Academic literature on the topic 'Cardiac Modelling ; Sinoatrial Node ; Sinus Node Dysfunction'
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Journal articles on the topic "Cardiac Modelling ; Sinoatrial Node ; Sinus Node Dysfunction"
1
Le Scouarnec, Solena, Naina Bhasin, Claude Vieyres, Thomas J. Hund, Shane R. Cunha, Olha Koval, Celine Marionneau, et al. "Dysfunction in ankyrin-B-dependent ion channel and transporter targeting causes human sinus node disease." Proceedings of the National Academy of Sciences 105, no. 40 (October 1, 2008): 15617–22. http://dx.doi.org/10.1073/pnas.0805500105.
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The identification of nearly a dozen ion channel genes involved in the genesis of human atrial and ventricular arrhythmias has been critical for the diagnosis and treatment of fatal cardiovascular diseases. In contrast, very little is known about the genetic and molecular mechanisms underlying human sinus node dysfunction (SND). Here, we report a genetic and molecular mechanism for human SND. We mapped two families with highly penetrant and severe SND to the human ANK2 (ankyrin-B/AnkB) locus. Mice heterozygous for AnkB phenocopy human SND displayed severe bradycardia and rate variability. AnkB is essential for normal membrane organization of sinoatrial node cell channels and transporters, and AnkB is required for physiological cardiac pacing. Finally, dysfunction in AnkB-based trafficking pathways causes abnormal sinoatrial node (SAN) electrical activity and SND. Together, our findings associate abnormal channel targeting with human SND and highlight the critical role of local membrane organization for sinoatrial node excitability.
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Zhang, Hengtao, Albert Y. Sun, Jong J. Kim, Victoria Graham, Elizabeth A. Finch, Igor Nepliouev, Guiling Zhao, et al. "STIM1–Ca2+ signaling modulates automaticity of the mouse sinoatrial node." Proceedings of the National Academy of Sciences 112, no. 41 (September 30, 2015): E5618—E5627. http://dx.doi.org/10.1073/pnas.1503847112.
Full textAbstract:
Cardiac pacemaking is governed by specialized cardiomyocytes located in the sinoatrial node (SAN). SAN cells (SANCs) integrate voltage-gated currents from channels on the membrane surface (membrane clock) with rhythmic Ca2+ release from internal Ca2+ stores (Ca2+ clock) to adjust heart rate to meet hemodynamic demand. Here, we report that stromal interaction molecule 1 (STIM1) and Orai1 channels, key components of store-operated Ca2+ entry, are selectively expressed in SANCs. Cardiac-specific deletion of STIM1 in mice resulted in depletion of sarcoplasmic reticulum (SR) Ca2+ stores of SANCs and led to SAN dysfunction, as was evident by a reduction in heart rate, sinus arrest, and an exaggerated autonomic response to cholinergic signaling. Moreover, STIM1 influenced SAN function by regulating ionic fluxes in SANCs, including activation of a store-operated Ca2+ current, a reduction in L-type Ca2+ current, and enhancing the activities of Na+/Ca2+ exchanger. In conclusion, these studies reveal that STIM1 is a multifunctional regulator of Ca2+ dynamics in SANCs that links SR Ca2+ store content with electrical events occurring in the plasma membrane, thereby contributing to automaticity of the SAN.
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Wu, Jingjing, Yanmin Zhang, Xinzhao Zhang, Longxian Cheng, Wim J. Lammers, Andrew A. Grace, James A. Fraser, Henggui Zhang, Christopher L. H. Huang, and Ming Lei. "Altered sinoatrial node function and intra-atrial conduction in murine gain-of-function Scn5a+/ΔKPQ hearts suggest an overlap syndrome." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 7 (April 1, 2012): H1510—H1523. http://dx.doi.org/10.1152/ajpheart.00357.2011.
