Saeki Y, Sawaguchi J, Akita S, Takamura TA, Fujibayashi K, Wakasa M, Akao H, Kitayama M, Kawai Y, Kajinami K. Initial decrease in the lipoprotein(a) level is a novel prognostic biomarker in patients with acute coronary syndrome. World J Cardiol 2024; 16(6): 329-338 [PMID: 38993583 DOI: 10.4330/wjc.v16.i6.329]
Corresponding Author of This Article
Kouji Kajinami, FACP, FAHA, MD, Professor, Department of Cardiology, Kanazawa Medical University, 1-1 Daigaku, Uchinada 9200293, Japan. kajinami@kanazawa-med.ac.jp
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
Observational Study
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Saeki Y, Sawaguchi J, Akita S, Takamura TA, Fujibayashi K, Wakasa M, Akao H, Kitayama M, Kawai Y, Kajinami K. Initial decrease in the lipoprotein(a) level is a novel prognostic biomarker in patients with acute coronary syndrome. World J Cardiol 2024; 16(6): 329-338 [PMID: 38993583 DOI: 10.4330/wjc.v16.i6.329]
Yasuhiko Saeki, Jun Sawaguchi, Satori Akita, Taka-aki Takamura, Kosuke Fujibayashi, Minoru Wakasa, Hironobu Akao, Yasuyuki Kawai, Kouji Kajinami, Department of Cardiology, Kanazawa Medical University, Uchinada 9200293, Japan
Michihiko Kitayama, Trans-catheter Cardiovascular Therapeutics, Kanazawa Medical University, Uchinada 9200293, Japan
Author contributions: Saeki Y contributed to principal investigator (conceptualization, data curation, formal data analysis and interpretation, and drafting of the manuscript); Sawaguchi J contributed to associate investigator (conceptualization, data curation, formal data analysis, and interpretation); Takamura TA, Kitayama M, and Kawai Y contributed to coronary interventionalists (data curation and project administration regarding percutaneous coronary intervention procedures and patient management); Akita S, Fujibayashi K, Wakasa M, and Akao H contributed to staff cardiologists (data curation, preliminary data analysis, and interpretation); Kajinami K contributed to director (supervision of the overall study and manuscript editing/finalization).
Supported bythe Vehicle Racing Commemorative Foundation, No. 2013–2015; Grant for Collaborative Research from Kanazawa Medical University, No. C2015-4; and Grants-in-Aid for Scientific Research (C) from the Japan Society for the Promotion of Science to Dr. Kouji Kajinami, No. 18K08051 and No. 21K08139.
Institutional review board statement: The study protocol conformed to the ethical guidelines of the 1975 Declaration of Helsinki and was approved by the Ethics Committee of our institution (Approval No. I-115).
Informed consent statement: Written informed consent was obtained from all patients prior to enrollment.
Conflict-of-interest statement: There are no conflicts of interest to disclose.
Data sharing statement: Data used to support the findings of this study are available from the corresponding author upon request.
STROBE statement: The authors have read the STROBE Statement—checklist of items, and the manuscript was prepared and revised according to the STROBE Statement—checklist of items.
Corresponding author: Kouji Kajinami, FACP, FAHA, MD, Professor, Department of Cardiology, Kanazawa Medical University, 1-1 Daigaku, Uchinada 9200293, Japan. kajinami@kanazawa-med.ac.jp
Received: February 6, 2024 Revised: April 22, 2024 Accepted: April 28, 2024 Published online: June 26, 2024 Processing time: 140 Days and 5.6 Hours
Core Tip
Core Tip: Two hundred and forty-nine patients with acute coronary syndrome were enrolled in the study. Lipoprotein(a) [Lp(a)] levels were measured before percutaneous coronary intervention (PCI) to 48 h after using an isoform-independent assay. Lp(a) levels decreased significantly from pre-PCI (0 h) to 12 h after, and then increased up to 48 h after. The changes from 0 to 12 h [Lp(a)Δ0-12] were significantly correlated with basal creatinine and Lp(a). Among the tertiles classified according to the changes from 0 to 12 h [Lp(a)Δ0-12], major adverse cardiac events (MACE) were significantly more frequent in the lowest Lp(a)Δ0-12 group than in the other two groups. Multivariate analysis revealed that Lp(a)Δ0-12 and basal creatinine were independent determinants of subsequent MACE.