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Copy file name to clipboardExpand all lines: docs/references.bib
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keywords = {Empagliflozin, Long QT syndrome type 3, Late sodium current, Nav1.5, Arrhythmia, Cardioprotection},
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abstract = {Background Sodium/glucose cotransporter 2 inhibitors (SGLT2is) like empagliflozin have demonstrated cardioprotective effects in patients with or without diabetes. SGLT2is have been shown to selectively inhibit the late component of cardiac sodium current (late INa). Induction of late INa is the primary mechanism in the pathophysiology of congenital long QT syndrome type 3 (LQT3) gain-of-function mutations in the SCN5A gene encoding Nav1.5. We investigated empagliflozin's effect on late INa in thirteen known LQT3 mutations located in distinct regions of the channel. Methods The whole-cell patch-clamp technique was used to investigate the effect of empagliflozin on late INa in recombinantly expressed Nav1.5 channels containing different LQT3 mutations. Molecular modeling of human Nav1.5 and simulations in a mathematical model of human ventricular myocytes were used to extrapolate our experimental results to excitation-contraction coupling. Results Empagliflozin selectively inhibited late INa in LQT3 mutations in the inactivation gate region of Nav1.5, without affecting peak current or channel kinetics. In contrast, empagliflozin inhibited both peak and late INa in mutations in the S4 voltage-sensing regions, altered channel gating, and slowed recovery from inactivation. Empagliflozin had no effect on late/peak INa or channel kinetics in channels with mutations in the putative empagliflozin binding region. Simulation results predict that empagliflozin may have a desirable therapeutic effect in LQT3 mutations in the inactivation gate region. Conclusions Empagliflozin selectively inhibits late INa, without affecting channel kinetics, in LQT3 mutations in the inactivation gate region. Empagliflozin may thus be a promising precision medicine approach for patients with specific LQT3 mutations.}
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}
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@inproceedings{monopoli2025arrhythmic,
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title = {Arrhythmic Mitral Valve Syndrome: Insights from Left Ventricular End-Systolic Shape Analysis},
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author = {Monopoli, Giulia and Sadeghinia, Mohammad Javad and Westrum Aabel, Eivind and Ribe, Margareth and Castrini, Anna Isotta and Hasselberg, Nina and Bugge, Cecilie and Five, Christian and Haugaa, Kristina and Balaban, Gabriel and others},
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booktitle = {International Conference on Functional Imaging and Modeling of the Heart},
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pages = {26--36},
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year = {2025},
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organization = {Springer}
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}
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@article{monopoli2025deepvalve,
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title = {DeepValve: The first automatic detection pipeline for the mitral valve in Cardiac Magnetic Resonance imaging},
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author = {Monopoli, Giulia and Haas, Daniel and Singh, Ashay and Aabel, Eivind Westrum and Ribe, Margareth and Castrini, Anna Isotta and Hasselberg, Nina Eide and Bugge, Cecilie and Five, Christian and Haugaa, Kristina and others},
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journal = {Computers in Biology and Medicine},
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volume = {192},
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pages = {110211},
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year = {2025},
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publisher = {Elsevier}
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}
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@article{odeigah2024computational,
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title = {A computational study of right ventricular mechanics in a rat model of pulmonary arterial hypertension},
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author = {Odeigah, Oscar O and Kwan, Ethan D and Garcia, Kristen M and Finsberg, Henrik and Valdez-Jasso, Daniela and Sundnes, Joakim},
Copy file name to clipboardExpand all lines: docs/repositories.md
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## 2025
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-[A software benchmark for cardiac elastodynamics](https://github.com/finsberg/cardiac_benchmark) {cite}`arostica2025117485`
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-[Arrhythmic Mitral Valve Syndrome: Insights from Left Ventricular End-Systolic Shape Analysis](https://github.com/ComputationalPhysiology/MAD-SSA) {cite}`monopoli2025arrhythmic`
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-[DeepValve: an automatic detection pipeline for the mitral valve in cardiac magnetic resonance imaging](https://github.com/giuliamonopoli/deepvalve-paper) {cite}`monopoli2025deepvalve`
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## 2024
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-[The sodium/glucose cotransporter 2 inhibitor Empagliflozin inhibits long QT 3 late sodium currents in a mutation specific manner](https://github.com/andygedwards/LQT3-SGLT2i) {cite}`LUNSONGA202599`
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