients with CCS, gradually higher levels of EDS and MT were independently associated with increased risk of MACE, including mortality. [ABSTRACT FROM AUTHOR]

Published
2021
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24. Growth Differentiation Factor 15 at 1 Month After an Acute Coronary Syndrome Is Associated With Increased Risk of Major Bleeding

Author

Lindholm, D., Hagström, E., James, S.K., Becker, R.C., Cannon, C.P., Himmelmann, A., Katus, H.A., Maurer, G., López-Sendón, J.L., Steg, P.G., Storey, R.F., Siegbahn, A., and Wallentin, L.

Subjects
embryonic structures
Abstract

BACKGROUND: Growth differentiation factor-15 (GDF-15) is related to major bleeding when measured at initial presentation in patients with acute coronary syndromes (ACSs) treated with dual antiplatelet therapy. It is unknown whether follow-up measurements provide additional information. The objective of this study was to investigate whether GDF-15 measured 1 month after an ACS provides additional information beyond the baseline levels with regard to the risk of major bleeding. METHODS AND RESULTS: GDF-15 was measured at baseline and at 1 month after an ACS in 4049 patients included in the PLATelet inhibition and patient Outcomes (PLATO) trial. The association between 1-month GDF-15 level and non-coronary artery bypass grafting surgery-related major bleeding was assessed by a multivariable Cox model, adjusting for baseline GDF-15, age, anemia, impaired renal function, history of gastrointestinal bleeding, and sex. Elevated GDF-15 (>1800 ng/L) at 1 month was associated with an increased risk of non-coronary artery bypass grafting-related major bleeding (3.9% versus 1.2%; hazard ratio, 3.38; 95% CI, 1.89-6.06), independent of baseline GDF-15. Patients who had elevated GDF-15 levels at baseline and subsequent nonelevated GDF-15 at 1 month had a similar risk as patients who had nonelevated levels at both measurements. CONCLUSIONS: GDF-15 at 1 month after an ACS is related to the risk of bleeding during DAPT and provides additional information on the bleeding risk beyond baseline GDF-15 levels. GDF-15 levels may therefore be useful as part of decision support concerning long-term antithrombotic treatment in patients post-ACS. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00391872.

Published
2017

25. Equal clinical performance of a novel point-of-care cardiac troponin I (cTnI) assay with a commonly used high-sensitivity cTnI assay

Author

Venge, P., van Lippen, L., Blaschke, S., Christ, M., Geier, F., Giannitsis, E., Hagström, E., Khellaf, M., Mair, J., Pariente, D., Scharnhorst, V., Semjonow, V., Venge, P., van Lippen, L., Blaschke, S., Christ, M., Geier, F., Giannitsis, E., Hagström, E., Khellaf, M., Mair, J., Pariente, D., Scharnhorst, V., and Semjonow, V.

Abstract

BACKGROUND: Efficient rule-out of acute myocardial infarction (MI) facilitates early disposition of chest pain patients in emergency departments (ED). Point-of-care (POC) cardiac troponin (cTn) may improve patient throughput. We compared the diagnostic accuracy of a novel cTnI test (Minicare cTnI, Philips), with current POC cTnI (I-Stat, Abbott) and high-sensitivity central laboratory cTnI (hs-cTnI; Architect, Abbott) assays.METHODS: The clinical performance of the assays were compared in samples from 450 patients from a previous clinical evaluation of Minicare cTnI.RESULTS: Minicare cTnI correlated with Architect hs-cTnI (r(2)=0.85, p<0.0001) and I-Stat cTnI (r(2)=0.93, p<0.0001). Areas under the receiver operating characteristics curves were 0.87-0.91 at admission (p=ns) and 0.96-0.97 3h after admission (p=ns). The negative predictive values (NPV) at admission were 95% ((92-97%, 95% CI) for Minicare cTnI and increased to 99% (97-100%) at 2-4h, and similar to Architect hs-cTnI (98%, 96-100%), but higher than I-Stat cTnI (95%, 92-97%; p<0.01). Negative likelihood ratios (LR-) after 2-4h were 0.06 (0.02-0.17, 95% CI) for Minicare cTnI, 0.11 (0.05-0.24) for Architect hs-cTnI (p=0.02) and 0.28 (0.18-0.43) for I-Stat cTnI (p<0.0001). The clinical concordances between Minicare cTnI and Architect hs-cTnI were 92% (admission) and 95% (2-4h), with lower concordances between Minicare cTnI and I-Stat cTnI (83% and 78%, respectively; p=0.007).CONCLUSIONS: The Minicare cTnI POC assay may become useful for prompt and safe ruling-out of AMI in ED patients with suspected AMI using a guideline supported 0/3h sampling protocol.

