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  • Ovid Technologies (Wolters Kluwer Health)  (22)
  • 1
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    Rotors Detected by Phase Analysis of Filtered, Epicardial Atrial Fibrillation Electrograms Colocalize With Regions of Conduction Block
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Circulation: Arrhythmia and Electrophysiology Vol. 11, No. 10 ( 2018-10)
    Details
    In: Circulation: Arrhythmia and Electrophysiology, Ovid Technologies (Wolters Kluwer Health), Vol. 11, No. 10 ( 2018-10)
    Abstract: Several recent studies suggest rotors detected by phase mapping may act as main drivers of persistent atrial fibrillation. However, the electrophysiological nature of detected rotors remains unclear. We performed a direct, 1:1 comparison between phase and activation time mapping in high-density, epicardial, direct-contact mapping files of human atrial fibrillation. Methods: Thirty-eight unipolar electrogram files of 10 s duration were recorded in patients with atrial fibrillation (n=20 patients) using a 16×16 electrode array placed on the epicardial surface of the left atrial posterior wall or the right atrial free wall. Phase maps and isochrone wave maps were constructed for all recordings. For each detected phase singularity (PS) with a lifespan of 〉 1 cycle length, the corresponding conduction pattern was investigated in the isochrone wave maps. Results: When using sinusoidal recomposition and Hilbert Transform, 138 PSs were detected. One hundred and four out of 138 PSs were detected within 1 electrode distance (1.5 mm) from a line of conduction block between nonrotating wavefronts detected by activation mapping. Far fewer rotating wavefronts were detected when rotating activity was identified based on wave mapping (18 out of 8219 detected waves). Fourteen out of these 18 cases were detected as PSs in phase mapping. Phase analysis of filtered electrograms produced by simulated wavefronts separated by conduction block also identified PSs on the line of conduction block. Conclusions: PSs identified by phase analysis of filtered epicardial electrograms colocalize with conduction block lines identified by activation mapping. Detection of PSs using phase analysis has a low specificity for identifying rotating wavefronts during human atrial fibrillation using activation mapping.
    Type of Medium: Online Resource
    ISSN: 1941-3149 , 1941-3084
    URL: Article
    DOI: 10.1161/CIRCEP.117.005858
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2425487-3
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  • 2
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    Development of a Substrate of Atrial Fibrillation During Chronic Atrioventricular Block in the Goat
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Circulation Vol. 111, No. 1 ( 2005-01-04), p. 30-37
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 111, No. 1 ( 2005-01-04), p. 30-37
    Abstract: Background— Atrial dilatation is an important risk factor for atrial fibrillation (AF). In the present study, we monitored the electrophysiological changes during progressive atrial dilatation in chronically instrumented goats. Methods and Results— In 8 goats, 2 screw-in leads with piezoelectric crystals were implanted transvenously in the right atrium. After 2 weeks, atrial diameter and effective refractory period were measured. AF paroxysms were induced by burst pacing to determine the baseline AF cycle length and stability of AF. After His-bundle ablation, the above measurements were repeated once a week. After 4 weeks of complete AV block, the free wall of the right atrium was mapped and the atrium was fixed in formalin for histological analysis. After His-bundle ablation, the ventricular rate decreased from 113.8±4.8 to 44.6±2.5 bpm. Right atrial diameter increased gradually by 13.5±3.9% during 4 weeks of AV block ( P 〈 0.01). The duration of induced AF paroxysms increased from 4.6 seconds to 6.4 minutes ( P 〈 0.05). Atrial effective refractory period and AF cycle length remained constant. Spontaneous paroxysms of AF were not observed. Atrial mapping during rapid pacing revealed that slow conduction ( 〈 30 cm/s) was present in 3.7±1.0% of the mapped area (control, 0.9±0.5%, P 〈 0.05). Histological analysis showed hypertrophy without atrial fibrosis. Connexin40 and connexin43 expression was unchanged. Conclusions— Chronic AV block in the goat leads to progressive atrial dilatation, prolongation of induced AF paroxysms, and local conduction delays. The increase in AF stability was not a result of a shortening of atrial refractoriness or atrial fibrosis.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000151517.43137.97
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
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  • 3
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    Intrapericardial Delivery of Amiodarone and Sotalol: Atrial Transmural Drug Distribution and Electrophysiological Effects
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Journal of Cardiovascular Pharmacology Vol. 54, No. 4 ( 2009-10), p. 355-363
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 54, No. 4 ( 2009-10), p. 355-363
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0b013e3181bad042
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 4
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    Increased Vulnerability to Atrial Fibrillation in Transgenic Mice With Selective Atrial Fibrosis Caused by Overexpression of TGF-β1
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Circulation Research Vol. 94, No. 11 ( 2004-06-11), p. 1458-1465
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 94, No. 11 ( 2004-06-11), p. 1458-1465
