Endothelial dysfunction predicts bleeding and cardiovascular death in acute coronary syndrome.

Acute coronary syndrome Bleeding event Cardiovascular death Cardiovascular event Endothelial dysfunction

Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 04 2023
Historique:
received: 12 09 2022
revised: 25 01 2023
accepted: 30 01 2023
pubmed: 4 2 2023
medline: 8 3 2023
entrez: 3 2 2023
Statut: ppublish

Résumé

Recently, there has been increasing awareness that bleeding may lead to adverse outcomes. Endothelial dysfunction is associated with increased risk of cardiovascular and bleeding events. This study aimed to investigate the association of endothelial dysfunction with major bleeding and specific causes of death in addition to major adverse cardiovascular events in patients with acute coronary syndrome. This single-centre retrospective observational study was conducted at a tertiary-care hospital; patients with acute coronary syndrome were included between June 2010 and November 2014 (median follow-up, 6.1 years). The reactive hyperaemia index was assessed before their discharge; reactive hyperaemia index <1.67 was defined as endothelial dysfunction. The main outcomes were the incidence of major bleeding, all-cause death, cardiovascular death, non-cardiovascular death, resuscitated cardiac arrest, non-fatal myocardial infarction, non-fatal stroke, and hospitalisation for heart failure. Among the included 674 patients with acute coronary syndrome, 264 (39.2%) had endothelial dysfunction. Multivariable Cox-hazard analyses revealed an independent predictive value of endothelial dysfunction for major bleeding (hazard ratio 2.29, 95% confidence interval 1.17-4.48, P = 0.016) and major adverse cardiovascular events (hazard ratio 2.04, 95% confidence interval 1.43-2.89, P < 0.001). The endothelial dysfunction group patients had a 2.5-fold greater risk of cardiovascular death; however, no association was found with non-cardiovascular death. Endothelial dysfunction assessed using reactive hyperaemia index predicted future major cardiovascular event as well as major bleeding and cardiovascular death in patients with acute coronary syndrome.

Sections du résumé

BACKGROUNDS
Recently, there has been increasing awareness that bleeding may lead to adverse outcomes. Endothelial dysfunction is associated with increased risk of cardiovascular and bleeding events. This study aimed to investigate the association of endothelial dysfunction with major bleeding and specific causes of death in addition to major adverse cardiovascular events in patients with acute coronary syndrome.
METHODS
This single-centre retrospective observational study was conducted at a tertiary-care hospital; patients with acute coronary syndrome were included between June 2010 and November 2014 (median follow-up, 6.1 years). The reactive hyperaemia index was assessed before their discharge; reactive hyperaemia index <1.67 was defined as endothelial dysfunction. The main outcomes were the incidence of major bleeding, all-cause death, cardiovascular death, non-cardiovascular death, resuscitated cardiac arrest, non-fatal myocardial infarction, non-fatal stroke, and hospitalisation for heart failure.
RESULTS
Among the included 674 patients with acute coronary syndrome, 264 (39.2%) had endothelial dysfunction. Multivariable Cox-hazard analyses revealed an independent predictive value of endothelial dysfunction for major bleeding (hazard ratio 2.29, 95% confidence interval 1.17-4.48, P = 0.016) and major adverse cardiovascular events (hazard ratio 2.04, 95% confidence interval 1.43-2.89, P < 0.001). The endothelial dysfunction group patients had a 2.5-fold greater risk of cardiovascular death; however, no association was found with non-cardiovascular death.
CONCLUSION
Endothelial dysfunction assessed using reactive hyperaemia index predicted future major cardiovascular event as well as major bleeding and cardiovascular death in patients with acute coronary syndrome.

Identifiants

pubmed: 36736671
pii: S0167-5273(23)00121-3
doi: 10.1016/j.ijcard.2023.01.079
pii:
doi:

Types de publication

Observational Study Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

11-17

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest None declared.

Auteurs

Tomohiro Yoshii (T)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan; National Cerebral and Cardiovascular Center, 6-1 Kishibe Shinmachi, Suita, Osaka, Japan.

Yasushi Matsuzawa (Y)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan. Electronic address: matsu@yokohama-cu.ac.jp.

So Kato (S)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Ryosuke Sato (R)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Youhei Hanajima (Y)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Shinnosuke Kikuchi (S)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Hidefumi Nakahashi (H)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Masaaki Konishi (M)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Eiichi Akiyama (E)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Yugo Minamimoto (Y)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Yuichiro Kimura (Y)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Kozo Okada (K)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Nobuhiko Maejima (N)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Noriaki Iwahashi (N)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Toshiaki Ebina (T)

Department of Laboratory Medicine and Clinical Investigation, Yokohama City University Medical Center, Yokohama, Japan.

Kiyoshi Hibi (K)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Masami Kosuge (M)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

Toshihiro Misumi (T)

Department of Biostatistics, Yokohama City University School of Medicine, Yokohama, Japan.

Kouichi Tamura (K)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Kazuo Kimura (K)

Division of Cardiology, Yokohama City University Medical Center, 4-57, Urafune-cho, Minami-ku, Yokohama, Japan.

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