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Mutations in SCN5A, the gene encoding the pore-forming subunit of cardiac Na+ channels, cause a spectrum of arrhythmic syndromes. Of these, sinoatrial node (SAN) dysfunction occurs in patients with both loss- and gain-of-function SCN5A mutations . We explored for corresponding alterations in SAN function and intracardiac conduction and clarified possible mechanisms underlying these in an established mouse long QT syndrome type 3 model carrying a mutation equivalent to human SCN5A-ΔKPQ. Electrophysiological characterizations of SAN function in living animals and in vitro sinoatrial preparations were compared with cellular SAN and two-dimensional tissue models exploring the consequences of Scn5a+/ΔKPQ mutations. Scn5a+/ΔKPQ mice showed prolonged electrocardiographic QT and corrected QT intervals confirming long QT phenotypes. They showed frequent episodes of sinus bradycardia, sinus pause/arrest, and significantly longer sinus node recovery times, suggesting compromised pacemaker activity compared with wild-type mice. Electrocardiographic waveforms suggested depressed intra-atrial, atrioventricular node, and intraventricular conduction in Scn5a+/ΔKPQ mice . Isolated Scn5a+/ΔKPQ sinoatrial preparations similarly showed lower mean intrinsic heart rates and overall slower conduction through the SAN to the surrounding atrium than did wild-type preparations. Computer simulations of both single SAN cells as well as two-dimensional SAN-atrial models could reproduce the experimental observations of impaired pacemaker and sinoatrial conduction in terms of changes produced by both augmented tail and reduced total Na+ currents, respectively. In conclusion, the gain-of-function long QT syndrome type 3 murine Scn5a+/ΔKPQ cardiac system, in overlap with corresponding features reported in loss-of-function Na+ channel mutations, shows compromised SAN pacemaker and conduction function explicable in modeling studies through a combination of augmented tail and reduced peak Na+ currents.
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Duba, Ayyappa S., Suneetha Jasty, Ankit Mahajan, Vijay Kodadhala, Raza Khan, Prithviraj Rai, and Mohammad Ghazvini. "Rare Case of Rapidly Worsening REM Sleep Induced Bradycardia." Case Reports in Cardiology 2015 (2015): 1–3. http://dx.doi.org/10.1155/2015/546712.
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Sinoatrial arrest also known as sinus pause occurs when sinoatrial node of the heart transiently ceases to generate the electrical impulse necessary for the myocardium to contract. It may last from 2.0 seconds to several minutes. Etiologies of sinoatrial arrest can be complex and heterogeneous. During rapid eye movement (REM) sleep, sinus arrests unrelated to apnea or hypopnea are very rare and only a few cases have been reported. Here we report a case of 36-year-old male with no significant past medical history who presented to our hospital after a syncopal episode at night. Physical examination showed no cardiac or neurological abnormalities and initial EKG and neuroimaging were normal. Overnight telemonitor recorded several episodes of bradyarrhythmia with sinus arrest that progressively lengthened over time. Sleep study was done which confirmed that sinus arrests occurred more during REM sleep and are unrelated to apnea or hypopnea. Electrophysiology studies showed sinus nodal dysfunction with no junctional escape, subsequently a dual chamber pacemaker placed for rapidly worsening case of REM sleep induced bradycardia.
5
di Bernardo, Diego, and Maria G. Signorini. "A Model of Two Nonlinear Coupled Oscillators for the Study of Heartbeat Dynamics." International Journal of Bifurcation and Chaos 08, no. 10 (October 1998): 1975–85. http://dx.doi.org/10.1142/s0218127498001637.
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The cardiac conduction system may be assumed to be a network of self-excitatory pacemakers, with the SinoAtrial (SA) node having the highest intrinsic rate. Subsidiary pacemakers with slower firing frequencies are located in the AtrioVentricular (AV) node and the His-Purkinje system. Under physiological conditions, the SA node is the dominant pace-maker and impulses travel from this node to the ventricle through the AV junction, which is traditionally regarded as a passive conduit. We consider the Av node as an active pace-maker and develop a model of two nonlinear coupled oscillators in order to describe the interaction between the SA and the AV node. These two nonlinear oscillators are based on a modification of the van der Pol osciallator, so that the generated waveforms resemble the action potentials of cells in the SA and the AV node respectively. A bifurcation analysis of this model is performed and the pathophysiological different kinds of heartbeat pathologies (1°, 2° (both Wenckebach and non-Wenckebach) and 3° AV blocks, sinus arrest, atrials bigeminy, etc.). This simple nonlinear model helps to improve the understanding of the complex phenomena involved in heart rhythm generation as well as of heart rate control and function.
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Zhang, Heng, Miao Hao, Lingkang Li, Keyan Chen, Jing Qi, Wei Chen, Xintong Cai, Chen Chen, Zhuang Liu, and Ping Hou. "Shenxian-Shengmai Oral Liquid Improves Sinoatrial Node Dysfunction through the PKC/NOX-2 Signaling Pathway." Evidence-Based Complementary and Alternative Medicine 2021 (April 10, 2021): 1–10. http://dx.doi.org/10.1155/2021/5572140.
