Journal articles: 'Cardiac Modelling ; Sinoatrial Node ; Sinus Node Dysfunction'

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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Ballesteros, A., Á. S. Rosero, H. Sáiz, E. García-Parreño, G. Carlos, and E. Manrique. "Lithium and EKG abnormalities. A review." European Psychiatry 41, S1 (April 2017): S750. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1394.

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IntroductionThe literature concerning possible cardio-toxic effects of lithium therapy in man is reviewed.MethodologyA review was conducted to clarify the mechanisms associated with the occurrence of conducting abnormalities when using lithium and investigating (if so) whether these alterations depend on the dose. The literature search was conducted in PubMed data reviewing articles between 1982 and 2015.Results(1) Related to pathopsychiology/risk factors: reports indicate T wave morphology changes with lithium therapy. Of particular concern are cases of sinus mode dysfunction or sinoatrial block and the appearance or aggravation of ventricular irritability. The incidence of cardiac complications, in general terms, may increase with age. Recent findings (a retrospective study of bipolar patients) of lithium-associated hypocalcaemia showed that hypocalcaemia resulting from medical diseases and bipolar patients with lithium-associated hypocalcaemia had significantly higher frequencies of conduction defects. (2) Related/unrelated to dose: therapeutic and toxic levels of lithium have infrequently been associated with serious cardiac dysfunction. Several case reports demonstrate two important points about Brugada syndrome unmasking: electrocardiograph abnormality severity may correspond to lithium levels and unmasking may occur in the therapeutic range of lithium. Other report shows a case of lithium induced sinus-node dysfunction in a patient with serum lithium levels in therapeutic range.ConclusionsLithium abnormalities are rare and mostly not related to dose. Conducting heart anomalies may occur, especially when several factors are present (such as age or co-morbid illnesses that affect calcium serum levels).Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Al Abed, Amr, Tianruo Guo, Nigel H. Lovell, and Socrates Dokos. "Optimisation of Ionic Models to Fit Tissue Action Potentials: Application to 3D Atrial Modelling." Computational and Mathematical Methods in Medicine 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/951234.

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A 3D model of atrial electrical activity has been developed with spatially heterogeneous electrophysiological properties. The atrial geometry, reconstructed from the male Visible Human dataset, included gross anatomical features such as the central and peripheral sinoatrial node (SAN), intra-atrial connections, pulmonary veins, inferior and superior vena cava, and the coronary sinus. Membrane potentials of myocytes from spontaneously active or electrically pacedin vitrorabbit cardiac tissue preparations were recorded using intracellular glass microelectrodes. Action potentials of central and peripheral SAN, right and left atrial, and pulmonary vein myocytes were each fitted using a generic ionic model having three phenomenological ionic current components: one time-dependent inward, one time-dependent outward, and one leakage current. To bridge the gap between the single-cell ionic models and the gross electrical behaviour of the 3D whole-atrial model, a simplified 2D tissue disc with heterogeneous regions was optimised to arrive at parameters for each cell type under electrotonic load. Parameters were then incorporated into the 3D atrial model, which as a result exhibited a spontaneously active SAN able to rhythmically excite the atria. The tissue-based optimisation of ionic models and the modelling process outlined are generic and applicable to image-based computer reconstruction and simulation of excitable tissue.

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Chaudhary, Rahul, Jalaj Garg, Parasuram Krishnamoorthy, Neeraj Shah, Gregg Lanier, Mathew W. Martinez, and Ronald Freudenberger. "Ivabradine." Journal of Cardiovascular Pharmacology and Therapeutics 21, no. 4 (December 31, 2015): 335–43. http://dx.doi.org/10.1177/1074248415624157.

