Evidence map›Paper›PMID 40873617›Full record

ArticleFrontiers in cardiovascular medicine2025

Prognostic role of angiotensin-II receptor type 1 and endothelin-1 receptor type A agonistic autoantibodies in patients with acute myocardial infarction.

Francesco Tona, Giovanni Civieri, Marta Vadori, Giulia Masiero, Laura Iop, Martina Perazzolo Marra, Annagrazia Cecere, Marika Martini, Donatella Tansella, Giacomo Bernava and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Transient Increase in ATInternational journal of molecular sciences · 2026
    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

14 authors.

Francesco Tona *Cardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Giovanni Civieri *Cardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Marta VadoriTransplant Immunology Unit, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Giulia MasieroCardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Laura IopTranslational Biomedicine Group, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Martina Perazzolo MarraCardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Annagrazia CecereCardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Marika MartiniCardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Donatella TansellaCardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Giacomo BernavaTranslational Biomedicine Group, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Benedetta SchiavonCardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Loira LeoniCardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Emanuele CozziTransplant Immunology Unit, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
Sabino IlicetoCardiology Division, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Functional autoantibodies against angiotensin II type 1 (AT1R-AAs) and endothelin-1 type A (ETAR-AAs) receptors are associated with microvascular obstruction and myocardial remodeling after ST-elevation myocardial infarction (STEMI). However, their role in the long-term prognosis after STEMI has not been investigated. Methods: This is a prospective observational study enrolling STEMI patients undergoing early primary PCI. The incidence of major adverse cardiovascular events (MACE) was investigated during the follow-up. Autoantibody seropositivity was defined as a level >10 U/ml. Results: 200 STEMI patients (89% male, median age 61 years) were enrolled. 110 (55%) were seronegative for both autoantibodies, 44 (22%) were seropositive for one autoantibody, and 46 (23%) were seropositive for both autoantibodies. Over a median follow-up of 1.2 years, the incidence of MACE was higher in patients with double (31%) and single (25%) seropositivity than in seronegative patients (13%, Conclusion: AT1R-AAs and ETAR-AAs are associated with an increased risk of MACE after STEMI. Assessment of autoantibody levels paves the way for future therapies targeting specific molecular pathways associated with poor prognosis after an acute coronary event.

Indexed as

acute coronary syndromeadverse prognosisautoantibodiesautoimmunitycoronary microcirculationG protein coupled receptorsno-reflow

Identifiers

PMID40873617
PMCPMC12378766

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