Posts Tagged: atrial fibrillation

Calcium Signaling and Cardiac Arrhythmias

Calcium Signaling and Cardiac Arrhythmias

Andrew P. Landstrom, Dobromir Dobrev, Xander H.T. Wehrens

Ryanodine receptor type-2 (RyR2) macromolecular complex. Cartoon representing RyR2 pore-forming subunits with accessory proteins that bind to and/or modulate channel function. CaM indicates calmodulin; CaMKII, Ca2+/calmodulin-dependent protein kinase II; CASQ2, calsequestrin-2; FKBP12.6, FK506-binding protein-12.6; JCTN, junctin; JPH2, juncophilin-2; PKA, protein kinase A; PM, plasma membrane; PP, protein phosphatase; SR, sarcoplasmic reticulum; TECRL, trans-2,3-enoyl-CoA reductase-like protein; and TRDN; triadin. [Powerpoint File]

Calcium Signaling and Cardiac Arrhythmias

Calcium Signaling and Cardiac Arrhythmias

Andrew P. Landstrom, Dobromir Dobrev, Xander H.T. Wehrens

Role of calcium-handling in excitation–contraction (EC) coupling. A, Schematic overview of key Ca2+-handling proteins involved in EC coupling. B, Schematic diagram of Ca2+ release unit and major components of the JMC (junctional membrane complex). The transverse tubule (TT) and sarcoplasmic reticulum (SR) membranes approximate to form the dyad. BIN1 indicates bridging integrator 1; Cav1.2, L-type Ca2+ channel; CAV3, caveolin-3; JPH2, juncophilin-2; NCX1, Na+/Ca2+ exchanger type-1; PM, plasma membrane; PMCA, plasmalemmal Ca2+-ATPase; RyR2, ryanodine receptor type-2; and SERCA2a, sarco/endoplasmic reticulum ATPase type-2a.* [Powerpoint File]

Atrial Fibrillation Epidemiology, Pathophysiology, and Clinical Outcomes

Atrial Fibrillation: Epidemiology, Pathophysiology, and Clinical Outcomes

Laila Staerk, Jason A. Sherer, Darae Ko, Emelia J. Benjamin, Robert H. Helm

Atrial fibrillation (AF) risk factors (RFs) induce structural and histopathologic changes to the atrium that are characterized by fibrosis, inflammation, and cellular and molecular changes. Such changes increase susceptibility to AF. Persistent AF further induces electric and structural remodeling that promotes perpetuation of AF. AF also may lead to the development of additional AF risk factors that further alters the atrial substrate. Finally, AF is associated with several clinical outcomes. *There are limited data supporting the association. BMI, body mass index; ERP, effective refractory period; HF, heart failure; IL, interleukin; MI, myocardial infarction; OSA, obstructive sleep apnea; SEE, systemic embolism event; TNF, tumor necrosis factor; and VTE, venous thromboembolism. [Powerpoint File]

Cardioembolic Stroke

Cardioembolic Stroke

Hooman Kamel, Jeff S. Healey

Overlap among cryptogenic stroke, embolic stroke of undetermined source, and cardioembolic stroke. [Powerpiont File]

Atrial Fibrillation Therapy Now and in the Future: Drugs, Biologicals, and Ablation

Atrial Fibrillation Therapy Now and in the Future: Drugs, Biologicals, and Ablation

Christopher E. Woods, Jeffrey Olgin

Emerging imaging modalities for atrial fibrillation (AF). A, MRI-based fibrosis imaging of the atria showing the University of Utah Atrial Fibrillation LGE-MRI–based staging system in human. Green areas indicate areas of fibrosis (adapted from Vergara et al72 with permission of the publisher). B, Left atrial rotor with counterclockwise activation in human mapped computationally using the proprietary focal impulse and rotor modulation mapping system (RhythmView, Topera Medical, Lexington, MA; adapted from Narayan et al17 with permission of the publisher). C, Phase mapping of posterior human left atrium during paroxysmal AF showing 2 successive rotations of a rotor near the right pulmonary vein ostia using 252-electrode vest was applied to the patient’s torso for body-surface mapping. The core of the rotor is depicted with a white star. The phases of the voltage propagation period are color coded with blue representing the depolarizing period and green representing the end of the repolarization (adapted from Haissaguerre et al77 with permission of the publisher). D, Endoscopic optical mapping of pulmonary vein (top left) and left ventricle (top right) in swine-isolated heart with a balloon tipped catheter via transeptal approach. Propagation map at successive time points from ventricular image for 1 beat shown below (C.E. Woods, MD, PhD, unpublished data, 2013; courtesy of AUST Development, LLC). Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation. [Powerpoint File]

Mathematical Approaches to Understanding and Imaging Atrial Fibrillation: Significance for Mechanisms and Management

Mathematical Approaches to Understanding and Imaging Atrial Fibrillation: Significance for Mechanisms and Management

