{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T03:30:36Z","timestamp":1791862236785,"version":"4.3.4"},"reference-count":21,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","funder":[{"name":"NIH","award":["5R33HL139929-05"],"award-info":[{"award-number":["5R33HL139929-05"]}]}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2026,1,6]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Cardiac allograft vasculopathy is an important cause of mortality after heart transplantation (HT). Dyslipidemia is a major contributor to the development of cardiac allograft vasculopathy. The safety and effectiveness of proprotein convertase subtilisin\/kexin 9 inhibition to lower cholesterol and to prevent cardiac allograft vasculopathy early after HT are not well established.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>In this investigator-initiated, prospective, multicenter, double-blind randomized trial, participants were randomized early after HT to receive either alirocumab or placebo in addition to rosuvastatin. Before randomization and at 1 year, all participants underwent invasive coronary assessment, including angiography, fractional flow reserve, coronary flow reserve, the index of microcirculatory resistance, and intravascular ultrasound with near-infrared spectroscopy. Lipid values were assessed at baseline and at prespecified intervals. The primary end point was the change in coronary artery plaque volume from baseline to 1 year after HT based on serial intravascular ultrasound.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      A total of 114 HT recipients were included (57 assigned to alirocumab and 57 assigned to placebo). Baseline characteristics were well matched between the 2 groups. The low-density lipoprotein cholesterol levels decreased significantly from baseline to 1 year in the alirocumab arm (72.7\u00b131.7 to 31.5\u00b120.7 mg\/dL;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001) and did not change with placebo (69.0\u00b122.4 to 69.2\u00b128.1 mg\/dL;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.92). Plaque volume increased numerically in both groups from baseline to 12 months (alirocumab, 176.3\u00b195.2 to 184.5\u00b1105.4 mm\u00b3;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.23; placebo 173.7\u00b196.7 to 183.1\u00b1109.8 mm\n                      <jats:sup>3<\/jats:sup>\n                      ;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.15). The change in plaque volume (mean difference in differences) did not differ between groups (1.01 [0.89\u20131.14];\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.86). Fractional flow reserve, coronary flow reserve, and the index of microcirculatory resistance did not change significantly with the addition of alirocumab. There were no significant adverse events related to alirocumab.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Proprotein convertase subtilisin\/kexin 9 inhibition with alirocumab in addition to statin therapy early after HT safely lowers low-density lipoprotein cholesterol but did not reduce coronary artery plaque progression after 1 year compared with rosuvastatin alone in patients with a low baseline low-density lipoprotein cholesterol.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>REGISTRATION:<\/jats:title>\n                    <jats:p>\n                      URL:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/www.clinicaltrials.gov\">https:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n                      ; Unique identifier: NCT03537742.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.125.077603","type":"journal-article","created":{"date-parts":[[2025,11,10]],"date-time":"2025-11-10T16:00:07Z","timestamp":1762790407000},"page":"7-17","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":19,"title":["Cardiac Allograft Vasculopathy Inhibition With Alirocumab: The CAVIAR Trial"],"prefix":"10.1161","volume":"153","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1799-1368","authenticated-orcid":true,"given":"William F.","family":"Fearon","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."},{"name":"VA Palo Alto Health Care System, CA (W.F.F.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kosei","family":"Terada","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kuniaki","family":"Takahashi","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anette","family":"Skoda","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9782-4449","authenticated-orcid":true,"given":"Helen I.","family":"Luikart","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1516-5209","authenticated-orcid":true,"given":"Cynthia A.","family":"Lamendola","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4571-1925","authenticated-orcid":true,"given":"Frederik M.","family":"Zimmermann","sequence":"additional","affiliation":[{"name":"Department of Cardiology, St. Antonius Hospital, Nieuwegein, the Netherlands (F.M.Z.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9633-1303","authenticated-orcid":true,"given":"Takehiro","family":"Hashikata","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3834-8665","authenticated-orcid":true,"given":"Kan","family":"Saito","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akihiro","family":"Yoshida","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brandon","family":"Varr","sequence":"additional","affiliation":[{"name":"Kaiser Permanente, Santa Clara, CA (B.V., C.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1922-7240","authenticated-orcid":true,"given":"Joshua W.","family":"Knowles","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, CA (W.F.F., K.T., K.T., A.S., H.I.L., C.A.L., T.H., K.S., A.Y., J.W.K., Y.H., J.T., K.K.K.)."},{"name":"Stanford Diabetes Research Center, Stanford 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