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Jonathan M. Kalman - One of the best experts on this subject based on the ideXlab platform.
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Sinus Node Dysfunction
Cardiac Pacing for the Clinician, 2008Co-Authors: Irene H. Stevenson, Paul B. Sparks, Jonathan M. KalmanAbstract:primary indication for pacemaker implantation in industrialized countries. The only effective treatment for symptomatic Sinus Node dysfunction is cardiac pacing. However, despite the widespread use of pacing therapy for this group of patients, the optimal pacing mode, pacing system and site of ventricular stimulation for Sinus Node dysfunction remains controversial. The available data for the diagnosis and treatment of Sinus Node dysfunction are reviewed in this chapter.
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Sinus Node Disease: An Idiopathic Right Atrial Myopathy
Trends in cardiovascular medicine, 2007Co-Authors: Kurt C. Roberts-thomson, Prashanthan Sanders, Jonathan M. KalmanAbstract:Sinus Node disease was previously thought to be a disease limited to the Sinus Node and its atrial connections. However, recent reports have demonstrated Sinus Node disease as a disease of the entire right atrial myocardium. These patients have widespread electrophysiological abnormalities of their atria, including prolonged refractory periods and slowed conduction. In addition to these electrical changes, there are significant structural changes, such as fibrosis and fatty infiltration, which can be detected endocardially as regions of fractionated signals, low-voltage electrograms, and electrically silent areas. In most cases, the etiology of these changes is unknown. These changes may contribute to the high prevalence of atrial fibrillation seen in patients with Sinus Node disease.
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Remodeling of Sinus Node Function in Patients With Congestive Heart Failure Reduction in Sinus Node Reserve
Circulation, 2004Co-Authors: Prashanthan Sanders, Peter M. Kistler, Joseph B. Morton, Steven J. Spence, Jonathan M. KalmanAbstract:Background— Experimental and clinical studies have demonstrated diffuse atrial remodeling in congestive heart failure (CHF). We hypothesized that patients with CHF would demonstrate derangement of Sinus Node function. Methods and Results— Eighteen patients with symptomatic CHF (left ventricular ejection fraction, 26±5%) and 18 age-matched control subjects were studied. Under autonomic blockade, the following were evaluated: intrinsic Sinus cycle length, corrected Sinus Node recovery time (CSNRT), sinoatrial conduction time, number and duration of fractionated electograms or double potentials along the crista terminalis, and location of the earliest Sinus activity. Electroanatomic mapping was performed to evaluate the location and nature of the Sinus Node complex, to characterize sinoatrial propagation, and to evaluate conduction abnormalities and voltage amplitude along the crista terminalis. Patients with CHF demonstrated the following findings compared with age-matched control subjects: prolongation of ...
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A mathematical model of Sinus Node function: validation by recording of Sinus Node electrograms
American Journal of Physiology-Heart and Circulatory Physiology, 1994Co-Authors: Jonathan M. Kalman, M Munawar, J M Chen, J M Power, A M TonkinAbstract:We have applied a mathematical function to model Sinus Node recovery after atrial pacing at different cycle lengths in 13 autonomically denervated, anesthetized canines. This model provides “pure” ...
Ralph Lazzara - One of the best experts on this subject based on the ideXlab platform.
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Current concepts of anatomy and electrophysiology of the Sinus Node
Journal of Interventional Cardiac Electrophysiology, 2016Co-Authors: Cliona Murphy, Ralph LazzaraAbstract:The sinoatrial Node, or Sinus Node, of humans is the principal pacemaker of the heart. Over the last century, studies have unraveled the complex molecular architecture of the Sinus Node and the expression of unique ion channels within its specialized myocytes. Aim of this review is to describe the embriology, the anatomy, the histology and the electrophisiology of the Sinus Node.
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Sinus Node dysfunction in a heart transplant patient secondary to severe Sinus Node artery obstruction--a case report.
Angiology, 2003Co-Authors: Can Hasdemir, Krishnaswamy Chandrasekaran, Ralph Lazzara, Dwight ReynoldsAbstract:A case of Sinus Node dysfunction is reported secondary to severe Sinus Node artery obstruction 3 years after orthotopic heart transplantation. The patient first presented with frequent dizzy spells and presyncopal episodes for 3 months and then recurrent syncope in the presence of an acute myocardial infarction. Coronary angiography showed a diffusely narrowed Sinus Node artery without any apparent collateral vessels. The Sinus Node artery had had only minimal distal disease 3 months previously. A dual chamber permanent pacemaker was implanted with significant improvement in clinical symptoms.
