58 results on '"Mahmoodi, Bakhtawar K."'
Search Results
52. Increased risk of arterial thromboembolism after a prior episode of venous thromboembolism: results from the Prevention of REnal and Vascular ENd stage Disease (PREVEND) Study.
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Schouwenburg, Inge M., Gansevoort, Ron T., Mahmoodi, Bakhtawar K., Visser, Margaretha M., Kluin-Nelemans, Hanneke C., Lijfering, Willem M., and Veeger, Nic J. G. M.
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THROMBOEMBOLISM risk factors ,CHRONIC kidney failure ,ANTICOAGULANTS ,CARDIOVASCULAR diseases risk factors ,MEDICAL statistics ,FOLLOW-up studies (Medicine) - Abstract
Large population-based studies are needed to establish the magnitude and duration of the recently suggested association between arterial and venous thromboembolism. In 1997-98, all inhabitants of Groningen, the Netherlands, aged 28-75 years ( n = 85 421), were invited to participate in a study that followed and monitored responding subjects ( n = 40 856) for venous and arterial thromboembolism until 2009. Thromboembolism was verified with national registries of hospital discharge diagnoses and death certificates, anticoagulation clinic and medical records. During a median follow-up of 10·7 years, 549 participants developed venous thromboembolism and 3283 developed arterial thromboembolism. Annual incidence of arterial thromboembolism after venous thromboembolism was 2·03% [95% confidence interval ( CI), 1·48-2·71], compared to 0·87% (95% CI, 0·84-0·90) in subjects without venous thromboembolism. The hazard ratio ( HR) of arterial thromboembolism after venous thromboembolism was 1·40 (95% CI, 1·04-1·88) after adjustment for age, sex and cardiovascular risk factors. This risk was highest during the first year after venous thromboembolism [annual incidence, 3·00% (95% CI, 1·64-5·04); adjusted HR, 2·01 (95% CI, 1·19-3·40)] and after an unprovoked event [annual incidence, 2·53% (95% CI, 1·68-3·66); adjusted HR, 1·62 (95% CI, 1·11-2·34)]. This study showed that subjects with venous thromboembolism are at increased risk for arterial thromboembolism, particularly in the first year after venous thromboembolism and after an unprovoked event. [ABSTRACT FROM AUTHOR]
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- 2012
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53. Lipid levels do not influence the risk of venous thromboembolism
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van Schouwenburg, Inge M., Mahmoodi, Bakhtawar K., Gansevoort, Ron T., Muntinghe, Friso L.H., Dullaart, Robin P.F., Kluin-Nelemans, Hanneke C., Veeger, Nic J.G.M., and Meijer, Karina
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- 2012
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54. Cardiovascular Risk Factors Associated With Venous Thromboembolism
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Gregson, John, Kaptoge, Stephen, Bolton, Thomas, Pennells, Lisa, Willeit, Peter, Burgess, Stephen, Bell, Steven, Sweeting, Michael, Rimm, Eric B, Kabrhel, Christopher, Zöller, Bengt, Assmann, Gerd, Gudnason, Vilmundur, Folsom, Aaron R, Arndt, Volker, Fletcher, Astrid, Norman, Paul E, Nordestgaard, Børge G, Kitamura, Akihiko, Mahmoodi, Bakhtawar K, Whincup, Peter H, Knuiman, Matthew, Salomaa, Veikko, Meisinger, Christa, Koenig, Wolfgang, Kavousi, Maryam, Völzke, Henry, Cooper, Jackie A, Ninomiya, Toshiharu, Casiglia, Edoardo, Rodriguez, Beatriz, Ben-Shlomo, Yoav, Després, Jean-Pierre, Simons, Leon, Barrett-Connor, Elizabeth, Björkelund, Cecilia, Notdurfter, Marlene, Kromhout, Daan, Price, Jackie, Sutherland, Susan E, Sundström, Johan, Kauhanen, Jussi, Gallacher, John, Beulens, Joline WJ, Dankner, Rachel, Cooper, Cyrus, Giampaoli, Simona, Deen, Jason F, Gómez De La Cámara, Agustín, 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, Njølstad, Inger, Lawlor, Deborah A, Van Der Schouw, Yvonne T, Selmer, Randi Marie, Trevisan, Maurizio, Verschuren, WM Monique, Greenland, Philip, Wassertheil-Smoller, Sylvia, Lowe, Gordon DO, Wood, Angela M, Butterworth, Adam S, Thompson, Simon G, Danesh, John, Di Angelantonio, Emanuele, Meade, Tom, and Emerging Risk Factors Collaboration
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2. Zero hunger ,Adult ,Male ,Venous Thrombosis ,Smoking ,Coronary Disease ,Venous Thromboembolism ,Middle Aged ,16. Peace & justice ,United Kingdom ,3. Good health ,Body Mass Index ,Cardiovascular Diseases ,Risk Factors ,Outcome Assessment, Health Care ,Diabetes Mellitus ,Humans ,Female ,Obesity ,Prospective Studies ,Pulmonary Embolism - 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; 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.
