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Myocardial Ischemia

Cardiovascular Medicine · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed9 referencesApproximately 4 min read

A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

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 (812 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

A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary artery disease), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction).

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: Heart Disease, Ischemic; Disease, Ischemic Heart; Diseases, Ischemic Heart; Heart Diseases, Ischemic; Ischemic Heart Diseases; Ischemia, Myocardial; Ischemias, Myocardial; Myocardial Ischemias.

Where it fits in the MeSH classification

Broader topics
Heart Diseases; Vascular Diseases
Narrower topics
Acute Coronary Syndrome; Angina Pectoris; Coronary Disease; Kounis Syndrome; Myocardial Infarction; Myocardial Reperfusion Injury
See also
Myocardial Infarction; Myocardial Revascularization; Myocardial Reperfusion; Myocardial Stunning; Ischemic Preconditioning, Myocardial

Related concepts

  • Coronary Artery Disease
  • Coronary Thrombosis
  • Myocardial Infarction

Research landscape

PubMed indexes 503,252 records tagged with the MeSH heading “Myocardial Ischemia” (counts retrieved 2026-10-29). 73,372 of them (14.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 193,554 records.

Reviews account for 65,676 records (13.1%) and meta-analyses for 7,828. Randomized controlled trials number 23,974 (4.8%) as a share of all records on the topic.

PubMed records by publication periodthrough 1999: 193,554 records; 2000-2009: 110,121 records; 2010-2019: 126,205 records; 2020 onward: 73,372 records193,554through 1999110,1212000-2009126,2052010-201973,3722020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 1999193,554
2000-2009110,121
2010-2019126,205
2020 onward73,372
Share of records by publication typeReviews: 13.1 percent; Meta-analyses: 1.6 percent; Randomized controlled trials: 4.8 percentReviews13.1% (65,676)Meta-analyses1.6% (7,828)Randomized controlled trials4.8% (23,974)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 503,252 PubMed records
TypeRecordsShare
Reviews65,67613.1%
Meta-analyses7,8281.6%
Randomized controlled trials23,9744.8%

Method: PubMed query "Myocardial Ischemia"[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 comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Integrative simulation analysis of myocardial ischaemia-reperfusion injury
Shimayoshi T, Takeuchi A, Matsuoka S
2026Research article
Design not recorded in structured metadata
1cc by
PMID 42625359 · DOI · PMC13577699
Exercise After Coronary Stenting: Potential Effects on in-Stent Restenosis
Spadafora L, Cacciatore S, Salvi M, Russo F, Lo Sasso L, Lauretti A, et al.
2026Review article
Design not recorded in structured metadata
1cc by
PMID 42616220 · DOI · PMC13490258
Artificial intelligence-enhanced management system for secondary prevention of coronary heart disease: a randomized clinical trial
Ba Z, Yuan J, Zhao S, Liu M, Chen G, Lian X, et al.
2026Randomized controlled trial
Design not recorded in structured metadata
1cc by
PMID 42613609 · DOI · PMC13488134

Integrative simulation analysis of myocardial ischaemia-reperfusion injury [1]

Research article Shimayoshi T, Takeuchi A, Matsuoka S · · 2026 · cited 1 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Cardiac ischaemia, reduced coronary blood flow, causes significant damages to the heart, and paradoxically reperfusion, restored flow after ischaemia, often results in more severe injury.
Closing excerpt
It was found that correcting ATP supply-consumption imbalance during reperfusion, that is, preservation of mitochondrial NADH production, attenuation of ATP consumption or activation of the Na+/K+ pump, was effective at mitigating the injury.
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 (295 words)

Cardiac ischaemia, reduced coronary blood flow, causes significant damages to the heart, and paradoxically reperfusion, restored flow after ischaemia, often results in more severe injury. Although the mechanisms underlying cardiac ischaemia-reperfusion injury have been intensively investigated, effective therapeutic strategies applicable during reperfusion to mitigate this damage have not been established yet. To obtain more insights into the mechanisms underlying ischaemia-reperfusion injury, and to explore effective methods to relieve reperfusion injury, we developed a comprehensive mathematical model of ventricular myocyte, implementing excitation-contraction (E-C) coupling, cytosolic and mitochondrial pH regulation, pH dependence of major components of E-C coupling and cellular energy metabolism, including mitochondrial oxidative phosphorylation. The mathematical model successfully reproduced experimentally observed findings on cardiac ischaemia-reperfusion injury, such as intracellular and extracellular acidosis, cytosolic Na+ overload, cytosolic Ca2+ overload, mitochondrial dysfunction, action potential shortening and contraction failure. It was found that the reperfusion-induced exacerbation of Na+ i, Ca2+ i overloads was mainly caused by insufficient production of NADH, which is used in mitochondrial oxidative phosphorylation to synthesize ATP for Na+/K+ pump and sarcoplasmic/endoplasmic reticulum Ca2+ pump (SERCA) to expel accumulated cytosolic Na+ and Ca2+, respectively. It was suggested that the preservation of mitochondrial NADH production, attenuation of ATP consumption via SERCA or contraction for a short period or activation of the Na+/K+ pump during reperfusion mitigates reperfusion injury. KEY POINTS: Experimental data on cardiac ischaemia-reperfusion injury are available. No effective methods applicable during reperfusion were available for mitigating the injury. We developed a comprehensive cardiomyocyte model to simulate the injury. Na+ and Ca2+ overloads and contraction failure could be reproduced by the model. It was found that correcting ATP supply-consumption imbalance during reperfusion, that is, preservation of mitochondrial NADH production, attenuation of ATP consumption or activation of the Na+/K+ pump, was effective at mitigating the injury.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42625359 · DOI · PMC13577699

