Evolocumab in HIV-Infected Patients With Dyslipidemia: Primary Results of the Randomized, Double-Blind BEIJERINCK Study.


Journal

Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365

Informations de publication

Date de publication:
26 05 2020
Historique:
received: 14 02 2020
revised: 16 03 2020
accepted: 17 03 2020
pubmed: 3 4 2020
medline: 12 1 2021
entrez: 3 4 2020
Statut: ppublish

Résumé

People living with human immunodeficiency virus (PLHIV) are at increased risk of atherosclerotic cardiovascular disease (ASCVD) and are prone to statin-related adverse events from drug-drug interactions with certain antiretroviral regimens. This study sought to evaluate the efficacy and safety of evolocumab in dyslipidemic PLHIV. BEIJERINCK (EvolocumaB Effect on LDL-C Lowering in SubJEcts with Human Immunodeficiency VirRus and INcreased Cardiovascular RisK) is a randomized, double-blind, multinational trial comparing monthly subcutaneous evolocumab 420 mg with placebo in PLHIV with hypercholesterolemia/mixed dyslipidemia taking maximally-tolerated statin therapy. The primary endpoint was the percent change (baseline to week 24) in low-density lipoprotein cholesterol (LDL-C); secondary endpoints included achievement of LDL-C <70 mg/dl and percent change in other plasma lipid and lipoprotein levels. Treatment-emergent adverse events were also examined. A total of 464 patients were analyzed (mean age of 56.4 years, 82.5% male, mean duration with HIV of 17.4 years). ASCVD was documented in 35.6% of patients, and statin intolerance/contraindications to statin use were present in 20.7% of patients. Evolocumab reduced LDL-C by 56.9% (95% confidence interval: 61.6% to 52.3%) from baseline to week 24 versus placebo. An LDL-C level of <70 mg/dl was achieved in 73.3% of patients in the evolocumab group versus 7.9% in the placebo group. Evolocumab also significantly reduced other atherogenic lipid levels, including non-high-density lipoprotein cholesterol, apolipoprotein B, and lipoprotein(a) (all p < 0.0001). Evolocumab was well tolerated, and treatment-emergent adverse events patient incidence was similar among evolocumab and placebo groups. Evolocumab was safe and significantly reduced lipid levels in dyslipidemic PLHIV on maximally-tolerated statin therapy. Evolocumab is an effective therapy for lowering atherogenic lipoproteins in PLHIV with high cardiovascular risk. (Safety, Tolerability & Efficacy on LDL-C of Evolocumab in Subjects With HIV & Hyperlipidemia/Mixed Dyslipidemia; NCT02833844).

Sections du résumé

BACKGROUND
People living with human immunodeficiency virus (PLHIV) are at increased risk of atherosclerotic cardiovascular disease (ASCVD) and are prone to statin-related adverse events from drug-drug interactions with certain antiretroviral regimens.
OBJECTIVES
This study sought to evaluate the efficacy and safety of evolocumab in dyslipidemic PLHIV.
METHODS
BEIJERINCK (EvolocumaB Effect on LDL-C Lowering in SubJEcts with Human Immunodeficiency VirRus and INcreased Cardiovascular RisK) is a randomized, double-blind, multinational trial comparing monthly subcutaneous evolocumab 420 mg with placebo in PLHIV with hypercholesterolemia/mixed dyslipidemia taking maximally-tolerated statin therapy. The primary endpoint was the percent change (baseline to week 24) in low-density lipoprotein cholesterol (LDL-C); secondary endpoints included achievement of LDL-C <70 mg/dl and percent change in other plasma lipid and lipoprotein levels. Treatment-emergent adverse events were also examined.
RESULTS
A total of 464 patients were analyzed (mean age of 56.4 years, 82.5% male, mean duration with HIV of 17.4 years). ASCVD was documented in 35.6% of patients, and statin intolerance/contraindications to statin use were present in 20.7% of patients. Evolocumab reduced LDL-C by 56.9% (95% confidence interval: 61.6% to 52.3%) from baseline to week 24 versus placebo. An LDL-C level of <70 mg/dl was achieved in 73.3% of patients in the evolocumab group versus 7.9% in the placebo group. Evolocumab also significantly reduced other atherogenic lipid levels, including non-high-density lipoprotein cholesterol, apolipoprotein B, and lipoprotein(a) (all p < 0.0001). Evolocumab was well tolerated, and treatment-emergent adverse events patient incidence was similar among evolocumab and placebo groups.
CONCLUSIONS
Evolocumab was safe and significantly reduced lipid levels in dyslipidemic PLHIV on maximally-tolerated statin therapy. Evolocumab is an effective therapy for lowering atherogenic lipoproteins in PLHIV with high cardiovascular risk. (Safety, Tolerability & Efficacy on LDL-C of Evolocumab in Subjects With HIV & Hyperlipidemia/Mixed Dyslipidemia; NCT02833844).