Prashanthan Sanders - One of the best experts on this subject based on the ideXlab platform.
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Sinus Node revisited.
Current opinion in cardiology, 2011Co-Authors: Dennis H. Lau, Kurt C. Roberts-thomson, Prashanthan SandersAbstract:Purpose of review Sinus Node disease (SND) is a common clinical condition and is the most common indication for permanent pacemaker implantation. This review aims to revisit the complex Sinus Node anatomy, the evolving understanding of its pacemaking mechanisms, the atrial myopathy in SND and Sinus Node remodeling. Recent findings Recent high-density noncontact mapping of the human Sinus Node showed multiple origins of Sinus activation and exit sites with preferential pathways of conduction. Perhaps, a newly described discrete paranodal area containing a molecular mixture of nodal and atrial cells may account for this long recognized discrepancy between the anatomical and functional Sinus Node. The funny current (I(f)) driven 'membrane clock' is not solely responsible for Sinus Node automaticity, following recent recognition of the importance of the 'calcium clock'. Several molecular links to Sinus Node remodeling have recently been identified: loss of connexin-43 expression and down-regulation of I(ca,L) in aging; reduced I(f) and down-regulation of I(f) encoding HCN4 and HCN2 subunits in heart failure; and calcium clock malfunction with down-regulated HCN4, HCN2 and minK in atrial fibrillation. Summary Ongoing research with improved technology and techniques continues to unravel new understandings and challenges to the century old discovery of the anatomical Sinus Node.
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Sinus Node Disease: An Idiopathic Right Atrial Myopathy
Trends in cardiovascular medicine, 2007Co-Authors: Kurt C. Roberts-thomson, Prashanthan Sanders, Jonathan M. KalmanAbstract:Sinus Node disease was previously thought to be a disease limited to the Sinus Node and its atrial connections. However, recent reports have demonstrated Sinus Node disease as a disease of the entire right atrial myocardium. These patients have widespread electrophysiological abnormalities of their atria, including prolonged refractory periods and slowed conduction. In addition to these electrical changes, there are significant structural changes, such as fibrosis and fatty infiltration, which can be detected endocardially as regions of fractionated signals, low-voltage electrograms, and electrically silent areas. In most cases, the etiology of these changes is unknown. These changes may contribute to the high prevalence of atrial fibrillation seen in patients with Sinus Node disease.
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Remodeling of Sinus Node Function in Patients With Congestive Heart Failure Reduction in Sinus Node Reserve
Circulation, 2004Co-Authors: Prashanthan Sanders, Peter M. Kistler, Joseph B. Morton, Steven J. Spence, Jonathan M. KalmanAbstract:Background— Experimental and clinical studies have demonstrated diffuse atrial remodeling in congestive heart failure (CHF). We hypothesized that patients with CHF would demonstrate derangement of Sinus Node function. Methods and Results— Eighteen patients with symptomatic CHF (left ventricular ejection fraction, 26±5%) and 18 age-matched control subjects were studied. Under autonomic blockade, the following were evaluated: intrinsic Sinus cycle length, corrected Sinus Node recovery time (CSNRT), sinoatrial conduction time, number and duration of fractionated electograms or double potentials along the crista terminalis, and location of the earliest Sinus activity. Electroanatomic mapping was performed to evaluate the location and nature of the Sinus Node complex, to characterize sinoatrial propagation, and to evaluate conduction abnormalities and voltage amplitude along the crista terminalis. Patients with CHF demonstrated the following findings compared with age-matched control subjects: prolongation of ...
Shih-ann Chen - One of the best experts on this subject based on the ideXlab platform.
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Sinus Node injury as a complication of superior vena cava isolation.
Journal of cardiovascular electrophysiology, 2005Co-Authors: Mary Gertrude Ong, Ching-tai Tai, Yenn-jiang Lin, Kun-tai Lee, Shih-lin Chang, Shih-ann ChenAbstract:We report a case with SVC ectopy initiating AF; the origin and breakout point of the Sinus Node was inside the SVC, and the SVC ectopy was conducted through the same path as the Sinus Node activation to depolarize the right atrium. Injury to the Sinus Node happened after successful isolation of SVC.
Richard B. Schuessler - One of the best experts on this subject based on the ideXlab platform.
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Abnormal Sinus Node function in clinical arrhythmias.