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Heart failure affects over 5 million people in the United States and carries a high rate of mortality. Ivabradine, a new agent has been added to the current medical options for managing heart failure. It is a selective funny current ( If) inhibitor in sinoatrial node and slows its firing rate, prolonging diastolic depolarization without a negative inotropic effect. Ivabradine was only recently approved by Food and Drug administration after the results of Systolic Heart Failure Treatment with the If Inhibitor Ivabradine (SHIFT) trial, for a reduction in rehospitalizations from chronic heart failure. This trial assessed patients with stable heart failure with reduced ejection fraction and a heart rate of at least 70 beats per minute at rest on maximally tolerated beta-blocker therapy and demonstrated statistically significant reduction in heart failure hospitalization and deaths. Additionally, ivabradine has been associated with reduced cardiac remodeling, reduced heart rate variability, improvement in exercise tolerance, improved heart failure class of New York Heart Association, and better quality of life. It has also been tried in other conditions, such as inappropriate sinus tachycardia and cardiogenic shock, and is currently in phase II trial for patients with newly diagnosed multiple organ dysfunction syndrome.

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Polishchuk, O., T. Amelina, and N. Zhyriada. "Psychological charactheristics of personality and internal pattern of the disease in patients with different types of heart rhythm disorders." Bukovinian Medical Herald 25, no. 2(98) (August 26, 2021): 96–102. http://dx.doi.org/10.24061/2413-0737.xxv.2.98.2021.15.

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Abstacts. We investigated psychological characteristics: anxiety, depression rate, hostility and aggression, subjective control level, dispositional optimism, and types of attitude to the disease in patients with different types of heart rhythm disorders.Objective. To determine psychological characteristics of personality, characteristics of the internal pattern of the disease, and quality of life in patients with different types of heart rhythm disorders.Results. 352 patients were examined. They were divided into 4 groups depending on the type of heart rate disorders: extrasystole (frequent – over 30 per 1 hour), atrial fibrillation, paroxysmal tachycardia, and deterioration of impulse conductivity, accompanied by bradycardia (sinoatrial block and sinus node dysfunction syndrome). All patients underwent a comprehensive psychodiagnostic study using the Toronto Alexithymia Scale, the Spielberger-Khanin Personal and Reactive Anxiety Scale, the Hospital Anxiety and Depression Scale (HADS), the Depression, Anxiety and Stress Questionnaire (DASS-21), the Bass-Darky test for aggressiveness and hostility diagnostics, study of the type of attitude to the disease (LOBI), the Rotter's Locus of Control Scale and the Dispositional Optimism Scale. It was found that with the same level of personality anxiety, patients with atrial fibrillation and life-threatening heart block demonstrated high levels of situational anxiety and depression. The index of aggression was the highest in patients with bradyarrhythmias and paroxysmal tachycardias. Harmonious, anxious and sensitive types of attitude to the disease are more common within all studied groups of patients with cardiac arrhythmias. Low levels of internality in health are observed in patients with extrasystole, especially in patients with atrial fibrillation. The Dispositional Optimism Test demonstrated a medium level of optimism among patients with extrasystole and paroxysmal tachycardia and a low level in patients with atrial fibrillation and cardiac conduction disorders.Conclusion. As a result of a comprehensive psychodiagnostic study, the psychological characteristics of the individual and the type of attitude to the disease in patients with various types of cardiac arrhythmias were determined. Mentioned disparities form the relevant internal pattern of the disease, which should be taken into account when planning treatment and rehabilitation measures.

