10 research outputs found
Assimilation of alternative sulfur sources in fungi
- Author
- A Kahnert
- AR Autry
- B Schmidt
- BD Faison
- C Hall
- C Miech
- C Oldfield
- CS Piddington
- D Schlenk
- DA Hogan
- DK Wicht
- E Aranda
- E Eichhorn
- E Zahra
- EJ Sampson
- F Baldi
- F Elmi
- GA Marzluf
- GL Waddell
- H Ichinose
- H SchÀfer
- HS Scott
- J Gahan
- J Prietzel
- JR Myette
- JR Ploeg van der
- L Bezalel
- M ĂsterĂ„s
- MA Kertesz
- MA Vairavamurthy
- MR Uria-Nickelsen
- N Sood
- O CarriĂłn
- RP Schreiner
- S Holt
- S Sollner
- SA Korban
- SV1 Shvetsova
- T Linder
- T Linder
- T Linder
- T Murakami-Nitta
- T Stressler
- Tomas Linder
- VM Boer
- Y Gherbawy
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2018
- Field of study
Fungi are well known for their metabolic versatility, whether it is the degradation of complex organic substrates or the biosynthesis of intricate secondary metabolites. The vast majority of studies concerning fungal metabolic pathways for sulfur assimilation have focused on conventional sources of sulfur such as inorganic sulfur ions and sulfur-containing biomolecules. Less is known about the metabolic pathways involved in the assimilation of so-called âalternativeâ sulfur sources such as sulfides, sulfoxides, sulfones, sulfonates, sulfate esters and sulfamates. This review summarizes our current knowledge regarding the structural diversity of sulfur compounds assimilated by fungi as well as the biochemistry and genetics of metabolic pathways involved in this process. Shared sequence homology between bacterial and fungal sulfur assimilation genes have lead to the identification of several candidate genes in fungi while other enzyme activities and pathways so far appear to be specific to the fungal kingdom. Increased knowledge of how fungi catabolize this group of compounds will ultimately contribute to a more complete understanding of sulfur cycling in nature as well as the environmental fate of sulfur-containing xenobiotics
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
- Author
- A Abbate
- A Abhyankar
- A Adams
- A Agafina
- A Akyea-Djamson
- A Alan
- A Alfieri
- A Alfrey
- A Alvarisqueta
- A Amos
- A Anadiotis
- A Anneveldt
- A Antolick
- A Arthur
- A Aslam
- Abaci F
- Abdullakutty J
- Abhaichand R
- Abib E Jr
- Aboufakher R
- Abrantes J
- Abreu M
- Abulencia K
- Acampora D
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- Accini Mendoza Jl
- Aceto L
- Acevedo B
- Acevedo L
- Acheatel R
- Actis Mv
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- Adjic Nc
- Affaki Gs
- Agarwal Dk
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- Aguilar M
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- Ahire N
- Ahmad I
- Ahmed Sh
- Ahn Y
- Aish B
- Aiub F
- Aiub J
- Ajax K
- Ajioka M
- Akai Y
- Akatova E
- Akrap B
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- Al-Khalili F
- Albisu J
- Alcalde Jm
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- Alfonso T
- Allen J
- Alllison Dc
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- Amerena J
- Andersen K
- Andor M
- Angelova I
- Angiolillo D
- Anita S
- Anker Sd
- Antalik L
- Antonicelli R
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- Apostolovic S
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- Yong H
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- Youssef G
- Yuan Z
- Yunoki C
- Yupanqui H
- Z Zhai
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- Zadionchenko V
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- Zhou H
- Zidova M
- Zielinski M
- Zieve F
- Zineldine A.
