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  • 101. Watkins, David
    et al.
    Gallant, Caroline
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Individual Genomes on the Horizon2010Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 363, nr 2, s. 195-196Artikel i tidskrift (Refereegranskat)
  • 102.
    Westermark, Gunilla T.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Korsgren, Olle
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Westermark, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Amyloid and Transplanted Islets Reply2008Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 359, nr 25, s. 2729-2731Artikel i tidskrift (Refereegranskat)
  • 103. Westermark, Gunilla T.
    et al.
    Westermark, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Berne, Christian
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Korsgren, Olle
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Widespread amyloid deposition in transplanted human pancreatic islets2008Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 359, nr 9, s. 977-979Artikel i tidskrift (Refereegranskat)
  • 104. White, Harvey D.
    et al.
    Held, Claes
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Stewart, Ralph
    Tarka, Elizabeth
    Brown, Rebekkah
    Davies, Richard Y.
    Budaj, Andrzej
    Harrington, Robert A.
    Steg, P. Gabriel
    Ardis-Sino, Diego
    Armstrong, Paul W.
    Avezum, Alvaro
    Aylward, Philip E.
    Bryce, Alfonso
    Chen, Hong
    Chen, Ming-Fong
    Corbalan, Ramon
    Dalby, Anthony J.
    Danchin, Nicolas
    De Winter, Robbert J.
    Denchev, Stefan
    Diaz, Rafael
    Elisaf, Moses
    Flather, Marcus D.
    Goudev, Assen R.
    Granger, Christopher B.
    Grinfeld, Liliana
    Hochman, Judith S.
    Husted, Steen
    Kim, Hyo-Soo
    Koenig, Wolfgang
    Linhart, Ales
    Lonn, Eva
    Lopez-Sendon, Jose
    Manolis, Athanasios J.
    Mohler, Emile R., III
    Nicolau, Jose C.
    Pais, Prem
    Parkhomenko, Alexander
    Pedersen, Terje R.
    Pella, Daniel
    Ramos-Corrales, Marco A.
    Ruda, Mikhail
    Sereg, Mtys
    Siddique, Saulat
    Sinnaeve, Peter
    Smith, Peter
    Sritara, Piyamitr
    Swart, Henk P.
    Sy, Rody G.
    Teramoto, Tamio
    Tse, Hung-Fat
    Watson, David
    Weaver, W. Douglas
    Weiss, Robert
    Viigimaa, Margus
    Vinereanu, Dragos
    Zhu, Junren
    Cannon, Christopher P.
    Wallentin, Lars
    Survival with Cardiac-Resynchronization Therapy in Mild Heart Failure2014Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 370, nr 18, s. 1702-1711Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Elevated lipoprotein-associated phospholipase A(2) activity promotes the development of vulnerable atherosclerotic plaques, and elevated plasma levels of this enzyme are associated with an increased risk of coronary events. Darapladib is a selective oral inhibitor of lipoprotein-associated phospholipase A(2). Methods: In a double-blind trial, we randomly assigned 15,828 patients with stable coronary heart disease to receive either once-daily darapladib (at a dose of 160 mg) or placebo. The primary end point was a composite of cardiovascular death, myocardial infarction, or stroke. Secondary end points included the components of the primary end point as well as major coronary events (death from coronary heart disease, myocardial infarction, or urgent coronary revascularization for myocardial ischemia) and total coronary events (death from coronary heart disease, myocardial infarction, hospitalization for unstable angina, or any coronary revascularization). Results: During a median follow-up period of 3.7 years, the primary end point occurred in 769 of 7924 patients (9.7%) in the darapladib group and 819 of 7904 patients (10.4%) in the placebo group (hazard ratio in the darapladib group, 0.94; 95% confidence interval [CI], 0.85 to 1.03; P=0.20). There were also no significant between-group differences in the rates of the individual components of the primary end point or in all-cause mortality. Darapladib, as compared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95% CI, 0.82 to 1.00; P=0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95% CI, 0.84 to 0.98; P=0.02). ConclusionsIn patients with stable coronary heart disease, darapladib did not significantly reduce the risk of the primary composite end point of cardiovascular death, myocardial infarction, or stroke. (Funded by GlaxoSmithKline; STABILITY ClinicalTrials.gov number, NCT00799903.)

