Lipid profile and risk factors for neoatherosclerosis after drug-eluting stent implantation in acute coronary syndrome.

Acute coronary syndrome Hyperlipidemia In-stent restenosis Lipoprotein (a) Neoatherosclerosis Non-high-density lipoprotein cholesterol

Journal

Journal of clinical lipidology
ISSN: 1933-2874
Titre abrégé: J Clin Lipidol
Pays: United States
ID NLM: 101300157

Informations de publication

Date de publication:
31 Aug 2024
Historique:
received: 21 02 2024
revised: 23 07 2024
accepted: 23 08 2024
medline: 16 9 2024
pubmed: 16 9 2024
entrez: 15 9 2024
Statut: aheadofprint

Résumé

Predictors of neoatherosclerosis in patients who received primary percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) remain unclear. The aim of this study is to investigate the frequency and risk factors of neoatherosclerosis 1-year after the onset of ACS. This study investigated 83 patients who underwent PCI for ACS followed by 1-year follow-up optical coherence tomography. The patients were categorized into the neoatherosclerosis (n = 11) and non-neoatherosclerosis groups (n = 72). Baseline characteristics, PCI procedures, medical therapies, and blood tests at 1-year, including detailed lipid profiles, were compared between the two groups. Diabetes mellitus was more prominent in the neoatherosclerosis than in the non-neoatherosclerosis group (45% vs. 17 %, respectively, p = 0.03). Total cholesterol (171 ± 37 mg/dL vs. 145 ± 25 mg/dL, respectively, p < 0.01), non-high-density lipoprotein cholesterol (HDL-C) (124 ± 36 mg/dL vs. 94 ± 24 mg/dL, respectively, p < 0.01), low-density lipoprotein cholesterol (94 ± 36 mg/dL vs. 72 ± 19 mg/dL, respectively, p < 0.01), and lipoprotein (a) (Lp[a]) (70 [19-112] mg/dL vs. 10 [3-25] mg/dL, respectively, p = 0.03) at follow-up were significantly higher in the neoatherosclerosis group. Multivariate analysis revealed that neoatherosclerosis was associated with high serum non-HDL-C (odds ratio [OR]: 1.075; 95 % confidence interval [CI]: 1.011-1.144; p < 0.01) and high serum Lp(a) levels (>30 mg/dL) (OR: 11.0; 95 % CI: 1.492-81.02; p = 0.02). Poorly controlled non-HDL-C and Lp(a) would be risk factors of neoatherosclerosis in patients 1-year after ACS.

Sections du résumé

BACKGROUND BACKGROUND
Predictors of neoatherosclerosis in patients who received primary percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) remain unclear.
OBJECTIVE OBJECTIVE
The aim of this study is to investigate the frequency and risk factors of neoatherosclerosis 1-year after the onset of ACS.
METHODS METHODS
This study investigated 83 patients who underwent PCI for ACS followed by 1-year follow-up optical coherence tomography. The patients were categorized into the neoatherosclerosis (n = 11) and non-neoatherosclerosis groups (n = 72). Baseline characteristics, PCI procedures, medical therapies, and blood tests at 1-year, including detailed lipid profiles, were compared between the two groups.
RESULTS RESULTS
Diabetes mellitus was more prominent in the neoatherosclerosis than in the non-neoatherosclerosis group (45% vs. 17 %, respectively, p = 0.03). Total cholesterol (171 ± 37 mg/dL vs. 145 ± 25 mg/dL, respectively, p < 0.01), non-high-density lipoprotein cholesterol (HDL-C) (124 ± 36 mg/dL vs. 94 ± 24 mg/dL, respectively, p < 0.01), low-density lipoprotein cholesterol (94 ± 36 mg/dL vs. 72 ± 19 mg/dL, respectively, p < 0.01), and lipoprotein (a) (Lp[a]) (70 [19-112] mg/dL vs. 10 [3-25] mg/dL, respectively, p = 0.03) at follow-up were significantly higher in the neoatherosclerosis group. Multivariate analysis revealed that neoatherosclerosis was associated with high serum non-HDL-C (odds ratio [OR]: 1.075; 95 % confidence interval [CI]: 1.011-1.144; p < 0.01) and high serum Lp(a) levels (>30 mg/dL) (OR: 11.0; 95 % CI: 1.492-81.02; p = 0.02).
CONCLUSION CONCLUSIONS
Poorly controlled non-HDL-C and Lp(a) would be risk factors of neoatherosclerosis in patients 1-year after ACS.

Identifiants

DOI: 10.1016/j.jacl.2024.08.011 PMID: 39278775
pubmed: 39278775
pii: S1933-2874(24)00238-1
doi: 10.1016/j.jacl.2024.08.011
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interest Sho Torii received research grants from Abbot Vascular Japan, Boston Scientific Japan, Medtronic, and received honoraria from Boston Scientific Japan. Gaku Nakazawa received honoraria from Abbot Medical, Boston Scientific, Terumo Corp., Daiichi-Sankyo, and OrbusNeich. Yuji Ikari received research grants from Boston Scientific, and received honoraria from AstraZeneca, Boston Scientific, Kaneka, Nipro, Novartis, Bayer, and Boehringer Ingelheim. The remaining authors have nothing to disclose.

Auteurs

Norihito Nakamura (N)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Katsuaki Sakai (K)

Nagasaki Heart Clinic, Nagasaki, Japan (Dr Sakai).

Sho Torii (S)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari). Electronic address: storii@tsc.u-tokai.ac.jp.

Yuki Aoki (Y)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Frederic Turcotte-Gosselin (F)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Kazuki Fujinuma (K)

Tokai University School of Medicine, Department of Clinical Engineering, Isehara, Japan (Drs Fujinuma and Ohwaki).

Ami Ohwaki (A)

Tokai University School of Medicine, Department of Clinical Engineering, Isehara, Japan (Drs Fujinuma and Ohwaki).

Kazuki Aihara (K)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Satoshi Noda (S)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Junichi Miyamoto (J)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Yu Sato (Y)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Manabu Shiozaki (M)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Makoto Natsumeda (M)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Yohei Ohno (Y)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Masataka Nakano (M)

Ageo Chuo Medical Center, Department of Cardiology, Saitama, Japan (Dr Nakano).

Fuminobu Yoshimachi (F)

Tokai Hachioji Hospital, Department of Cardiology, Hachioji, Japan (Dr Yoshimachi).

Gaku Nakazawa (G)

Kindai University Faculty of Medicine, Department of Cardiology, Osaka-Sayama, Japan (Dr Nakazawa).

Yuji Ikari (Y)

Tokai University School of Medicine, Department of Cardiology, Isehara, Japan (Drs Nakamura, Torii, Aoki, Turcotte-Gosselin, Aihara, Noda, Miyamoto, Sato, Shiozaki, Natsumeda, Ohno, and Ikari).

Classifications MeSH