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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005467naa a2200985 4500
001oai:DiVA.org:uu-225516
003SwePub
008140604s2014 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2255162 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 D.4 aut
2451 0a Survival with Cardiac-Resynchronization Therapy in Mild Heart Failure
264 1c 2014
338 a print2 rdacarrier
520 a 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.)
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Kardiologi0 (SwePub)302062 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cardiac and Cardiovascular Systems0 (SwePub)302062 hsv//eng
7001 a Held, Claes,d 1956-u Uppsala universitet,Uppsala kliniska forskningscentrum (UCR),Institutionen för medicinska vetenskaper4 aut0 (Swepub:uu)clahe947
7001 a Stewart, Ralph4 aut
7001 a Tarka, Elizabeth4 aut
7001 a Brown, Rebekkah4 aut
7001 a Davies, Richard Y.4 aut
7001 a Budaj, Andrzej4 aut
7001 a Harrington, Robert A.4 aut
7001 a Steg, P. Gabriel4 aut
7001 a Ardis-Sino, Diego4 aut
7001 a Armstrong, Paul W.4 aut
7001 a Avezum, Alvaro4 aut
7001 a Aylward, Philip E.4 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 J.4 aut
7001 a Danchin, Nicolas4 aut
7001 a De Winter, Robbert J.4 aut
7001 a Denchev, Stefan4 aut
7001 a Diaz, Rafael4 aut
7001 a Elisaf, Moses4 aut
7001 a Flather, Marcus D.4 aut
7001 a Goudev, Assen R.4 aut
7001 a Granger, Christopher B.4 aut
7001 a Grinfeld, Liliana4 aut
7001 a Hochman, Judith S.4 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 Lopez-Sendon, Jose4 aut
7001 a Manolis, Athanasios J.4 aut
7001 a Mohler, Emile R., III4 aut
7001 a Nicolau, Jose C.4 aut
7001 a Pais, Prem4 aut
7001 a Parkhomenko, Alexander4 aut
7001 a Pedersen, Terje R.4 aut
7001 a Pella, Daniel4 aut
7001 a Ramos-Corrales, Marco A.4 aut
7001 a Ruda, Mikhail4 aut
7001 a Sereg, Mtys4 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 P.4 aut
7001 a Sy, Rody G.4 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 P.4 aut
7001 a Wallentin, Lars4 aut
7102 a Uppsala universitetb Uppsala kliniska forskningscentrum (UCR)4 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-225516
8564 8u https://doi.org/10.1056/NEJMoa1315878

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