TY - JOUR
T1 - Impact of PCSK9 inhibition on coronary atheroma progression
T2 - Rationale and design of Global Assessment of Plaque Regression with a PCSK9 Antibody as Measured by Intravascular Ultrasound (GLAGOV)
AU - Puri, Rishi
AU - Nissen, Steven E.
AU - Somaratne, Ransi
AU - Cho, Leslie
AU - Kastelein, John J P
AU - Ballantyne, Christie M.
AU - Koenig, Wolfgang
AU - Anderson, Todd J.
AU - Yang, Jingyuan
AU - Kassahun, Helina
AU - Wasserman, Scott M.
AU - Scott, Robert
AU - Borgman, Marilyn
AU - Nicholls, Stephen J.
N1 - Funding Information:
R.S., J.Y., H.K., S.W., and R.S are employees and stockholders of Amgen, Inc. L.C. serves as a consultant for Amgen and Sanofi-Aventis. S.E.N. has received research support to perform clinical trials through the Cleveland Clinic Coordinating Center for Clinical Research (C5R) from Pfizer, AstraZeneca, Novartis, Roche, Daiichi-Sankyo, Takeda, Sanofi-Aventis, Resverlogix, and Eli Lilly, and is a consultant/advisor for many pharmaceutical companies but requires them to donate all honoraria or consulting fees directly to charity so that he receives neither income nor a tax deduction. J.J.P.K. reports consulting fees from Amgen during the conduct of the study and consulting fees from Cerenis, The Medicines Company, CSL Behring, Regeneron, Eli Lilly, Esperion, AstraZeneca, Pronova, Boehringer Ingelheim, Catabasis, Novartis, Merck, Isis Pharmaceuticals, Kowa, Sanofi, Gemphire, and Cymabay. W.K. has received consulting fees from Novartis, Pfizer, The Medicines Company, Amgen, AstraZeneca, MSD, GSK, and Sanderling Ventures; honorarium (lectures) from AstraZeneca, Novartis, MSD, Amgen, and Actavis, and research contracts with Abbott, Roche Diagnostics, Beckmann, and Singulex, and participates in several clinical trials (PEGASUS, LEADER, CANTOS, and FOURIER). C.M.B. has received grant/research support from Abbott Diagnostic, Amarin, Amgen, Eli Lilly, Esperion, Novartis, Pfizer, Otsuka, Regeneron, Roche Diagnostic, Sanofi-Synthelabo, Takeda, National Institutes of Health, the American Heart Association, and the ADA (all significant, paid to his institution). He also serves as a consultant to Abbott Diagnostics, Amarin, Amgen, Astra Zeneca, Eli Lilly, Esperion, Genzyme, Matinas BioPharma Inc, Merck, Novartis, Pfizer, Regeneron, Roche, and Sanofi-Synthelabo. T.J.A. reports research collaborations with Amgen, Merck, and Pfizer. S.J.N. reported receiving research support from AstraZeneca, Novartis, Eli Lilly, Anthera, LipoScience, Roche, and Resverlogix, and receiving honoraria from or serving as a consultant to AstraZeneca, Roche, Esperion, Abbott, Pfizer, Merck, Takeda, LipoScience, Omthera, Novo-Nordisk, Sanofi-Aventis, Atheronova, Anthera, CSL Behring, and Boehringer Ingelheim. All other authors have no declarations to make.
Publisher Copyright:
© 2016 Elsevier, Inc. All rights reserved.
PY - 2016/6
Y1 - 2016/6
N2 - Background Statin-mediated low-density lipoprotein cholesterol (LDL-C) lowering fails to prevent more than half of cardiovascular events in clinical trials. Serial plaque imaging studies have highlighted the benefits of aggressive LDL-C lowering, with plaque regression evident in up to two-thirds of patients with achieved LDL-C levels <70 mg/dL. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors permit LDL-C-lowering by a further 54% to 75% in statin-treated patients. The impact of achieving very low LDL-C levels with PCSK9 inhibitors on coronary atherosclerosis has not been investigated. Aims To test the hypothesis that incremental LDL-C lowering with the PCSK9 inhibitor, evolocumab, will result in a significantly greater change from baseline in coronary atheroma volume than placebo in subjects receiving maximally tolerated statin therapy. Methods A phase 3, multicenter, double-blind, randomized, placebo-controlled trial evaluating the impact of evolocumab on coronary atheroma volume as assessed by serial coronary intravascular ultrasound at baseline in patients undergoing a clinically indicated coronary angiogram with angiographic evidence of coronary atheroma, and after 78 weeks of treatment. Subjects (n = 968) were randomized 1:1 into 2 groups to receive monthly either evolocumab 420 mg or placebo subcutaneous injections. Conclusions The GLAGOV trial will explore whether greater degrees of plaque regression are achievable with ultrahigh-intensity LDL-C lowering after combination statin-PCSK9 inhibitor therapy. GLAGOV will provide important mechanistic, safety, and efficacy data prior to the eagerly anticipated clinical outcomes trials testing the PCSK9 inhibitor hypothesis (www.clinicaltrials.gov identifier NCT01813422).
AB - Background Statin-mediated low-density lipoprotein cholesterol (LDL-C) lowering fails to prevent more than half of cardiovascular events in clinical trials. Serial plaque imaging studies have highlighted the benefits of aggressive LDL-C lowering, with plaque regression evident in up to two-thirds of patients with achieved LDL-C levels <70 mg/dL. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors permit LDL-C-lowering by a further 54% to 75% in statin-treated patients. The impact of achieving very low LDL-C levels with PCSK9 inhibitors on coronary atherosclerosis has not been investigated. Aims To test the hypothesis that incremental LDL-C lowering with the PCSK9 inhibitor, evolocumab, will result in a significantly greater change from baseline in coronary atheroma volume than placebo in subjects receiving maximally tolerated statin therapy. Methods A phase 3, multicenter, double-blind, randomized, placebo-controlled trial evaluating the impact of evolocumab on coronary atheroma volume as assessed by serial coronary intravascular ultrasound at baseline in patients undergoing a clinically indicated coronary angiogram with angiographic evidence of coronary atheroma, and after 78 weeks of treatment. Subjects (n = 968) were randomized 1:1 into 2 groups to receive monthly either evolocumab 420 mg or placebo subcutaneous injections. Conclusions The GLAGOV trial will explore whether greater degrees of plaque regression are achievable with ultrahigh-intensity LDL-C lowering after combination statin-PCSK9 inhibitor therapy. GLAGOV will provide important mechanistic, safety, and efficacy data prior to the eagerly anticipated clinical outcomes trials testing the PCSK9 inhibitor hypothesis (www.clinicaltrials.gov identifier NCT01813422).
UR - http://www.scopus.com/inward/record.url?scp=84963616071&partnerID=8YFLogxK
U2 - 10.1016/j.ahj.2016.01.019
DO - 10.1016/j.ahj.2016.01.019
M3 - Article
C2 - 27264224
AN - SCOPUS:84963616071
VL - 176
SP - 83
EP - 92
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
ER -