Reduction of Myocardial Infarction and All-Cause Mortality Associated to Statins in Patients Without Obstructive CAD.


Journal

JACC. Cardiovascular imaging
ISSN: 1876-7591
Titre abrégé: JACC Cardiovasc Imaging
Pays: United States
ID NLM: 101467978

Informations de publication

Date de publication:
12 2021
Historique:
received: 19 04 2021
accepted: 07 05 2021
pubmed: 19 7 2021
medline: 22 2 2022
entrez: 18 7 2021
Statut: ppublish

Résumé

The aim of this work was to evaluate the prognostic impact of statin therapy in symptomatic patients without obstructive CAD. Information on the prognostic impact of post-coronary computed tomographic angiography (CTA) statin use in patients with no or nonobstructive coronary artery disease (CAD) is sparse. Patients undergoing CTA with suspected CAD in western Denmark from 2008 to 2017 with <50% coronary stenoses were identified. Information on post-CTA use of statin therapy and cardiovascular events were obtained from national registries. The study included 33,552 patients, median aged 56 years, 58% female, with no (n = 19,669) or nonobstructive (n = 13,883) CAD and a median follow-up of 3.5 years. The absolute risk of the combined end point of myocardial infarction (MI) or all-cause mortality was directly associated with the CAD burden with an event rate/1,000 patient-years of 4.13 (95% CI: 3.69-4.61) in no, 7.74 (95% CI: 6.88-8.71) in mild (coronary artery calcium score [CACS] 0-99), 13.72 (95% CI: 11.61-16.23) in moderate (CACS 100-399), and 32.47 (95% CI: 26.25-40.16) in severe (CACS ≥400) nonobstructive CAD. Statin therapy was associated with a multivariable adjusted HR for MI and death of 0.52 (95% CI: 0.36-0.75) in no, 0.44 (95% CI: 0.32-0.62) in mild, 0.51 (95% CI: 0.34-0.75) in moderate, and 0.52 (95% CI: 0.32-0.86) in severe nonobstructive CAD. The estimated numbers needed to treat to prevent the primary end point were 92 (95% CI: 61-182) in no, 36 (95% CI: 26-58) in mild, 24 (95% CI: 15-61) in moderate, and 13 (95% CI: 7-86) in severe nonobstructive CAD. Residual confounding may persist, but not to an extent explaining all of the observed risk reduction associated with statin treatment. The risk of MI and all-cause mortality in patients without obstructive CAD is directly associated with the CAD burden. Statin therapy is associated with a reduction of MI and all-cause death across the spectrum of CAD, however, the absolute benefit of treatment is directionally proportional with the CAD burden.

Sections du résumé

OBJECTIVES
The aim of this work was to evaluate the prognostic impact of statin therapy in symptomatic patients without obstructive CAD.
BACKGROUND
Information on the prognostic impact of post-coronary computed tomographic angiography (CTA) statin use in patients with no or nonobstructive coronary artery disease (CAD) is sparse.
METHODS
Patients undergoing CTA with suspected CAD in western Denmark from 2008 to 2017 with <50% coronary stenoses were identified. Information on post-CTA use of statin therapy and cardiovascular events were obtained from national registries.
RESULTS
The study included 33,552 patients, median aged 56 years, 58% female, with no (n = 19,669) or nonobstructive (n = 13,883) CAD and a median follow-up of 3.5 years. The absolute risk of the combined end point of myocardial infarction (MI) or all-cause mortality was directly associated with the CAD burden with an event rate/1,000 patient-years of 4.13 (95% CI: 3.69-4.61) in no, 7.74 (95% CI: 6.88-8.71) in mild (coronary artery calcium score [CACS] 0-99), 13.72 (95% CI: 11.61-16.23) in moderate (CACS 100-399), and 32.47 (95% CI: 26.25-40.16) in severe (CACS ≥400) nonobstructive CAD. Statin therapy was associated with a multivariable adjusted HR for MI and death of 0.52 (95% CI: 0.36-0.75) in no, 0.44 (95% CI: 0.32-0.62) in mild, 0.51 (95% CI: 0.34-0.75) in moderate, and 0.52 (95% CI: 0.32-0.86) in severe nonobstructive CAD. The estimated numbers needed to treat to prevent the primary end point were 92 (95% CI: 61-182) in no, 36 (95% CI: 26-58) in mild, 24 (95% CI: 15-61) in moderate, and 13 (95% CI: 7-86) in severe nonobstructive CAD. Residual confounding may persist, but not to an extent explaining all of the observed risk reduction associated with statin treatment.
CONCLUSIONS
The risk of MI and all-cause mortality in patients without obstructive CAD is directly associated with the CAD burden. Statin therapy is associated with a reduction of MI and all-cause death across the spectrum of CAD, however, the absolute benefit of treatment is directionally proportional with the CAD burden.

Identifiants

pubmed: 34274285
pii: S1936-878X(21)00487-3
doi: 10.1016/j.jcmg.2021.05.022
pii:
doi:

Substances chimiques

Hydroxymethylglutaryl-CoA Reductase Inhibitors 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2400-2410

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures This work was supported by a research grant to Dr Øvrehus by the Faculty of Health Sciences, University of Southern Denmark. Dr Grove has received speaker honoraria or consultancy fees from AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Pfizer, Merck Sharp & Dohme, MundiPharma, Portola Pharmaceuticals, and Roche; and an unrestricted research grant from Boehringer Ingelheim. Dr Nørgaard has received unrestricted institutional research grants from Siemens and Heart Flow. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Kristian A Øvrehus (KA)

Department of Cardiology, Odense University Hospital, Odense, Esbjerg, Denmark; Department of Clinical Medicine, Health, University of Southern Denmark, Odense, Denmark. Electronic address: kristian.altern.ovrehus@rsyd.dk.

Axel Diederichsen (A)

Department of Cardiology, Odense University Hospital, Odense, Esbjerg, Denmark; Department of Clinical Medicine, Health, University of Southern Denmark, Odense, Denmark.

Erik L Grove (EL)

Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Medicine, Health, Aarhus University, Aarhus, Denmark.

Flemming H Steffensen (FH)

Department of Cardiology, Lillebaelt Hospital-Vejle, Vejle, Denmark.

Martin B Mortensen (MB)

Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.

Jesper M Jensen (JM)

Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.

Hans Mickley (H)

Department of Cardiology, Odense University Hospital, Odense, Esbjerg, Denmark; Department of Clinical Medicine, Health, University of Southern Denmark, Odense, Denmark.

Lene H Nielsen (LH)

Department of Cardiology, Odense University Hospital, Odense, Esbjerg, Denmark.

Martin Busk (M)

Department of Cardiology, Lillebaelt Hospital-Vejle, Vejle, Denmark.

Niels Peter R Sand (NPR)

Department of Cardiology, Hospital of South West Jutland, Esbjerg, Denmark; Department of Regional Health Research, University of Southern Denmark, Esbjerg, Denmark.

Jess Lambrechtsen (J)

Department of Cardiology, Odense University Hospital Svendborg, Svendborg, Denmark.

Anders H Riis (AH)

Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.

Ina Trolle Andersen (IT)

Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.

Hans E Bøtker (HE)

Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Medicine, Health, Aarhus University, Aarhus, Denmark.

Bjarne L Nørgaard (BL)

Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Medicine, Health, Aarhus University, Aarhus, Denmark.

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