Natalia A. Trayanova

Geometric models of the atria. A, Volume image of the sheep atria acquired by serial surface imaging (resolution, 50 μm), with a representative slice. Subdivision of atria into different regions as represented by the different colors: right atrium (RA), green; left atrium (LA), blue; Bachman bundle (BB), red; and posterior LA (PLA), yellow. LAA indicates LA appendage; LSPV, left superior pulmonary vein; RAA, RA appendage; and RSPV, right superior pulmonary vein. Images reproduced from Zhao et al50,51 with permission of the publisher. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation. B, A model of the fibrotic human atria generated from a patient late gadolinium enhancement (LGE) MRI scan (top left) after segmentation (top right) into normal and fibrotic tissue (fibrotic lesions in red). Reproduced with permission from McDowell et al. [Powerpoint File]

Emerging Directions in the Genetics of Atrial Fibrillation

Emerging Directions in the Genetics of Atrial Fibrillation

Nathan R. Tucker, Patrick T. Ellinor

Known genetic pathways for atrial fibrillation (AF) pathogenesis. Schematic of known AF-related genes derived from previous studies. Genes listed include those where coding variation was identified in familial AF and candidate gene screens, as well as the genes suggested to be implicated in AF based on genome-wide association studies (GWAS). Names listed in red indicate those identified by familial studies and candidate gene screens, whereas those listed in gray are gene targets implicated by GWAS. [Powerpoint File]

Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

Jordi Heijman*, Niels Voigt*, Stanley Nattel, Dobromir Dobrev

Arrhythmogenic changes in atrial fibroblasts. Disease- and atrial fibrillation (AF)–related remodeling promotes fibroblast differentiation into myofibroblasts, involving altered expression of several ion channel proteins and microRNAs (miRs). Myofibroblasts facilitate AF maintenance by promoting re-entry through fibrosis/collagen deposition, as well as paracrine and direct electrotonic interactions with cardiomyocytes. Ado indicates aldosterone; Ang-II, angiotensin II; TGFβ1, transforming growth factor β1; TNFα, tumor necrosis factor α; TRPC3, transient receptor potential (TRP) canonical-3; and TRPM, TRP melastatin–related 7. [Powerpoint File]

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

Mark J. Shen, Douglas P. Zipes

Scheme of autonomic innervation of the heart. The cardiac sympathetic ganglia consist of cervical ganglia, stellate (cervicothoracic) ganglia, and thoracic ganglia. Parasympathetic innervation comes from the vagus nerves. Reprinted from Shen et al12 with permission of the publisher. Copyright © 2011, Nature Publishing Group. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation. [Powerpoint File]

Phenotypic Manifestations of Mutations in Genes Encoding Subunits of Cardiac Potassium Channels

Phenotypic Manifestations of Mutations in Genes Encoding Subunits of Cardiac Potassium Channels

Wataru Shimizu, Minoru Horie

Scheme showing the central dogma of protein synthesis. Numbers in parentheses (1 through 10) in the cartoon indicate diverse mechanisms underlying cardiac potassium channel diseases. For detailed explanation, see text. ER indicates endoplasmic reticulum; CM, cardiac cell membrane; G, Golgi apparatus; and N, cellular nucleus. [Powerpoint File]

Noninvasive Electrocardiographic Imaging of Arrhythmogenic Substrates in Humans

Noninvasive Electrocardiographic Imaging of Arrhythmogenic Substrates in Humans

Yoram Rudy

The electrocardiographic imaging (ECGI) procedure. Bottom, The electric data. A total of 250 electrocardiograms over the entire torso surface are recorded simultaneously to generate body surface potential maps every millisecond. Top, The geometric data. Computed tomography (CT) scan provides the epicardial geometry and body surface electrode positions in the same image. The electric and geometric data are combined and processed by the ECGI algorithms to reconstruct potentials, electrograms, activation isochrones, and repolarization patterns on the surface of the heart. Adapted from Ramanathan et al,4 with permission. [Powerpoint File]

Rotors and the Dynamics of Cardiac Fibrillation

Rotors and the Dynamics of Cardiac Fibrillation

Sandeep V. Pandit, José Jalife

Rotors and spirals, basic concepts. A, Schematic representation of reentry around a ring-like anatomic obstacle where the wavelength (black) is shorter than the path length, allowing for a fully excitable gap (white). B, Leading circle reentry around a functional obstacle, with centripetal forces pointing inwards toward a refractory center. C, Two-dimensional (2D) spiral wave, along with the rotor tip at the center (*). D, Schematic of a 3-dimensional scroll wave. E, Snapshot of the spiral wave: electrotonic effects of the core decrease conduction velocity (arrows), action potential duration (representative examples shown from positions 1, 2, and 3), and wavelength (the distance from the wavefront [black line] to the wave tail [dashed line]). Conduction velocity (CV) decreases and wavefront curvature becomes more pronounced, near the rotor, which is a phase singularity at the point where the wavefront and the wave tail meet (*). F, Computer simulation of reentry.38 Top, Snapshot of the transmembrane voltage distribution during simulated reentry in chronic atrial fibrillation (AF) conditions in a 2D sheet incorporating human atrial ionic math models. Bottom, Snapshot of inactivation variables of sodium current, “h.j,” during reentry. [Powerpoint File]