Multiscale computational analysis of the bioelectric consequences of myocardial ischaemia and infarction

Ferrero, J.M.; Trénor, Beatriz; Romero, Lucía

doi:10.1093/europace/eut405

Cited by 30 publications

(19 citation statements)

References 135 publications

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“…These two phases were modeled separately by mimicking ischemia induced changes on cardiac electrophysiology [31,32] at 10 and 45 minutes post-occlusion, respectively. In phase A, we considered: (i) hyperkalemia: an increase in extracellular potassium concentration; (ii) acidosis: decrease in the maximum conductivity of sodium and L-type calcium currents, and; (iii) hypoxia: activation of ATP dependent potassium current, I KATP [33,34]. In phase B, changes to sodium-calcium exchanger, sodium-potassium pump and intracellular calcium handling system were introduced in addition to the alterations seen in phase A.…”

Section: Methodsmentioning

confidence: 99%

Comparison of Electric- and Magnetic-Cardiograms Produced by Myocardial Ischemia in Models of the Human Ventricle and Torso

Alday

Zhang

et al. 2016

PLoS ONE

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Myocardial ventricular ischemia arises from a lack of blood supply to the heart, which may cause abnormal repolarization and excitation wave conduction patterns in the tissue, leading to cardiac arrhythmias and even sudden death. Current diagnosis of cardiac ischemia by the 12-lead electrocardiogram (ECG) has limitations as they are insensitive in many cases and may show unnoticeable differences to normal patterns. As the magnetic field provides extra information on cardiac excitation and is more sensitive to tangential currents to the surface of the chest, whereas the electric field is more sensitive to flux currents, it has been hypothesized that the magnetocardiogram (MCG) may provide a complementary method to the ECG in ischemic diagnosis. However, it is unclear yet about the differences in sensitivity regions of body surface ECG and MCG signals to ischemic conditions. The aim of this study was to investigate such differences by using 12-, 36- ECG and 36-MCG computed from multi-scale biophysically detailed computational models of the human ventricles and torso in both control and ischemic conditions. It was shown that ischemia produced changes in the ECG and MCG signals in the QRS complex, T-wave and ST-segment, with greater relative differences seen in the 36-lead ECG and MCG as compared to the 12-leads ECG (34% and 37% vs 26%, respectively). The 36-lead ECG showed more averaged sensitivity than the MCG in the change of T-wave due to ischemia (37% vs 32%, respectively), whereas the MCG showed greater sensitivity than the ECG in the change of the ST-segment (50% vs 40%, respectively). In addition, both MCG and ECG showed regional-dependent changes to ischemia, but with MCG showing a stronger correlation between ischemic region in the heart. In conclusion, MCG shows more sensitivity than ECG in response to ischemia, which may provide an alternative method for the diagnosis of ischemia.

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Section: Methodsmentioning

confidence: 99%

Comparison of Electric- and Magnetic-Cardiograms Produced by Myocardial Ischemia in Models of the Human Ventricle and Torso

Alday

Zhang

et al. 2016

PLoS ONE

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“…These complex ion channel representations have been incorporated into numerous cardiac model 'cells' from multiple species. The cellular level models have been widely replicated and coupled, creating mathematical representations of cardiac tissue in one, two or three dimensions, with the incorporation of complex anatomical heterogeneities including anisotropy, structural features and distinct cells with specifically associated electrophysiological characteristics (Trenor et al 2007;Romero et al 2009;Bers & Grandi, 2011;Niederer & Smith, 2012;Roberts et al 2012;Sugiura et al 2012;Trayanova et al 2012;Zhang et al 2012;Zhou & O'Rourke, 2012;Polakova & Sobie, 2013;Quail & Taylor, 2013;Romero et al 2013;Sato & Clancy, 2013;Tobon et al 2013;Ferrero et al 2014;Gomez et al 2014;Henriquez, 2014;Ramirez et al 2014;Trayanova & Boyle, 2014;Duncker et al 2015).…”

Section: Cellular Models To Study Cardiac Arrhythmia Mechanismsmentioning

confidence: 99%

Potassium currents in the heart: functional roles in repolarization, arrhythmia and therapeutics