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Sick sinus syndrome (SSS) is one of the common causes of cardiac syncope and sudden death; the occurrence of SSS is associated with the accumulation of ROS in the sinoatrial node (SAN). Shenxian-shengmai (SXSM) is a traditional Chinese medicine available as oral liquid that causes a significant increase in heart rate. The objective of this study is to observe the improvement of SXSM on SAN function in SSS mice and explore its potential mechanism. In the current study, SSS was simulated in mice by inducing SAN dysfunction using a micro-osmotic pump to inject angiotensin II (Ang II). The mouse model with SSS was used to determine the effect of SXSM on SAN function and to explore its potential mechanism. Furthermore, the HL-1 cell line, derived from mouse atrial myocytes, was used to simulate SAN pacemaker cells. Our results indicated that SXSM significantly increased the heart rate of SSS mice by reducing the AngII-induced accumulation of ROS in the SAN and by inhibiting the expression of HDAC4, thereby reducing the loss of HCN4, a critical component of the cardiac conduction system. MASSON staining revealed a reduction of SAN damage in SSS mice that were treated with SXSM compared with controls. In vitro experiments showed that AngII treatment caused an upregulation of the PKC/NOX-2 signaling pathway in HL-1 cells which could be prevented by pretreatment with SXSM. The protective effect of SXSM was attenuated upon treatment with the PCK agonist PMA. In conclusion, SXSM reduced the AngII-induced accumulation of ROS in the SAN through the PKC/NOX2 signaling pathway, improving the functioning of the SAN and preventing the decrease of heart rate in SSS mice.
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Bulgakova, E. S., T. V. Tvorogova, B. A. Rudenko, and O. M. Drapkina. "CAROTID ARTERY STENTING IN A PATIENT WITH SINUS BRADYCARDIA: CLINICAL CASE." Rational Pharmacotherapy in Cardiology 14, no. 3 (July 5, 2018): 356–60. http://dx.doi.org/10.20996/1819-6446-2018-14-3-356-360.
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Syndrome of hemodynamic depression is a frequent complication of the carotid artery endovascular intervention and, as a rule, is transient in nature. This article presents a clinical case of carotid artery stenting in a 63-year-old patient. The specific feature of this patient was the initial sinoatrial node dysfunction as a permanent sinus bradycardia. The examination verified multisite atherosclerosis, including coronary artery stenosis, manifested by the presence of stable angina, without history of myocardial infarction. Therefore, coronary endovascular treatment was firstly performed. Reexamination after coronary blood flow restoration revealed stable sinus bradycardia persistence without any positive or negative changes. According to anamnesis, examination and instrumental diagnostic results, indications for permanent cardiac pacing were not identified. Carotid artery stenting after the necessary preventive measures was successful. The article also considers possible risk factors of significant perioperative bradycardia during carotid angioplasty with stenting and measures preventing cardiac conduction perioperative worsening.
8
Chan, Chao-Shun, Yung-Kuo Lin, Yao-Chang Chen, Yen-Yu Lu, Shih-Ann Chen, and Yi-Jen Chen. "Heart Failure Differentially Modulates Natural (Sinoatrial Node) and Ectopic (Pulmonary Veins) Pacemakers: Mechanism and Therapeutic Implication for Atrial Fibrillation." International Journal of Molecular Sciences 20, no. 13 (June 30, 2019): 3224. http://dx.doi.org/10.3390/ijms20133224.
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Heart failure (HF) frequently coexists with atrial fibrillation (AF) and dysfunction of the sinoatrial node (SAN), the natural pacemaker. HF is associated with chronic adrenergic stimulation, neurohormonal activation, abnormal intracellular calcium handling, elevated cardiac filling pressure and atrial stretch, and fibrosis. Pulmonary veins (PVs), which are the points of onset of ectopic electrical activity, are the most crucial AF triggers. A crosstalk between the SAN and PVs determines PV arrhythmogenesis. HF has different effects on SAN and PV electrophysiological characteristics, which critically modulate the development of AF and sick sinus syndrome. This review provides updates to improve our current understanding of the effects of HF in the electrical activity of the SAN and PVs as well as therapeutic implications for AF.
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Glukhov, Alexey V., Vadim V. Fedorov, Mark E. Anderson, Peter J. Mohler, and Igor R. Efimov. "Functional anatomy of the murine sinus node: high-resolution optical mapping of ankyrin-B heterozygous mice." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 2 (August 2010): H482—H491. http://dx.doi.org/10.1152/ajpheart.00756.2009.
