ArticleJACC. Basic to translational science2017
Increased afterload following myocardial infarction promotes conduction-dependent arrhythmias that are unmasked by hypokalemia.
Article in JACC. Basic to translational science, 2017. 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
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The trial behind it
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Cardiac radiotherapy induces electrical conduction reprogramming in the absence of transmural fibrosis.Nature communications · 2021Trial
- Left ventricular deformation predicts major adverse cardiac events following acute myocardial infarction independently of afterload and ventricular-arterial coupling.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- Arrhythmogenic Remodeling in the Failing Heart.Cells · 2021Review
- Arrhythmogenic Mechanisms in Hypokalaemia: Insights From Pre-clinical Models.Frontiers in cardiovascular medicine · 2021Review
- Echocardiographic Left Ventricular Mass Estimation: Two-Dimensional Area-Length Method is Superior to M-Mode Linear Method in Swine Models of Cardiac Diseases.Journal of cardiovascular translational research · 2020Article
- Factors Promoting Conduction Slowing as Substrates for Block and Reentry in Infarcted Hearts.Biophysical journal · 2019Article
- Pathophysiology of Calcium Mediated Ventricular Arrhythmias and Novel Therapeutic Options with Focus on Gene Therapy.International journal of molecular sciences · 2019Review
- Arrhythmias and Heart Rate: Mechanisms and Significance of a Relationship.Arrhythmia & electrophysiology review · 2018Review
- Hypokalemia-Induced Arrhythmias and Heart Failure: New Insights and Implications for Therapy.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Although the pathophysiological significance of resistant hypertension in post-myocardial infarction (MI) patients is established, mechanisms by which increased afterload in that setting worsens outcome are unclear. With regards to sudden cardiac death, whether increased afterload alters the electrophysiological substrate following MI is unknown. We established a new large animal model of chronic post-MI remodeling with increased afterload which exhibits widespread deposition of fibrosis in remote areas from the anterior MI, mimicking the disease phenotype of patients with advanced ischemic heart disease. We identified the mode-of-initiation and mechanism of arrhythmias which were consistently unmasked by hypokalemia in this clinically-relevant model.
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Registered trials
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