Observational Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Cardiol. Jun 26, 2024; 16(6): 329-338
Published online Jun 26, 2024. doi: 10.4330/wjc.v16.i6.329
Initial decrease in the lipoprotein(a) level is a novel prognostic biomarker in patients with acute coronary syndrome
Yasuhiko Saeki, Jun Sawaguchi, Satori Akita, Taka-aki Takamura, Kosuke Fujibayashi, Minoru Wakasa, Hironobu Akao, Michihiko Kitayama, Yasuyuki Kawai, Kouji Kajinami
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 by the 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.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
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
Abstract
BACKGROUND

Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular diseases; however, its role in acute coronary syndrome (ACS) remains unclear.

AIM

To investigate the hypothesis that the Lp(a) levels are altered by various conditions during the acute phase of ACS, resulting in subsequent cardiovascular events.

METHODS

From September 2009 to May 2016, 377 patients with ACS who underwent emergent coronary angiography, and 249 who completed ≥ 1000 d of follow-up were enrolled. Lp(a) levels were measured using an isoform-independent assay at each time point from before percutaneous coronary intervention (PCI) to 48 h after PCI. The primary endpoint was the occurrence of major adverse cardiac events (MACE; cardiac death, other vascular death, ACS, and non-cardiac vascular events).

RESULTS

The mean circulating Lp(a) level decreased significantly from pre-PCI (0 h) to 12 h after (19.0 mg/dL to 17.8 mg/dL, P < 0.001), and then increased significantly up to 48 h after (19.3 mg/dL, P < 0.001). The changes from 0 to 12 h [Lp(a)Δ0-12] significantly correlated with the basal levels of creatinine [Spearman’s rank correlation coefficient (SRCC): -0.181, P < 0.01] and Lp(a) (SRCC: -0.306, P < 0.05). Among the tertiles classified according to Lp(a)Δ0-12, MACE was significantly more frequent in the lowest Lp(a)Δ0-12 group than in the remaining two tertile groups (66.2% vs 53.6%, P = 0.034). A multivariate analysis revealed that Lp(a)Δ0-12 [hazard ratio (HR): 0.96, 95% confidence interval (95%CI): 0.92-0.99] and basal creatinine (HR: 1.13, 95%CI: 1.05-1.22) were independent determinants of subsequent MACE.

CONCLUSION

Circulating Lp(a) levels in patients with ACS decreased significantly after emergent PCI, and a greater decrease was independently associated with a worse prognosis.

Keywords: Lipoprotein (a); Acute coronary syndrome; Percutaneous coronary intervention; Major adverse cardiac events; Prognosis

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.