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  1. Article ; Online: Mounting evidence that fibrosis generates a major mechanism for atrial fibrillation.

    Spach, Madison S

    Circulation research

    2007  Volume 101, Issue 8, Page(s) 743–745

    MeSH term(s) Aging/pathology ; Aging/physiology ; Animals ; Atrial Fibrillation/etiology ; Atrial Fibrillation/pathology ; Atrial Fibrillation/physiopathology ; Atrial Function, Left/physiology ; Fibrosis ; Heart Failure/complications ; Heart Failure/pathology ; Humans
    Language English
    Publishing date 2007-10-12
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.107.163956
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Transition from a continuous to discontinuous understanding of cardiac conduction.

    Spach, Madison S

    Circulation research

    2003  Volume 92, Issue 2, Page(s) 125–126

    MeSH term(s) Animals ; Anisotropy ; Electrophysiology/history ; Gap Junctions/physiology ; Heart Conduction System/physiology ; History, 20th Century ; Humans ; Membrane Potentials/physiology ; Models, Cardiovascular ; Signal Processing, Computer-Assisted ; Ventricular Function
    Language English
    Publishing date 2003-02-07
    Publishing country United States
    Document type Editorial ; Historical Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/01.res.0000056973.54305.67
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Mechanism of origin of conduction disturbances in aging human atrial bundles: experimental and model study.

    Spach, Madison S / Heidlage, J Francis / Dolber, Paul C / Barr, Roger C

    Heart rhythm

    2007  Volume 4, Issue 2, Page(s) 175–185

    Abstract: Background: Aging is associated with a significant increase in atrial tachyarrhythmias, especially atrial fibrillation. A macroscopic repolarization gradient created artificially by a stimulus at one site before a premature stimulus from a second site ... ...

    Abstract Background: Aging is associated with a significant increase in atrial tachyarrhythmias, especially atrial fibrillation. A macroscopic repolarization gradient created artificially by a stimulus at one site before a premature stimulus from a second site is widely considered to be part of the experimental protocol necessary for the initiation of such arrhythmias in the laboratory. How such gradients occur naturally in aging atrial tissue is unknown.
    Objective: The objective of this study was to determine if the pattern of cellular connectivity in aging human atrial bundles produces a mechanism for variable early premature responses.
    Methods: Extracellular and intracellular potentials were recorded after control and premature stimuli at a single site in aging human atrial bundles. We also measured cellular geometry, the distribution of connexins, and the distribution of collagenous septa. A model of the atrial bundles was constructed based on the morphological results. Action potential propagation and the sodium current were analyzed after premature stimuli in the model.
    Results: Similar extracellular potential waveform responses occurred after early premature stimuli in the aging bundles and in the model. Variable premature conduction patterns were accounted for by the single model of aging atrial structure. A major feature of the model results was that the conduction events and the magnitude of the sodium current at multiple sites were very sensitive to small changes in the location and the timing of premature stimuli.
    Conclusion: In aging human atrial bundles stimulated from only a single site, premature stimuli induce variable arrhythmogenic conduction responses. The generation of these responses is greatly enhanced by remodeling of cellular connectivity during aging. The results provide insight into sodium current structural interactions as a general mechanism of arrhythmogenic atrial responses to premature stimuli.
    MeSH term(s) Action Potentials ; Aged ; Aging/metabolism ; Aging/physiology ; Anisotropy ; Cardiac Complexes, Premature/metabolism ; Cardiac Complexes, Premature/physiopathology ; Connexins/metabolism ; Female ; Heart Atria/metabolism ; Heart Atria/physiopathology ; Heart Atria/ultrastructure ; Heart Conduction System/metabolism ; Heart Conduction System/physiopathology ; Heart Conduction System/ultrastructure ; Humans ; Ion Channels/physiology ; Male ; Membrane Potentials/physiology ; Middle Aged ; Models, Cardiovascular
    Chemical Substances Connexins ; Ion Channels
    Language English
    Publishing date 2007-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2006.10.023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Cell size and communication: role in structural and electrical development and remodeling of the heart.

    Spach, Madison S / Heidlage, J Francis / Barr, Roger C / Dolber, Paul C

    Heart rhythm

    2004  Volume 1, Issue 4, Page(s) 500–515

    Abstract: With the advent of new information about alterations of cardiac gap junctions in disease conditions associated with arrhythmias, there have been major advances in the genetic and metabolic manipulation of gap junctions. In contrast, in naturally ... ...

