Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (600 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Necrosis of the myocardium caused by an obstruction of the blood supply to the heart (coronary circulation).
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Infarction, Myocardial; Infarctions, Myocardial; Myocardial Infarctions; Heart Attack; Heart Attacks; Myocardial Infarct; Infarct, Myocardial; Infarcts, Myocardial.
Where it fits in the MeSH classification
- Broader topics
- Myocardial Ischemia; Infarction
- Narrower topics
- Anterior Wall Myocardial Infarction; Inferior Wall Myocardial Infarction; MINOCA; Non-ST Elevated Myocardial Infarction; Shock, Cardiogenic; ST Elevation Myocardial Infarction
- See also
- Heart Rupture, Post-Infarction
Related concepts
- Necrosis
- Myocardium
- Coronary Circulation
Research landscape
PubMed indexes 207,315 records tagged with the MeSH heading “Myocardial Infarction” (counts retrieved 2026-10-29). 32,093 of them (15.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 83,493 records.
Reviews account for 23,447 records (11.3%) and meta-analyses for 3,422. Randomized controlled trials number 10,038 (4.8%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 83,493 |
| 2000-2009 | 41,121 |
| 2010-2019 | 50,608 |
| 2020 onward | 32,093 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 23,447 | 11.3% |
| Meta-analyses | 3,422 | 1.7% |
| Randomized controlled trials | 10,038 | 4.8% |
Method: PubMed query "Myocardial Infarction"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42270610 · DOI · PMC13254370 |
| Depth of neutrophil mobilization stratifies survival in ST-elevation myocardial infarction | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42399420 · DOI · PMC13461374 |
| Spontaneous Coronary Reperfusion in STEMI After Pre-Hospital Loading Dose of Triple Antithrombotic Therapy | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42470298 · DOI · PMC13379941 |
Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Histaminylation is a newly discovered monoaminylation catalyzed by transglutaminase 2 (TGM2), and its role in myocardial fibrosis has not yet been elucidated.
- Closing excerpt
- This study also highlights a novel role of histamine in maintaining stress environment mechanical stability.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (245 words)
Histaminylation is a newly discovered monoaminylation catalyzed by transglutaminase 2 (TGM2), and its role in myocardial fibrosis has not yet been elucidated. Here, we identified histaminylation in cardiac type I collagen isolated from mice 7 days after acute myocardial infarction (AMI) by mass spectrometry. Using histamine-deficient Hdc-/- mice, we demonstrated an increase in TGM2-mediated γ-glutamyl-ε-lysine crosslinks and a higher myocardial Young's modulus in the scar region of Hdc-/- mice than in wild-type controls, indicating that histaminylation might restrain the role of TGM2 in cardiac fibrogenesis after AMI. Furthermore, we reconstituted an in vitro crosslinking system, yielding unmodified collagen and histaminylated collagen. The results of mechanical indentation and electron microscopy demonstrated that histaminylation could reduce crosslink formation, lower matrix stiffness, and alter viscoelasticity. Subsequently, primary murine cardiac fibroblasts were cultured under cyclic stretch with TGF-β on different substrates, and the results revealed that histaminylated collagen strongly attenuated TGF-β-induced fibroblast-to-myofibroblast transition and reduced focal adhesion assembly. Mechanically, integrated single-cell and bulk RNA-seq analyses indicated that the PIEZO1/ITGB1 mechanotransduction axis was upregulated and mediated downstream signal transduction in the infarcted hearts of Hdc-/- mice. Finally, local delivery of a histamine-releasing hydrogel to Hdc-/- mice after AMI could significantly reinstate collagen histaminylation and reduce crosslink abundance and cardiac dysfunction. Collectively, these data reveal that collagen histaminylation limits TGM2-dependent crosslinking, softens the extracellular matrix, and inhibits the PIEZO1/ITGB1 axis, thereby mitigating myocardial fibrosis after AMI. This study also highlights a novel role of histamine in maintaining stress environment mechanical stability.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42270610 · DOI · PMC13254370
Depth of neutrophil mobilization stratifies survival in ST-elevation myocardial infarction [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Systemic inflammatory responses shape clinical outcomes in acute cardiovascular disease.
- Closing excerpt
- Immature granulocytes also remained independently associated with survival in multivariate models incorporating risk factors, enabling the immediate identification of vulnerable patients with ST-elevation myocardial infarction upon hospital admission.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)
Systemic inflammatory responses shape clinical outcomes in acute cardiovascular disease. Because of their functional plasticity and rapid turnover, neutrophils have emerged as dynamic indicators of inflammatory stress. Here we profile the appearance of distinct neutrophil maturation stages in patients with ST-elevation myocardial infarction, heart failure and stroke. Our data reveal the mobilization of immature neutrophils in all groups; however, patients with ST-elevation myocardial infarction exhibited the most pronounced engagement of this response, including the appearance of CD16lowCD10neg preneutrophils (preNeus), the final mitotic neutrophil progenitor, which was associated with disease outcome. Plasma cytokine profiling identified a coordinated inflammatory signature associated with preNeu mobilization, consistent with emergency granulopoiesis. PreNeus were identifiable as immature granulocytes in routine blood count analysis, where they predicted 30-day mortality better than established biomarkers in two clinical cohorts. Immature granulocytes also remained independently associated with survival in multivariate models incorporating risk factors, enabling the immediate identification of vulnerable patients with ST-elevation myocardial infarction upon hospital admission.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42399420 · DOI · PMC13461374
Spontaneous Coronary Reperfusion in STEMI After Pre-Hospital Loading Dose of Triple Antithrombotic Therapy [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundTo evaluate the incidence and prognosis of spontaneous coronary reperfusion in STEMI using pre-hospital loading dose of P2Y12 inhibitors.
