ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2008
Repolarization abnormalities and afterdepolarizations in a canine model of sudden cardiac death.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Acute GLP-1 Agonism Induces Arrhythmogenic Electrical Activity in Aged Mice Heart Through Impaired Cellular Na+ and Ca2+ Handlings: The Role of CK2 Hyperphosphorylation.Anatolian journal of cardiology · 2025Article
- Animal models of arrhythmia: classic electrophysiology to genetically modified large animals.Nature reviews. Cardiology · 2019Review
- Translational Models of Arrhythmia Mechanisms and Susceptibility: Success and Challenges of Modeling Human Disease.Frontiers in cardiovascular medicine · 2019Review
- Mechanisms Underlying Interactions Between Low-Frequency Oscillations and Beat-to-Beat Variability of Celullar Ventricular Repolarization in Response to Sympathetic Stimulation: Implications for Arrhythmogenesis.Frontiers in physiology · 2019Article
- Divergent effects of adrenaline in human induced pluripotent stem cell-derived cardiomyocytes obtained from hypertrophic cardiomyopathy.Disease models & mechanisms · 2018Article
- Dysfunction of the β2-spectrin-based pathway in human heart failure.American journal of physiology. Heart and circulatory physiology · 2016Article
- Chronic Omega-3 Polyunsaturated Fatty Acid Treatment Variably Affects Cellular Repolarization in a Healed Post-MI Arrhythmia Model.Frontiers in physiology · 2016Article
- Heart failure duration progressively modulates the arrhythmia substrate through structural and electrical remodeling.Life sciences · 2015Article
- Myocardial electrotonic response to submaximal exercise in dogs with healed myocardial infarctions: evidence for β-adrenoceptor mediated enhanced coupling during exercise testing.Frontiers in physiology · 2015Article
- Ibandronate and ventricular arrhythmia risk.Journal of cardiovascular electrophysiology · 2014Article
- Differential effects of the peroxynitrite donor, SIN-1, on atrial and ventricular myocyte electrophysiology.Journal of cardiovascular pharmacology · 2013Article
- Article
- Endurance exercise training normalizes repolarization and calcium-handling abnormalities, preventing ventricular fibrillation in a model of sudden cardiac death.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Synchronization of early afterdepolarizations and arrhythmogenesis in heterogeneous cardiac tissue models.Biophysical journal · 2012Article
- Dietary omega-3 fatty acids and susceptibility to ventricular fibrillation: lack of protection and a proarrhythmic effect.Circulation. Arrhythmia and electrophysiology · 2012Article
- Shortened Ca2+ signaling refractoriness underlies cellular arrhythmogenesis in a postinfarction model of sudden cardiac death.Circulation research · 2012Article
- Early afterdepolarizations and cardiac arrhythmias.Heart rhythm · 2010Article
- Effects of dietary omega-3 fatty acids on ventricular function in dogs with healed myocardial infarctions: in vivo and in vitro studies.American journal of physiology. Heart and circulatory physiology · 2010Article
- Redox modification of ryanodine receptors underlies calcium alternans in a canine model of sudden cardiac death.Cardiovascular research · 2009Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Ventricular tachyarrhythmias are the most common cause of sudden cardiac death (SCD); a healed myocardial infarction increases the risk of SCD. We determined the contribution of specific repolarization abnormalities to ventricular tachyarrhythmias in a postinfarction model of SCD. For our methods, we used a postinfarction canine model of SCD, where an exercise and ischemia test was used to stratify animals as either susceptible (VF(+)) or resistant (VF(-)) to sustained ventricular tachyarrhythmias. Our results show no changes in global left ventricular contractility or volumes occurred after infarction. At 8-10 wk postmyocardial infarction, myocytes were isolated from the left ventricular midmyocardial wall and studied. In the VF(+) animals, myocyte action potential (AP) prolongation occurred at 50 and 90% repolarization (P < 0.05) and was associated with increased variability of AP duration and afterdepolarizations. Multiple repolarizing K(+) currents (I(Kr), I(to)) and inward I(K1) were also reduced (P < 0.05) in myocytes from VF(+) animals compared with control, noninfarcted dogs. In contrast, only I(to) was reduced in VF(-) myocytes compared with controls (P < 0.05). While afterdepolarizations were not elicited at baseline in myocytes from VF(-) animals, afterdepolarizations were consistently elicited after the addition of an I(Kr) blocker. In conclusion, the loss of repolarization reserve via reductions in multiple repolarizing currents in the VF(+) myocytes leads to AP prolongation, repolarization instability, and afterdepolarizations in myocytes from animals susceptible to SCD. These abnormalities may provide a substrate for initiation of postmyocardial infarction ventricular tachyarrhythmias.
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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.