  • 105. White, Harvey D
    et al.
    Held, Claes
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Stewart, Ralph
    Tarka, Elizabeth
    Brown, Rebekkah
    Davies, Richard Y
    Budaj, Andrzej
    Harrington, Robert A
    Steg, P Gabriel
    Ardissino, Diego
    Armstrong, Paul W
    Avezum, Alvaro
    Aylward, Philip E
    Bryce, Alfonso
    Chen, Hong
    Chen, Ming-Fong
    Corbalan, Ramon
    Dalby, Anthony J
    Danchin, Nicolas
    De Winter, Robbert J
    Denchev, Stefan
    Diaz, Rafael
    Elisaf, Moses
    Flather, Marcus D
    Goudev, Assen R
    Granger, Christopher B
    Grinfeld, Liliana
    Hochman, Judith S
    Husted, Steen
    Kim, Hyo-Soo
    Koenig, Wolfgang
    Linhart, Ales
    Lonn, Eva
    López-Sendón, José
    Manolis, Athanasios J
    Mohler, Emile R
    Nicolau, José C
    Pais, Prem
    Parkhomenko, Alexander
    Pedersen, Terje R
    Pella, Daniel
    Ramos-Corrales, Marco A
    Ruda, Mikhail
    Sereg, Mátyás
    Siddique, Saulat
    Sinnaeve, Peter
    Smith, Peter
    Sritara, Piyamitr
    Swart, Henk P
    Sy, Rody G
    Teramoto, Tamio
    Tse, Hung-Fat
    Watson, David
    Weaver, W Douglas
    Weiss, Robert
    Viigimaa, Margus
    Vinereanu, Dragos
    Zhu, Junren
    Cannon, Christopher P
    Wallentin, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Darapladib for preventing ischemic events in stable coronary heart disease2014Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 370, nr 18, s. 1702-1711Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND:

    Elevated lipoprotein-associated phospholipase A2 activity promotes the development of vulnerable atherosclerotic plaques, and elevated plasma levels of this enzyme are associated with an increased risk of coronary events. Darapladib is a selective oral inhibitor of lipoprotein-associated phospholipase A2.

    METHODS:

    In a double-blind trial, we randomly assigned 15,828 patients with stable coronary heart disease to receive either once-daily darapladib (at a dose of 160 mg) or placebo. The primary end point was a composite of cardiovascular death, myocardial infarction, or stroke. Secondary end points included the components of the primary end point as well as major coronary events (death from coronary heart disease, myocardial infarction, or urgent coronary revascularization for myocardial ischemia) and total coronary events (death from coronary heart disease, myocardial infarction, hospitalization for unstable angina, or any coronary revascularization).

    RESULTS:

    During a median follow-up period of 3.7 years, the primary end point occurred in 769 of 7924 patients (9.7%) in the darapladib group and 819 of 7904 patients (10.4%) in the placebo group (hazard ratio in the darapladib group, 0.94; 95% confidence interval [CI], 0.85 to 1.03; P=0.20). There were also no significant between-group differences in the rates of the individual components of the primary end point or in all-cause mortality. Darapladib, as compared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95% CI, 0.82 to 1.00; P=0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95% CI, 0.84 to 0.98; P=0.02).

    CONCLUSIONS:

    In patients with stable coronary heart disease, darapladib did not significantly reduce the risk of the primary composite end point of cardiovascular death, myocardial infarction, or stroke. (Funded by GlaxoSmithKline; STABILITY ClinicalTrials.gov number, NCT00799903.).

