Apabetalone lowers serum alkaline phosphatase and improves cardiovascular risk in patients with cardiovascular disease.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
11 2019
Historique:
received: 06 04 2019
revised: 19 08 2019
accepted: 12 09 2019
pubmed: 1 10 2019
medline: 4 8 2020
entrez: 1 10 2019
Statut: ppublish

Résumé

In patients with cardiovascular disease, considerable residual risk remains despite evidence-based secondary prevention measures. Alkaline phosphatase (ALP) has been suggested as a modifiable cardiovascular risk factor. We sought to determine whether cardiovascular risk reduction by the bromodomain and extra-terminal (BET) protein inhibitor apabetalone is associated with the concomitant lowering of serum ALP. In a post-hoc analysis of 795 patients with established coronary heart disease and statin treatment, who participated in phase 2 placebo-controlled trials of apabetalone, we determined the effect of assigned treatment for up to 24 weeks on the incidence of major adverse cardiovascular events (MACE) and serum ALP. Baseline ALP (median 72 U/L) predicted MACE (death, non-fatal myocardial infarction, coronary revascularization, or hospitalization for cardiovascular causes), independent of high-sensitivity C-reactive protein (hsCRP), sex, age, race, study, cardiovascular risk factors, chronic kidney disease (CKD), liver function markers and treatment allocation (hazard ratio [HR] per standard deviation [SD] 1.6, 95% CI 1.19-2.16, p = 0.002). Mean placebo-corrected decreases in ALP from baseline were 9.2% (p < 0.001) after 12-14 weeks and 7.7% (p < 0.001) after 24-26 weeks of apabetalone treatment. In the apabetalone group, a 1-SD reduction in ALP was associated with a HR for MACE of 0.64 (95% CI 0.46-0.90, p = 0.009). Serum ALP predicts residual cardiovascular risk, independent of hsCRP, established cardiovascular risk factors and CKD, in patients with cardiovascular disease on statin treatment. Apabetalone lowers serum ALP, which was associated with a lower risk of cardiovascular events. Whether the beneficial cardiovascular effects of apabetalone are causally related to ALP reduction remains undetermined.

Sections du résumé

BACKGROUND AND AIMS
In patients with cardiovascular disease, considerable residual risk remains despite evidence-based secondary prevention measures. Alkaline phosphatase (ALP) has been suggested as a modifiable cardiovascular risk factor. We sought to determine whether cardiovascular risk reduction by the bromodomain and extra-terminal (BET) protein inhibitor apabetalone is associated with the concomitant lowering of serum ALP.
METHODS
In a post-hoc analysis of 795 patients with established coronary heart disease and statin treatment, who participated in phase 2 placebo-controlled trials of apabetalone, we determined the effect of assigned treatment for up to 24 weeks on the incidence of major adverse cardiovascular events (MACE) and serum ALP.
RESULTS
Baseline ALP (median 72 U/L) predicted MACE (death, non-fatal myocardial infarction, coronary revascularization, or hospitalization for cardiovascular causes), independent of high-sensitivity C-reactive protein (hsCRP), sex, age, race, study, cardiovascular risk factors, chronic kidney disease (CKD), liver function markers and treatment allocation (hazard ratio [HR] per standard deviation [SD] 1.6, 95% CI 1.19-2.16, p = 0.002). Mean placebo-corrected decreases in ALP from baseline were 9.2% (p < 0.001) after 12-14 weeks and 7.7% (p < 0.001) after 24-26 weeks of apabetalone treatment. In the apabetalone group, a 1-SD reduction in ALP was associated with a HR for MACE of 0.64 (95% CI 0.46-0.90, p = 0.009).
CONCLUSIONS
Serum ALP predicts residual cardiovascular risk, independent of hsCRP, established cardiovascular risk factors and CKD, in patients with cardiovascular disease on statin treatment. Apabetalone lowers serum ALP, which was associated with a lower risk of cardiovascular events. Whether the beneficial cardiovascular effects of apabetalone are causally related to ALP reduction remains undetermined.

Identifiants

pubmed: 31568963
pii: S0021-9150(19)31476-5
doi: 10.1016/j.atherosclerosis.2019.09.002
pii:
doi:

Substances chimiques

Biomarkers 0
Hydroxymethylglutaryl-CoA Reductase Inhibitors 0
Quinazolinones 0
apabetalone 8R4A7GDZ1D
Alkaline Phosphatase EC 3.1.3.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

59-65

Informations de copyright

Crown Copyright © 2019. Published by Elsevier B.V. All rights reserved.

Auteurs

Mathias Haarhaus (M)

Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. Electronic address: mathias.loberg-haarhaus@sll.se.

Kausik K Ray (KK)

Imperial Centre for Cardiovascular Disease Prevention, School of Public Health, Imperial College London, London, UK.

Stephen J Nicholls (SJ)

South Australian Health and Medical Research Institute, University of Adelaide, PO Box 11060, Adelaide, SA, 5001, Australia.

Gregory G Schwartz (GG)

University of Colorado School of Medicine, Aurora, CO, USA.

Ewelina Kulikowski (E)

Resverlogix Corp, Calgary, AB, Canada.

Jan O Johansson (JO)

Resverlogix Inc, San Francisco, CA, USA.

Michael Sweeney (M)

Resverlogix Inc, San Francisco, CA, USA.

Christopher Halliday (C)

Resverlogix Corp, Calgary, AB, Canada.

Kenneth Lebioda (K)

Resverlogix Corp, Calgary, AB, Canada.

Norman Wong (N)

Resverlogix Corp, Calgary, AB, Canada.

Vincent Brandenburg (V)

Department of Cardiology and Nephrology, Rhein-Maas Klinikum Wuerselen, Wuerselen, Germany.

Srinivasan Beddhu (S)

Division of Nephrology and Hypertension and Medical Service, Veterans Affairs Salt Lake City Healthcare System, Salt Lake City, UT, USA.

Marcello Tonelli (M)

Department of Medicine, University of Calgary, Calgary, AB, Canada.

Carmine Zoccali (C)

CNR-IFC Clin Epid Renal Diseases and Hypertension, Reggio C. c/o Ospedali Riuniti, 89124, Reggio C. Italy.

Kamyar Kalantar-Zadeh (K)

Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology and Hypertension, University of California Irvine Medical Center, Orange, CA, USA; Nephrology Section, Tibor Rubin Veterans Affairs Medical Center, Long Beach, CA, USA; Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA, USA. Electronic address: kkz@uci.edu.

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Classifications MeSH