Evidence map›Paper›PMID 39368019›Full record

ArticleHeart and vessels2025

Anti-inflammatory effects of proprotein convertase subtilisin/kexin 9 inhibitor therapy in the early phase of acute myocardial infarction.

Tomohiro Shimizu, Tetsuji Morishita, Hiroyasu Uzui, Yusuke Sato, Tatsuhiro Kataoka, Machiko Miyoshi, Junya Yamaguchi, Yuichiro Shiomi, Hiroyuki Ikeda, Naoto Tama and 3 more

Abstract read
In one paragraph

Article in Heart and vessels, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Tomohiro ShimizuDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Tetsuji MorishitaDepartment of Internal Medicine, Matsunami General Hospital, Gifu, 501-6062, Japan.
Hiroyasu UzuiDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan. huzui@u-fukui.ac.jp.ORCID http://orcid.org/0000-0001-7634-6911
Yusuke SatoDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Tatsuhiro KataokaDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Machiko MiyoshiDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Junya YamaguchiDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Yuichiro ShiomiDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Hiroyuki IkedaDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Naoto TamaDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Kanae HasegawaDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Kentaro IshidaDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.
Hiroshi TadaDepartment of Cardiovascular Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, Matsuoka Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan.

Funding

Japan Society for the Promotion of Science JP16K09456
6 · The paper itself

Abstract

This study examined the anti-inflammatory and endothelial function-enhancing effects of proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitor therapy in the early phase after acute myocardial infarction (AMI) by assessing changes in tumor necrosis factor-α (TNF-α) levels and the L-arginine/asymmetric-dimethylarginine (ADMA) ratio. This retrospective, single-center cohort study included patients who underwent successful timely primary percutaneous coronary intervention (PCI) for first-onset AMI between September 2017 and March 2018. The PCSK9 inhibitor group comprised patients who received 75 mg alirocumab up to 7 days after AMI, while the standard therapy group comprised patients who did not. We evaluated the change in TNF-α levels and the L-arginine/ADMA ratio at the time of hospital admission and prior to discharge. PCSK9 inhibitor therapy in the early phase after AMI suppressed TNF-α levels (standard therapy group, 1.64 ± 2.14 pg/mL vs. PCSK9 inhibitor group, 0.26 ± 0.33 pg/mL; p = 0.033) and increased the L-arginine/ADMA ratio (standard therapy group, - 13.0 ± 39.7 vs. PCSK9 inhibitor group, 23.2 ± 39.7; p = 0.042). Upon multiple regression analysis adjusted for sex, age, and peak creatine kinase levels, PCSK9 inhibitor therapy was associated with TNF-α suppression (p = 0.025; β = - 0.235, 95% confidence interval [CI], - 0.436 to - 0.033). The L-arginine/ADMA ratio was also analyzed using multiple regression, adjusted for sex, age, peak creatine kinase levels, and smoking, showing a significant improvement in the ratio (p = 0.018; β = 41.913, 95% CI, 10.337-73.491). Moreover, a weak negative correlation was suggested between the change in TNF-α levels and the change in L-arginine/ADMA ratio (r = - 0.393, p = 0.058). PCSK9 inhibitor therapy in the early phase after AMI suppresses TNF-α levels and improves the L-arginine/ADMA ratio, potentially indicating anti-inflammatory and endothelial function-enhancing effects.

Indexed as

Antibodies, Monoclonal, HumanizedMyocardial InfarctionPCSK9 InhibitorsAgedAnti-Inflammatory AgentsArginineBiomarkersFemaleHumansMaleMiddle AgedPercutaneous Coronary InterventionProprotein Convertase 9Retrospective StudiesTime FactorsTreatment OutcomealirocumabAntibodies, Monoclonal, HumanizedAnti-Inflammatory AgentsArginineBiomarkersN,N-dimethylargininePCSK9 InhibitorsPCSK9 protein, humanProprotein Convertase 9Tumor Necrosis Factor-alphaAcute myocardial infarctionl-arginine/asymmetric-dimethylarginineProprotein convertase subtilisin/kexin 9 inhibitorTumor necrosis factor-α

Identifiers

PMID39368019
PMCPMC11923012

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.