Exercise After Coronary Stenting: Potential Effects on in-Stent Restenosis [2]

Review article Spadafora L, Cacciatore S, Salvi M, Russo F, Lo Sasso L, Lauretti A, et al. · · 2026 · cited 1 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Purpose of reviewStructured exercise is a cornerstone of secondary prevention after percutaneous coronary intervention (PCI), yet its specific relationship with in-stent restenosis (ISR) is less well characterized.
Closing excerpt
Larger, contemporary trials with standardized intracoronary imaging endpoints are needed to clarify whether, and in which patient subsets, exercise meaningfully affects the biology of ISR.
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 (225 words)

Purpose of reviewStructured exercise is a cornerstone of secondary prevention after percutaneous coronary intervention (PCI), yet its specific relationship with in-stent restenosis (ISR) is less well characterized. This narrative review summarizes the biological rationale, clinical evidence, safety, and practical prescription of exercise training in patients with coronary stents, with a focus on its potential impact on ISR.Recent findingsExercise training improves endothelial nitric oxide bioavailability, reduces systemic inflammation, and favorably modulates neointimal proliferation in experimental and clinical studies. Pooled clinical data suggest that exercise-based cardiac rehabilitation after PCI is associated with a reduction in angiographically defined restenosis, although individual trials, largely from the bare-metal and early drug-eluting stent (DES) eras, have shown inconsistent results on binary restenosis endpoints. Available contemporary data do not suggest an excess risk of stent thrombosis, clinically relevant arrhythmias, or adverse ventricular remodeling when exercise is initiated in clinically stable patients using an individualized and supervised approach. The direct anti-restenotic effect of exercise remains biologically plausible and clinically suggestive but is not yet firmly established, particularly in the contemporary thin-strut DES era. Nevertheless, the well-documented benefits of exercise on functional capacity, endothelial health, and cardiovascular prognosis justify its role as an essential, time-sensitive component of post-PCI care. Larger, contemporary trials with standardized intracoronary imaging endpoints are needed to clarify whether, and in which patient subsets, exercise meaningfully affects the biology of ISR.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42616220 · DOI · PMC13490258

Artificial intelligence-enhanced management system for secondary prevention of coronary heart disease: a randomized clinical trial [3]

Randomized controlled trial Ba Z, Yuan J, Zhao S, Liu M, Chen G, Lian X, et al. · · 2026 · cited 1 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundSecondary prevention of coronary heart disease (CHD) remains suboptimal due to fragmented care and therapeutic inertia.
Closing excerpt
Registered on 11 November 2024.
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 (292 words)

BackgroundSecondary prevention of coronary heart disease (CHD) remains suboptimal due to fragmented care and therapeutic inertia. While digital health interventions offer a promising strategy, few existing tools provide comprehensive, closed-loop management of multidimensional risk factors without increasing clinician workload. This study aimed to evaluate the efficacy of an artificial intelligence (AI)-enhanced management system (AIM-CHD) in improving multidimensional risk factor control among patients with CHD.MethodsThis single-center, open-label, parallel-group, randomized clinical trial was conducted from November 2024 to June 2025 in China. A total of 1100 adults with confirmed CHD were randomized 1:1 to receive either the AIM-CHD intervention (n = 549) or usual care (n = 551) for 3 months. The AIM-CHD system featured automated multi-source data capture, guideline-directed risk stratification, and closed-loop feedback via smartphone. The primary outcome was the low-density lipoprotein cholesterol (LDL-C) level at 3 months. Secondary outcomes included goal attainment rates for LDL-C (ResultsOf 1100 randomized participants (mean age 61 years; 75.3% male), 943 (85.7%) completed the 3-month follow-up. The intervention group achieved a significantly lower mean LDL-C level compared with the control group (60.4 ± 23.4 vs. 63.7 ± 26.0 mg/dL), with an adjusted mean difference of - 3.2 mg/dL (95% CI, - 6.2 to - 0.3; p = 0.03). Furthermore, participants in the intervention group were more likely to achieve the LDL-C target (71% vs. 64%; RR, 1.10; 95% CI, 1.01-1.20; p = 0.03) and the BP target (45% vs. 35%; RR, 1.27; 95% CI, 1.09-1.48; p = 0.002). No significant differences were observed for HbA1c, BMI, or medication adherence.ConclusionsThe AIM-CHD system significantly improved short-term lipid and BP control compared with usual care. These findings support interoperable, low-burden digital management systems as a scalable strategy in routine secondary prevention.Trial registrationClinicalTrials.gov Identifier: NCT06686056. Registered on 11 November 2024.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42613609 · DOI · PMC13488134