Published
2017

26. Psychosocial stress and major cardiovascular events in patients with stable coronary heart disease

Author

Hagström, E., primary, Norlund, F., additional, Stebbins, A., additional, Armstrong, P. W., additional, Chiswell, K., additional, Granger, C. B., additional, López‐Sendón, J., additional, Pella, D., additional, Soffer, J., additional, Sy, R., additional, Wallentin, L., additional, White, H. D., additional, Stewart, R. A. H., additional, and Held, C., additional

Published
2017
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28. L’università dell’Utopia. La Statale di Milano negli anni Settanta

Author

Coen Porosini, A., Dionigi, R., Generali, D., Botta, M., Capanna, M., Bellini, R., Baldini, F., Carrozzini, G., Veneziano, R., Martignoni, G. M., Giannitrapani, P., Vedibene, M., Brebbia, G., Meazza, C., Petitot, J., Sini, C., Bianca, M., Broggini, G., Cambria, F., Rodríguez, R. A., Fabbrichesi, R., Handjaras, L., Maiorca, B., Biuso, A. G., Agazzi, E., Heinzmann, G., Coliva, A., Gonzalez, W. J., Arrojo, M. J., Coniglione, F., Negro, M., Chiffi, D., Sabatini, N., Schiavio, F., Taramelli, R., Lenk, H., Maring, M., Cambi, F., Buzzoni, M., Galuzzi, M., Quaranta, M., Renzi, E., Ferri, M. B., Paladini, A., Giannì, I., Scaramuzza, G., Dino, O., DALLA VIGNA, PIERRE ALESSANDRO, Paganini, G., Galli, S. B., Pozzi, P., Kemp, P., Lazzari, M., Marinotti, A., Colonnello, P., Piccari, P., Quarta, A., Vinti, C., Micheli, G., Bazhanov, V. A., Panza, M., Cimino, G., Luzzini, F., Vaccari, E., Wolenski, J., Rossi, A., Bertagna, G., Bartolini, R., Tussi, T., Scolozzi, E., Hagström, E., Ponzellini, V., Patti, A., Barile, S., Veca, S., Frascanetti Brondino, Y., Visconti, K., Orecchia, A. M., Sandrini, M. G., Dobner, C., Moccia, N., Brondino, M., Velázquez, L., Brondino, L., Papi, F., Brissa, E., de Paoli, M., Riccobono, M. G., Santi, G., Pasetti, C., and Martignoni, G.

Published
2015

29. Association of vitamin D status with arterial blood pressure and hypertension risk: a mendelian randomisation study

Author

Ks, Vimaleswaran, Cavadino A, Dj, Berry, LifeLines Cohort Study investigators, Jorde R, Ak, Dieffenbach, Lu C, Ac, Alves, Hj, Heerspink, Tikkanen E, Eriksson J, Wong A, Mangino M, Ka, Jablonski, Im, Nolte, Dk, Houston, Ts, Ahluwalia, Pj, Most, Pasko D, Zgaga L, Thiering E, Vitart V, Rm, Fraser, Je, Huffman, Ra, Boer, Schöttker B, Ku, Saum, Mi, Mccarthy, Dupuis J, Kh, Herzig, Sebert S, Pouta A, Laitinen J, Me, Kleber, Navis G, Lorentzon M, Jameson K, Arden N, Ja, Cooper, Acharya J, Hardy R, Raitakari O, Ripatti S, Lk, Billings, Lahti J, Osmond C, Bw, Penninx, Rejnmark L, Kk, Lohman, Paternoster L, Rp, Stolk, Dg, Hernandez, Byberg L, Hagström E, Melhus H, Ingelsson E, Mellström D, Ljunggren O, Tzoulaki I, McLachlan S, Theodoratou E, Cm, Tiesler, Jula A, Navarro P, Af, Wright, Polasek O, International Consortium for Blood Pressure (ICBP), Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, Global Blood Pressure Genetics (Global BPGen) consortium, Caroline Hayward, Jf, Wilson, Rudan I, Salomaa V, Heinrich J, Campbell H, Jf, Price, Karlsson M, Lind L, Michaëlsson K, Bandinelli S, Tm, Frayling, Ca, Hartman, Ti, Sørensen, Sb, Kritchevsky, Bl, Langdahl, Jg, Eriksson, Jc, Florez, Td, Spector, Lehtimäki T, Kuh D, Se, Humphries, Cooper C, Ohlsson C, März W, Mh, Borst, Kumari M, Mika Kivimaki, Tj, Wang, Power C, Brenner H, Grimnes G, van der Harst P, Snieder H, Ad, Hingorani, Pilz S, Jc, Whittaker, Järvelin MR, and Hyppönen E

