Micro-Magnetocardiography System With a Single-Chip SQUID Magnetometer Array for QT Analysis and Diagnosis of Myocardial Injury in Small Animals

Komamura, Kazuo; Adachi, Yoshiaki; Miyamoto, Masatoshi; Kawai, Jun; Haruta, Yasuhiro; Uehara, Gen

doi:10.1109/tbcas.2008.2003979

Cited by 10 publications

(2 citation statements)

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“…Magnetocardiography (MCG) can be used to diagnose and predict the risk of cardiac arrhythmias in humans (Steinhoff et al, 2004 ; Sato et al, 2012 ; Kwong et al, 2013 ; Ito et al, 2014 ; Yoshida et al, 2015 ). A micromagnetometer array with a superconducting quantum interference device (SQUID) can be used for non-contact recording of MCGs from mice and has the potential for high-throughput use to screen for pro- or anti-arrhythmic effects of pharmacological agents (Komamura et al, 2008 ). Given the evidence presented here, it is clear that increased ROS can lead to intracellular organelle dysfunction and arrhythmias in cardio-metabolic disorders such as diabetes mellitus and hypertension.…”

Section: Clinical Relevance and Future Perspectivesmentioning

confidence: 99%

Reactive Oxygen Species, Endoplasmic Reticulum Stress and Mitochondrial Dysfunction: The Link with Cardiac Arrhythmogenesis

et al. 2016

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Background: Cardiac arrhythmias represent a significant problem globally, leading to cerebrovascular accidents, myocardial infarction, and sudden cardiac death. There is increasing evidence to suggest that increased oxidative stress from reactive oxygen species (ROS), which is elevated in conditions such as diabetes and hypertension, can lead to arrhythmogenesis.Method: A literature review was undertaken to screen for articles that investigated the effects of ROS on cardiac ion channel function, remodeling and arrhythmogenesis.Results: Prolonged endoplasmic reticulum stress is observed in heart failure, leading to increased production of ROS. Mitochondrial ROS, which is elevated in diabetes and hypertension, can stimulate its own production in a positive feedback loop, termed ROS-induced ROS release. Together with activation of mitochondrial inner membrane anion channels, it leads to mitochondrial depolarization. Abnormal function of these organelles can then activate downstream signaling pathways, ultimately culminating in altered function or expression of cardiac ion channels responsible for generating the cardiac action potential (AP). Vascular and cardiac endothelial cells become dysfunctional, leading to altered paracrine signaling to influence the electrophysiology of adjacent cardiomyocytes. All of these changes can in turn produce abnormalities in AP repolarization or conduction, thereby increasing likelihood of triggered activity and reentry.Conclusion: ROS plays a significant role in producing arrhythmic substrate. Therapeutic strategies targeting upstream events include production of a strong reducing environment or the use of pharmacological agents that target organelle-specific proteins and ion channels. These may relieve oxidative stress and in turn prevent arrhythmic complications in patients with diabetes, hypertension, and heart failure.

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Section: Clinical Relevance and Future Perspectivesmentioning

confidence: 99%

Reactive Oxygen Species, Endoplasmic Reticulum Stress and Mitochondrial Dysfunction: The Link with Cardiac Arrhythmogenesis

et al. 2016

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“…Magnetocardiography is used as a clinical tool for the analysis of fetal heart function showing the complex relationship between the maternal and fetal heartbeat [ 133 , 134 ]. Micro-magnetocardiography has been performed on adult rodents, [ 135 , 136 ] but has not been used to detect prenatal heart function in animal models. The expense of this method deters its use.…”

Section: Electrodes and Application To Study Cardiogenesismentioning

confidence: 99%

Probing the Electrophysiology of the Developing Heart

Watanabe

Rollins

Polo‐Parada

et al. 2016

JCDD

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Many diseases that result in dysfunction and dysmorphology of the heart originate in the embryo. However, the embryonic heart presents a challenging subject for study: especially challenging is its electrophysiology. Electrophysiological maturation of the embryonic heart without disturbing its physiological function requires the creation and deployment of novel technologies along with the use of classical techniques on a range of animal models. Each tool has its strengths and limitations and has contributed to making key discoveries to expand our understanding of cardiac development. Further progress in understanding the mechanisms that regulate the normal and abnormal development of the electrophysiology of the heart requires integration of this functional information with the more extensively elucidated structural and molecular changes.

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