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: 4 complete abstracts (964 words), 10 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
Coagulation of blood in any of the coronary vessels. The presence of a blood clot (thrombus) often leads to 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: Thrombosis, Coronary; Coronary Thromboses; Thromboses, Coronary.
Where it fits in the MeSH classification
- Broader topics
- Coronary Disease; Thrombosis
Related concepts
- Coronary Vessels
- Thrombus
- Myocardial Infarction
Research landscape
PubMed indexes 8,561 records tagged with the MeSH heading “Coronary Thrombosis” (counts retrieved 2026-10-29). 597 of them (7.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 2,927 records.
Reviews account for 1,562 records (18.2%) and meta-analyses for 160. Randomized controlled trials number 464 (5.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,477 |
| 2000-2009 | 2,560 |
| 2010-2019 | 2,927 |
| 2020 onward | 597 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,562 | 18.2% |
| Meta-analyses | 160 | 1.9% |
| Randomized controlled trials | 464 | 5.4% |
Method: PubMed query "Coronary Thrombosis"[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 |
|---|---|---|---|---|
| New Insights into Mechanisms of Action for Omega-3 Fatty Acids in Atherothrombotic Cardiovascular Disease | 2019 | Review article Design not recorded in structured metadata | 82 | cc by PMID 30637567 · DOI · PMC6330561 |
| Thrombus aspiration in hyperglycemic ST-elevation myocardial infarction (STEMI) patients: clinical outcomes at 1-year follow-up | 2018 | Research article Design not recorded in structured metadata | 53 | cc by PMID 30497513 · DOI · PMC6262961 |
| Simultaneous bright- and black-blood whole-heart MRI for noncontrast enhanced coronary lumen and thrombus visualization | 2018 | Research article Design not recorded in structured metadata | 42 | cc by PMID 28722267 · DOI · PMC5811778 |
| Stent Thrombosis: A Narrative Review From Pathophysiology to Therapy | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 41910580 · DOI · PMC13045374 |
New Insights into Mechanisms of Action for Omega-3 Fatty Acids in Atherothrombotic Cardiovascular Disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Purpose of reviewTreatment of hypercholesterolemia with statins results in significant reductions in cardiovascular risk; however, individuals with well-controlled low-density lipoprotein cholesterol (LDL-C) levels, but persistent high triglycerides (TG), remain at increased risk.
- Closing excerpt
- Additional mechanistic trials will provide further insights into their role in reducing cardiovascular risk in subjects with well-managed LDL-C but elevated TG levels.
- 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 (271 words)
Purpose of reviewTreatment of hypercholesterolemia with statins results in significant reductions in cardiovascular risk; however, individuals with well-controlled low-density lipoprotein cholesterol (LDL-C) levels, but persistent high triglycerides (TG), remain at increased risk. Genetic and epidemiologic studies have shown that elevated fasting TG levels are associated with incident cardiovascular events. At effective doses, omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), lower TG levels but may have additional atheroprotective properties compared to other TG-lowering therapies such as niacin and fibrates. The purpose of this review is to evaluate mechanisms related to the potential benefits of omega-3 fatty acids in atherothrombotic disease.Recent findingsLarge randomized clinical trials are currently under way to test the cardiovascular benefits of omega-3 fatty acids at a pharmacologic dosage (4 g/day). A large randomized trial with a prescription EPA-only formulation was shown to reduce a composite of cardiovascular events by 25% in statin-treated patients with established cardiovascular disease or diabetes and other CV risk factors. EPA and DHA have distinct tissue distributions as well as disparate effects on membrane structure and lipid dynamics, rates of lipid oxidation, and signal transduction pathways. Compared to other TG-lowering therapies, EPA has been found to inhibit cholesterol crystal formation, inflammation, and oxidative modification of atherogenic lipoprotein particles. The anti-inflammatory and endothelial benefits of EPA are enhanced in combination with a statin. Omega-3 fatty acids like EPA only at a pharmacologic dose reduce fasting TG and interfere with mechanisms of atherosclerosis that results in reduced cardiovascular events. Additional mechanistic trials will provide further insights into their role in reducing cardiovascular risk in subjects with well-managed LDL-C but elevated TG levels.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30637567 · DOI · PMC6330561
Thrombus aspiration in hyperglycemic ST-elevation myocardial infarction (STEMI) patients: clinical outcomes at 1-year follow-up [2]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectivesWe evaluate whether the thrombus aspiration (TA) before primary percutaneous coronary intervention (PPCI) may improve STEMI outcomes in hyperglycemic patients.