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Gowran, A., T. Kulikova, FC Lewis, G. Foldes, L. Fuentes, LE Viiri, V. Spinelli, et al. "Poster session 3Cell growth, differentiation and stem cells - Heart511The role of the endocannabinoid system in modelling muscular dystrophy cardiac disease with induced pluripotent stem cells.512An emerging role of T lymphocytes in cardiac regenerative processes in heart failure due to dilated cardiomyopathy513Canonical wnt signaling reverses the ‘aged/senescent’ human endogenous cardiac stem cell phenotype514Hippo signalling modulates survival of human induced pluripotent stem cell-derived cardiomyocytes515Biocompatibility of mesenchymal stem cells with a spider silk matrix and its potential use as scaffold for cardiac tissue regeneration516A snapshot of genome-wide transcription in human induced pluripotent stem cell-derived hepatocyte-like cells (iPSC-HLCs)517Can NOS/sGC/cGK1 pathway trigger the differentiation and maturation of mouse embryonic stem cells (ESCs)?518Introduction of external Ik1 to human-induced pluripotent stem cell-derived cardiomyocytes via Ik1-expressing HEK293519Cell therapy of the heart studied using adult myocardial slices in vitro520Enhancement of the paracrine potential of human adipose derived stem cells when cultured as spheroid bodies521Mechanosensitivity of cardiomyocyte progenitor cells: the strain response in 2D and 3D environments522The effect of the vascular-like network on the maturation of the human induced pluripotent stem cell derived cardiomyocytes.Transcriptional control and RNA species - Heart525Gene expression regulation in heart failure: from pathobiology to bioinformatics526Human transcriptome in idiopathic dilated cardiomyopathy - a novel high throughput screening527A high-throghput approach unveils putative miRNA-mediated mitochondria-targeted cardioprotective circuits activated by T3 in the post ischemia reperfusion setting528The effect of uraemia on the expression of miR-212/132 and the calcineurin pathway in the rat heartCytokines and cellular inflammation - Heart531Lack of growth differentiation factor 15 aggravates adverse cardiac remodeling upon pressure-overload in mice532Blocking heteromerization of platelet chemokines ccl5 and cxcl4 reduces inflammation and preserves heart function after myocardial infarction533Is there an association between low-dose aspirin use and clinical outcome in HFPEF? Implications of modulating monocyte function and inflammatory mediator release534N-terminal truncated intracellular matrix metalloproteinase-2 expression in diabetic heart.535Expression of CD39 and CD73 on peripheral T-cell subsets in calcific aortic stenosis536Mast cells in the atrial myocardium of patients with atrial fibrillation: a comparison with patients in sinus rhythm539Characteristics of the inflammatory response in patients with coronary artery disease and arterial hypertension540Pro-inflammatory cytokines as cardiovascular events predictors in rheumatoid arthritis and asymptomatic atherosclerosis541Characterization of FVB/N murinic bone marrow-derived macrophage polarization into M1 and M2 phenotypes542The biological expression and thoracic anterior pain syndromeSignal transduction - Heart545The association of heat shock protein 90 and TGFbeta receptor I is involved in collagen production during cardiac remodelling in aortic-banded mice546Loss of the inhibitory GalphaO protein in the rostral ventrolateral medulla of the brainstem leads to abnormalities in cardiovascular reflexes and altered ventricular excitablitiy547Selenoprotein P regulates pressure overload-induced cardiac remodeling548Study of adenylyl cyclase activity in erythrocyte membranes in patients with chronic heart failure549Direct thrombin inhibitors inhibit atrial myocardium hypertrophy in a rat model of heart failure and atrial remodeling550Tissue factor / FVIIa transactivates the IGF-1R by a Src-dependent phosphorylation of caveolin-1551Notch signaling is differently altered in endothelial and smooth muscle cells of ascending aortic aneurysm patients552Frizzled 5 expression is essential for endothelial proliferation and migration553Modulation of vascular function and ROS production by novel synthetic benzopyran analogues in diabetes mellitusExtracellular matrix and fibrosis - Heart556Cardiac fibroblasts as inflammatory supporter cells trigger cardiac