Full textAbstract:
The mouse is widely used as a genetic platform to investigate the molecular mechanisms of sinoatrial node (SAN) pacemaking. Recently, it has been shown that isolated SAN cells from the ankyrin-B (AnkB)-deficient mice display severe pacemaking dysfunction similar to individuals harboring ankyrin 2 allele variants. However, these results have been limited to isolated SAN cells only and thus did not evaluate the functional anatomy of the widely distributed atrial pacemaker complex (e.g., the dynamic interaction of primary and subsidiary pacemakers). We studied pacemaker function in an intact mouse atrial preparation, which included the SAN, atrioventricular junction (AVJ), and both atria, excluding most of the septum. Optical mapping with a voltage-sensitive dye and CMOS camera ULTIMA-L was used to map spontaneous pacemaker activity with or without autonomic modulation in wild-type (WT) mice ( n = 7) and in the AnkB heterozygous (AnkB+/−; n = 9) mouse model of human SAN disease. In WT mice, isoproterenol accelerated the SAN rate (for 10 μM: from 325 ± 19 to 510 ± 33 beat/min, P < 0.01) and shifted the leading pacemaker site superiorly by 0.77 ± 0.11 mm within the SAN. ACh decreased the SAN rate (from 333 ± 26 to 96 ± 22 beats/min, P < 0.01) and shifted the leading pacemaker either inferiorly within the SAN or abruptly toward the AVJ. After isoproterenol, AnkB+/− mice exhibited a larger beat-to-beat variability (SD of a cycle length: 13.4 ± 3.6 vs. 2.5 ± 0.8 ms, P < 0.01 vs. WT mice), disorganized shift of the leading pacemaker (2.04 ± 0.37 mm, P < 0.05 vs. WT mice), and competing multiple pacemakers, resulting in beat-to-beat changes of the leading pacemaker location site between the SAN and AVJ regions. Notably, AnkB+/− mice also displayed a reduced sensitivity to ACh (rate slowing by 32 ± 12% vs. 67 ± 4%, P < 0.05, AnkB+/− vs. WT mice, respectively). In conclusion, AnkB dysfunction results in SAN abnormalities in an isolated mouse atria preparation. While AnkB dysfunction dramatically alters single SAN cell function, the mechanisms underlying cardiac automaticity are clearly complex, and phenotypes may be partially compensated by the dynamic interaction of cells within the pacemaker complex. These new findings highlight the importance of the functional anatomy of the entire atrial distributed pacemaker complex, including the SAN and AVJ, and clearly demonstrate the role of AnkB in cardiac automaticity.
10
Lang, Di, and Alexey V. Glukhov. "Cellular and Molecular Mechanisms of Functional Hierarchy of Pacemaker Clusters in the Sinoatrial Node: New Insights into Sick Sinus Syndrome." Journal of Cardiovascular Development and Disease 8, no. 4 (April 13, 2021): 43. http://dx.doi.org/10.3390/jcdd8040043.
Full textAbstract:
The sinoatrial node (SAN), the primary pacemaker of the heart, consists of a heterogeneous population of specialized cardiac myocytes that can spontaneously produce action potentials, generating the rhythm of the heart and coordinating heart contractions. Spontaneous beating can be observed from very early embryonic stage and under a series of genetic programing, the complex heterogeneous SAN cells are formed with specific biomarker proteins and generate robust automaticity. The SAN is capable to adjust its pacemaking rate in response to environmental and autonomic changes to regulate the heart’s performance and maintain physiological needs of the body. Importantly, the origin of the action potential in the SAN is not static, but rather dynamically changes according to the prevailing conditions. Changes in the heart rate are associated with a shift of the leading pacemaker location within the SAN and accompanied by alterations in P wave morphology and PQ interval on ECG. Pacemaker shift occurs in response to different interventions: neurohormonal modulation, cardiac glycosides, pharmacological agents, mechanical stretch, a change in temperature, and a change in extracellular electrolyte concentrations. It was linked with the presence of distinct anatomically and functionally defined intranodal pacemaker clusters that are responsible for the generation of the heart rhythm at different rates. Recent studies indicate that on the cellular level, different pacemaker clusters rely on a complex interplay between the calcium (referred to local subsarcolemmal Ca2+ releases generated by the sarcoplasmic reticulum via ryanodine receptors) and voltage (referred to sarcolemmal electrogenic proteins) components of so-called “coupled clock pacemaker system” that is used to describe a complex mechanism of SAN pacemaking. In this review, we examine the structural, functional, and molecular evidence for hierarchical pacemaker clustering within the SAN. We also demonstrate the unique molecular signatures of intranodal pacemaker clusters, highlighting their importance for physiological rhythm regulation as well as their role in the development of SAN dysfunction, also known as sick sinus syndrome.