- Closing excerpt
- The significant increase of pre-admission cardiac arrests observed in the TIMI 3 group could be specifically explored as it might be a concern regarding future pre-hospital reperfusion therapy strategies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (197 words)
BackgroundTo evaluate the incidence and prognosis of spontaneous coronary reperfusion in STEMI using pre-hospital loading dose of P2Y12 inhibitors.MethodsThis prospective bi-centric study included STEMI patients who referred for primary PCI from June 1, to November 1, 2022. All patients received before hospital admission loading dose of aspirin, heparin and P2Y12 inhibitor. The primary outcome was incidence of spontaneous coronary reperfusion (TIMI 3 flow) before primary PCI. Major in-hospital and 1-year events were secondary outcomes.ResultsWithin the study period, 263 patients were admitted with ongoing STEMI and 49 of them (18.6%) had spontaneous coronary reperfusion with no significant difference between loading dose of ticagrelor (n = 226; 85.9%) or clopidogrel (n = 27, 10.3%) and TIMI 3 flow (n = 41; 18.1% vs. n = 7; 25.9%, p = 0.53; respectively). Peak of T-hs troponin (p ConclusionSpontaneous reperfusion at admission was observed in about 20% of STEMI patients who received a pre-hospital loading dose of antithrombotic therapy including P2Y12 inhibitors, and was associated with markers of decrease of infarct size. The significant increase of pre-admission cardiac arrests observed in the TIMI 3 group could be specifically explored as it might be a concern regarding future pre-hospital reperfusion therapy strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42470298 · DOI · PMC13379941
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The global prevalence of myocardial infarction: a systematic review and meta-analysis [4]
- Research article Intravascular imaging-guided coronary drug-eluting stent implantation: an updated network meta-analysis [5]
- Research article P2Y12 Inhibitor or Aspirin Monotherapy for Secondary Prevention of Coronary Events [6]
- Research article Venoarterial extracorporeal membrane oxygenation in patients with infarct-related cardiogenic shock: an individual patient data meta-analysis of randomised trials [7]
- Research article Integrative single-cell meta-analysis reveals disease-relevant vascular cell states and markers in human atherosclerosis [8]
- Research article Temporary mechanical circulatory support in infarct-related cardiogenic shock: an individual patient data meta-analysis of randomised trials with 6-month follow-up [9]
References
- Zhu J, Sun D, Zeng G, Wu K, Yang X, Zhu X, et al.. Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis. . 2026. PMID 42270610 · DOI · PMC13254370
- Richter M, von Göwels J, Fähndrich M, Lipgens Fernandez C, Grohn K, Welzel M, et al.. Depth of neutrophil mobilization stratifies survival in ST-elevation myocardial infarction. . 2026. PMID 42399420 · DOI · PMC13461374
- Meunier PA, Juenin L, Moulis L, Roubille F, Robert P, Macia JC, et al.. Spontaneous Coronary Reperfusion in STEMI After Pre-Hospital Loading Dose of Triple Antithrombotic Therapy. . 2026. PMID 42470298 · DOI · PMC13379941
- Salari N, Morddarvanjoghi F, Abdolmaleki A, Rasoulpoor S, Khaleghi AA, Hezarkhani LA, et al.. The global prevalence of myocardial infarction: a systematic review and meta-analysis. BMC Cardiovasc Disord. 2023. PMID 37087452 · DOI · PMC10122825
- Stone GW, Christiansen EH, Ali ZA, Andreasen LN, Maehara A, Ahmad Y, et al.. Intravascular imaging-guided coronary drug-eluting stent implantation: an updated network meta-analysis. Lancet. 2024. PMID 38401549 · DOI
- Gragnano F, Cao D, Pirondini L, Franzone A, Kim HS, von Scheidt M, et al.. P2Y12 Inhibitor or Aspirin Monotherapy for Secondary Prevention of Coronary Events. J Am Coll Cardiol. 2023. PMID 37407118 · DOI
- Zeymer U, Freund A, Hochadel M, Ostadal P, Belohlavek J, Rokyta R, et al.. Venoarterial extracorporeal membrane oxygenation in patients with infarct-related cardiogenic shock: an individual patient data meta-analysis of randomised trials. Lancet. 2023. PMID 37643628 · DOI
- Mosquera JV, Auguste G, Wong D, Turner AW, Hodonsky CJ, Alvarez-Yela AC, et al.. Integrative single-cell meta-analysis reveals disease-relevant vascular cell states and markers in human atherosclerosis. Cell Rep. 2023. PMID 37950869 · DOI · PMC12335892
- Thiele H, Møller JE, Henriques JPS, Bogerd M, Seyfarth M, Burkhoff D, et al.. Temporary mechanical circulatory support in infarct-related cardiogenic shock: an individual patient data meta-analysis of randomised trials with 6-month follow-up. Lancet. 2024. PMID 39236726 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.