Impact of serum lipoprotein (a) level on coronary plaque progression and cardiovascular events in statin-treated patients with acute coronary syndrome: a yokohama-acs substudy.


Journal

Journal of cardiology
ISSN: 1876-4738
Titre abrégé: J Cardiol
Pays: Netherlands
ID NLM: 8804703

Informations de publication

Date de publication:
07 2020
Historique:
received: 24 09 2019
revised: 03 01 2020
accepted: 13 01 2020
pubmed: 11 2 2020
medline: 18 5 2021
entrez: 11 2 2020
Statut: ppublish

Résumé

Lipoprotein (a) [Lp(a)] has been reported to be a residual risk factor in patients who have achieved target lipid levels. The aim of the present study was to investigate the associations of Lp(a) with plaque progression and major cardiovascular events in patients with acute coronary syndromes (ACS). The Yokohama-ACS study included 102 patients with ACS who underwent intravascular ultrasound (IVUS) at baseline and at 10-month follow-up after percutaneous coronary intervention (PCI). The patients were randomly assigned to receive either moderate- or low-intensity statin therapy. IVUS was performed to measure the plaque volume at non-culprit lesions. We enrolled 76 patients for whom Lp(a) levels at 10-month follow-up were available. The patients were divided into 2 groups according whether their Lp(a) levels were ≤20 mg/dl [low Lp(a) group; n = 49] or >20 mg/dl [high Lp(a) group; n = 27]. Baseline characteristics and low-density lipoprotein cholesterol levels at 10-month follow-up were similar in the low Lp(a) group and high Lp(a) group (87 ± 29 mg/dl vs. 93 ± 27 mg/dl, p = 0.42). The low Lp(a) group had significant plaque regression, whereas the high Lp(a) group showed slight plaque progression (-6.8% vs. 2.5%, p = 0.02). Ninety-five percent of the prognostic data were obtained 5 years after PCI. The cumulative event-free survival rate was significantly lower in the high Lp(a) group (p = 0.02; log-rank test). Lp(a) levels may be an alternative predictor of further plaque regression and the likelihood of major adverse cardiovascular events in statin-treated ACS patients.

Sections du résumé

BACKGROUND
Lipoprotein (a) [Lp(a)] has been reported to be a residual risk factor in patients who have achieved target lipid levels. The aim of the present study was to investigate the associations of Lp(a) with plaque progression and major cardiovascular events in patients with acute coronary syndromes (ACS).
METHODS
The Yokohama-ACS study included 102 patients with ACS who underwent intravascular ultrasound (IVUS) at baseline and at 10-month follow-up after percutaneous coronary intervention (PCI). The patients were randomly assigned to receive either moderate- or low-intensity statin therapy. IVUS was performed to measure the plaque volume at non-culprit lesions. We enrolled 76 patients for whom Lp(a) levels at 10-month follow-up were available.
RESULTS
The patients were divided into 2 groups according whether their Lp(a) levels were ≤20 mg/dl [low Lp(a) group; n = 49] or >20 mg/dl [high Lp(a) group; n = 27]. Baseline characteristics and low-density lipoprotein cholesterol levels at 10-month follow-up were similar in the low Lp(a) group and high Lp(a) group (87 ± 29 mg/dl vs. 93 ± 27 mg/dl, p = 0.42). The low Lp(a) group had significant plaque regression, whereas the high Lp(a) group showed slight plaque progression (-6.8% vs. 2.5%, p = 0.02). Ninety-five percent of the prognostic data were obtained 5 years after PCI. The cumulative event-free survival rate was significantly lower in the high Lp(a) group (p = 0.02; log-rank test).
CONCLUSIONS
Lp(a) levels may be an alternative predictor of further plaque regression and the likelihood of major adverse cardiovascular events in statin-treated ACS patients.

Identifiants

pubmed: 32037254
pii: S0914-5087(20)30020-4
doi: 10.1016/j.jjcc.2020.01.005
pii:
doi:

Substances chimiques

Hydroxymethylglutaryl-CoA Reductase Inhibitors 0
Lipoprotein(a) 0

Banques de données

ClinicalTrials.gov
['NCT00549926']

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

66-72

Informations de copyright

Copyright © 2020. Published by Elsevier Ltd.

Auteurs

Kensuke Matsushita (K)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan; Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Kiyoshi Hibi (K)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan. Electronic address: hibikiyo@yokohama-cu.ac.jp.

Naohiro Komura (N)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.

Yuichiro Kimura (Y)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.

Yasushi Matsuzawa (Y)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.

Masaaki Konishi (M)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.

Nobuhiko Maejima (N)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.

Noriaki Iwahashi (N)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.

Masami Kosuge (M)

Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.

Toshiaki Ebina (T)

Division of Cardiology, Yokohama City University Medical Center, 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, Yokohama, Japan.

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