  • 106. Wykrzykowska, Joanna J
    et al.
    Kraak, Robin P
    Hofma, Sjoerd H
    van der Schaaf, Rene J
    Arkenbout, E Karin
    IJsselmuiden, Alexander J
    Elias, Joëlle
    van Dongen, Ivo M
    Tijssen, Ruben Y G
    Koch, Karel T
    Baan, Jan
    Vis, M Marije
    de Winter, Robbert J
    Piek, Jan J
    Tijssen, Jan G P
    Henriques, Jose P S
    Bioresorbable Scaffolds versus Metallic Stents in Routine PCI.2017Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 376, nr 24, s. 2319-2328Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Bioresorbable vascular scaffolds were developed to overcome the shortcomings of drug-eluting stents in percutaneous coronary intervention (PCI). We performed an investigator-initiated, randomized trial to compare an everolimus-eluting bioresorbable scaffold with an everolimus-eluting metallic stent in the context of routine clinical practice.

    METHODS: We randomly assigned 1845 patients undergoing PCI to receive either a bioresorbable vascular scaffold (924 patients) or a metallic stent (921 patients). The primary end point was target-vessel failure (a composite of cardiac death, target-vessel myocardial infarction, or target-vessel revascularization). The data and safety monitoring board recommended early reporting of the study results because of safety concerns. This report provides descriptive information on end-point events.

    RESULTS: The median follow-up was 707 days. Target-vessel failure occurred in 105 patients in the scaffold group and in 94 patients in the stent group (2-year cumulative event rates, 11.7% and 10.7%, respectively; hazard ratio, 1.12; 95% confidence interval [CI], 0.85 to 1.48; P=0.43); event rates were based on Kaplan-Meier estimates in time-to-event analyses. Cardiac death occurred in 18 patients in the scaffold group and in 23 patients in the stent group (2-year cumulative event rates, 2.0% and 2.7%, respectively), target-vessel myocardial infarction occurred in 48 patients in the scaffold group and in 30 patients in the stent group (2-year cumulative event rates, 5.5% and 3.2%), and target-vessel revascularization occurred in 76 patients in the scaffold group and in 65 patients in the stent group (2-year cumulative event rates, 8.7% and 7.5%). Definite or probable device thrombosis occurred in 31 patients in the scaffold group as compared with 8 patients in the stent group (2-year cumulative event rates, 3.5% vs. 0.9%; hazard ratio, 3.87; 95% CI, 1.78 to 8.42; P<0.001).

    CONCLUSIONS: In this preliminary report of a trial involving patients undergoing PCI, there was no significant difference in the rate of target-vessel failure between the patients who received a bioresorbable scaffold and the patients who received a metallic stent. The bioresorbable scaffold was associated with a higher incidence of device thrombosis than the metallic stent through 2 years of follow-up. (Funded by Abbott Vascular; AIDA ClinicalTrials.gov number, NCT01858077 .).

  • 107. Yao, James C.
    et al.
    Ito, Tetsuhide
    Öberg, Kjell
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Advances in Pancreatic Neuroendocrine Tumor Treatment REPLY2011Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 364, nr 19, s. 1874-1875Artikel i tidskrift (Refereegranskat)
  • 108. Yao, James C.
    et al.
    Shah, Manisha H.
    Ito, Tetsuhide
    Bohas, Catherine Lombard
    Wolin, Edward M.
    Van Cutsem, Eric
    Hobday, Timothy J.
    Okusaka, Takuji
    Capdevila, Jaume
    de Vries, Elisabeth G. E.
    Tomassetti, Paola
    Pavel, Marianne E.
    Hoosen, Sakina
    Haas, Tomas
    Lincy, Jeremie
    Lebwohl, David
    Öberg, Kjell
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Medicin.
    Everolimus for advanced pancreatic neuroendocrine tumors2011Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 364, nr 6, s. 514-523Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Everolimus, an oral inhibitor of mammalian target of rapamycin (mTOR), has shown antitumor activity in patients with advanced pancreatic neuroendocrine tumors, in two phase 2 studies. We evaluated the agent in a prospective, randomized, phase 3 study.

    METHODS: We randomly assigned 410 patients who had advanced, low-grade or intermediate-grade pancreatic neuroendocrine tumors with radiologic progression within the previous 12 months to receive everolimus, at a dose of 10 mg once daily (207 patients), or placebo (203 patients), both in conjunction with best supportive care. The primary end point was progression-free survival in an intention-to-treat analysis. In the case of patients in whom radiologic progression occurred during the study, the treatment assignments could be revealed, and patients who had been randomly assigned to placebo were offered open-label everolimus.

