ArticleCirculation. Arrhythmia and electrophysiology2015
Targeted antioxidant treatment decreases cardiac alternans associated with chronic myocardial infarction.
Article in Circulation. Arrhythmia and electrophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- PITX2C deficiency promotes arrhythmogenic remodelling via oxidative stress in atrial myocytes.Journal of molecular and cellular cardiology plus · 2026Article
- Berberine Stabilizes the Arrhythmogenic Substrate in Obese Rats by Klotho-Mediated Attenuation of Oxidative Stress and Inflammation.International journal of molecular sciences · 2026Article
- Optical mapping: pioneering the frontier of preclinical antiarrhythmic drug evaluation.iScience · 2026Review
- Review
- Role of Mitochondrial ROS for Calcium Alternans in Atrial Myocytes.Biomolecules · 2024Article
- Huoxin pill prevents acute myocardial ischaemia injury via inhibition of Wnt/β-catenin signaling.Journal of cellular and molecular medicine · 2021Article
- Aging Attenuates Cardiac Contractility and Affects Therapeutic Consequences for Myocardial Infarction.Aging and disease · 2020Review
- Integrating Literature-Based Knowledge Database and Expression Data to Explore Molecular Pathways Connecting PPARG and Myocardial Infarction.PPAR research · 2020Article
- Cardiac Alternans: Mechanisms and Clinical Utility in Arrhythmia Prevention.Journal of the American Heart Association · 2019Review
- Pyruvate enhancement of cardiac performance: Cellular mechanisms and clinical application.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- The histone H3K9 methyltransferase SUV39H links SIRT1 repression to myocardial infarction.Nature communications · 2017Article
- Reversible redox modifications of ryanodine receptor ameliorate ventricular arrhythmias in the ischemic-reperfused heart.American journal of physiology. Heart and circulatory physiology · 2016Article
- Mesenchymal stem cells suppress cardiac alternans by activation of PI3K mediated nitroso-redox pathway.Journal of molecular and cellular cardiology · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIn myocardial infarction (MI), repolarization alternans is a potent arrhythmia substrate that has been linked to Ca2+ cycling proteins, such as sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), located in the sarcoplasmic reticulum. MI is also associated with oxidative stress and increased xanthine oxidase (XO) activity, an important source of reactive oxygen species (ROS) in the sarcoplasmic reticulum that may reduce SERCA2a function. We hypothesize that in chronic MI, XO-mediated oxidation of SERCA2a is a mechanism of cardiac alternans. METHODS AND
resultsMale Lewis rats underwent ligation of the left anterior descending coronary artery (n=54) or sham procedure (n=24). At 4 weeks, optical mapping of intracellular Ca2+ and ROS was performed. ECG T-wave alternans (ECG ALT) and Ca2+ transient alternans (Ca2+ALT) were induced by rapid pacing (300-120 ms) before and after the XO inhibitor allopurinol (ALLO, 50 µmol/L). In MI, ECG ALT (2.32±0.41%) and Ca2+ ALT (22.3±4.5%) were significantly greater compared with sham (0.18±0.08%, P<0.001; 0.79±0.32%, P<0.01). Additionally, ROS was increased by 137% (P<0.01) and oxidation of SERCA2a by 30% (P<0.05) in MI compared with sham. Treatment with ALLO significantly decreased ECG ALT (-77±9%, P<0.05) and Ca2+ ALT (-56±7%, P<0.05) and, importantly, reduced ROS (-65%, P<0.01) and oxidation of SERCA2a (-38%, P<0.05). CaMKII inhibition and general antioxidant treatment had no effect on ECG ALT and Ca2+ ALT.
conclusionsThese results demonstrate, for the first time, that in MI, increased ROS from XO is a significant cause of repolarization alternans. This suggests that targeting XO ROS production may be effective at preventing arrhythmia substrates in chronic MI.
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