inflammation in heart failure557A role for galectin-3 in calcific aortic valve stenosis558Omega-3 polyunsaturated fatty acids- can they decrease risk for ventricular fibrillation?559Serum levels of elastin derived peptides and circulating elastin-antielastin immune complexes in sera of patients with coronary artery disease560Endocardial fibroelastosis is secondary to hemodynamic alterations in the chick model of hypoplastic left heart syndrome561Dynamics of serum levels of matrix metalloproteinases in primary anterior STEMI patients564Deletion of the alpha-7 nicotinic acetylcholine receptor changes the vascular remodeling induced by transverse aortic constriction in mice.565Extracellular matrix remodelling in response to venous hypertension: proteomics of human varicose veinsIon channels, ion exchangers and cellular electrophysiology - Heart568Microtubule-associated protein RP/EB family member 1 modulates sodium channel trafficking and cardiac conduction569Investigation of electrophysiological abnormalities in a rabbit athlete's heart model570Upregulation of expression of multiple genes in the atrioventricular node of streptozotocin-induced diabetic rat571miR-1 as a regulator of sinoatrial rhythm in endurance training adaptation572Selective sodium-calcium exchanger inhibition reduces myocardial dysfunction associated with hypokalaemia and ventricular fibrillation573Effect of racemic and levo-methadone on action potential of human ventricular cardiomyocytes574Acute temperature effects on the chick embryonic heart functionVasculogenesis, angiogenesis and arteriogenesis577Clinical improvement and enhanced collateral vessel growth after monocyte transplantation in mice578The role of HIF-1 alpha, VEGF and obstructive sleep apnoea in the development of coronary collateral circulation579Initiating cardiac repair with a trans-coronary sinus catheter intervention in an ischemia/reperfusion porcine animal model580Early adaptation of pre-existing collaterals after acute arteriolar and venular microocclusion: an in vivo study in chick chorioallantoic membraneEndothelium583EDH-type responses to the activator of potassium KCa2.3 and KCa3.1 channels SKA-31 in the small mesenteric artery from spontaneously hypertensive rats584The peculiarities of endothelial dysfunction in patients with chronic renocardial syndrome585Endothelial dysfunction, atherosclerosis of the carotid arteries and level of leptin in patient with coronary heart disease in combination with hepatic steatosis depend from body mass index.586Role of non-coding RNAs in thoracic aortic aneurysm associated with bicuspid aortic valve587Cigarette smoke extract abrogates atheroprotective effects of high laminar flow on endothelial function588The prognostic value of anti-connective tissue antibodies in coronary heart disease and asymptomatic atherosclerosis589Novel potential properties of bioactive peptides from spanish dry-cured ham on the endothelium.Lipids592Intermediate density lipoprotein is associated with monocyte subset distribution in patients with stable atherosclerosis593The characteristics of dyslipidemia in rheumatoid arthritisAtherosclerosis596Macrophages differentiated in vitro are heterogeneous: morphological and functional profile in patients with coronary artery disease597Palmitoylethanolamide promotes anti-inflammatory phenotype of macrophages and attenuates plaque formation in ApoE-/- mice598Amiodarone versus esmolol in the perioperative period: an in vitro study of coronary artery bypass grafts599BMPRII signaling of fibrocytes, a mesenchymal progenitor cell population, is increased in STEMI and dyslipidemia600The characteristics of atherogenesis and systemic inflammation in rheumatoid arthritis601Role of adenosine-to-inosine RNA editing in human atherosclerosis602Presence of bacterial DNA in thrombus aspirates of patients with myocardial infarction603Novel E-selectin binding polymers reduce atherosclerotic lesions in ApoE(-/-) mice604Differential expression of the plasminogen receptor Plg-RKT in monocyte and macrophage subsets - possible functional consequences in atherogenesis605Apelin-13 treatment enhances the stability of atherosclerotic plaques606Mast cells are increased in the media of coronary lesions in patients with myocardial infarction and favor atherosclerotic plaque instability607Association of neutrophil to lymphocyte ratio with presence of