Dissertations / Theses on the topic "Cardiac Modelling ; Sinoatrial Node ; Sinus Node Dysfunction"
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Wang, Ruoxi. "Computational investigation of the mechanisms underlying the cardiac pacemaker and its dysfunction." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/computational-investigation-of-the-mechanisms-underlying-the-cardiac-pacemaker-and-its-dysfunction(0a24969e-f175-42dc-8703-068753bfdb34).html.
Full textAbstract:
The sinoatrial node is the primary cardiac pacemaker, which is responsible for generating spontaneous depolarisation of cellular membranes, leading to pacemaking action potentials that control the initiation and regulation of the rhythms of the heart. Previous studies in experimental electrophysiology have gathered a large amount of experimental data about the mechanisms of cardiac pacemaking activities at the molecular, ionic and cellular levels, however, the precise mechanisms underlying the genesis of spontaneous pacemaking action potentials still remain controversial. Mathematical models of the electrophysiology provide a unique alternative tool complimentary to experimental investigations, enabling us to analyse the fundamental physiological mechanisms of cardiac pacemaking activities in an efficient way that would be more difficult to conduct in experimental approaches. In this thesis, an integrated model, incorporating the detailed cellular ion channel kinetics, multi-compartment intracellular Ca2+ handling system and cell morphology, was developed for simulating the spontaneous pacemaking action potentials as well as the stochastic nature of local Ca2+ dynamics in the murine SA node cells. By using the model, the ionic mechanisms underlying the automaticity of primary cardiac pacemaking cells were investigated, the individual role of the ‘membrane clock’ (the cell membrane events) and ‘Ca2+ clock’ (intracellular Ca2+ activities) on generating the pacemaking action potentials were examined. In addition, the model also considered the regulation of the autonomic nervous systems on cardiac pacemaking action potentials. For the first time, competitive regulation of electrical action potentials of the murine SA node cells by the circadian sympathetic and parasympathetic systems during 24-hours were investigated. Furthermore, the individual role of the neurotransmitters, ACh- and ISO-induced actions on variant ion channel and Ca2+ handling in regulating cardiac pacemaking action potentials were also analysed. At the tissue level, an anatomically detailed 2D model of the intact SA node and atrium was developed to investigate the ionic mechanisms underlying sinus node dysfunctions in variant genetic defect conditions. Effects of these genetic defects in impairing cardiac pacemaker ability in pacing and driving the surrounding atrium as seen in the sinus node dysfunction were investigated.
Book chapters on the topic "Cardiac Modelling ; Sinoatrial Node ; Sinus Node Dysfunction"
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Potpara, Tatjana. "Sinus node disease: ECG patterns and diagnosis." In ESC CardioMed, edited by Giuseppe Boriani, 1949–52. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0449.
Full textAbstract:
A healthy sinus node (SN) is the physiological principal site of electrical impulse formation in the heart, owing to its ability to sustain a regular generation of spontaneous depolarization at faster rates than other latent cardiac pacemakers. Structural disease (or senescence) of the SN and sinoatrial junction may cause SN disease (SND). The electrocardiographic (ECG) manifestations of SND are usually intermittent and can be easily missed. The ECG patterns of SND include: (1) periods of spontaneous, often pronounced, sinus bradycardia; (2) sinus pause due to sinus arrest or sinoatrial exit block; and (3) tachycardia-bradycardia syndrome. There is no standardized set of diagnostic criteria for SND. Since the symptoms of SND are non-specific, and the initial ECG may not be diagnostic, establishing a correlation between symptoms and the underlying heart rhythm at the time of symptoms is essential for the diagnosis, provided that any potentially reversible cause(s) of transient SN dysfunction have been excluded (or identified and treated). Invasive electrophysiological studies are not routinely used for the evaluation of SND, due to a limited sensitivity, and may be considered in patients with a mismatch of symptoms and ECG findings. When reversible causes have been excluded, SND should be distinguished from ‘physiological’ bradycardia (particularly in well-trained athletes), neurocardiogenic syncope with a pronounced cardioinhibitory component, or carotid sinus hypersensitivity. Carotid sinus hypersensitivity can be established by carotid sinus massage resulting in a pause of longer than 3 s or a symptomatic drop in blood pressure, or both.