- Zirlik A
- Zucchetti C
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2017
- Field of study
Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1ÎČ, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1ÎČ innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
Inequality in carbon intensity in EU-28: analysis based on club convergence
- Author
- A Acaravci
- A Stegman
- B Ozcan
- C Liu
- CC Lee
- CO Criado
- D Romero-Ăvila
- DT Quah
- DT Quah
- E Panopoulou
- Firat Emir
- G Montasser El
- H Heidari
- J Westerlund
- JE Aldy
- JW Burnett
- M Camarero
- M Christidou
- MC Strazicich
- Mehmet Balcilar
- MJ Herrerias
- MR Barassi
- Muhammad Shahbaz
- N Apergis
- NC Yavuz
- PC Phillips
- PC Phillips
- PN Van
- R Ezcurra
- R Ulucak
- RA Begum
- S Acar
- S Acar
- S Farhani
- S Yu
- SA Solarin
- SN Durlauf
- T Jobert
- X Li
- Y Wang
- Z Korban
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Assimilation of alternative sulfur sources in fungi
- Author
- A Kahnert
- AR Autry
- B Schmidt
- BD Faison
- C Hall
- C Miech
- C Oldfield
- CS Piddington
- D Schlenk
- DA Hogan
- DK Wicht
- E Aranda
- E Eichhorn
- E Zahra
- EJ Sampson
- F Baldi
- F Elmi
- GA Marzluf
- GL Waddell
- H Ichinose
- H SchÀfer
- HS Scott
- J Gahan
- J Prietzel
- JR Myette
- JR Ploeg van der
- L Bezalel
- M ĂsterĂ„s
- MA Kertesz
- MA Vairavamurthy
- MR Uria-Nickelsen
- N Sood
- O CarriĂłn
- RP Schreiner
- S Holt
- S Sollner
- SA Korban
- SV1 Shvetsova
- T Linder
- T Linder
- T Linder
- T Murakami-Nitta
- T Stressler
- Tomas Linder
- VM Boer
- Y Gherbawy
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Hybridization and genetic variation in Danish populations of European crab apple (Malus sylvestris)
- Author
- A Estoup
- A Young
- AM Bowcock
- Anders S. Larsen
- B Charlesworth
- BE Juniper
- BFJ Manly
- BR Stephan
- BS Weir
- CFE Bacles
- CJ Jones
- Conny B. Asmussen
- CR Linder
- CS Campbell
- DB Goldstein
- DI Jarvis
- Ditte C. Olrik
- E Coart
- ED KjĂŠr
- EE Dickson
- Els Coart
- Erik D. KjĂŠr
- F Austerlitz
- F Balloux
- Food and Agriculture Organization
- FT Ledig
- G Eriksson
- G Muir
- H Kugler
- I Wagner
- I Wagner
- I Wagner
- I Wagner
- J Nielsen
- JC Gower
- JD Nason
- JF Storz
- JJ Doyle
- JK McKay
- JK Pritchard
- JL Hamrick
- JM Rhymer
- JS Coleman
- JS Jensen
- K Remmy
- L Gianfranceschi
- L Graudal
- L Triest
- LH Rieseberg
- LH Rieseberg
- M Heuertz
- M Lynch
- M Nei
- M Nei
- M Perron
- M Raymond
- M Slatkin
- MA Beaumont
- MAAF
- MO Winfield
- MW Chase
- National Research Council
- OJ Hardy
- OJ Hardy
- P Guilford
- PE Smouse
- R Liebhard
- RM ButtenschĂžn
- S Holm
- S Mariette
- S Wright
- S Ădum
- SA Flint-Garcia
- SS Korban
- SW Guo
- T Myking
- VV Ponomarenko
- Y Michalakis
- Y Watano
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Malus sieversii: the origin, flavonoid synthesis mechanism, and breeding of red-skinned and red-fleshed apples
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- A Gonzalez
- AG Brown
- AM Takos
- B Winkel-Shirley
- BC Sheng
- BE Ubi
- C Zhang
- CP Bondonnoa
- CY Zhang
- CY Zhang
- D Chagné
- DA Hyson
- E Sadilova
- E Tacken
- F Laurens
- FS Cheng
- G Giomaro
- G Williamson
- GM Volk
- H Flachowsky
- H Flachowsky
- H Sato
- H Umemura
- H Umemura
- H Xu
- HS Aldwinckle
- I Elsharkawy
- I Szankowski
- J Almeida
- J Boyer
- J Thomasraese
- J Yang
- J Zhao
- JA Vinson
- JG Schaart
- JJ Luby
- JL Hamrick
- K Lin-Wang
- K Sekido
- K Sekido
- K Yi
- L Jaakola
- LG Klein
- M Ghislain
- M Jezek
- M NeumĂŒller
- M Yang
- MB Crane
- MC King
- MG Hertog
- MG Hertog
- MV Eberhardt
- N Duan
- N Nesi
- N Wang
- N Wang
- N Wang
- N Wang
- N Yamagishi
- NS Van
- NS Van
- P Knekt
- PK Boss
- PL Forsline
- PL Forsline
- PL Forsline
- PM Krisetherton
- Q Zhen
- R Tsao
- R Velasco
- R Zamora-Ros
- RK Volz
- RK Volz
- RV Espley
- RV Espley
- RV Espley