    RESULTS: The median progression-free survival was 11.0 months with everolimus as compared with 4.6 months with placebo (hazard ratio for disease progression or death from any cause with everolimus, 0.35; 95% confidence interval [CI], 0.27 to 0.45; P<0.001), representing a 65% reduction in the estimated risk of progression or death. Estimates of the proportion of patients who were alive and progression-free at 18 months were 34% (95% CI, 26 to 43) with everolimus as compared with 9% (95% CI, 4 to 16) with placebo. Drug-related adverse events were mostly grade 1 or 2 and included stomatitis (in 64% of patients in the everolimus group vs. 17% in the placebo group), rash (49% vs. 10%), diarrhea (34% vs. 10%), fatigue (31% vs. 14%), and infections (23% vs. 6%), which were primarily upper respiratory. Grade 3 or 4 events that were more frequent with everolimus than with placebo included anemia (6% vs. 0%) and hyperglycemia (5% vs. 2%). The median exposure to everolimus was longer than exposure to placebo by a factor of 2.3 (38 weeks vs. 16 weeks).

    CONCLUSIONS: Everolimus, as compared with placebo, significantly prolonged progression-free survival among patients with progressive advanced pancreatic neuroendocrine tumors and was associated with a low rate of severe adverse events. (Funded by Novartis Oncology; RADIANT-3 ClinicalTrials.gov number, NCT00510068.).

  • 109.
    Yusuf, Salim
    et al.
    McMaster Univ, Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON, Canada.;McMaster Univ, Dept Med, Hamilton, ON, Canada..
    Lonn, Eva
    McMaster Univ, Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON, Canada.;McMaster Univ, Dept Med, Hamilton, ON, Canada..
    Pais, Prem
    St Johns Res Inst, Bangalore, Karnataka, India..
    Bosch, Jackie
    McMaster Univ, Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON, Canada.;McMaster Univ, Sch Rehabil Sci, Hamilton, ON, Canada..
    Lopez-Jaramillo, Patricio
    Univ Santander, Fdn Oftalmol Santander, Bucaramanga, Colombia.;Univ Santander, Inst Masira, Sch Med, Bucaramanga, Colombia..
    Zhu, Jun
    Chinese Acad Med Sci, Fu Wai Hosp, Beijing 100730, Peoples R China.;Peking Union Med Coll, Beijing 100021, Peoples R China..
    Xavier, Denis
    St Johns Res Inst, Bangalore, Karnataka, India.;St Johns Med Coll, Bangalore, Karnataka, India..
    Avezum, Alvaro
    Dante Pazzanese Inst Cardiol, Sao Paulo, Brazil..
    Leiter, Lawrence A.
    Univ Toronto, St Michaels Hosp, Li Ka Shing Knowledge Inst, Toronto, ON, Canada.;Univ Toronto, St Michaels Hosp, Keenan Res Ctr Biomed Sci, Toronto, ON, Canada..
    Piegas, Leopoldo S.
    HCor Heart Hosp, Sao Paulo, Brazil..
    Parkhomenko, Alexander
    Inst Cardiol, Kiev, Ukraine..
    Keltai, Matyas
    Semmelweis Univ, Hungarian Inst Cardiol, H-1085 Budapest, Hungary..
    Keltai, Katalin
    Semmelweis Univ, Hungarian Inst Cardiol, H-1085 Budapest, Hungary..
    Sliwa, Karen
    Univ Cape Town, Hatter Inst Cardiovasc Res Africa, Dept Med, Soweto Cardiovasc Res Grp, ZA-7925 Cape Town, South Africa..
    Chazova, Irina
    Inst Clin Cardiol, Russian Cardiol Res Complex, Moscow, Russia..
    Peters, Ron J. G.
    Univ Amsterdam, Acad Med Ctr, Dept Cardiol, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands..
    Held, Claes
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Yusoff, Khalid
    Univ Teknologi Majlis Amansh Rakyat, Selayang, Malaysia.;Univ Coll Sedaya Int Univ, Kuala Lumpur, Malaysia..
    Lewis, Basil S.
    Technion Israel Inst Technol, Ruth & Bruce Rappaport Sch Med, Lady Davis Carmel Med Ctr, Haifa, Israel..
    Jansky, Petr
    Univ Hosp Motol, Prague, Czech Republic..
    Khunti, Kamlesh
    Univ Leicester, Diabet Res Ctr, Leicester, Leics, England..
    Toff, William D.
    Univ Leicester, Dept Cardiovasc Sci, Leicester, Leics, England.;Glenfield Hosp, Natl Inst Hlth Res, Leicester Cardiovasc Biomed Res Unit, Leicester, Leics, England..
    Reid, Christopher M.
    Monash Ctr Cardiovasc Res & Educ Therapeut, Primary Care Diabet & Vasc Med, Melbourne, Vic, Australia.;Curtin Univ, Sch Publ Hlth, Perth, WA 6845, Australia..
    Varigos, John
    Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia..
    Accini, Jose L.
    Univ Norte, Barranquilla, Colombia..
    McKelvie, Robert
    McMaster Univ, Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON, Canada.;McMaster Univ, Dept Med, Hamilton, ON, Canada..
    Pogue, Janice
    McMaster Univ, Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON, Canada.;McMaster Univ, Dept Clin Epidemiol & Biostat, Hamilton, ON, Canada..
    Jung, Hyejung
    McMaster Univ, Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON, Canada..
    Liu, Lisheng
    Chinese Acad Med Sci, Fu Wai Hosp, Beijing 100730, Peoples R China.;Peking Union Med Coll, Beijing 100021, Peoples R China..
    Diaz, Rafael
    Inst Cardiovasc Rosario, Rosario, Santa Fe, Argentina..
    Dans, Antonio
    Univ Philippines, Coll Med, Manila, Philippines..
    Dagenais, Gilles
    Univ Laval, Inst Univ Cardiol & Pneumol Quebec, Quebec City, PQ, Canada..
    Blood-Pressure and Cholesterol Lowering in Persons without Cardiovascular Disease2016Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 374, nr 21, s. 2032-2043Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND Elevated blood pressure and elevated low-density lipoprotein (LDL) cholesterol increase the risk of cardiovascular disease. Lowering both should reduce the risk of cardiovascular events substantially.

