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Article ; Online: Synchronization of Triggered Waves in Atrial Tissue.

Shiferaw, Yohannes / Aistrup, Gary L / Wasserstrom, John A

2018 Volume 115, Issue 6, Page(s) 1130–1141

Abstract: ... by Ca influx from the L-type Ca channel and occur during the action potential. However, the consequences ...

Abstract	When an atrial cell is paced rapidly, calcium (Ca) waves can form on the cell boundary and propagate to the cell interior. These waves are referred to as "triggered waves" because they are initiated by Ca influx from the L-type Ca channel and occur during the action potential. However, the consequences of triggered waves in atrial tissue are not known. Here, we develop a phenomenological model of Ca cycling in atrial myocytes that accounts for the formation of triggered waves. Using this model, we show that a fundamental requirement for triggered waves to induce abnormal electrical activity in tissue is that these waves must be synchronized over large populations of cells. This is partly because triggered waves induce a long action potential duration (APD) followed by a short APD. Thus, if these events are not synchronized between cells, then they will on average cancel and have minimal effects on the APD in tissue. Using our computational model, we identify two distinct mechanisms for triggered wave synchronization. The first relies on cycle length (CL) variability, which can prolong the CL at a given beat. In cardiac tissue, we show that CL prolongation leads to a substantial amplification of APD because of the synchronization of triggered waves. A second synchronization mechanism applies in a parameter regime in which the cell exhibits stochastic alternans in which a triggered wave fires, on average, only every other beat. In this scenario, we identify a slow synchronization mechanism that relies on the bidirectional feedback between the APD in tissue and triggered wave initiation. On large cables, this synchronization mechanism leads to spatially discordant APD alternans with spatial variations on a scale of hundreds of cells. We argue that these spatial patterns can potentially serve as an arrhythmogenic substrate for the initiation of atrial fibrillation.
MeSH term(s)	Atrial Function ; Calcium Signaling ; Electrophysiological Phenomena ; Feedback, Physiological ; Heart Atria/cytology ; Models, Cardiovascular
Language	English
Publishing date	2018-08-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2018.08.015
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Article ; Online: Remodeling Promotes Proarrhythmic Disruption of Calcium Homeostasis in Failing Atrial Myocytes.

Shiferaw, Yohannes / Aistrup, Gary L / Louch, William E / Wasserstrom, J A

Biophysical journal

2019 Volume 118, Issue 2, Page(s) 476–491

Abstract: ... that disruption of the spatial relationship between L-type Ca channels (LCCs) and ryanodine receptors results ...

Abstract	It is well known that heart failure (HF) typically coexists with atrial fibrillation (AF). However, until now, no clear mechanism has been established that relates HF to AF. In this study, we apply a multiscale computational framework to establish a mechanistic link between atrial myocyte structural remodeling in HF and AF. Using a spatially distributed model of calcium (Ca) signaling, we show that disruption of the spatial relationship between L-type Ca channels (LCCs) and ryanodine receptors results in markedly increased Ca content of the sarcoplasmic reticulum (SR). This increase in SR load is due to changes in the balance between Ca entry via LCCs and Ca extrusion due to the sodium-calcium exchanger after an altered spatial relationship between these signaling proteins. Next, we show that the increased SR load in atrial myocytes predisposes these cells to subcellular Ca waves that occur during the action potential (AP) and are triggered by LCC openings. These waves are common in atrial cells because of the absence of a well-developed t-tubule system in most of these cells. This distinct spatial architecture allows for the presence of a large pool of orphaned ryanodine receptors, which can fire and sustain Ca waves during the AP. Finally, we incorporate our atrial cell model in two-dimensional tissue simulations and demonstrate that triggered wave generation in cells leads to electrical waves in tissue that tend to fractionate to form wavelets of excitation. This fractionation is driven by the underlying stochasticity of subcellular Ca waves, which perturbs AP repolarization and consequently induces localized conduction block in tissue. We outline the mechanism for this effect and argue that it may explain the propensity for atrial arrhythmias in HF.
MeSH term(s)	Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/pathology ; Atrial Remodeling ; Calcium/metabolism ; Heart Atria/pathology ; Homeostasis ; Models, Cardiovascular ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-12-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2019.12.012
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Article ; Online: Mechanism for Triggered Waves in Atrial Myocytes.

Shiferaw, Yohannes / Aistrup, Gary L / Wasserstrom, J Andrew

Biophysical journal

2017 Volume 113, Issue 3, Page(s) 656–670

Abstract: Excitation-contraction coupling in atrial cells is mediated by calcium (Ca) signaling between L ... to as "triggered waves" because they are initiated by L-type Ca channel openings during the action potential ...