Abstract

BACKGROUND: Low plasma 25-hydroxyvitamin D (25[OH]D) concentration is associated with high arterial blood pressure and hypertension risk, but whether this association is causal is unknown. We used a mendelian randomisation approach to test whether 25(OH)D concentration is causally associated with blood pressure and hypertension risk. METHODS: In this mendelian randomisation study, we generated an allele score (25[OH]D synthesis score) based on variants of genes that affect 25(OH)D synthesis or substrate availability (CYP2R1 and DHCR7), which we used as a proxy for 25(OH)D concentration. We meta-analysed data for up to 108 173 individuals from 35 studies in the D-CarDia collaboration to investigate associations between the allele score and blood pressure measurements. We complemented these analyses with previously published summary statistics from the International Consortium on Blood Pressure (ICBP), the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, and the Global Blood Pressure Genetics (Global BPGen) consortium. FINDINGS: In phenotypic analyses (up to n=49 363), increased 25(OH)D concentration was associated with decreased systolic blood pressure (β per 10% increase, -0·12 mm Hg, 95% CI -0·20 to -0·04; p=0·003) and reduced odds of hypertension (odds ratio [OR] 0·98, 95% CI 0·97-0·99; p=0·0003), but not with decreased diastolic blood pressure (β per 10% increase, -0·02 mm Hg, -0·08 to 0·03; p=0·37). In meta-analyses in which we combined data from D-CarDia and the ICBP (n=146 581, after exclusion of overlapping studies), each 25(OH)D-increasing allele of the synthesis score was associated with a change of -0·10 mm Hg in systolic blood pressure (-0·21 to -0·0001; p=0·0498) and a change of -0·08 mm Hg in diastolic blood pressure (-0·15 to -0·02; p=0·01). When D-CarDia and consortia data for hypertension were meta-analysed together (n=142 255), the synthesis score was associated with a reduced odds of hypertension (OR per allele, 0·98, 0·96-0·99; p=0·001). In instrumental variable analysis, each 10% increase in genetically instrumented 25(OH)D concentration was associated with a change of -0·29 mm Hg in diastolic blood pressure (-0·52 to -0·07; p=0·01), a change of -0·37 mm Hg in systolic blood pressure (-0·73 to 0·003; p=0·052), and an 8·1% decreased odds of hypertension (OR 0·92, 0·87-0·97; p=0·002). INTERPRETATION: Increased plasma concentrations of 25(OH)D might reduce the risk of hypertension. This finding warrants further investigation in an independent, similarly powered study. FUNDING: British Heart Foundation, UK Medical Research Council, and Academy of Finland.

Published
2014

30. Association of vitamin D status with arterial blood pressure and hypertension risk: A mendelian randomisation study

Author

Vimaleswaran, K.S., Cavadino, A., Berry, D.J., Jorde, R., Dieffenbach, A.K., Lu, C., Alves, A.C., Heerspink, H.J., Tikkanen, E., Eriksson, J., Wong, A., Mangino, M., Jablonski, K.A., Nolte, I.M., Houston, D.K., Ahluwalia, T.S., van der Most, P.J., Pasko, D., Zgaga, L., Thiering, E., Vitart, V., Fraser, R.M., Huffman, J.E., de Boer, R.A., Schöttker, B., Saum, K.U., McCarthy, M.I., Dupuis, J., Herzig, K.H., Sebert, S., Pouta, A., Laitinen, J., Kleber, M.E., Navis, G., Lorentzon, M., Jameson, K., Arden, N., Cooper, J.A., Acharya, J., Hardy, R., Raitakari, O., Ripatti, S., Billings, L.K., Lahti, J., Osmond, C., Penninx, B.W., Rejnmark, L., Lohman, K.K., Paternoster, L., Stolk, R.P., Hernandez, D.G., Byberg, L., Hagström, E., Melhus, H., Ingelsson, E., Mellström, D., Ljunggren, O., Tzoulaki, I., McLachlan, S., Theodoratou, E., Tiesler, C.M., Jula, A., Navarro, P., Wright, A.F., Polasek, O., ICBP Consortium (), CHARGE Consortium (), Global BPgen Consortium (), Wilson, J.F., Rudan, I., Salomaa, V., Heinrich, J., Campbell, H., Price, J.F., Karlsson, M., Lind, L., Michaelsson, K., Bandinelli, S., Frayling, T.M., Hartman, C.A., Sørensen, T.I., Kritchevsky, S.B., Langdahl, B.L., Eriksson, J.G., Florez, J.C, Spector, T.D., Lehtimäki, T., Kuh, D., Humphries, S.E., Cooper, C., Ohlsson, C., Marz, W., de Borst, M.H., Kumari, M., Kivimaki, M., Wang, T.J., Power, C., Brenner, H., Grimnes, G., van der Harst, P., Snieder, H., Hingorani, A.D., Pilz, S., Whittaker, J.C., Jarvelin, M.R., and Hyppönen, E.

