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FältnamnIndikatorerMetadata
00005418naa a2200985 4500
001oai:DiVA.org:uu-236340
003SwePub
008141118s2014 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2363402 URI
0247 a https://doi.org/10.1056/NEJMoa13158782 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a White, Harvey D4 aut
2451 0a Darapladib for preventing ischemic events in stable coronary heart disease
264 1c 2014
338 a print2 rdacarrier
520 a 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.).
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng
7001 a Held, Claesu Uppsala universitet,Kardiologi,Uppsala kliniska forskningscentrum (UCR)4 aut0 (Swepub:uu)clahe947
7001 a Stewart, Ralph4 aut
7001 a Tarka, Elizabeth4 aut
7001 a Brown, Rebekkah4 aut
7001 a Davies, Richard Y4 aut
7001 a Budaj, Andrzej4 aut
7001 a Harrington, Robert A4 aut
7001 a Steg, P Gabriel4 aut
7001 a Ardissino, Diego4 aut
7001 a Armstrong, Paul W4 aut
7001 a Avezum, Alvaro4 aut
7001 a Aylward, Philip E4 aut
7001 a Bryce, Alfonso4 aut
7001 a Chen, Hong4 aut
7001 a Chen, Ming-Fong4 aut
7001 a Corbalan, Ramon4 aut
7001 a Dalby, Anthony J4 aut
7001 a Danchin, Nicolas4 aut
7001 a De Winter, Robbert J4 aut
7001 a Denchev, Stefan4 aut
7001 a Diaz, Rafael4 aut
7001 a Elisaf, Moses4 aut
7001 a Flather, Marcus D4 aut
7001 a Goudev, Assen R4 aut
7001 a Granger, Christopher B4 aut
7001 a Grinfeld, Liliana4 aut
7001 a Hochman, Judith S4 aut
7001 a Husted, Steen4 aut
7001 a Kim, Hyo-Soo4 aut
7001 a Koenig, Wolfgang4 aut
7001 a Linhart, Ales4 aut
7001 a Lonn, Eva4 aut
7001 a López-Sendón, José4 aut
7001 a Manolis, Athanasios J4 aut
7001 a Mohler, Emile R4 aut
7001 a Nicolau, José C4 aut
7001 a Pais, Prem4 aut
7001 a Parkhomenko, Alexander4 aut
7001 a Pedersen, Terje R4 aut
7001 a Pella, Daniel4 aut
7001 a Ramos-Corrales, Marco A4 aut
7001 a Ruda, Mikhail4 aut
7001 a Sereg, Mátyás4 aut
7001 a Siddique, Saulat4 aut
7001 a Sinnaeve, Peter4 aut
7001 a Smith, Peter4 aut
7001 a Sritara, Piyamitr4 aut
7001 a Swart, Henk P4 aut
7001 a Sy, Rody G4 aut
7001 a Teramoto, Tamio4 aut
7001 a Tse, Hung-Fat4 aut
7001 a Watson, David4 aut
7001 a Weaver, W Douglas4 aut
7001 a Weiss, Robert4 aut
7001 a Viigimaa, Margus4 aut
7001 a Vinereanu, Dragos4 aut
7001 a Zhu, Junren4 aut
7001 a Cannon, Christopher P4 aut
7001 a Wallentin, Larsu Uppsala universitet,Kardiologi,Uppsala kliniska forskningscentrum (UCR)4 aut0 (Swepub:uu)larswall
7102 a Uppsala universitetb Kardiologi4 org
7730 t New England Journal of Medicineg 370:18, s. 1702-1711q 370:18<1702-1711x 0028-4793x 1533-4406
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-236340
8564 8u https://doi.org/10.1056/NEJMoa1315878

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