isolated coronary artery ectasiaCalcium fluxes and excitation-contraction coupling610The coxsackie- and adenovirus receptor (CAR) regulates calcium homeostasis in the developing heart611HMW-AGEs application acutely reduces ICaL in adult cardiomyocytes612Measuring electrical conductibility of cardiac T-tubular systems613Postnatal development of cardiac excitation-contraction coupling in rats614Role of altered Ca2+ homeostasis during adverse cardiac remodeling after ischemia/reperfusion615Experimental study of sarcoplasmic reticulum dysfunction and energetic metabolism in failing myocardium associated with diabetes mellitusHibernation, stunning and preconditioning618Volatile anesthetic preconditioning attenuates ischemic-reperfusion injury in type II diabetic patients undergoing on-pump heart surgery619The effect of early and delayed phase of remote ischemic preconditioning on ischemia-reperfusion injury in the isolated hearts of healthy and diabetic rats620Post-conditioning with 1668-thioate leads to attenuation of the inflammatory response and remodeling with less fibrosis and better left ventricular function in a murine model of myocardial infarction621Maturation-related changes in response to ischemia-reperfusion injury and in effects of classical ischemic preconditioning and remote preconditioningMitochondria and energetics624Phase changes in myocardial mitochondrial respiration caused by hypoxic preconditioning or periodic hypoxic training625Desmin mutations depress mitochondrial metabolism626Methylene blue modulates mitochondrial function and monoamine oxidases-related ROS production in diabetic rat hearts627Doxorubicin modulates the real-time oxygen consumption rate of freshly isolated adult rat and human ventricular cardiomyocytesCardiomyopathies and fibrosis630Effects of genetic or pharmacologic inhibition of the ubiquitin/proteasome system on myocardial proteostasis and cardiac function631Suppression of Wnt signalling in a desmoglein-2 transgenic mouse model for arrhythmogenic cardiomyopathy632Cold-induced cardiac hypertrophy is reversed after thermo-neutral deacclimatization633CD45 is a sensitive marker to diagnose lymphocytic myocarditis in endomyocardial biopsies of living patients and in autopsies634Atrial epicardial adipose tissue derives from epicardial progenitors635Caloric restriction ameliorates cardiac function, sympathetic cardiac innervation and beta-adrenergic receptor signaling in an experimental model of post-ischemic heart failure636High fat diet improves cardiac remodelling and function after extensive myocardial infarction in mice637Epigenetic therapy reduces cardiac hypertrophy in murine models of heart failure638Imbalance of the VHL/HIF signaling in WT1+ Epicardial Progenitors results in coronary vascular defects, fibrosis and cardiac hypertrophy639Diastolic dysfunction is the first stage of the developing heart failure640Colchicine aggravates coxsackievirus B3 infection in miceArterial and pulmonary hypertension642Osteopontin as a marker of pulmonary hypertension in patients with coronary heart disease combined with chronic obstructive pulmonary disease643Myocardial dynamic stiffness is increased in experimental pulmonary hypertension partly due to incomplete relaxation644Hypotensive effect of quercetin is possibly mediated by down-regulation of immunotroteasome subunits in aorta of spontaneously hypertensive rats645Urocortin-2 improves right ventricular function and attenuates experimental pulmonary arterial hypertension646A preclinical evaluation of the anti-hypertensive properties of an aqueous extract of Agathosma (Buchu)Biomarkers648The adiponectin level in hypertensive females with rheumatoid arthritis and its relationship with subclinical atherosclerosis649Markers for identification of renal dysfunction in the patients with chronic heart failure650cardio-hepatic syndromes in chronic heart failure: North Africa profile651To study other biomarkers that assess during myocardial infarction652Interconnections of apelin levels with parameters of lipid metabolism in hypertension patients653Plasma proteomics in hypertension: prediction and follow-up of albuminuria during chronic renin-angiotensin system suppression654Soluble RAGE levels in plasma of patients with cerebrovascular events." Cardiovascular Research 111, suppl 1 (July 1, 2016): S92—S116. http://dx.doi.org/10.1093/cvr/cvw150.

