Coronary artery plaque characteristics and treatment with biologic therapy in severe psoriasis: results from a prospective observational study.


Journal

Cardiovascular research
ISSN: 1755-3245
Titre abrégé: Cardiovasc Res
Pays: England
ID NLM: 0077427

Informations de publication

Date de publication:
15 03 2019
Historique:
received: 24 10 2018
revised: 17 12 2018
accepted: 12 01 2019
pubmed: 6 2 2019
medline: 12 3 2020
entrez: 6 2 2019
Statut: ppublish

Résumé

The use of biologic therapy has increased over the past decade well beyond primary autoimmune diseases. Indeed, a recent trial using an anti-IL-1beta antibody reduced second myocardial infarction (MI) in those who have had MI. Psoriasis is a chronic inflammatory disease often treated with biologics when severe, is associated with increased risk of MI, in part driven by high-risk coronary plaque phenotypes by coronary computed tomography angiography (CCTA). We hypothesized that we would observe a reduction in inflammatory-driven phenotypes of coronary plaque, including non-calcified coronary plaque burden and lipid-rich necrotic core in those treated with biologic therapy after one-year compared with non-biologic therapy. In a prospective, observational study, 290 participants were recruited from 1 January 2013 through 31 October 2018 with 215 completing one-year follow-up. Of the 238, 121 consecutive participants who were biologic treatment naïve at baseline were included. A blinded reader (blinded to patient demographics, visit and treatment) quantified total coronary plaque burden and plaque subcomponents (calcified and non-calcified) in the three main coronary vessels >2 mm using dedicated software (QAngio, Medis, Netherlands). Psoriasis patients were middle-aged [mean (standard deviation) age, 50.5 (12.1) years], mostly male (n = 70, 58%) with low cardiovascular risk by Framingham score [median (interquartile range, IQR), 3 (1-6)] and had moderate to severe skin disease at baseline [median (IQR) Psoriasis Area Severity Index, PASI, 8.6 (5.3-14.0)]. Biologic therapy was associated with a 6% reduction in non-calcified plaque burden (P = 0.005) reduction in necrotic core (P = 0.03), with no effect on fibrous burden (P = 0.71). Decrease in non-calcified plaque burden in the biologic treated group was significant compared with slow plaque progression in non-biologic treated (Δ, -0.07 mm2 vs. 0.06 mm2; P = 0.02) and associated with biologic treatment beyond adjustment for traditional cardiovascular risk factors (β = 0.20, P = 0.02). In this observational study, we demonstrate that biologic therapy in severe psoriasis was associated with favourable modulation of coronary plaque indices by CCTA. These findings highlight the importance of systemic inflammation in coronary artery disease and support the conduct of larger, randomized trials.

Identifiants

pubmed: 30721933
pii: 5306384
doi: 10.1093/cvr/cvz009
pmc: PMC6432047
doi:

Substances chimiques

Biological Products 0

Types de publication

Journal Article Observational Study Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

721-728

Commentaires et corrections

Type : CommentIn

Informations de copyright

Published by Oxford University Press on behalf of the European Society of Cardiology 2019. This work is written by US Government employees and is in the public domain in the US.

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Auteurs

Youssef A Elnabawi (YA)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Amit K Dey (AK)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Aditya Goyal (A)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Jacob W Groenendyk (JW)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Jonathan H Chung (JH)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Agastya D Belur (AD)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Justin Rodante (J)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Charlotte L Harrington (CL)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Heather L Teague (HL)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Yvonne Baumer (Y)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Andrew Keel (A)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Martin P Playford (MP)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Veit Sandfort (V)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Marcus Y Chen (MY)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Benjamin Lockshin (B)

DermAssociates, Silver Spring, MD, USA.

Joel M Gelfand (JM)

Department of Dermatology, University of Pennsylvania, Philadelphia, PA, USA.

David A Bluemke (DA)

Department of Radiology, University of Wisconsin, Madison, WI, USA.

Nehal N Mehta (NN)

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

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Classifications MeSH