    METHODS In a trial with 2-by-2 factorial design, we randomly assigned 12,705 participants at intermediate risk who did not have cardiovascular disease to rosuvastatin (10 mg per day) or placebo and to candesartan (16 mg per day) plus hydrochlorothiazide (12.5 mg per day) or placebo. In the analyses reported here, we compared the 3180 participants assigned to combined therapy (with rosuvastatin and the two antihypertensive agents) with the 3168 participants assigned to dual placebo. The first coprimary outcome was the composite of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke, and the second coprimary outcome additionally included heart failure, cardiac arrest, or revascularization. The median follow-up was 5.6 years.

    RESULTS The decrease in the LDL cholesterol level was 33.7 mg per deciliter (0.87 mmol per liter) greater in the combined-therapy group than in the dual-placebo group, and the decrease in systolic blood pressure was 6.2 mm Hg greater with combined therapy than with dual placebo. The first coprimary outcome occurred in 113 participants (3.6%) in the combined-therapy group and in 157 (5.0%) in the dual-placebo group (hazard ratio, 0.71; 95% confidence interval [CI], 0.56 to 0.90; P=0.005). The second coprimary outcome occurred in 136 participants (4.3%) and 187 participants (5.9%), respectively (hazard ratio, 0.72; 95% CI, 0.57 to 0.89; P=0.003). Muscle weakness and dizziness were more common in the combined-therapy group than in the dual-placebo group, but the overall rate of discontinuation of the trial regimen was similar in the two groups.

    CONCLUSIONS The combination of rosuvastatin (10 mg per day), candesartan (16 mg per day), and hydrochlorothiazide (12.5 mg per day) was associated with a significantly lower rate of cardiovascular events than dual placebo among persons at intermediate risk who did not have cardiovascular disease. (ClinicalTrials.gov number, NCT00468923.)