55. Association of chronic kidney disease with adverse outcomes.
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Hentschel, Viet Anh-Thu, Mundt, Heiko, Benck, Urs, Birck, Rainer, Krämer, Bernhard K., Izumi, Yuichiro, Ogawa, Masami, Itoh, Hidenori, Shimada, Hajime, Nonoguchi, Hiroshi, Xin Du, Ye Zhao, Wenjuan Huang, Lin Liu, Changchun Cao, Mahmoodi, Bakhtawar K., Fox, Caroline S., Astor, Brad C., Nelson, Robert G., and Matsushita, Kunihiro
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KIDNEY diseases , *MORTALITY , *HYPERTENSION , *META-analysis , *CHRONIC kidney failure - Abstract
Several letters to the editor, as well as the authors' reply on their article "Associations of Kidney Disease Measures With Mortality and End-Stage Renal Disease in Individuals With and Without Hypertension: A Meta-Analysis" published in the November 10, 2012 issue are presented.
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- 2013
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56. Association of Chromosome 9p21 With Subsequent Coronary Heart Disease Events.
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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 MP, 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 VV, Leiherer A, Lenzini PA, Levin D, Lyytikäinen LP, 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, Viviani 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 ML, 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, Maitland-van 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, Ten Berg JM, Thanassoulis G, Thiery J, van der Graaf Y, Visseren FLJ, Waltenberger J, Van der Harst P, Tardif JC, Sattar N, Lang CC, Pare G, Brophy JM, Anderson JL, März W, Wallentin L, Cameron VA, Horne BD, Samani NJ, Hingorani AD, and Asselbergs FW
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- Case-Control Studies, Coronary Artery Disease genetics, Female, Gene Frequency, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Myocardial Infarction genetics, Myocardial Infarction pathology, Odds Ratio, Risk Factors, Chromosomes, Human, Pair 9, Coronary Artery Disease pathology
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Background: 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., Methods: 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., Results: 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 interaction <0.001 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)., Conclusions: 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.
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- 2019
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57. Economic evaluation of the use of non-vitamin K oral anticoagulants in patients with atrial fibrillation on antiplatelet therapy: a modelling analysis using the healthcare system in the Netherlands.