- Closing excerpt
- 25th, June 2016.
- 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 (249 words)
ObjectivesWe evaluate whether the thrombus aspiration (TA) before primary percutaneous coronary intervention (PPCI) may improve STEMI outcomes in hyperglycemic patients.BackgroundThe management of hyperglycemic patients during STEMI is unclear.MethodsWe undertook an observational cohort study of 3166 first STEMI. Patients were grouped on the basis of whether they received TA or not. Moreover, among these patients we selected a subgroup of STEMI patients with hyperglycemia during the event (glycaemia > 140 mg/dl). The endpoint at 1 year included all-cause mortality, cardiac mortality and re-hospitalization for coronary disease, heart failure and stroke.ResultsOne-thousand STEMI patients undergoing PPCI to plus TA (TA-group) and 1504 STEMI patients treated with PPCI alone (no-TA group) completed the study. In overall study-population, Kaplan-Meier-analysis demonstrated no significant difference in mortality rates between patients with and without TA (P = 0.065). After multivariate Cox-analysis (HR: 0.94, 95% CI 0.641-1.383) and the addition of propensity matching (HR: 0.86 95% CI 0.412-1.798) TA was still not associated with decreased mortality. By contrast, in hyperglycemic subgroup STEMI patients (TA-group, n = 331; no-TA group, n = 566), Kaplan-Meier-analysis demonstrated a significantly lower mortality (P = 0.019) in TA-group than the no-TA group. After multivariate Cox-analysis (HR: 0.64, 95% CI 0.379-0.963) and the addition of propensity matching (HR: 0.54, 95% CI 0.294-0.984) TA was still associated with decreased mortality.ConclusionsTA was not associated with lower mortality in PPCI for STEMI when used in our large all-comer cohort. Conversely, TA during PPCI for STEMI reduces clinical outcomes in hyperglycemic patients. Trial registration NCT02817542. 25th, June 2016.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30497513 · DOI · PMC6262961
Simultaneous bright- and black-blood whole-heart MRI for noncontrast enhanced coronary lumen and thrombus visualization [3]
Abstract reading summary — source excerpts
- Opening excerpt
- PurposeTo develop a 3D whole-heart Bright-blood and black-blOOd phase SensiTive (BOOST) inversion recovery sequence for simultaneous noncontrast enhanced coronary lumen and thrombus/hemorrhage visualization.
- Closing excerpt
- This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
- 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 (213 words)
PurposeTo develop a 3D whole-heart Bright-blood and black-blOOd phase SensiTive (BOOST) inversion recovery sequence for simultaneous noncontrast enhanced coronary lumen and thrombus/hemorrhage visualization.MethodsThe proposed sequence alternates the acquisition of two bright-blood datasets preceded by different preparatory pulses to obtain variations in blood/myocardium contrast, which then are combined in a phase-sensitive inversion recovery (PSIR)-like reconstruction to obtain a third, coregistered, black-blood dataset. The bright-blood datasets are used for both visualization of the coronary lumen and motion estimation, whereas the complementary black-blood dataset potentially allows for thrombus/hemorrhage visualization. Furthermore, integration with 2D image-based navigation enables 100% scan efficiency and predictable scan times. The proposed sequence was compared to conventional coronary MR angiography (CMRA) and PSIR sequences in a standardized phantom and in healthy subjects. Feasibility for thrombus depiction was tested ex vivo.ResultsWith BOOST, the coronary lumen is visualized with significantly higher (P ConclusionA new PSIR sequence for noncontrast enhanced simultaneous coronary lumen and thrombus/hemorrhage detection was developed. The sequence provided improved coronary lumen depiction and showed potential for thrombus visualization. Magn Reson Med 79:1460-1472, 2018. © 2017 International Society for Magnetic Resonance in Medicine. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28722267 · DOI · PMC5811778
Stent Thrombosis: A Narrative Review From Pathophysiology to Therapy [4]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundStent thrombosis (ST) remains a rare but potentially life-threatening complication of percutaneous coronary intervention (PCI), associated with high rates of myocardial infarction and mortality.
- Closing excerpt
- Ongoing advances in device technology and pharmacological treatments, along with a growing understanding of inflammatory pathways, may further improve prevention and clinical outcomes.