- S Vimolmangkang
- SA Harris
- SA Kadir
- SK Brown
- SS Korban
- T Harada
- T Visser
- T Visser
- TJ Li
- TK Mcghie
- U Wienand
- VG Bus
- X Chen
- XB Xie
- XH An
- XH An
- XJ Liu
- XJ Liu
- XS Chen
- XS Chen
- XS Zhang
- XU Hai-Feng
- XY Zhang
- Y Ban
- Y Hamada
- Y Jiang
- Y Lespinasse
- Y Lespinasse
- Y Wang
- Y Xu
- YC Wang
- YF Chu
- YK Wang
- YM Zhang
- YY Li
- Z Huang
- Z Ju
- ZC Liu
- ZC Liu
- ZQ Zhou
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Self-incompatibility in woody horticultural species
- Author
- A Iezzoni
- A Serrhini
- A Speranza
- AA Ager
- AC Zeven
- AG Manganaris
- AG Stephenson
- AJ Lack
- AL Orr-Ewing
- AM Fuss
- AR Griffin
- AR Griffin
- B Bahai
- B Griffing
- B. Griffing
- BA Barlow
- BA Lalonde
- BA Mcclure
- BA Mcclure
- BH Rohitha
- BM Duggar
- BM Potts
- BM Potts
- BT Styles
- C Blinkenberg
- C Degani
- C Degani
- C Petersen
- CA Schroeder
- CF Bob
- D Charlesworth
- D Lewis
- D Lewis
- D Lewis
- D Schmitt
- D Suranyi
- DA Neill
- DF Dayton
- DG Rowlands
- DH Byrne
- DH Maggs
- DK Sharma
- DM OâMalley
- DV Beardsell
- DW Lane
- DW Schemske
- E Keep
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- E Keep
- E Pimienta
- E. Keep
- EA James
- EC Cornish
- EG Williams
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- F Mergen
- FG Dennis
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- FW Cope
- FW Martin
- G DeGrandi-Hoffman
- G DeGrandi-Hoffman
- GF Moran
- GJ Anderson
- GM Darrow
- H Fukui
- HF Chin
- Hiratsuka
- Hodgson
- Hogenboom
- HT Chan
- HY Wetzstein
- I. Modlibowska
- J Heslop-Harrison
- J Kenrick
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- J Kenrick
- J Weinberger
- JB Nasrallah
- JK Scott
- JL Brewbaker
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- JN Moore
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- JP Tilquin
- JW Beland
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- JW Raff
- JW Raff
- K Lundkvist
- K Ryugo
- K Yamashita
- K Yamashita
- K Yamashita
- Kaul
- KG Dwyer
- KG Stott
- KJ Patterson
- KS Bawa
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- L Thien
- LD Pryor
- LD Romberg
- LH Hammer
- LK Opeke
- M Gaget
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- M Trick
- MA Anderson
- MB Crane
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- MF Ellis
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- N Ramirez
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- O Reuveni
- Opeke L.K. and Jacob, V.J
- P Howland
- P Montalti
- P Spiegel-Roy
- PV Bolstad
- R Lande
- R Socias
- R.P. Overton
- RB Knox
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- RE Farmer Jr.
- REC Layne
- RF Stettler
- RF Stettler
- RI Bertin
- RJ Knight
- RJ Knight
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- RL Bell
- RL Hummel
- RL Innes
- RP Guries
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- S Hiratsuka
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- S Hiratsuka
- S Hiratsuka
- S Sutherland
- S-J Li
- SA Mehlenbacher
- SA Weinbaum
- SL Krebs
- SL Krebs
- SL Mau
- Socias i Company R., Kester, D.E. and Bradley
- Soost
- Soost R.K
- SP Vander
- SR Seavey
- SS Korban
- T Barry
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- W Wunnachit
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- Y Heslop-Harrison
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- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/1994
- Field of study
Evolocumab and clinical outcomes in patients with cardiovascular disease
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- Abelson M.
- Aboufakher R.
- Abrahamsen T. E.
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- Appel K.
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- Athyros V.
- Auerbach E.
- Awtry E.
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- Banikova A.
