ArticleComputational and mathematical methods in medicine2016
In Silico Investigation into Cellular Mechanisms of Cardiac Alternans in Myocardial Ischemia.
Article in Computational and mathematical methods in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 38 citations in OpenAlex.
- In silico study of the mechanisms of hypoxia and contractile dysfunction during ischemia and reperfusion of hiPSC cardiomyocytes.Disease models & mechanisms · 2024Article
- Variability in electrophysiological properties and conducting obstacles controls re-entry risk in heterogeneous ischaemic tissue.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2020Article
- Exploring Impaired SERCA Pump-Caused Alternation Occurrence in Ischemia.Computational and mathematical methods in medicine · 2019Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia is associated with pathophysiological conditions such as hyperkalemia, acidosis, and hypoxia. These physiological disorders may lead to changes on the functions of ionic channels, which in turn form the basis for cardiac alternans. In this paper, we investigated the roles of hyperkalemia and calcium handling components played in the genesis of alternans in ischemia at the cellular level by using computational simulations. The results show that hyperkalemic reduced cell excitability and delayed recovery from inactivation of depolarization currents. The inactivation time constant
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