    Abstract With the advent of new information about alterations of cardiac gap junctions in disease conditions associated with arrhythmias, there have been major advances in the genetic and metabolic manipulation of gap junctions. In contrast, in naturally occurring cardiac preparations, little is known about cell-to-cell transmission and the subcellular events of propagation or about structural mechanisms that may affect conduction events at this small size scale. Therefore, the aim of this article is to review results that produce the following unifying picture: changes in cardiac conduction due to remodeling cardiac morphology ultimately are limited to changes in three morphologic parameters: (1) cell geometry (size and shape), (2) gap junctions (distribution and conductivity), and (3) interstitial space (size and distribution). In this article, we consider changes in conduction that result from the remodeling of cell size and gap junction distribution that occurs with developmental ventricular hypertrophy from birth to maturity. We then go on to changes in longitudinal and transverse propagation in aging human atrial bundles that are produced by remodeling interstitial space due to deposition of collagenous septa. At present, experimental limitations in naturally occurring preparations prevent measurement of the conductance of individual gap junctional plaques, as well as the delays in conduction associated with cell-to-cell transmission. Therefore, we consider the development of mathematical electrical models based on documented cardiac microstructure to gain insight into the role of specific morphologic parameters in generating the changes in anisotropic propagation that we measured in the tissue preparations. A major antiarrhythmic implication of the results is that an "indirect" therapeutic target is interstitial collagen, because regulation of its deposition and turnover to prevent or alter microfibrosis can enhance side-to-side electrical coupling between small groups of cells in aging atrial bundles.
    MeSH term(s) Action Potentials ; Animals ; Cell Size ; Computer Simulation ; Gap Junctions ; Heart Conduction System/cytology ; Humans ; Membrane Potentials ; Models, Cardiovascular ; Myocardium/cytology ; Myocytes, Cardiac/physiology ; Ventricular Remodeling/physiology
    Language English
    Publishing date 2004-10
    Publishing country United States
    Document type Lectures ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2004.06.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The perplexing complexity of cardiac arrhythmias: beyond electrical remodeling.

    Adamson, Philip B / Barr, Roger C / Callans, David J / Chen, Peng-Sheng / Lathrop, David A / Makielski, Jonathan C / Nerbonne, Jeanne M / Nuss, H Bradley / Olgin, Jeffrey E / Przywara, Dennis A / Rosen, Michael R / Rozanski, George J / Spach, Madison S / Yamada, Kathryn A

    Heart rhythm

    2005  Volume 2, Issue 6, Page(s) 650–659

    Abstract: Cardiac arrhythmias continue to pose a major medical challenge and significant public health burden. Atrial fibrillation, the most prevalent arrhythmia, affects more than two million Americans annually and is associated with a twofold increase in ... ...

    Abstract Cardiac arrhythmias continue to pose a major medical challenge and significant public health burden. Atrial fibrillation, the most prevalent arrhythmia, affects more than two million Americans annually and is associated with a twofold increase in mortality. In addition, more than 250,000 Americans each year suffer ventricular arrhythmias, often resulting in sudden cardiac death. Despite the high incidence and societal impact of cardiac arrhythmias, presently there are insufficient insights into the molecular mechanisms involved in arrhythmia generation, propagation, and/or maintenance or into the molecular determinants of disease risk, prognosis, and progression. In addition, present therapeutic strategies for arrhythmia abatement often are ineffective or require palliative device therapy after persistent changes in the electrical and conduction characteristics of the heart have occurred, changes that appear to increase the risk for arrhythmia progression. This article reviews our present understanding of the complexity of mechanisms that regulate cardiac membrane excitability and cardiac function and explores the role of derangements in these mechanisms that interact to induce arrhythmogenic substrates. Approaches are recommended for future investigations focused on providing new mechanistic insights and therapeutic interventions.
    MeSH term(s) Arrhythmias, Cardiac/genetics ; Arrhythmias, Cardiac/physiopathology ; Disease Progression ; Extracellular Matrix/physiology ; Heart Conduction System/physiology ; Humans ; Ion Channels/physiology ; Prognosis ; Ventricular Remodeling/physiology
    Chemical Substances Ion Channels
    Language English
    Publishing date 2005-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2005.03.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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