Abstract

BACKGROUND: Low plasma 25-hydroxyvitamin D (25[OH]D) concentration is associated with high arterial blood pressure and hypertension risk, but whether this association is causal is unknown. We used a mendelian randomisation approach to test whether 25(OH)D concentration is causally associated with blood pressure and hypertension risk. METHODS: In this mendelian randomisation study, we generated an allele score (25[OH]D synthesis score) based on variants of genes that affect 25(OH)D synthesis or substrate availability (CYP2R1 and DHCR7), which we used as a proxy for 25(OH)D concentration. We meta-analysed data for up to 108 173 individuals from 35 studies in the D-CarDia collaboration to investigate associations between the allele score and blood pressure measurements. We complemented these analyses with previously published summary statistics from the International Consortium on Blood Pressure (ICBP), the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, and the Global Blood Pressure Genetics (Global BPGen) consortium. FINDINGS: In phenotypic analyses (up to n=49 363), increased 25(OH)D concentration was associated with decreased systolic blood pressure (β per 10% increase, -0·12 mm Hg, 95% CI -0·20 to -0·04; p=0·003) and reduced odds of hypertension (odds ratio [OR] 0·98, 95% CI 0·97-0·99; p=0·0003), but not with decreased diastolic blood pressure (β per 10% increase, -0·02 mm Hg, -0·08 to 0·03; p=0·37). In meta-analyses in which we combined data from D-CarDia and the ICBP (n=146 581, after exclusion of overlapping studies), each 25(OH)D-increasing allele of the synthesis score was associated with a change of -0·10 mm Hg in systolic blood pressure (-0·21 to -0·0001; p=0·0498) and a change of -0·08 mm Hg in diastolic blood pressure (-0·15 to -0·02; p=0·01). When D-CarDia and consortia data for hypertension were meta-analysed together (n=142 255), the synthesis score was associated with a reduced odds of hypertension (OR per allele, 0·98, 0·96-0·99; p=0·001). In instrumental variable analysis, each 10% increase in genetically instrumented 25(OH)D concentration was associated with a change of -0·29 mm Hg in diastolic blood pressure (-0·52 to -0·07; p=0·01), a change of -0·37 mm Hg in systolic blood pressure (-0·73 to 0·003; p=0·052), and an 8·1% decreased odds of hypertension (OR 0·92, 0·87-0·97; p=0·002). INTERPRETATION: Increased plasma concentrations of 25(OH)D might reduce the risk of hypertension. This finding warrants further investigation in an independent, similarly powered study. FUNDING: British Heart Foundation, UK Medical Research Council, and Academy of Finland.

Published
2014

31. Association of vitamin D status with arterial blood pressure and hypertension risk: A mendelian randomisation study

Author

Vimaleswaran, Kerani S., Cavadino, Alana, Berry, Diane J., Jorde, Rolf, Grimnes, Guri, Dieffenbach, Aida Karina, Lu, Chen, Alves, Alexessander Couto, Heerspink, Hiddo J. Lambers, Tikkanen, Emmi, Eriksson, Joel, Wong, Andrew, Mangino, Massimo, Jablonski, Kathleen A., Nolte, Ilja M., Houston, Denise K., Ahluwalia, Tarunveer Singh, van der Most, Peter J., Pasko, Dorota, Zgaga, Lina, Thiering, Elisabeth, Schöttker, B, Saum, KU, Brenner, H, Järvelin, MR, Tzoulaki, I, Snieder, H, Stolk, RP, Hartman, CA, de Boer, RA, van der Harst, P, Navis, G, de Borst, MH, Lorentzon, M, Mellström, D, Ohlsson, C, Hardy, R, Kuh, D, Cooper, JA, Acharya, J, Humphries, SE, Hingorani, AD, Kumari, M, Kivimaki, M, Spector, TD, Kritchevsky, SB, Lohman, KK, Sørensen, TIA, Frayling, TM, Campbell, H, Theodoratou, E, Fraser, RM, Wilson, JF, Rudan, I, Price, JF, McLachlan, S, Vitart, V, Navarro, P, Huffman, JE, Hayward, C, Wright, AF, Tiesler, CMT, Heinrich, J, McCarthy, MI, Ingelsson, E, Arden, N, Cooper, C, Dupuis, J, Herzig, KH, Sebert, S, Pouta, A, Laitinen, J, Kleber, ME, März, W, Jameson, K, Osmond, C, Raitakari, O, Ripatti, S, Lahti, J, Eriksson, JG, Penninx, BW, Billings, LK, Florez, JC, Rejnmark, L, Langdahl, BL, Paternoster, L, Hernandez, DG, Byberg, L, Michaelsson, K, Hagström, E, Melhus, H, Ljunggren, O, Lind, L, Jula, A, Polasek, O, Salomaa, V, Karlsson, M, Bandinelli, S, Lehtimäki, T, Wang, TJ, Pilz, S, and Whittaker, JC