Identifiants

pubmed: 32234462
pii: S0735-1097(20)34629-5
doi: 10.1016/j.jacc.2020.03.025
pii:
doi:

Substances chimiques

Anti-HIV Agents 0
Antibodies, Monoclonal, Humanized 0
Anticholesteremic Agents 0
Cholesterol, LDL 0
Hydroxymethylglutaryl-CoA Reductase Inhibitors 0
Triglycerides 0
evolocumab LKC0U3A8NJ

Banques de données

ClinicalTrials.gov
['NCT02833844']

Types de publication

Journal Article Multicenter Study Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2570-2584

Investigateurs

David Baker (D)
Mark Bloch (M)
Robert Finlayson (R)
Jennifer Hoy (J)
Kenneth Koh (K)
Norman Roth (N)
Stephane De Wit (S)
Eric Florence (E)
Linos Vandekerckhove (L)
Bruno Caramelli (B)
Jose Valdez Ramalho Madruga (JV)
Sandra Wagner Cardoso (S)
Greg Bondy (G)
Michael Gill (M)
George Tsoukas (G)
Sylvie Trottier (S)
Marek Smieja (M)
Franck Boccara (F)
Christine Katlama (C)
Fabrice Bonnet (F)
Francois Raffi (F)
Laurent Cotte (L)
Jean-Michel Molina (JM)
Jacques Reynes (J)
Antonios Papadopoulos (A)
Simeon Metallidis (S)
Vassilios Paparizos (V)
Vasileios Papastamopoulos (V)
Cristina Mussini (C)
Massimo Galli (M)
Andrea Antinori (A)
Antonio Di Biagio (A)
Pierluigi Viale (P)
Andrzej Horban (A)
Nuno Marques (N)
Daniel Coutinho (D)
Joaquim Oliveira (J)
Paula Freitas (P)
Liliana-Lucia Preotescu (LL)
Iosif Marincu (I)
Rodica Silaghi (R)
Sorin Rugina (S)
Noluthando Mwelase (N)
Sheena Kotze (S)
Jose Ignacio Bernardino de la Serna (JI)
Vicente Estrada Perez (V)
Esteban Martinez (E)
Adrian Curran (A)
Dominique Laurent Braun (DL)
Alexandra Calmy (A)
Enos Bernasconi (E)
Matthias Cavassini (M)
John Walsh (J)
Julie Fox (J)
Graeme Moyle (G)
Robert Rosenson (R)
Jamie Morano (J)
Jason Baker (J)
Gerald Pierone (G)
Carl Fichtenbaum (C)
Paul Benson (P)
Deborah Goldstein (D)
Joseph Sacco (J)
Princy Kumar (P)
Robert Grossberg (R)
Kara Chew (K)
Christopher DeFilippi (C)
Vilma Drelichman (V)
Norman Markowitz (N)
David Parenti (D)
Katherine Doktor (K)
Paul Thompson (P)

Commentaires et corrections

Type : CommentIn
Type : ErratumIn
Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Franck Boccara (F)

AP-HP, Hôpitaux de l'Est Parisien, Hôpital Saint-Antoine, Department of Cardiology, Sorbonne Université-INSERM UMR S_938, Centre de Recherche Saint-Antoine, Paris, France. Electronic address: franck.boccara@aphp.fr.

Princy N Kumar (PN)

Division of Infectious Diseases and Travel Medicine, Georgetown University School of Medicine, Washington, DC.

Bruno Caramelli (B)

Interdisciplinary Medicine in Cardiology Unit, InCor, University of São Paulo, São Paulo, Brazil.

Alexandra Calmy (A)

HIV/AIDS Unit, Division of Infectious Diseases, Geneva University Hospitals, Geneva, Switzerland.

J Antonio G López (JAG)

Global Development, Amgen Inc., Thousand Oaks, California.

Sarah Bray (S)

Global Development, Amgen Inc., Thousand Oaks, California.

Marcoli Cyrille (M)

Global Development, Amgen Inc., Thousand Oaks, California.

Robert S Rosenson (RS)

Cardiometabolics Unit, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai, New York, New York.

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Classifications MeSH