Evidence map›Paper›PMID 32955695›Full record

ArticleJournal of thrombosis and thrombolysis2021

Determinants of ST-segment elevation myocardial infarction as clinical presentation of acute coronary syndrome.

Osamu Kurihara, Masamichi Takano, Tsunekazu Kakuta, Tsunenari Soeda, Filippo Crea, Tom Adriaenssens, Holger M Nef, Niklas F Boeder, Erika Yamamoto, Hyung Oh Kim and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of thrombosis and thrombolysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 29% of its field
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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

17 authors at 9 institutions in 6 countries.

Osamu KuriharaCardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA, 02114, USA.
Masamichi TakanoCardiovascular Center, Nippon Medical School Chiba Hokusoh Hospital, 1715 Kamakari, Inzai, Chiba, 270-1694, Japan. takanom@nms.ac.jp.
Tsunekazu KakutaDivision of Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.
Tsunenari SoedaDepartment of Cardiovascular Medicine, Nara Medical University, Nara, Japan.
Filippo CreaFondazione Policlinico Universitario A Gemelli IRCCS, Rome, Italy.
Tom AdriaenssensDepartment of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium.
Holger M NefDepartment of Cardiology, University of Giessen, Giessen, Germany.
Niklas F BoederDepartment of Cardiology, University of Giessen, Giessen, Germany.
Erika YamamotoCardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA, 02114, USA.
Hyung Oh KimCardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA, 02114, USA.
Michele RussoCardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA, 02114, USA.
Iris McNultyCardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA, 02114, USA.
Makoto ArakiCardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA, 02114, USA.
Akihiro NakajimaCardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA, 02114, USA.
Hang LeeBiostatistics Center, Harvard Medical School, Massachusetts General Hospital, Boston, MA, USA.
Kyoichi MizunoMitsukoshi Health and Welfare Foundation, Tokyo, Japan.
Ik -Kyung JangCardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA, 02114, USA. ijang@mgh.harvard.edu.
Massachusetts General Hospital · USGiessen School of Theology · DEHarvard University · USChiba Hokusou Hospital · JPIstituti di Ricovero e Cura a Carattere Scientifico · ITKU Leuven · BEMitsukoshi Health and Welfare Foundation · JPNara Medical University · JPTsuchiura Kyodo General Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antiplatelet agents and statin therapies are widely used in patients with known cardiovascular disease. Plaque rupture (PR) and plaque erosion (PE) are the most frequent underlying mechanisms of acute coronary syndromes (ACS). The conditions and medications that are associated with ST-segment elevation myocardial infarction (STEMI) following PR or PE have not been systematically studied. A total of 838 ACS patients (494 with STEMI, 344 with NSTE-ACS) who were diagnosed with PR or PE by optical coherence tomography were included. The patients were categorized into two groups based on underlying pathology, and the baseline characteristics and culprit plaque morphology associated with STEMI were investigated within each group. Among 838 patients, 467 (55.7%) had PR, and 371 (44.3%) were diagnosed with PE. Among patients with PR, older age, hyperlipidemia, no antiplatelet therapy, higher level of low-density lipoprotein cholesterol, and greater lipid burden and macrophage infiltration were associated with increased probability of STEMI. Among patients with PE, no dual antiplatelet therapy and no statin therapy were associated with increased probability of STEMI. The incidence of STEMI caused by PR was significantly lower on antiplatelet therapy (P < 0.001), and the incidence of STEMI caused by PE was significantly lower on antiplatelet therapy (P < 0.001) or on statin therapy (P < 0.001). Antiplatelet therapy is associated with lower probability of STEMI, regardless of underlying pathology, and statin therapy is associated with lower probability of STEMI in PE as clinical presentation of ACS. Statin therapy prior to the onset of acute coronary syndromes (ACS) may reduce the probability of plaque rupture. Antiplatelet therapy prior to the onset of ACS is associated with reduced probability of ST-segment elevation myocardial infarction (STEMI) following both plaque rupture and plaque erosion, and dual antiplatelet therapy offers additional protection compared to a single antiplatelet agent in plaque erosion. The combination of statin and antiplatelet therapy may have an additive effect on reducing the probability of STEMI caused by plaque erosion. Yellow: lipid pool(necrotic core); red: fibrin-rich thrombus; gray; platelet-rich thrombus.

Indexed as

Acute Coronary SyndromeHydroxymethylglutaryl-CoA Reductase InhibitorsPlaque, AtheroscleroticST Elevation Myocardial InfarctionThrombosisAgedCoronary AngiographyHumansPlatelet Aggregation InhibitorsTomography, Optical CoherenceHydroxymethylglutaryl-CoA Reductase InhibitorsPlatelet Aggregation InhibitorsPlaque erosionPlaque ruptureST-segment elevation myocardial infarction

Identifiers

PMID32955695
OpenAlexW3087223271

What Socratic holds

Textmetadata
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.