Abstract

Background Low plasma 25-hydroxyvitamin D (25[OH]D) concentration is associated with high arterial blood pressure and hypertension risk, but whether this association is causal is unknown. We used a mendelian randomisation approach to test whether 25(OH)D concentration is causally associated with blood pressure and hypertension risk. Methods In this mendelian randomisation study, we generated an allele score (25[OH]D synthesis score) based on variants of genes that aff ect 25(OH)D synthesis or substrate availability (CYP2R1 and DHCR7), which we used as a proxy for 25(OH)D concentration. We meta-analysed data for up to 108 173 individuals from 35 studies in the D-CarDia collaboration to investigate associations between the allele score and blood pressure measurements. We complemented these analyses with previously published summary statistics from the International Consortium on Blood Pressure (ICBP), the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, and the Global Blood Pressure Genetics (Global BPGen) consortium. Findings In phenotypic analyses (up to n=49 363), increased 25(OH)D concentration was associated with decreased systolic blood pressure (β per 10% increase, –0·12 mm Hg, 95% CI –0·20 to –0·04; p=0·003) and reduced odds of hypertension (odds ratio [OR] 0·98, 95% CI 0·97–0·99; p=0·0003), but not with decreased diastolic blood pressure (β per 10% increase, –0·02 mm Hg, –0·08 to 0·03; p=0·37). In meta-analyses in which we combined data from D-CarDia and the ICBP (n=146 581, after exclusion of overlapping studies), each 25(OH)D-increasing allele of the synthesis score was associated with a change of –0·10 mm Hg in systolic blood pressure (–0·21 to –0·0001; p=0·0498) and a change of –0·08 mm Hg in diastolic blood pressure (–0·15 to –0·02; p=0·01). When D-CarDia and consortia data for hypertension were meta-analysed together (n=142 255), the synthesis score was associated with a reduced odds of hypertension (OR per allele, 0·98, 0·96–0·99; p=0·001). In instrumental variable analysis, each 10% increase in genetically instrumented 25(OH)D concentration was associated with a change of –0·29 mm Hg in diastolic blood pressure (–0·52 to –0·07; p=0·01), a change of –0·37 mm Hg in systolic blood pressure (–0·73 to 0·003; p=0·052), and an 8·1% decreased odds of hypertension (OR 0·92, 0·87–0·97; p=0·002). Interpretation Increased plasma concentrations of 25(OH)D might reduce the risk of hypertension. This fi nding warrants further investigation in an independent, similarly powered study.

Published
2014

33. Short-term network planning of distribution system with photovoltaic

Author

Huang, Yalin, Hagström, E., Alvehag, Karin, Martínez, Alberto Fernández, He, Y., Huang, Yalin, Hagström, E., Alvehag, Karin, Martínez, Alberto Fernández, and He, Y.

Abstract

The number of connections of photovoltaic (PV) to distribution network is increasing. Very few PV connection guidelines that distribution system operators (DSOs) can refer to have been found. This paper deals with network planning guidelines for distribution networks with PV. The paper aims to identify planning rules that are relatively easy to implement., QC 20140625

Published
2013
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34. Genetic variants and associations of 25-hydroxyvitamin D concentrations with major clinical outcomes

Author

Levin, GP, Robinson-Cohen, C, De Boer, IH, Houston, DK, Lohman, K, Liu, Y, Kritchevsky, SB, Cauley, JA, Tanaka, T, Ferrucci, L, Bandinelli, S, Patel, KV, Hagström, E, Michaëlsson, K, Melhus, H, Wang, T, Wolf, M, Psaty, BM, Siscovick, D, Kestenbaum, B, Levin, GP, Robinson-Cohen, C, De Boer, IH, Houston, DK, Lohman, K, Liu, Y, Kritchevsky, SB, Cauley, JA, Tanaka, T, Ferrucci, L, Bandinelli, S, Patel, KV, Hagström, E, Michaëlsson, K, Melhus, H, Wang, T, Wolf, M, Psaty, BM, Siscovick, D, and Kestenbaum, B

Abstract

Context: Lower serum 25-hydroxyvitaminDconcentrations are associatedwith greater risks of many chronic diseases across large, prospective community-based studies. Substrate 25-hydroxyvitamin D must be converted to 1,25-dihydroxyvitamin D for full biological activity, and complex metabolic pathways suggest that interindividual variability in vitamin D metabolism may alter the clinical consequences of measured serum 25-hydroxyvitamin D. Objective: To investigate whether common variation within genes encoding the vitamin D-binding protein, megalin, cubilin, CYP27B1, CYP24A1, and the vitamin D receptor (VDR) modify associations of low 25-hydroxyvitamin D with major clinical outcomes. Design, Setting, and Participants: Examination of 141 single-nucleotide polymorphisms in a discovery cohort of 1514 white participants (who were recruited from 4 US regions) from the community-based Cardiovascular Health Study. Participants had serum 25-hydroxyvitamin D measurements in 1992-1993 and were followed up for a median of 11 years (through 2006). Replication meta-analyses were conducted across the independent, community-based US Health, Aging, and Body Composition (n=922; follow-up: 1998-1999 through 2005), Italian Invecchiare in Chianti (n=835; follow-up: 1998-2000 through 2006), and Swedish Uppsala Longitudinal Study of Adult Men (n=970; follow-up: 1991-1995 through 2008) cohort studies. Main OutcomeMeasure: Composite outcome of incident hip facture, myocardial infarction, cancer, and mortality over long-term follow-up. Results: Interactions between 5 single-nucleotide polymorphisms and low 25-hydroxyvitamin D concentration were identified in the discovery phase and 1 involving a variant in the VDR gene replicated in independent meta-analysis. Among Cardiovascular Health Study participants, low 25-hydroxyvitamin D concentration was associated with hazard ratios for risk of the composite outcome of 1.40 (95% CI, 1.12-1.74) for those who had 1 minor allele at rs7968585 and 1.82 (9