- 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 (231 words)
BackgroundStent thrombosis (ST) remains a rare but potentially life-threatening complication of percutaneous coronary intervention (PCI), associated with high rates of myocardial infarction and mortality. Despite advances in stent technology and antithrombotic therapy, its multifactorial pathophysiology and optimal management remain challenging.MethodsWe performed a narrative review of the current literature focusing on the pathophysiological mechanisms, clinical predictors, and contemporary management strategies of ST. Particular attention was given to stent-related, pharmacological, and patient-related factors, as well as emerging therapeutic approaches and preventive strategies.ResultsST arises from the complex interplay between mechanical factors (e.g., stent malapposition, underexpansion, and neoatherosclerosis), pharmacological aspects (e.g., premature discontinuation or inadequate response to dual antiplatelet therapy), and patient-related conditions, including hypercoagulability and systemic inflammation. In the acute setting, prompt PCI with restoration of coronary flow remains the cornerstone of treatment, while intravascular imaging plays a key role in identifying underlying mechanisms and optimizing outcomes. Preventive strategies rely on procedural optimization, appropriate antithrombotic therapy, and careful patient selection. New-generation drug-eluting stents and imaging-guided PCI have reduced ST incidence, whereas emerging approaches-including drug-coated balloons, subcutaneous antiplatelet agents, and anti-inflammatory therapies-represent promising adjunctive strategies, although ST-specific benefits are not yet fully established.ConclusionsST is a multifactorial complication requiring an integrated approach combining optimized PCI techniques, tailored antithrombotic therapy, and careful risk stratification. Ongoing advances in device technology and pharmacological treatments, along with a growing understanding of inflammatory pathways, may further improve prevention and clinical outcomes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41910580 · DOI · PMC13045374
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 Stent thrombosis in randomized clinical trials of drug-eluting stents [5]
- Research article Consensus and future directions on the definition of high on-treatment platelet reactivity to adenosine diphosphate [6]
- Research article Analysis of 14 trials comparing sirolimus-eluting stents with bare-metal stents [7]
- Research article Stent thrombosis and restenosis: what have we learned and where are we going? The Andreas Grüntzig Lecture ESC 2014 [8]
- Research article Vascular inflammation and repair: implications for re-endothelialization, restenosis, and stent thrombosis [9]
- Research article Mechanisms of plaque vulnerability and rupture [10]
References
- Preston Mason R. New Insights into Mechanisms of Action for Omega-3 Fatty Acids in Atherothrombotic Cardiovascular Disease. . 2019. PMID 30637567 · DOI · PMC6330561
- Sardu C, Barbieri M, Balestrieri ML, Siniscalchi M, Paolisso P, Calabrò P, et al.. Thrombus aspiration in hyperglycemic ST-elevation myocardial infarction (STEMI) patients: clinical outcomes at 1-year follow-up. . 2018. PMID 30497513 · DOI · PMC6262961
- Ginami G, Neji R, Phinikaridou A, Whitaker J, Botnar RM, Botnar RM, et al.. Simultaneous bright- and black-blood whole-heart MRI for noncontrast enhanced coronary lumen and thrombus visualization. . 2018. PMID 28722267 · DOI · PMC5811778
- Cecchi E, Granchietti AG, Mazzotta R, Garofalo M, Panichella G, Iula G, et al.. Stent Thrombosis: A Narrative Review From Pathophysiology to Therapy. . 2026. PMID 41910580 · DOI · PMC13045374
- Mauri L, Hsieh WH, Massaro JM, Ho KK, D'Agostino R, Cutlip DE. Stent thrombosis in randomized clinical trials of drug-eluting stents. N Engl J Med. 2007. PMID 17296821 · DOI
- Bonello L, Tantry US, Marcucci R, Blindt R, Angiolillo DJ, Becker R, et al.. Consensus and future directions on the definition of high on-treatment platelet reactivity to adenosine diphosphate. J Am Coll Cardiol. 2010. PMID 20828644 · DOI
- Kastrati A, Mehilli J, Pache J, Kaiser C, Valgimigli M, Kelbaek H, et al.. Analysis of 14 trials comparing sirolimus-eluting stents with bare-metal stents. N Engl J Med. 2007. PMID 17296823 · DOI
- Byrne RA, Joner M, Kastrati A. Stent thrombosis and restenosis: what have we learned and where are we going? The Andreas Grüntzig Lecture ESC 2014. Eur Heart J. 2015. PMID 26417060 · DOI · PMC4677274
- Inoue T, Croce K, Morooka T, Sakuma M, Node K, Simon DI. Vascular inflammation and repair: implications for re-endothelialization, restenosis, and stent thrombosis. JACC Cardiovasc Interv. 2011. PMID 22017929 · DOI · PMC3341937
- Shah PK. Mechanisms of plaque vulnerability and rupture. J Am Coll Cardiol. 2003. PMID 12644336 · 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.