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16

Wallace, Michael J., Mona El Refaey, Pietro Mesirca, Thomas J. Hund, Matteo E. Mangoni, and Peter J. Mohler. "Genetic Complexity of Sinoatrial Node Dysfunction." Frontiers in Genetics 12 (April 1, 2021). http://dx.doi.org/10.3389/fgene.2021.654925.

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The pacemaker cells of the cardiac sinoatrial node (SAN) are essential for normal cardiac automaticity. Dysfunction in cardiac pacemaking results in human sinoatrial node dysfunction (SND). SND more generally occurs in the elderly population and is associated with impaired pacemaker function causing abnormal heart rhythm. Individuals with SND have a variety of symptoms including sinus bradycardia, sinus arrest, SAN block, bradycardia/tachycardia syndrome, and syncope. Importantly, individuals with SND report chronotropic incompetence in response to stress and/or exercise. SND may be genetic or secondary to systemic or cardiovascular conditions. Current management of patients with SND is limited to the relief of arrhythmia symptoms and pacemaker implantation if indicated. Lack of effective therapeutic measures that target the underlying causes of SND renders management of these patients challenging due to its progressive nature and has highlighted a critical need to improve our understanding of its underlying mechanistic basis of SND. This review focuses on current information on the genetics underlying SND, followed by future implications of this knowledge in the management of individuals with SND.

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Li, Haojie, Jianyu Qu, Yitong Yu, Heng Zhang, Chenfei Rao, Sheng Liu, Lihui Zheng, Bin Lu, and Zhe Zheng. "Sinoatrial nodal artery injury in thoracoscopic epicardial ablation for atrial fibrillation." European Journal of Cardio-Thoracic Surgery, October 28, 2020. http://dx.doi.org/10.1093/ejcts/ezaa317.

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Abstract OBJECTIVES This study aimed to clarify the incidence of sinoatrial nodal artery (SANa) injury in thoracoscopic epicardial surgical ablation for atrial fibrillation (AF) and its impact on postoperative outcomes, which have not been previously elucidated. METHODS We enrolled 103 consecutively patients with AF who underwent thoracoscopic epicardial ablation at our institution. In these patients, we evaluated the postoperative incidence of SANa injury by using enhanced cardiac computed tomography. For patients with confirmed SANa injury, 3-day continuous electrocardiographic monitoring and exercise stress tests were performed to assess the sinus rhythm maintenance and sinus node function. RESULTS Thirteen patients (12.6%) had a confirmed SANa injury (left anterior type in 6 patients, left posterior type in 2 patients and double-branch type in 5 patients). After a median follow-up of 24 months, the patients with SANa injury were not found to be associated with lower sinus rhythm maintenance (hazard ratio 1.09, 95% confidential interval 0.36–3.31) as compared with those without SANa injury after adjustment for patient characteristics. Sinus node function was evaluated in 7 patients with SANa injury who remained in sinus rhythm after the procedure, and no sinus node dysfunction was confirmed in the 3-day electrocardiographic monitoring and exercise stress tests at a median follow-up of 12 months. CONCLUSIONS The prevalence of SANa injury in the patients who underwent thoracoscopic epicardial ablation for AF was relatively low, and the incidence of SANa injury was not associated with postoperative restoration of sinus rhythm and sinoatrial node dysfunction. More studies are required to better understand SANa injury.

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Patel, Nilesh, Faisal Majeed, and Anupam Ashutosh Sule. "Seizure Triggered by Sick Sinus Syndrome." BMJ Case Reports, November 4, 2017, bcr—2017–222011. http://dx.doi.org/10.1136/bcr-2017-222011.

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Sick sinus syndrome (SSS) is a dysfunction of sinoatrial node resulting in symptomatic bradycardia or sinus pauses causing decreased cardiac output with cerebral hypoperfusion and usually presents as syncope, presyncope or fatigue. The occurrence of a seizure is very rare. A 69-year-old man suffered two episodes of generalised tonic–clonic seizures. MRI and electroencephalogram failed to reveal the cause of seizures. In the emergency room, he experienced presyncope simultaneous to bradycardia and sinus pauses. He was stabilised with atropine and dopamine infusion and underwent definitive therapy with a permanent dual-chamber pacemaker with complete symptom resolution. Diagnostic confounders include convulsive syncope and ictal bradycardia. Syncope may be accompanied by myoclonic jerks (convulsive syncope), but postictal confusion is absent. Bradycardia may be seen during the postictal period (ictal bradycardia syndrome), but protracted sinus dysfunction is not present. Hypoperfusion due to significant SSS triggered seizures in this patient who may have an underlying predisposition.