Published
2012

39. MHC variability supports dog domestication from a large number of wolves: high diversity in Asia.

Author

Niskanen, A K, Hagström, E, Lohi, H, Ruokonen, M, Esparza-Salas, R, Aspi, J, and Savolainen, P

Subjects
*DOMESTICATION of dogs, *DOGS, *MAJOR histocompatibility complex, *ALLELES, *WOLVES, *MITOCHONDRIAL DNA, *POLYMERASE chain reaction
Abstract

The process of dog domestication is still somewhat unresolved. Earlier studies indicate that domestic dogs from all over the world have a common origin in Asia. So far, major histocompatibility complex (MHC) diversity has not been studied in detail in Asian dogs, although high levels of genetic diversity are expected at the domestication locality. We sequenced the second exon of the canine MHC gene DLA-DRB1 from 128 Asian dogs and compared our data with a previously published large data set of MHC alleles, mostly from European dogs. Our results show that Asian dogs have a higher MHC diversity than European dogs. We also estimated that there is only a small probability that new alleles have arisen by mutation since domestication. Based on the assumption that all of the currently known 102 DLA-DRB1 alleles come from the founding wolf population, we simulated the number of founding wolf individuals. Our simulations indicate an effective population size of at least 500 founding wolves, suggesting that the founding wolf population was large or that backcrossing has taken place. [ABSTRACT FROM AUTHOR]

Published
2013
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46. Eligibility for lipid-lowering therapy when applying systemic coronary risk estimation 2 according to guidelines on apparently healthy middle-aged individuals.

Author

Yari A, Ueda P, Lundman P, Alfredsson J, Ravn-Fischer A, Söderberg S, Yndigegn T, Hagström E, and Jernberg T

Subjects
Humans, Middle Aged, Male, Female, Risk Assessment, Sweden epidemiology, Hypolipidemic Agents therapeutic use, Dyslipidemias epidemiology, Dyslipidemias drug therapy, Dyslipidemias blood, Dyslipidemias diagnosis, Heart Disease Risk Factors, Computed Tomography Angiography, Biomarkers blood, Patient Selection, Risk Factors, Lipids blood, Age Factors, Eligibility Determination, Coronary Artery Disease epidemiology, Coronary Artery Disease diagnostic imaging, Coronary Artery Disease prevention & control, Practice Guidelines as Topic, Coronary Angiography
Abstract

Aims: To estimate the proportion eligible for lipid-lowering therapy (LLT) when using the systemic coronary risk estimation 2 (SCORE2) on apparently healthy individuals., Methods and Results: Individuals aged 50-64 years were randomly invited to The Swedish Cardiopulmonary Bioimage Study (n = 30 154). Participants with previous atherosclerotic cardiovascular disease (CVD), diabetes mellitus, or chronic kidney disease were excluded. The 10-year risk of CVD was estimated using the SCORE2 equation and the multicell chart. Eligibility for LLT was estimated according to the 2021 European Society of Cardiology CVD prevention guidelines. Presence of coronary atherosclerosis was determined using coronary computed tomography angiography (CCTA). Among 26 570 apparently healthy individuals, 32% had high and 4% had very high 10-year CVD risk, according to the SCORE2 equation. Among high- and very-high-risk individuals, 99% had low-density lipoprotein cholesterol levels above guideline goals making 35% of the total population eligible for LLT. Of those eligible, undergoing imaging, 38% had no signs of coronary atherosclerosis according to CCTA. Using the SCORE2 chart, 52% of the population were eligible for LLT, of which 44% had no signs of coronary atherosclerosis. In those with high or very high risk, ongoing LLT was reported in 7% and another 11% received LLT within 6 months after study participation., Conclusion: Nearly all apparently healthy individuals with high and very high CVD risk, or 35% of the total population, were eligible for LLT according to guidelines, and a large proportion had no signs of atherosclerosis. Compared with the SCORE2 equation, the SCORE2 chart resulted in more individuals being eligible for LLT., Competing Interests: Conflict of interest: A.Y. reports institutional research grant from MSD, outside the submitted work. A.R.-F. reports grants from Amarin and Bayer and payment for lectures and expert testimony from Amarin, Amgen, Astra Zeneca, Boehringer Ingelheim, Novartis, Novo Nordisk, Orion Pharma, Pfizer, and Sanofi. J.A. reports lecture fee from Boehringer Ingelheim, Astra Zeneca, MSD, Bayer, and Novartis and advisory board reimbursement from Astra Zeneca and Novartis. S.S. reports consultancy and speakers honoraria from Actelion Ltd. E.H. reports institutional research grants from Pfizer and Amgen and small personal fees from Amarin, Amgen, Astra Zeneca, Bayer, and Novo Nordisk. T.J. reports research grant funding from MSD (significant). All other authors declare no conflict of interest., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Published
2024
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47. Lipoproteins and lipoprotein lipid composition are associated with stages of dysglycemia and subclinical coronary atherosclerosis.