Journal of cardiovascular electrophysiology, 2003Co-Authors: Richard B. SchuesslerAbstract:Abnormal Sinus Node Function. To understand abnormal Sinus Node function in clinical atrial arrhythmias, it is essential to understand the normal function of the Sinus Node. Much of our understanding of the Sinus Node comes from work done in rabbits. In small animals, the Node is a thin structure and can be modeled in two dimensions. However, in canines and humans, the Node is a more complex structure completely surrounded by myocytes. Recent data suggest that the Node may be insulated from the surrounding atrial myocytes, except at a limited number of exit sites. A model of the Node with discrete exit sites explains how atrial activation can be initiated from multiple sites simultaneously. Within the Node there may exist specialized pathways that explain the complex conduction within the Node. Multiple cell types, with different intrinsic rates, combined with the nonuniform distribution of autonomic receptors, provide a basis for understanding the dynamics of heart rate control and the initiation of atrial activation. In addition, this model of the Sinus Node provides a framework to propose novel mechanisms underlying various atrial arrhythmias, such as atrial premature depolarizations or Sinus Node reentry. (J Cardiovasc Electrophysiol, Vol. 14, pp. 215-217, February 2003)
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Differential Expression of Gap Junction Proteins in the Canine Sinus Node
Circulation research, 1998Co-Authors: F. Kwong, Richard B. Schuessler, Karen G. Green, James G. Laing, Eric C. Beyer, John P. Boineau, Jeffrey E. SaffitzAbstract:Abstract —Electrical coupling of pacemaker cells at gap junctions appears to play an important role in Sinus Node function. Although the major cardiac gap junction protein, connexin43 (Cx43), is expressed abundantly in atrial and ventricular muscle, its expression in the Sinus Node has been a subject of controversy. The objectives of the present study were to determine whether Cx43 is expressed by Sinus Node myocytes, to characterize the spectrum of connexin expression phenotypes in Sinus Node pacemaker cells, and to define the spatial distribution of different connexin phenotypes in the intact Sinus Node. To fulfill these objectives, we performed high-resolution immunohistochemical analysis of disaggregated adult canine Sinus Node preparations. Using enhanced tissue preservation and antigen retrieval techniques, we also performed immunohistochemical studies on sections of intact canine Sinus Node tissue. Analysis of disaggregated Sinus Node preparations revealed three populations of pacemaker cells distinguished on the basis of connexin immunohistochemical phenotype: ≈55% of cells expressed only connexin40 (Cx40); 30% to 35% of cells expressed Cx43, connexin45 (Cx45), and Cx40; and the remaining cells had no detectable connexin expression. In immunostained sections of intact Sinus Node, Cx43- and Cx45-positive cells were limited in their distribution and were observed in discrete bundles that appeared to abut atrial myocytes. In contrast, Cx40 immunoreactive signal was widely distributed in the Sinus Node region. These results indicate that subsets of pacemaker cells express distinct connexin phenotypes. Differential expression of connexins could create regions within the Sinus Node with different conduction properties, thereby contributing to the nonuniform conduction properties seen in this tissue.
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Structural determinants of slow conduction in the canine Sinus Node.
Journal of cardiovascular electrophysiology, 1997Co-Authors: Jeffrey E. Saffitz, Karen G. Green, Richard B. SchuesslerAbstract:Structure of Sinus Node Gap Junctions. Introduction: To elucidate the role of tissue structure as a determinant of the unique conduction properties of the Sinus Node. we compared the spatial distribution of intercellular connections at gap junctions in the Sinus Node to the more rapidly conducting crista terminalis and left ventricle, which have been studied previously. Methods and Results: Samples of four canine Sinus Nodes were prepared for electron microscopy. The total number and spatial orientation of neighboring myocytes connected by ultrastructurally identified intercalated disks and gap junctions to nine randomly selected index cells were determined by sequentially examining subserial sections. Sinus Node cells were sparsely interconnected compared to the extent of interconnections observed previously in other tissues. A typical Sinus Node cell was connected to only 4.8 ± 0.7 neighbors compared with 11.3 ± 2.2 cells in the left ventricle and 6.4 ± 1.7 cells in the crista terminalis. Sinus Node interconnections occurred at small intercalated disks that usually connected cells in partial side-to-side and end-to-end juxtaposition. In contrast, left ventricular myocytes are interconnected at large intercalated disks that adjoin many cells in pure side-to-side and end-to-end orientations. Crista terminalis myocytes are connected primarily in end-to-end fashion. The aggregate gap junction profile length per unit myocyte area was 26.5 times greater in the left ventricle and 5.0 times greater in the crista terminalis than in the Sinus Node. Conclusion: Sinus Node myocytes exhibit small, sparsely distributed gap junctions that interconnect cells in complex patterns of lateral and terminal apposition. These structural features are consistent with the unique conduction properties of the Sinus Node.