Observational studyBlood advances2024
Thromboinflammation is associated with clinical outcome after ST-elevation myocardial infarction.
Observational study in Blood advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03539133 (Systemic Organ Communication in STEMI), which is not on this map. Cited by 17 papers.
What it found
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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.
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.
Systemic Organ Communication in STEMI
Who cites it
17 citing papers in PubMed.
- Emerging evidence of neutrophil extracellular traps in essential hypertension and target organ damage: pathophysiological insights and therapeutic implications.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- Panax notoginseng saponins inhibit platelet activation and thrombosis while preserving hemostasis: involvement of platelet oxylipin metabolic reprogramming.BMC complementary medicine and therapies · 2026Article
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- Circulating S100A8/A9 drives faster platelet COX-1 recovery via MRP4, impairing the duration of aspirin response.Blood advances · 2026Article
- A transgenic mouse model for reticulated platelet detection reveals expansion after myocardial ischemia/reperfusion.Blood vessels, thrombosis & hemostasis · 2026Article
- Thromboinflammation is associated with high thrombotic risk in patients with newly diagnosed myeloproliferative neoplasms.Leukemia · 2026Article
- The Phoenix Heart-PICSO and the Rebirth of Embryonic Life in the Ischemic Myocardium.Journal of cardiovascular development and disease · 2026Review
- The systemic immune-inflammation index in coronary heart disease: a narrative review of thromboinflammation, phenotype-dependent utility, and clinical translation.Frontiers in cardiovascular medicine · 2026Review
- Inflammatory responses driven by neutrophil extracellular traps in cardiovascular diseases: molecular mechanisms, emerging biomarkers, and therapeutic targets.Frontiers in immunology · 2026Review
- Prognostic Value of Circulating NETosis Biomarkers in ST-Elevation Myocardial Infarction: Citrullinated Histone H3 Outperforms Cell-Free DNA and Nucleosomes.Journal of inflammation research · 2026Article
- Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Association between neutrophil extracellular traps, the Von Willebrand factor axis, and clinical outcome in stable coronary artery disease.Frontiers in cardiovascular medicine · 2026Article
- Article
- METAB-HTX: prospective, longitudinal cohort study evaluating cardiac and systemic metabolism after heart transplantation.ESC heart failure · 2025Article
- GALMs confirm predictive power of thromboinflammation in STEMI.Blood advances · 2025Article
- Generalized additive logit models for clinical prediction.Blood advances · 2025Article
- Inflammatory and neutrophil extracellular trap markers to predict cardiac events after ST-segment elevation myocardial infarction.PloS one · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractPlatelets are crucial in thrombus formation during ST-elevation myocardial infarction (STEMI). In addition, they also play an important role in postischemic thromboinflammation, which is determined by the interplay between activated platelets and neutrophils. The latter form neutrophil extracellular traps, which are detectable in plasma as citrullinated histone H3-deoxyribonucleic acid-DNA complexes. Prediction of the risk of recurrent events is important in precision medicine. Therefore, we investigated whether circulating thromboinflammatory markers predict clinical outcome after STEMI. We performed a prospective, multicentric, observational, all-comer study of patients with STEMI (n = 361). Thromboinflammation, measured as H3Cit-DNA complexes, was assessed on day 1 after presentation with STEMI as well as 5 days and 6 months after STEMI by enzyme-linked immunosorbent assay. Twelve months of clinical follow-up was conducted. Multivariate analysis was performed investigating which variables were independently associated with major adverse cardiac events (MACEs). Patients were aged 64 ± 12 years; 80% were male; and 40% had diabetes mellitus. Thromboinflammation was enhanced during index hospitalization compared with 6-months follow-up (137.4 ± 100.0 μg/L vs 53.7 ± 54.7 μg/L; P < .001). Additionally, patients within the highest tertile of thromboinflammation at day 1 after STEMI showed worse outcome during follow-up (hazard ratio, 2.57; 95% confidence interval, 1.72-3.85; P < .001). Receiver operating characteristic analysis revealed a cutoff value of 219.3 μg/L. In multivariate logistic regression analysis, thromboinflammation was independently associated with outcome after STEMI. To sum it up, thromboinflammation is enhanced in STEMI. It identifies patients at high risk of MACE. Therefore, thromboinflammation might be a promising target and marker in precision medicine. The trial was registered at www.clinicaltrials.gov as #NCT03539133.
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