Author

Gigante B, Chen Q, Björkbacka H, Björnson E, Brinck J, Chorell E, Djekic D, Edsfeldt A, Engström G, Eriksson JW, Gottsäter A, Gummesson A, Hagström E, Hedin U, Jernberg T, Johnston N, Nilsson L, Nyström F, Otten J, Rosengren A, Söderberg S, Haglöw JT, and Östgren CJ

Abstract

Background: Dyslipidaemia in patients with diabetes contributes to the risk of atherosclerotic cardiovascular disease. We aimed to identify a dyslipidemic profile associated with both dysglycemia and subclinical coronary atherosclerosis., Methods: Study participants (n = 5050) were classified in three groups: normoglycemia, pre-diabetes, and diabetes. A coronary artery calcium score (CACS) > 0 defined subclinical coronary atherosclerosis. Two independent methods were used to identify, among 225 lipid biomarkers, those that were associated with pre-diabetes and diabetes and were further tested for association by zero inflated Poisson regression with CACS and with CACS burden in study participants with CACS>0. Estimates were adjusted for cardiovascular risk factors with an interaction term for dispensed lipid lowering drugs., Results: Thirty-two biomarkers associated with prediabetes and diabetes were further investigated for association with CACS. HDL diameter [multi-adjusted OR of 0.85 and 95 %CI (0.78-0.92)] as well as free cholesterol, phospholipids and total lipids in extra large HDL were inversely associated with CACS. There was a borderline significant interaction between small HDL and dispensed lipid lowering drugs on the presence of CACS, with and multi-adjusted OR of 0.53 and 95 %CI (0.36-0.77). None of the 32 glycemic profile-related lipid biomarkers associated with the relative increase of CACS in those with CACS>0. No consistent association was observed between non-HDL lipoproteins and CACS., Conclusions: Changes in composition and relative concentration of HDL associated with both dysglycemia and subclinical coronary atherosclerosis. Treatment with lipid lowering drugs may contribute to reduce the risk associated with high circulating levels of small HDL., Competing Interests: Declaration of competing interest None., (Copyright © 2024. Published by Elsevier B.V.)

Published
2024
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48. Intensive early and sustained lowering of non-high-density lipoprotein cholesterol after myocardial infarction and prognosis: the SWEDEHEART registry.

Author

Schubert J, Leosdottir M, Lindahl B, Westerbergh J, Melhus H, Modica A, Cater N, Brinck J, Ray KK, and Hagström E

Subjects
Humans, Male, Female, Aged, Middle Aged, Prognosis, Cholesterol, LDL blood, Sweden epidemiology, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Cholesterol, HDL blood, Cholesterol, HDL metabolism, Cholesterol blood, Myocardial Infarction blood, Myocardial Infarction mortality, Registries
Abstract

Background and Aims: Non-HDL-C provides an estimate of lipid-associated risk and is a secondary treatment target after myocardial infarction (MI). The aim was to study the relationship between non-HDL-C levels after MI and risk of adverse outcomes., Methods: From the SWEDEHEART registry, 56 262 patients with MI were included. Outcomes were major adverse cardiovascular event (MACE: death, MI, and ischaemic stroke), death, and non-fatal MI. Non-HDL-C was assessed at admission, 2 months, and 1 year. Target achievement (<2.2 mmol/L) of non-HDL-C, timing thereof, and outcomes were assessed., Results: During median follow-up of 5.4 years, 9549 had MACE, 5427 died, and 3946 had MI. Long-term hazard ratio (HR) for MACE in the lowest vs. the highest quartile of achieved non-HDL-C at 1 year was 0.76 [95% confidence interval (CI) 0.71-0.81]. Short-term results were consistent also when assessing non-HDL-C levels at 2 months, including early events up to 1 year (HR 0.80, 95% CI 0.68-0.92). Similar results were observed for all outcomes. Patients achieving both early and sustained targets had lowest risk of outcomes (HR 0.80, 95% CI 0.74-0.86) vs. patients achieving target early or late (HR for both 0.86, 95% CI 0.79-0.93)., Conclusions: The lowest achieved levels both at 2 months and at 1 year of non-HDL-C were associated with better outcome. The lowest risk was observed when target was achieved within 2 months of MI and sustained thereafter. These findings challenge the current stepwise approach for cholesterol lowering after MI, which inevitably results in delaying goal attainment and possible harm., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Published
2024
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49. Management and outcome in foreign-born vs native-born patients with myocardial infarction in Sweden.

Author

Zwackman S, Häggström J, Hagström E, Jernberg T, Karlsson JE, Lawesson SS, Leosdottir M, Ravn-Fischer A, Eriksson M, and Alfredsson J

Subjects
Humans, Male, Sweden epidemiology, Female, Aged, Middle Aged, Emigrants and Immigrants statistics & numerical data, Follow-Up Studies, Risk Factors, Disease Management, Survival Rate trends, Cause of Death trends, Myocardial Infarction epidemiology, Myocardial Infarction ethnology, Myocardial Infarction therapy, Registries
Abstract