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Alugubelli, N., A. Kanwal, R. Allamneni, D. J. Schamp, G. R. Meininger, and A. Saini. "P696Incidence of sinus node dysfunction with cancer chemotherapy: a systematic review of literature." European Heart Journal 40, Supplement_1 (October 1, 2019). http://dx.doi.org/10.1093/eurheartj/ehz747.0301.

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Abstract Background Introduction of newer classes of chemotherapeutic agents has led to improved survival in many cancers, often at the cost of increased side effects. With the advent of cardio-oncology, there has been growing focus on cardiac side effects of chemotherapy like cardiomyopathy, QT prolongation, VT and AF. However, data on cancer chemotherapy related sinus node dysfunction (SND) is limited. Objective To assess the incidence of chemotherapy related SND through a systematic review of available literature. Methods We performed a systematic review of PUBMED database for studies reporting SND (including sinus bradycardia, sinus pauses, sinoatrial exit blocks or asystole) with use of chemotherapeutic agents. Weighted average incidence of SND was calculated from studies. Case reports were reported independently. Results 2012 articles were reviewed of which 38 were eligible for data extraction. Incidence of SND varied significantly between drug classes. However, specific drugs were associated with increased incidence of SND like anthracyclines (Epirubicin 8.3%), antimetabolites (5 Fluorouracil 20%), tyrosine kinase inhibitors (crizotinib 43%), antimicrotubule agents (paclitaxel 29%) and angiogenesis inhibitors (Thalidomide 22%). The weighted average incidence is shown in table. Drug type Drug Type of cancers No. of studies Total No. Weighted average of incidence of sinus arrhythmias No. of case reports Anthracyclines Epirubicin Breast, Hodgkin's disease 1 24 8.3% 1 Idarubicin CML – – – 1 Unclassified anthracyclines Ewing sarcoma 2 370 4.31% – Antimetabolites 5 Fluorouracil Esophageal, gastric, colon, rectal 1 5 20% 1 Capecitabine Rectal cancer – – – 1 Methotrexate Osteosarcoma – – – 1 Cytarabine AML – – – 1 Antimicrotubule agent Paclitaxel Ovarian cancer 2 4505 29.36% – Kinase inhibitors Crizotinib Lung 2 1095 43% 4 Alectinib Lung 1 225 5% – Ibrutinib Mantle cell lymphoma – – – 1 Monoclonal antibodies Infliximab Ulcerative colitis – – – 1 Angiogenesis inhibitors Thalidomide Multiple myeloma 4 83 21.62% 2 Endostar Metastatic colorectal and gastric 1 23 13% – Selective estrogen modulators Tamoxifene Extracranial meningioma – – – 1 Antiandrogen Abiraterone Prostate cancer 1 17 6% – Other drugs Crisnatol mesylate Advanced solid tumors 1 43 2.3% – Mitoxantrone AML – – – 1 Combination drugs Bevacizumab +Vorinostat Malignant Glioma 1 40 3% – All-trans-retinoic acid+idarubicin AML – – – 2 Tivantinib+Erlotinib Advanced solid malignancies 1 32 23.1% – Paclitaxel+Carboplatin+Bevacizumab Lung – – – 1 Paclitaxel+Carboplatin Ovarian 1 79 2.9% – Daunorubicin+Amsacrine AML – – – 1 CHOP Diffuse large B cell lymphoma – – – 1 Conclusion There is cumulative evidence of increased incidence of SND with certain chemotherapeutics. In pre-existing SND, certain drugs and combinations must be avoided and alternative agents, should be considered. Future studies are needed to evaluate the role of remote cardiac monitoring and permanent pacing in specific situations where no safer alternatives exist.

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Journal articles on the topic 'Cardiac Modelling ; Sinoatrial Node ; Sinus Node Dysfunction'

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