{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T21:21:40Z","timestamp":1790284900108,"version":"4.1.0"},"reference-count":27,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2023,4,21]],"date-time":"2023-04-21T00:00:00Z","timestamp":1682035200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,6,21]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Icosapent ethyl (IPE) significantly reduced ischaemic events in statin-treated patients with atherosclerosis or diabetes and elevated triglycerides in REDUCE-IT, including large reductions in myocardial infarction and elective, urgent, and emergent coronary revascularization. However, the mechanisms driving this clinical benefit are not fully known. The EVAPORATE trial demonstrated that IPE significantly reduced plaque burden. No study to date has assessed the impact of IPE on coronary physiology. Fractional flow reserve (FFR) derived from coronary computed tomography angiography (CTA) data sets (FFRCT) applies computational fluid dynamics to calculate FFR values in epicardial coronary arteries. Our objective was to assess the impact of IPE on coronary physiology assessed by FFRCT using imaging data from EVAPORATE.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>A total of 47 patients and of 507 coronary lesions at baseline, 9 months, and 18 months with coronary CTA and FFRCT were studied in a blinded core lab. The pre-specified primary endpoint was the FFRCT value in the distal coronary segment from baseline to follow-up in the most diseased vessel per patient using IPE compared with placebo. The pre-specified secondary endpoint was the change in translesional FFRCT (\u0394FFRCT) across the most severe (minimum 30% diameter stenosis) coronary lesion per vessel. Baseline FFRCT was similar for IPE compared with placebo (0.83 \u00b1 0.08 vs. 0.84 \u00b1 0.08, P = 0.55). There was significant improvement in the primary endpoint, as IPE improved mean distal segment FFRCT at 9- and 18-month follow-up compared with placebo (0.01 \u00b1 0.05 vs. \u22120.05 \u00b1 0.09, P = 0.02, and \u22120.01 \u00b1 0.09 vs. \u22120.09 \u00b1 0.12, P = 0.03, respectively). \u0394FFRCT in 140 coronary lesions was improved, although not statistically significant, with IPE compared with placebo (\u22120.06 \u00b1 0.08 vs. \u22120.09 \u00b1 0.1, P = 0.054).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Icosapent ethyl demonstrated significant benefits in coronary physiology compared with placebo. This early and sustained improvement in FFRCT at 9- and 18-month follow-up provides mechanistic insight into the clinical benefit observed in the REDUCE-IT trial. Furthermore, this is the first assessment of FFRCT to determine drug effect.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ehjci\/jead063","type":"journal-article","created":{"date-parts":[[2023,4,21]],"date-time":"2023-04-21T09:32:35Z","timestamp":1682069555000},"page":"866-873","source":"Crossref","is-referenced-by-count":32,"title":["Benefit of icosapent ethyl on coronary physiology assessed by computed tomography angiography fractional flow reserve: EVAPORATE-FFRCT"],"prefix":"10.1093","volume":"24","author":[{"given":"Mark G","family":"Rabbat","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Cardiology, Loyola University Medical Center, 2160 S. 1st Avenue , Maywood, IL 60153 , USA"},{"name":"Department of Medicine, Division of Cardiology, Edward Hines Jr. VA Hospital, 5000 South 5th Avenue , Hines, IL , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suvasini","family":"Lakshmanan","sequence":"additional","affiliation":[{"name":"Department of Medicine, Lundquist Institute at Harbor-UCLA Medical Center, 1124 W Carson Street, Torrance, CA 90502 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9076-2321","authenticated-orcid":false,"given":"Mina M","family":"Benjamin","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, Loyola University Medical Center, 2160 S. 1st Avenue , Maywood, IL 60153 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gheorghe","family":"Doros","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Baim Institute for clinical research, Boston University, 930 Commonwealth Ave #3 , Boston, MA 02215 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2720-3508","authenticated-orcid":false,"given":"April","family":"Kinninger","sequence":"additional","affiliation":[{"name":"Department of Medicine, Lundquist Institute at Harbor-UCLA Medical Center, 1124 W Carson Street, Torrance, CA 90502 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew J","family":"Budoff","sequence":"additional","affiliation":[{"name":"Department of Medicine, Lundquist Institute at Harbor-UCLA Medical Center, 1124 W Carson Street, Torrance, CA 90502 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1278-6245","authenticated-orcid":false,"given":"Deepak L","family":"Bhatt","sequence":"additional","affiliation":[{"name":"Mount Sinai Heart, Icahn School of Medicine at Mount Sinai, 1 Gustave Levy Place, Box 1030, New York , NY 10029 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,4,22]]},"reference":[{"key":"2023062113351910900_jead063-B1","doi-asserted-by":"crossref","first-page":"774","DOI":"10.1093\/eurheartj\/ehu500","article-title":"Triglycerides on the rise: should we swap seats on the seesaw?","volume":"36","author":"Libby","year":"2015","journal-title":"Eur Heart J"},{"key":"2023062113351910900_jead063-B2","doi-asserted-by":"crossref","first-page":"100","DOI":"10.1161\/CIRCOUTCOMES.115.002104","article-title":"Elevated triglyceride level is independently associated with increased all-cause mortality in patients with established coronary heart disease: twenty-two-year follow-up of the bezafibrate infarction prevention study and registry","volume":"9","author":"Klempfner","year":"2016","journal-title":"Circ Cardiovasc Qual 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statin-treated patients with high residual cardiovascular risk","volume":"7","author":"Toth","year":"2018","journal-title":"J Am Heart Assoc"},{"key":"2023062113351910900_jead063-B6","doi-asserted-by":"crossref","first-page":"11","DOI":"10.1056\/NEJMoa1812792","article-title":"Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia","volume":"380","author":"Bhatt","year":"2019","journal-title":"N Engl J Med"},{"key":"2023062113351910900_jead063-B7","doi-asserted-by":"crossref","first-page":"2791","DOI":"10.1016\/j.jacc.2019.02.032","article-title":"Effects of icosapent ethyl on total ischemic events: from REDUCE-IT","volume":"73","author":"Bhatt","year":"2019","journal-title":"J Am Coll Cardiol"},{"key":"2023062113351910900_jead063-B8","doi-asserted-by":"crossref","first-page":"1159","DOI":"10.1016\/j.jacc.2019.06.043","article-title":"Reduction in first and total ischemic events with icosapent ethyl across baseline triglyceride 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