Aims: Previous studies on disparities in healthcare and outcomes have shown conflicting results. The aim of this study was to assess differences in baseline characteristics, management, and outcomes in myocardial infarction (MI) patients, by country of birth., Methods and Results: In total, 194 259 MI patients (64% male, 15% foreign-born) from the nationwide SWEDEHEART (The Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies) registry were included and compared by geographic region of birth. The primary outcome was 1-year major adverse cardiovascular events (MACEs) including all-cause death, MI, and stroke. Secondary outcomes were long-term MACE (up to 12 years), the individual components of MACE, 30-day mortality, management, and risk factors. Logistic regression, Cox proportional hazard models, and propensity score match (PSM), accounting for baseline differences, were used. Foreign-born patients were younger, often male, and had a higher cardiovascular (CV) risk factor burden, including smoking, diabetes, and hypertension. In PSM analyses, Asia-born patients had higher likelihood of revascularization [odds ratio 1.16, 95% confidence interval (CI) 1.04-1.30], statins and beta-blocker prescription at discharge, and a 34% lower risk of 30-day mortality. Furthermore, no statistically significant differences were found in primary outcomes except for Asia-born patients having lower risk of 1-year MACE [hazard ratio (HR) 0.85, 95% CI 0.73-0.98], driven by lower mortality (HR 0.72, 95% CI 0.57-0.91). The results persisted over the long-term follow-up., Conclusion: This study shows that in a system with universal healthcare coverage in which acute and secondary preventive treatments do not differ by country of birth, foreign-born patients, despite higher CV risk factor burden, will do at least as well as native-born patients., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Published
2024
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50. Structured diabetes care routines in cardiac rehabilitation are associated with increased diabetes detection and improved treatment after myocardial infarction: a nationwide observational study.

Author

Sharad B, Eckerdal N, Magnusson M, Michelsen HÖ, Jujic A, Lidin M, Mellbin L, Shaat N, Pingel R, Wallert J, Hagström E, and Leósdóttir M

Subjects
Humans, Male, Female, Middle Aged, Sweden epidemiology, Aged, Treatment Outcome, Time Factors, Predictive Value of Tests, Glycemic Control, Health Care Surveys, Practice Patterns, Physicians', Blood Glucose metabolism, Blood Glucose drug effects, Myocardial Infarction diagnosis, Myocardial Infarction rehabilitation, Myocardial Infarction therapy, Myocardial Infarction epidemiology, Myocardial Infarction blood, Registries, Cardiac Rehabilitation, Glucose Tolerance Test, Hypoglycemic Agents therapeutic use, Glycated Hemoglobin metabolism, Diabetes Mellitus diagnosis, Diabetes Mellitus epidemiology, Diabetes Mellitus blood, Diabetes Mellitus therapy, Biomarkers blood
Abstract

Background: Despite the detrimental impact of abnormal glucose metabolism on cardiovascular prognosis after myocardial infarction (MI), diabetes is both underdiagnosed and undertreated. We investigated associations between structured diabetes care routines in cardiac rehabilitation (CR) and detection and treatment of diabetes at one-year post-MI., Methods: Center-level data was derived from the Perfect-CR survey, which evaluated work routines applied at Swedish CR centers (n = 76). Work routines involving diabetes care included: (1) routine assessment of fasting glucose and/or HbA1c, (2) routine use of oral glucose tolerance test (OGTT), (3) having regular case rounds with diabetologists, and (4) whether glucose-lowering medication was adjusted by CR physicians. Patient-level data was obtained from the national MI registry SWEDEHEART (n = 7601, 76% male, mean age 62.6 years) and included all post-MI patients irrespective of diabetes diagnosis. Using mixed-effects regression we estimated differences between patients exposed versus. not exposed to the four above-mentioned diabetes care routines. Outcomes were newly detected diabetes and the proportion of patients receiving oral glucose-lowering medication at one-year post-MI., Results: Routine assessment of fasting glucose/HbA1c was performed at 63.2% (n = 48) of the centers, while 38.2% (n = 29) reported using OGTT for detecting glucose abnormalities. Glucose-lowering medication adjusted by CR physicians (n = 13, 17.1%) or regular case rounds with diabetologists (n = 7, 9.2%) were less frequently reported. In total, 4.0% of all patients (n = 304) were diagnosed with diabetes during follow-up and 17.9% (n = 1361) were on oral glucose-lowering treatment one-year post-MI. Routine use of OGTT was associated with a higher rate of newly detected diabetes at one-year (risk ratio [95% confidence interval]: 1.62 [1.26, 1.98], p = 0.0007). At one-year a higher proportion of patients were receiving oral glucose-lowering medication at centers using OGTT (1.22 [1.07, 1.37], p = 0.0046) and where such medication was adjusted by CR physicians (1.31 [1.06, 1.56], p = 0.0155). Compared to having none of the structured diabetes care routines, the more routines implemented the higher the rate of newly detected diabetes (from 0 routines: 2.7% to 4 routines: 6.3%; p for trend = 0.0014)., Conclusions: Having structured routines for diabetes care implemented within CR can improve detection and treatment of diabetes post-MI. A cluster-randomized trial is warranted to ascertain causality., (© 2024. The Author(s).)

Published
2024
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