Chiamvimonvat

Chen‐Izu

Clancy

et al. 2017

The Journal of Physiology

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This is the second of the two White Papers from the fourth UC Davis Cardiovascular Symposium Systems Approach to Understanding Cardiac Excitation-Contraction Coupling and Arrhythmias (3-4 March 2016), a biennial event that brings together leading experts in different fields of cardiovascular research. The theme of the 2016 symposium was 'K channels and regulation', and the objectives of the conference were severalfold: (1) to identify current knowledge gaps; (2) to understand what may go wrong in the diseased heart and why; (3) to identify possible novel therapeutic targets; and (4) to further the development of systems biology approaches to decipher the molecular mechanisms and treatment of cardiac arrhythmias. The sessions of the Symposium focusing on the functional roles of the cardiac K channel in health and disease, as well as K channels as therapeutic targets, were contributed by Ye Chen-Izu, Gideon Koren, James Weiss, David Paterson, David Christini, Dobromir Dobrev, Jordi Heijman, Thomas O'Hara, Crystal Ripplinger, Zhilin Qu, Jamie Vandenberg, Colleen Clancy, Isabelle Deschenes, Leighton Izu, Tamas Banyasz, Andras Varro, Heike Wulff, Eleonora Grandi, Michael Sanguinetti, Donald Bers, Jeanne Nerbonne and Nipavan Chiamvimonvat as speakers and panel discussants. This article summarizes state-of-the-art knowledge and controversies on the functional roles of cardiac K channels in normal and diseased heart. We endeavour to integrate current knowledge at multiple scales, from the single cell to the whole organ levels, and from both experimental and computational studies.

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“…As we all know, cardiovascular disease is one of the world's major killer diseases, such as cardiac infarction and myocardial hypertrophy, accounting for approximately 20% of deaths every year in the world (Ferrero et al, 2014). Of note, a large number of animal experiments and clinical trials have shown that myocyte apoptosis is an important event after acute myocardial infarction and may be responsible for a significant portion of myocyte death during the acute ischemic stage, as well as progressive loss of surviving myocytes during the subacute and chronic stages (Bathgate-Siryk et al, 2014;Takemura & Fujiwara, 2004).…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effects of fucoidan against hypoxia-induced apoptosis in H9c2 cardiomyoblast cells

Zhang

Xie

et al. 2015

Pharmaceutical Biology

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Context: Cardiomyocyte apoptosis plays a critical role in the progress of heart diseases. Fucoidan, a complex-sulfated polysaccharide, has been reported to possess potential cardioprotective efficacy in vivo. Objective: The present study determines whether fucoidan could provide cardioprotection on hypoxia-induced cardiomyocyte apoptosis. Materials and methods: H9c2 cardiomyoblast cells were incubated with various concentrations (15, 30, and 60 lg/ml) of fucoidan in a humidified incubator at 37 C with 95% O 2 and 5% CO 2 . After 6 h, hypoxia was processed and the cardioprotective effects of fucoidan were evaluated by applying MTT, ELISA, Hoechst 33258 nucleus staining, and western blot.Results: Following a 6 h exposure of H9c2 to hypoxic condition, significant reduction was found in cell survival (0.57-fold) and superoxide dismutase (SOD) activity (0.56-fold), which were associated with the increase of malondialdehyde (MDA) level (2.58-fold), creatine phosphokinase (CK, 3.57-fold), and lactate dehydrogenase (LDH) activities (2.39-fold). Moreover, hypoxiainduced apoptosis was confirmed by Hoechst 33258 nuclear staining, and these changes were accompanied by the increase of Bcl-2 (1.27-fold) and Bax expression (2.6-fold). However, preincubation of the cells with fucoidan prior to hypoxia exposure elevated the cell viability (30 lg/ml, 1.18-fold; 60 lg/ml, 1.32-fold) and SOD activity (30 lg/ml, 1.12-fold; 60 lg/ml, 1.25-fold), but decreased the MDA level (30 lg/ml, 0.70-fold; 60 lg/ml, 0.80-fold), CK (30 lg/ml, 0.69-fold; 60 lg/ml, 0.76-fold), and LDH (30 lg/ml, 0.67-fold; 60 lg/ml, 0.86-fold) leakages. Hoechst 33258 nuclear staining observations demonstrated the same protective effect of fucoidan on hypoxia-induced myocardial injury. Also, cardioprotective effects of fucoidan were reflected by increasing Bcl-2 (60 lg/ml, 1.84-fold), as well as decreasing Bax (60 lg/ml, 0.6-fold). Conclusion: Fucoidan had protective effect against hypoxia-induced cardiomyocytes apoptosis, and the mechanism might involve protections of the cell from oxidative injury.

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Multiscale computational analysis of the bioelectric consequences of myocardial ischaemia and infarction

Cited by 30 publications

References 135 publications

Comparison of Electric- and Magnetic-Cardiograms Produced by Myocardial Ischemia in Models of the Human Ventricle and Torso

Comparison of Electric- and Magnetic-Cardiograms Produced by Myocardial Ischemia in Models of the Human Ventricle and Torso

Potassium currents in the heart: functional roles in repolarization, arrhythmia and therapeutics

Cardioprotective effects of fucoidan against hypoxia-induced apoptosis in H9c2 cardiomyoblast cells

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