  • 110. Yusuf, Salim
    et al.
    Mehta, Shamir R.
    Chrolavicius, Susan
    Afzal, Rizwan
    Pogue, Janice
    Granger, Christopher B.
    Budaj, Andrzej
    Peters, Ron J. G.
    Bassand, Jean-Pierre
    Wallentin, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Joyner, Campbell
    Fox, Keith A. A.
    Comparison of fondaparinux and enoxaparin in acute coronary syndromes2006Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 354, nr 14, s. 1464-1476Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The combined use of anticoagulants, antiplatelet agents, and invasive coronary procedures reduces ischemic coronary events but also increases bleeding in patients with acute coronary syndromes. We therefore assessed whether fondaparinux would preserve the anti-ischemic benefits of enoxaparin while reducing bleeding. METHODS: We randomly assigned 20,078 patients with acute coronary syndromes to receive either fondaparinux (2.5 mg daily) or enoxaparin (1 mg per kilogram of body weight twice daily) for a mean of six days and evaluated death, myocardial infarction, or refractory ischemia at nine days (the primary outcome); major bleeding; and their combination. Patients were followed for up to six months. RESULTS: The number of patients with primary-outcome events was similar in the two groups (579 with fondaparinux [5.8 percent] vs. 573 with enoxaparin [5.7 percent]; hazard ratio in the fondaparinux group, 1.01; 95 percent confidence interval, 0.90 to 1.13), satisfying the noninferiority criteria. The number of events meeting this combined outcome showed a nonsignificant trend toward a lower value in the fondaparinux group at 30 days (805 vs. 864, P=0.13) and at the end of the study (1222 vs. 1308, P=0.06). The rate of major bleeding at nine days was markedly lower with fondaparinux than with enoxaparin (217 events [2.2 percent] vs. 412 events [4.1 percent]; hazard ratio, 0.52; P<0.001). The composite of the primary outcome and major bleeding at nine days favored fondaparinux (737 events [7.3 percent] vs. 905 events [9.0 percent]; hazard ratio, 0.81; P<0.001). Fondaparinux was associated with a significantly reduced number of deaths at 30 days (295 vs. 352, P=0.02) and at 180 days (574 vs. 638, P=0.05). CONCLUSIONS: Fondaparinux is similar to enoxaparin in reducing the risk of ischemic events at nine days, but it substantially reduces major bleeding and improves long term mortality and morbidity. (ClinicalTrials.gov number, NCT00139815.).

  • 111.
    Zander, Cecilia Soussi
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi, Medicinsk genetik.
    Soussi, Thierry
    Breast-cancer stromal cells with TP53 mutations2008Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 358, nr 15, s. 1635-1635Artikel i tidskrift (Övrigt vetenskapligt)
  • 112.
    Zander, Cecilia Soussi
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi.
    Soussi, Thierry
    Breast-cancer stromal cells with TP53 mutations.2008Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 358, nr 15Artikel i tidskrift (Refereegranskat)
  • 113. Zeisler, Harald
    et al.
    Llurba, Elisa
    Chantraine, Frederic
    Vatish, Manu
    Staff, Anne Cathrine
    Sennström, Maria
    Olovsson, Matts
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Obstetrik & gynekologi.
    Brennecke, Shaun P
    Stepan, Holger
    Allegranza, Deirdre
    Dilba, Peter
    Schoedl, Maria
    Hund, Martin
    Verlohren, Stefan
    Predictive Value of the sFlt-1:PlGF Ratio in Women with Suspected Preeclampsia2016Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 374, nr 1, s. 13-22Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The ratio of soluble fms-like tyrosine kinase 1 (sFlt-1) to placental growth factor (PlGF) is elevated in pregnant women before the clinical onset of preeclampsia, but its predictive value in women with suspected preeclampsia is unclear.