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 β blockers after myocardial infarction with mildly reduced ejection fraction: an individual patient data meta-analysis of randomised controlled trials [4]
    Rossello X, Prescott EIB, Kristensen AMD, Latini R, Fuster V, Fagerland MW, et al. · Lancet · 2025 · cited 73 times (Europe PMC)
  • Research article Clopidogrel versus aspirin for secondary prevention of coronary artery disease: a systematic review and individual patient data meta-analysis [5]
    Valgimigli M, Choi KH, Giacoppo D, Gragnano F, Kimura T, Watanabe H, et al. · Lancet · 2025 · cited 64 times (Europe PMC)
  • Research article Beta-Blockers after Myocardial Infarction with Normal Ejection Fraction [6]
    Kristensen AMD, Rossello X, Atar D, Yndigegn T, Kimura T, Latini R, et al. · N Engl J Med · 2026 · cited 59 times (Europe PMC)
  • Research article Systematic review and meta-analysis of respiratory viral triggers for acute myocardial infarction and stroke [7]
    Nguyen TQ, Vlasenko D, Shetty AN, Zhao E, Reid CM, Clothier HJ, et al. · Cardiovasc Res · 2025 · cited 20 times (Europe PMC)
  • Research article Glucagon-like peptide-1 receptor agonist in myocardial infarction and atherosclerotic cardiovascular disease risk reduction: a comprehensive meta-analysis of number needed to treat, efficacy and safety [8]
    Tang ASP, Hsu JTY, Chong SKS, Quek J, Shek G, Sulaimi F, et al. · Cardiovasc Diabetol · 2025 · cited 20 times (Europe PMC)
  • Research article Advanced Analyses of Coronary Computed Tomography Angiography to Predict Future Cardiac Events: A Meta-Analysis [9]
    Bianchini E, Alqahtani F, Alsubai S, Del Sole PA, Elzomor H, Sharif R, et al. · JACC Cardiovasc Imaging · 2025 · cited 17 times (Europe PMC)

References

  1. Shimayoshi T, Takeuchi A, Matsuoka S. Integrative simulation analysis of myocardial ischaemia-reperfusion injury. . 2026. PMID 42625359 · DOI · PMC13577699
  2. Spadafora L, Cacciatore S, Salvi M, Russo F, Lo Sasso L, Lauretti A, et al.. Exercise After Coronary Stenting: Potential Effects on in-Stent Restenosis. . 2026. PMID 42616220 · DOI · PMC13490258
  3. Ba Z, Yuan J, Zhao S, Liu M, Chen G, Lian X, et al.. Artificial intelligence-enhanced management system for secondary prevention of coronary heart disease: a randomized clinical trial. . 2026. PMID 42613609 · DOI · PMC13488134
  4. Rossello X, Prescott EIB, Kristensen AMD, Latini R, Fuster V, Fagerland MW, et al.. β blockers after myocardial infarction with mildly reduced ejection fraction: an individual patient data meta-analysis of randomised controlled trials. Lancet. 2025. PMID 40897190 · DOI
  5. Valgimigli M, Choi KH, Giacoppo D, Gragnano F, Kimura T, Watanabe H, et al.. Clopidogrel versus aspirin for secondary prevention of coronary artery disease: a systematic review and individual patient data meta-analysis. Lancet. 2025. PMID 40902613 · DOI
  6. Kristensen AMD, Rossello X, Atar D, Yndigegn T, Kimura T, Latini R, et al.. Beta-Blockers after Myocardial Infarction with Normal Ejection Fraction. N Engl J Med. 2026. PMID 41211954 · DOI
  7. Nguyen TQ, Vlasenko D, Shetty AN, Zhao E, Reid CM, Clothier HJ, et al.. Systematic review and meta-analysis of respiratory viral triggers for acute myocardial infarction and stroke. Cardiovasc Res. 2025. PMID 40570137 · DOI · PMC12352309
  8. Tang ASP, Hsu JTY, Chong SKS, Quek J, Shek G, Sulaimi F, et al.. Glucagon-like peptide-1 receptor agonist in myocardial infarction and atherosclerotic cardiovascular disease risk reduction: a comprehensive meta-analysis of number needed to treat, efficacy and safety. Cardiovasc Diabetol. 2025. PMID 40652242 · DOI · PMC12255114
  9. Bianchini E, Alqahtani F, Alsubai S, Del Sole PA, Elzomor H, Sharif R, et al.. Advanced Analyses of Coronary Computed Tomography Angiography to Predict Future Cardiac Events: A Meta-Analysis. JACC Cardiovasc Imaging. 2025. PMID 40758074 · 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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At a glance

503,252
PubMed records on this heading
15%
published since 2020
65,676
review articles
23,974
randomized trials
9
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

Related topics See all →

  • Acute Coronary SyndromeCardiovascular Medicine
  • Coronary DiseaseCardiovascular Medicine
  • Coronary ThrombosisCardiovascular Medicine
  • Myocardial InfarctionCardiovascular Medicine
  • Angina PectorisCardiovascular Medicine

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