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Bennaghmouch N, de Veer AJWM, Mahmoodi BK, Jofre-Bonet M, Lip GYH, Bode K, and Ten Berg JM
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- Administration, Oral, Atrial Fibrillation complications, Atrial Fibrillation economics, Cost-Benefit Analysis, Humans, Netherlands, Stroke economics, Vitamin K, Anticoagulants administration & dosage, Atrial Fibrillation drug therapy, Platelet Aggregation Inhibitors administration & dosage, Quality-Adjusted Life Years, Stroke prevention & control
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Aims: Non-vitamin K oral anticoagulants (NOACs) have consistently demonstrated superior efficacy in terms of stroke prevention and safety in terms of bleeding over vitamin K antagonist (VKA) in patients with non-valvular atrial fibrillation (AF). The potential use of NOACs in AF patients requiring antiplatelet therapy (APT) has only been assessed in small meta-analyses reporting consistent benefits of NOACs over VKAs. However, the prescription costs of NOACs are higher than those of VKAs. The aim of his study was to estimate the cost-effectiveness (CE) of NOACs compared to VKAs in patients with non-valvular AF also requiring APT with the Dutch healthcare system used as a surrogate of many European healthcare systems., Methods and Results: A decision tree was constructed to analyse the CE of NOACs compared to VKAs in patients with non-valvular AF with an indication for APT over a horizon of 1 year. Beside the base-case analysis, univariate probabilistic sensitivity and two sensitivity analyses were performed: first, we assessed the impact of VKA home monitoring; second, we varied the NOACs price assuming patent expiration. Use of NOACs instead of VKA is associated with a health gain of 0.0171 quality-adjusted life years (QALYs) and with an incremental cost of €357, resulting in an incremental cost-effectiveness ratio of €20 919, which is almost equal to the generally accepted CE threshold of €20 000 used in the Netherlands. The probability that NOACs are cost-effective at a conservative willingness-to-pay threshold of €20 000 per QALY was 50%. Introducing home monitoring increased VKAs costs so much that NOACs became the dominant option (less costly and more effective). Price drops associated to patent expiration of NOACs increased its CE., Conclusion: This analysis suggests that the use of NOACs is a cost-effective alternative of VKAs in patients with AF needing APT. Our findings in the Netherlands healthcare system are probably consistent with other European populations., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com.)
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- 2019
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58. High absolute risks and predictors of venous and arterial thromboembolic events in patients with nephrotic syndrome: results from a large retrospective cohort study.
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Mahmoodi BK, ten Kate MK, Waanders F, Veeger NJ, Brouwer JL, Vogt L, Navis G, and van der Meer J
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- Adult, Cohort Studies, Female, Follow-Up Studies, Humans, Male, Middle Aged, Nephrotic Syndrome diagnosis, Odds Ratio, Prognosis, Retrospective Studies, Risk Factors, Thromboembolism etiology, Venous Thromboembolism, Arteries, Nephrotic Syndrome complications, Predictive Value of Tests, Thromboembolism diagnosis
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Background: No data are available on the absolute risk of either venous thromboembolism (VTE) or arterial thromboembolism (ATE) in patients with nephrotic syndrome. Reported risks are based on multiple case reports and small studies with mostly short-term follow-up. We assessed the absolute risk of VTE and ATE in a large, single-center, retrospective cohort study and attempted to identify predictive factors in these patients., Methods and Results: A total of 298 consecutive patients with nephrotic syndrome (59% men; mean age, 42+/-18 years) were enrolled. Mean follow-up was 10+/-9 years. Nephrotic syndrome was defined by proteinuria > or =3.5 g/d, and patients were classified according to underlying histological lesions accounting for nephrotic syndrome. Objectively verified symptomatic thromboembolic events were the primary study outcome. Annual incidences of VTE and ATE were 1.02% (95% confidence interval, 0.68 to 1.46) and 1.48% (95% confidence interval, 1.07 to 1.99), respectively. Over the first 6 months of follow-up, these rates were 9.85% and 5.52%, respectively. Proteinuria and serum albumin levels tended to be related to VTE; however, only the predictive value of the ratio of proteinuria to serum albumin was significant (hazard ratio, 5.6; 95% confidence interval, 1.2 to 26.2; P=0.03). In contrast, neither the degree of proteinuria nor serum albumin levels were related to ATE. Sex, age, hypertension, diabetes, smoking, prior ATE, and estimated glomerular filtration rate predicted ATE (P< or =0.02)., Conclusions: This study verifies high absolute risks of symptomatic VTE and ATE that were remarkably elevated within the first 6 months. Whereas the ratio of proteinuria to serum albumin predicted VTE, estimated glomerular filtration rate and multiple classic risk factors for atherosclerosis were predictors of ATE.
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- 2008
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