Abstract	Excitation-contraction coupling in atrial cells is mediated by calcium (Ca) signaling between L-type Ca channels and Ryanodine receptors that occurs mainly at the cell boundary. This unique architecture dictates essential aspects of Ca signaling under both normal and diseased conditions. In this study we apply laser scanning confocal microscopy, along with an experimentally based computational model, to understand the Ca cycling dynamics of an atrial cell subjected to rapid pacing. Our main finding is that when an atrial cell is paced under Ca overload conditions, Ca waves can then nucleate on the cell boundary and propagate to the cell interior. These propagating Ca waves are referred to as "triggered waves" because they are initiated by L-type Ca channel openings during the action potential. These excitations are distinct from spontaneous Ca waves originating from random fluctuations of Ryanodine receptor channels, and which occur after much longer waiting times. Furthermore, we argue that the onset of these triggered waves is a highly nonlinear function of the sarcoplasmic reticulum Ca load. This strong nonlinearity leads to aperiodic response of Ca at rapid pacing rates that is caused by the complex interplay between paced Ca release and triggered waves. We argue further that this feature of atrial cells leads to dynamic instabilities that may underlie atrial arrhythmias. These studies will serve as a starting point to explore the nonlinear dynamics of atrial cells and will yield insights into the trigger and maintenance of atrial fibrillation.
MeSH term(s)	Animals ; Atrial Fibrillation/pathology ; Calcium Signaling/drug effects ; Dogs ; Heart Atria/cytology ; Isoproterenol/pharmacology ; Models, Biological ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/pathology ; Nonlinear Dynamics
Chemical Substances	Isoproterenol (L628TT009W)
Language	English
Publishing date	2017-08-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2017.06.026
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Zs.A 235: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Phosphatidylinositol-4,5-Bisphosphate Binding to Amphiphysin-II Modulates T-Tubule Remodeling: Implications for Heart Failure.

Zhou, Junlan / Singh, Neha / Monnier, Chloe / Marszalec, William / Gao, Li / Jin, Jing / Frisk, Michael / Louch, William E / Verma, Suresh / Krishnamurthy, Prasanna / Nico, Elsa / Mulla, Maaz / Aistrup, Gary L / Kishore, Raj / Wasserstrom, J Andrew

Frontiers in physiology

2021 Volume 12, Page(s) 782767

Abstract: BIN1 (amphyphysin-II) is a structural protein involved in T-tubule (TT) formation and phosphatidylinositol-4,5-bisphosphate (PIP2) is responsible for localization of BIN1 to sarcolemma. The goal of this study was to determine if PIP2-mediated targeting ... ...

Abstract	BIN1 (amphyphysin-II) is a structural protein involved in T-tubule (TT) formation and phosphatidylinositol-4,5-bisphosphate (PIP2) is responsible for localization of BIN1 to sarcolemma. The goal of this study was to determine if PIP2-mediated targeting of BIN1 to sarcolemma is compromised during the development of heart failure (HF) and is responsible for TT remodeling. Immunohistochemistry showed co-localization of BIN1, Cav1.2, PIP2, and phospholipase-Cβ1 (PLCβ1) in TTs in normal rat and human ventricular myocytes. PIP2 levels were reduced in spontaneously hypertensive rats during HF progression compared to age-matched controls. A PIP Strip assay of two native mouse cardiac-specific isoforms of BIN1 including the longest (cardiac BIN1 #4) and shortest (cardiac BIN1 #1) isoforms as well human skeletal BIN1 showed that all bound PIP2. In addition, overexpression of all three BIN1 isoforms caused tubule formation in HL-1 cells. A triple-lysine motif in a short loop segment between two helices was mutated and replaced by negative charges which abolished tubule formation, suggesting a possible location for PIP2 interaction aside from known consensus binding sites. Pharmacological PIP2 depletion in rat ventricular myocytes caused TT loss and was associated with changes in Ca
Language	English
Publishing date	2021-12-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.782767
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Article ; Online: Intracellular Ca2+ waves, afterdepolarizations, and triggered arrhythmias.

Shiferaw, Yohannes / Aistrup, Gary L / Wasserstrom, J Andrew

Cardiovascular research

2012 Volume 95, Issue 3, Page(s) 265–268

MeSH term(s)	Action Potentials ; Animals ; Arrhythmias, Cardiac/etiology ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/physiopathology ; Calcium Signaling ; Humans ; Myocytes, Cardiac/metabolism ; Risk Factors ; Sarcoplasmic Reticulum/metabolism ; Time Factors
Language	English
Publishing date	2012-04-27
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvs155
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Article ; Online: Interventricular differences in sodium current and its potential role in Brugada syndrome.