    METHODS: We performed a prospective, multicenter, observational study to derive and validate a ratio of serum sFlt-1 to PlGF that would be predictive of the absence or presence of preeclampsia in the short term in women with singleton pregnancies in whom preeclampsia was suspected (24 weeks 0 days to 36 weeks 6 days of gestation). Primary objectives were to assess whether low sFlt-1:PlGF ratios (at or below a derived cutoff) predict the absence of preeclampsia within 1 week after the first visit and whether high ratios (above the cutoff) predict the presence of preeclampsia within 4 weeks.

    RESULTS: In the development cohort (500 women), we identified an sFlt-1:PlGF ratio cutoff of 38 as having important predictive value. In a subsequent validation study among an additional 550 women, an sFlt-1:PlGF ratio of 38 or lower had a negative predictive value (i.e., no preeclampsia in the subsequent week) of 99.3% (95% confidence interval [CI], 97.9 to 99.9), with 80.0% sensitivity (95% CI, 51.9 to 95.7) and 78.3% specificity (95% CI, 74.6 to 81.7). The positive predictive value of an sFlt-1:PlGF ratio above 38 for a diagnosis of preeclampsia within 4 weeks was 36.7% (95% CI, 28.4 to 45.7), with 66.2% sensitivity (95% CI, 54.0 to 77.0) and 83.1% specificity (95% CI, 79.4 to 86.3).

    CONCLUSIONS: An sFlt-1:PlGF ratio of 38 or lower can be used to predict the short-term absence of preeclampsia in women in whom the syndrome is suspected clinically. (Funded by Roche Diagnostics.).

  • 114.
    Zethelius, Björn
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Berglund, Lars
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Basu, Samar
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Venge, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Arnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Use of multiple biomarkers to improve the prediction of death from cardiovascular causes2008Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 358, nr 20, s. 2107-2116Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The incremental usefulness of adding multiple biomarkers from different disease pathways for predicting the risk of death from cardiovascular causes has not, to our knowledge, been evaluated among the elderly. METHODS: We used data from the Uppsala Longitudinal Study of Adult Men (ULSAM), a community-based cohort of elderly men, to investigate whether a combination of biomarkers that reflect myocardial cell damage, left ventricular dysfunction, renal failure, and inflammation (troponin I, N-terminal pro-brain natriuretic peptide, cystatin C, and C-reactive protein, respectively) improved the risk stratification of a person beyond an assessment that was based on the established risk factors for cardiovascular disease (age, systolic blood pressure, use or nonuse of antihypertensive treatment, total cholesterol, high-density lipoprotein cholesterol, use or nonuse of lipid-lowering treatment, presence or absence of diabetes, smoking status, and body-mass index). RESULTS: During follow-up (median, 10.0 years), 315 of the 1135 participants in our study (mean age, 71 years at baseline) died; 136 deaths were the result of cardiovascular disease. In Cox proportional-hazards models adjusted for established risk factors, all of the biomarkers significantly predicted the risk of death from cardiovascular causes. The C statistic increased significantly when the four biomarkers were incorporated into a model with established risk factors, both in the whole cohort (C statistic with biomarkers vs. without biomarkers, 0.766 vs. 0.664; P<0.001) and in the group of 661 participants who did not have cardiovascular disease at baseline (0.748 vs. 0.688, P=0.03). The improvement in risk assessment remained strong when it was estimated by other statistical measures of model discrimination, calibration, and global fit. CONCLUSIONS: Our data suggest that in elderly men with or without prevalent cardiovascular disease, the simultaneous addition of several biomarkers of cardiovascular and renal abnormalities substantially improves the risk stratification for death from cardiovascular causes beyond that of a model that is based only on established risk factors.

  • 115.
    Zethelius, Björn
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Venge, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Arnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Multiple biomarkers and cardiovascular risk - Reply2008Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 359, nr 7, s. 761-761Artikel i tidskrift (Refereegranskat)
  • 116.
    Zetterström, Henrik
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Högman, C F
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Hedlund, K
    Clinical usefulness of red cells preserved in protein-poor media1978Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, ISSN ISSN 0028-4793, Vol. 299, s. 1377-1382Artikel i tidskrift (Refereegranskat)
123 101 - 116 av 116
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