ReviewJournal of cellular and molecular medicine2025
The Role of Infarct Border Zone Remodelling in Ventricular Arrhythmias: Bridging Basic Research and Clinical Applications.
Review in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed.
- NEAT1 Coordinates a PDLIM5-CACNA1C Regulatory Program Associated with a Potentially Arrhythmogenic Cardiomyocyte State in the Border Zone During Early Myocardial Infarction.International journal of molecular sciences · 2026Article
- Trem2 regulates macrophage phenotype via the JAK2/STAT3 signaling pathway to ameliorate ventricular remodeling after acute myocardial infarction.Molecular biology reports · 2026Article
- Post-MI Remodeling Mechanics of Left Ventricle: Microstructure-Informed Models, Identifiability, and Uncertainty for Patient-Specific Prediction.Bioengineering (Basel, Switzerland) · 2026Review
- From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death.Life (Basel, Switzerland) · 2026Review
- Metabolic regulation of macrophage polarization in myocardial infarction: from mechanisms to targeted therapies.Journal of translational medicine · 2026Review
- Inflammation-Mediated Mechanisms of Arrhythmias After Acute Myocardial Infarction.Reviews in cardiovascular medicine · 2026Review
- The Irreversible March of Time: Ischemic Delay and Impact on Outcomes in ST-Segment Elevation Myocardial Infarction.Journal of cardiovascular development and disease · 2025Review
- Gene Therapy for Cardiac Arrhythmias: Mechanisms, Modalities and Therapeutic Applications.Medical sciences (Basel, Switzerland) · 2025Review
- Inflammasome Signaling in Cardiac Arrhythmias: Linking Inflammation, Fibrosis, and Electrical Remodeling.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Patients who experience post-myocardial infarction (MI) and present with a left ventricular ejection fraction of less than 35% are classified as being at high risk for sudden cardiac death due to ventricular arrhythmias (VAs). The expansion of scar tissue and the extension of the infarct border zone (IBZ) following MI play critical roles in the progression of heart failure and the onset of VAs. Various aspects of structural remodelling, including cardiac fibrosis, along with electrophysiological changes such as alterations in gap junctions, ion channels, and autonomic nervous system function within the IBZ may contribute to abnormal impulse generation and conduction, thereby increasing susceptibility to arrhythmias. Currently, management strategies for VAs primarily encompass pharmacologic interventions (e.g., β-blockers, amiodarone), device-based approaches (e.g., ICD implantation), or catheter ablation techniques as outlined by ESC Guidelines. In this review, we systematically summarise both structural characteristics inherent in ischaemic myocardial substrates and clinical treatment strategies regarding VAs. We propose that early prevention strategies aimed at mitigating arrhythmogenic substrate formation represent an innovative approach to treating VAs following MI.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.