Calloe, Kirstine / Aistrup, Gary L / Di Diego, José M / Goodrow, Robert J / Treat, Jacqueline A / Cordeiro, Jonathan M

Physiological reports

2018 Volume 6, Issue 14, Page(s) e13787

Abstract: Brugada syndrome (BrS) is an inherited disease associated with ST elevation in the right precordial leads, polymorphic ventricular tachycardia (PVT), and sudden cardiac death in adults. Mutations in the cardiac sodium channel account for a large fraction ...

Abstract	Brugada syndrome (BrS) is an inherited disease associated with ST elevation in the right precordial leads, polymorphic ventricular tachycardia (PVT), and sudden cardiac death in adults. Mutations in the cardiac sodium channel account for a large fraction of BrS cases. BrS manifests in the right ventricle (RV), which led us to examine the biophysical and molecular properties of sodium channel in myocytes isolated from the left (LV) and right ventricle. Patch clamp was used to record sodium current (I
MeSH term(s)	Action Potentials ; Animals ; Brugada Syndrome/physiopathology ; Cells, Cultured ; Dogs ; Endocardium/cytology ; Female ; Heart Ventricles/cytology ; Male ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/physiology ; NAV1.5 Voltage-Gated Sodium Channel/genetics ; NAV1.5 Voltage-Gated Sodium Channel/metabolism ; Pericardium/cytology ; Sodium/metabolism
Chemical Substances	NAV1.5 Voltage-Gated Sodium Channel ; Sodium (9NEZ333N27)
Language	English
Publishing date	2018-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.13787
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Article ; Online: Arrhythmia triggers in heart failure: the smoking gun of [Ca2+]i dysregulation.

Aistrup, Gary L / Balke, C William / Wasserstrom, J Andrew

Heart rhythm

2011 Volume 8, Issue 11, Page(s) 1804–1808

Abstract: Among the most serious problems associated with heart failure is the increased likelihood of life-threatening arrhythmias. Both triggered and reentrant arrhythmias in heart failure may arise as a result of aberrant intracellular Ca cycling. This article ... ...

Abstract	Among the most serious problems associated with heart failure is the increased likelihood of life-threatening arrhythmias. Both triggered and reentrant arrhythmias in heart failure may arise as a result of aberrant intracellular Ca cycling. This article presents some new ideas, based on recent studies, about how altered Ca cycling in heart failure might serve as the cellular basis for arrhythmogenesis.
MeSH term(s)	Action Potentials ; Arrhythmias, Cardiac/complications ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/pathology ; Calcium/metabolism ; Calcium Signaling/physiology ; Heart Failure/etiology ; Heart Failure/metabolism ; Heart Failure/pathology ; Humans ; Myocytes, Cardiac/metabolism
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2011-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2229357-7
ISSN	1556-3871 ; 1547-5271
ISSN (online)	1556-3871
ISSN	1547-5271
DOI	10.1016/j.hrthm.2011.06.012
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Article ; Online: Searching for "order" in atrial fibrillation using electrogram morphology recurrence plots.

Gordon, David / Goldberger, Jeffrey J / Arora, Rishi / Aistrup, Gary L / Ng, Jason

Computers in biology and medicine

2015 Volume 65, Page(s) 220–228

Abstract: ... laminarity (LAM), average diagonal line length (L), trapping time (TT), divergence (DIV), and Shannon׳s ... of the activation morphologies resulted in significant decreases in DET, LAM, L, TT, and ENTR and significant ...

Abstract	Background: Bipolar electrograms recorded during atrial fibrillation (AF) can have an appearance of chaotic/random behavior. The aim of this study was to use a novel electrogram morphology recurrence (EMR) analysis to quantify the level of order in the morphology patterns in AF. Methods: Rapid atrial pacing was performed in seven dogs at 600bpm for 3 weeks leading to sustained AF. Open chest high density electrical recordings were made in multiple atrial sites. EMR plots of bipolar electrograms at each site were created by cross-correlating morphologies of each detected activations with morphologies of every other activation. The following features of the EMR plots were quantified: recurrence rate (RR), determinism (DET), laminarity (LAM), average diagonal line length (L), trapping time (TT), divergence (DIV), and Shannon׳s entropy (ENTR). For each recording site, these measures were calculated for the normal sequence of morphologies and also after random shuffling of the electrogram orders. Results: Electrograms recordings from a total of 3961 sites had average cycle lengths of 104±22ms resulting in an average of 100±19 activations detected per 10-s recording and an average RR of 0.38±0.28 (range 0.02-1.00). Shuffling the order of the activation morphologies resulted in significant decreases in DET, LAM, L, TT, and ENTR and significant increases in DIV. Conclusions: EMR plots of AF electrograms show varying rates of recurrence with patterns that suggest an underlying deterministic structure to the activation sequences. A better understanding of AF dynamics could lead to improved methods in mapping and treating AF.
MeSH term(s)	Animals ; Atrial Fibrillation/physiopathology ; Dogs ; Electrocardiography ; Humans ; Myocardial Contraction
Language	English
Publishing date	2015-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	127557-4
ISSN	1879-0534 ; 0010-4825
ISSN (online)	1879-0534
ISSN	0010-4825
DOI	10.1016/j.compbiomed.2015.07.018
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Article ; Online: Triggered Ca