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- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2017
- Field of study
peer reviewedBACKGROUND Evolocumab is a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%. Whether it prevents cardiovascular events is uncertain. METHODS We conducted a randomized, double-blind, placebo-controlled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin therapy. Patients were randomly assigned to receive evolocumab (either 140 mg every 2 weeks or 420 mg monthly) or matching placebo as subcutaneous injections. The primary efficacy end point was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. The key secondary efficacy end point was the composite of cardiovascular death, myocardial infarction, or stroke. The median duration of follow-up was 2.2 years. RESULTS At 48 weeks, the least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with placebo, was 59%, from a median baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P<0.001). Relative to placebo, evolocumab treatment significantly reduced the risk of the primary end point (1344 patients [9.8%] vs. 1563 patients [11.3%]; hazard ratio, 0.85; 95% confidence interval [CI], 0.79 to 0.92; P<0.001) and the key secondary end point (816 [5.9%] vs. 1013 [7.4%]; hazard ratio, 0.80; 95% CI, 0.73 to 0.88; P<0.001). The results were consistent across key subgroups, including the subgroup of patients in the lowest quartile for baseline LDL cholesterol levels (median, 74 mg per deciliter [1.9 mmol per liter]). There was no significant difference between the study groups with regard to adverse events (including new-onset diabetes and neurocognitive events), with the exception of injection-site reactions, which were more common with evolocumab (2.1% vs. 1.6%). CONCLUSIONS In our trial, inhibition of PCSK9 with evolocumab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per deciliter (0.78 mmol per liter) and reduced the risk of cardiovascular events. These findings show that patients with atherosclerotic cardiovascular disease benefit from lowering of LDL cholesterol levels below current targets. © 2017 Massachusetts Medical Society
Evolocumab and clinical outcomes in patients with cardiovascular disease
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- Zarich S
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- Zdrenghea D
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- Ziegler O
- Zilahi Z
- Zrazhevskiy K
- Ăstergren J
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2017
- Field of study
BACKGROUND Evolocumab is a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%. Whether it prevents cardiovascular events is uncertain. METHODS We conducted a randomized, double-blind, placebo-controlled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin therapy. Patients were randomly assigned to receive evolocumab (either 140 mg every 2 weeks or 420 mg monthly) or matching placebo as subcutaneous injections. The primary efficacy end point was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. The key secondary efficacy end point was the composite of cardiovascular death, myocardial infarction, or stroke. The median duration of follow-up was 2.2 years. RESULTS At 48 weeks, the least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with placebo, was 59%, from a median baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P<0.001). Relative to placebo, evolocumab treatment significantly reduced the risk of the primary end point (1344 patients [9.8%] vs. 1563 patients [11.3%]; hazard ratio, 0.85; 95% confidence interval [CI], 0.79 to 0.92; P<0.001) and the key secondary end point (816 [5.9%] vs. 1013 [7.4%]; hazard ratio, 0.80; 95% CI, 0.73 to 0.88; P<0.001). The results were consistent across key subgroups, including the subgroup of patients in the lowest quartile for baseline LDL cholesterol levels (median, 74 mg per deciliter [1.9 mmol per liter]). There was no significant difference between the study groups with regard to adverse events (including new-onset diabetes and neurocognitive events), with the exception of injection-site reactions, which were more common with evolocumab (2.1% vs. 1.6%). CONCLUSIONS In our trial, inhibition of PCSK9 with evolocumab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per deciliter (0.78 mmol per liter) and reduced the risk of cardiovascular events. These findings show that patients with atherosclerotic cardiovascular disease benefit from lowering of LDL cholesterol levels below current targets
Ezetimibe added to statin therapy after acute coronary syndromes
- Author
- Aagnes I
- Aambakk MB
- Aase O
- Aaser E
- Abdel-Latief A
- Abell T
- Aboufakher R
- Abramson B
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- Zanolin D
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- Zweiker R
- Ă ngman K
- Ădes I
- Ăstberg S
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2015
- Field of study
BACKGROUND: Statin therapy reduces low-density lipoprotein (LDL) cholesterol levels and the risk of cardiovascular events, but whether the addition of ezetimibe, a nonstatin drug that reduces intestinal cholesterol absorption, can reduce the rate of cardiovascular events further is not known. METHODS: We conducted a double-blind, randomized trial involving 18,144 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and had LDL cholesterol levels of 50 to 100 mg per deciliter (1.3 to 2.6 mmol per liter) if they were receiving lipid-lowering therapy or 50 to 125 mg per deciliter (1.3 to 3.2 mmol per liter) if they were not receiving lipid-lowering therapy. The combination of simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-ezetimibe) was compared with simvastatin (40 mg) and placebo (simvastatin monotherapy). The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary revascularization ( 6530 days after randomization), or nonfatal stroke. The median follow-up was 6 years. RESULTS: The median time-weighted average LDL cholesterol level during the study was 53.7 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (P<0.001). The Kaplan-Meier event rate for the primary end point at 7 years was 32.7% in the simvastatin-ezetimibe group, as compared with 34.7% in the simvastatin-monotherapy group (absolute risk difference, 2.0 percentage points; hazard ratio, 0.936; 95% confidence interval, 0.89 to 0.99; P = 0.016). Rates of pre-specified muscle, gallbladder, and hepatic adverse effects and cancer were similar in the two groups. CONCLUSIONS: When added to statin therapy, ezetimibe resulted in incremental lowering of LDL cholesterol levels and improved cardiovascular outcomes. Moreover, lowering LDL cholesterol to levels below previous targets provided additional benefit