Gussak, Georg / Marszalec, William / Yoo, Shin / Modi, Rishi / O'Callaghan, Caitlin / Aistrup, Gary L / Cordeiro, Jonathan M / Goodrow, Robert / Kanaporis, Giedrius / Blatter, Lothar A / Shiferaw, Yohannes / Arora, Rishi / Zhou, Junlan / Burrell, Amy R / Wasserstrom, J Andrew

Circulation. Arrhythmia and electrophysiology

2020 Volume 13, Issue 6, Page(s) e008179

Abstract: Background: We have identified a novel form of abnormal Ca: Methods: Simultaneous recordings of intracellular Ca: Results: At 3.3 to 5 Hz, TCWs occurred during the AP and often outlasted several AP cycles. Maximum diastolic potential was reduced, ... ...

Abstract	Background: We have identified a novel form of abnormal Ca Methods: Simultaneous recordings of intracellular Ca Results: At 3.3 to 5 Hz, TCWs occurred during the AP and often outlasted several AP cycles. Maximum diastolic potential was reduced, and AP duration was significantly prolonged during TCWs. All electrophysiological responses to TCWs were abolished by SEA0400 and ORM10103, indicating that Na-Ca exchange current caused depolarization. The time constant of recovery from inactivation of Ca Conclusions: Triggered Ca
MeSH term(s)	Action Potentials ; Animals ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/physiopathology ; Calcium Signaling ; Computer Simulation ; Diastole ; Dogs ; Female ; Heart Rate ; Male ; Models, Cardiovascular ; Myocytes, Cardiac/metabolism ; Sodium-Calcium Exchanger/metabolism ; Time Factors
Chemical Substances	Sodium-Calcium Exchanger
Language	English
Publishing date	2020-05-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2426129-4
ISSN	1941-3084 ; 1941-3149
ISSN (online)	1941-3084
ISSN	1941-3149
DOI	10.1161/CIRCEP.119.008179
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Article: Digitalis: new actions for an old drug.

Wasserstrom, J Andrew / Aistrup, Gary L

American journal of physiology. Heart and circulatory physiology

2005 Volume 289, Issue 5, Page(s) H1781–93

Abstract: The mechanisms by which digitalis causes its therapeutic and toxic actions have been studied for nearly a half century, revealing a great deal about cardiac cell regulation of intracellular ions via the Na-K-ATPase (NKA) and how it is altered by cardiac ... ...

Abstract	The mechanisms by which digitalis causes its therapeutic and toxic actions have been studied for nearly a half century, revealing a great deal about cardiac cell regulation of intracellular ions via the Na-K-ATPase (NKA) and how it is altered by cardiac glycosides. However, recent observations suggest that digitalis may have additional effects on cardiac cell function in both the short and long term that include intracellular effects, interactions with specific NKA isoforms in different cellular locations, effects on intracellular (including nuclear) signaling, and long-term regulation of intracellular ionic balances through circulating ouabain-like compounds. The purpose of this review is to examine the current status of a number of the newest and most interesting developments in the study of digitalis with a particular focus on cardiac function, although we will also discuss some of the new advances in other relevant cardiovascular effects. This new information has important implications for both our understanding of ionic regulation in normal and diseased hearts as well as for potential avenues for the development of future therapeutic interventions for the treatment of heart failure.
MeSH term(s)	Animals ; Anti-Arrhythmia Agents/pharmacology ; Anti-Arrhythmia Agents/therapeutic use ; Cardiotonic Agents/pharmacology ; Cardiotonic Agents/therapeutic use ; Digitalis Glycosides/pharmacology ; Digitalis Glycosides/therapeutic use ; Hemodynamics/drug effects ; Humans ; Receptors, Neurokinin-2/antagonists & inhibitors ; Signal Transduction/drug effects
Chemical Substances	Anti-Arrhythmia Agents ; Cardiotonic Agents ; Digitalis Glycosides ; Receptors, Neurokinin-2
Language	English
Publishing date	2005-10-10
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	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00707.2004
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