    Abstract: Studies on patients and large animal models suggest the importance of atrial fibrosis in the development of atrial fibrillation (AF). To investigate whether increased fibrosis is sufficient to produce a substrate for AF, we have studied cardiac electrophysiology (EP) and inducibility of atrial arrhythmias in MHC-TGFcys 33 ser transgenic mice (Tx), which have increased fibrosis in the atrium but not in the ventricles. In anesthetized mice, wild-type (Wt) and Tx did not show significant differences in surface ECG parameters. With transesophageal atrial pacing, no significant differences were observed in EP parameters, except for a significant decrease in corrected sinus node recovery time in Tx mice. Burst pacing induced AF in 14 of 29 Tx mice, whereas AF was not induced in Wt littermates ( P 〈 0.01). In Langendorff perfused hearts, atrial conduction was studied using a 16-electrode array. Epicardial conduction velocity was significantly decreased in the Tx RA compared with the Wt RA. In the Tx LA, conduction velocity was not significantly different from Wt, but conduction was more heterogeneous. Action potential characteristics recorded with intracellular microelectrodes did not reveal differences between Wt and Tx mice in either atrium. Thus, in this transgenic mouse model, selective atrial fibrosis is sufficient to increase AF inducibility.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.0000129579.59664.9d
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1467838-X
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  • 5
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    Abstract 17767: A MiR-31-dependent Loss of Dystrophin & Nnos in the Human Atria Plays a Key Role in Atrial Fibrillation-induced Electrical Remodelling
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: Background: Management of atrial fibrillation (AF) remains a challenge. AF remodels the atrial electrical properties, thereby increasing resistance to treatment. Although remodeling has long been a target for therapeutic intervention in AF, the mechanisms driving this phenomenon are incompletely understood. Methods & Results: Using atrial samples from 351 patients (73 AF), and 67 goats (34 AF), we show that atrial-specific upregulation of miR31 causes dystrophin (DYS) translational repression and accelerates mRNA degradation of neuronal nitric oxide synthase (nNOS) leading to a profound reduction in NO availability. Six prediction algorithms and reporter assays established DYS and nNOS as miR-31 targets. In atrial myocytes from patients with AF (hAFm), both DYS and nNOS bind to miR-31 within the RNA induced silencing complex (RISC). In actinomycin D-treated myocytes from patients in sinus rhythm (hSRm), miR31 accelerated nNOS (but not DYS) mRNA decay. mRNA of nNOS (but not DYS) & protein content of nNOS, DYS & DYS associated proteins were significantly reduced in hAFm. Inhibition of miR31 in hAFm restored both DYS & nNOS protein. Protection of the nNOS miR31 binding site with a target site blocker (TSB) restored nNOS mRNA and protein (but not DYS), whereas, DYS-TSB increased both DYS and nNOS protein (but not mRNA), in keeping with an effect of DYS restoration on nNOS protein stability. Indeed, K48-linked polyubiquitination of nNOS was increased in hAFm & prevented by proteasome inhibition with MG132. NOS: inhibition (SMTC, 100 nmol) or transfection with a miR31 mimic was employed to evaluate the impact of these findings on atrial electrical properties. Both interventions shortened action potential duration (APD90) and abolished rate-dependency of the APD90 in hSRm but not in hAFm. By contrast, miR31 inhibition restored APD & APD rate-dependency in hAFm (both reversed by SMTC) but had no effect on hSRm. In mice (n=126), nNOS gene deletion or inhibition shortened atrial APD90 & lead to a 2-fold increase in AF inducibility in response to atrial burst pacing. Conclusions: These findings identify atrial-specific upregulation of miR31 in human AF as a key mechanism causing atrial loss of dystrophin and nNOS, which, in turn, lead to the electrical phenotype begetting AF.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.17767
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
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  • 6
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    Atrial Sources of Reactive Oxygen Species Vary With the Duration and Substrate of Atrial Fibrillation : Implications for the Antiarrhythmic Effect of Statins
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Circulation Vol. 124, No. 10 ( 2011-09-06), p. 1107-1117
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 124, No. 10 ( 2011-09-06), p. 1107-1117
    Abstract: An altered nitric oxide–redox balance has been implicated in the pathogenesis of atrial fibrillation (AF). Statins inhibit NOX2-NADPH oxidases and prevent postoperative AF but are less effective in AF secondary prevention; the mechanisms underlying these findings are poorly understood. Methods and Results— By using goat models of pacing-induced AF or of atrial structural remodeling secondary to atrioventricular block and right atrial samples from 130 patients undergoing cardiac surgery, we found that the mechanisms responsible for the NO-redox imbalance differ between atria and with the duration and substrate of AF. Rac1 and NADPH oxidase activity and the protein level of NOX2 and p22phox were significantly increased in the left atrium of goats after 2 weeks of AF and in patients who developed postoperative AF in the absence of differences in leukocytes infiltration. Conversely, in the presence of longstanding AF or atrioventricular block, uncoupled nitric oxide synthase activity (secondary to reduced BH 4 content and/or increased arginase activity) and mitochondrial oxidases accounted for the biatrial increase in reactive oxygen species. Atorvastatin caused a mevalonate-reversible inhibition of Rac1 and NOX2-NADPH oxidase activity in right atrial samples from patients who developed postoperative AF, but it did not affect reactive oxygen species, nitric oxide synthase uncoupling, or BH 4 in patients with permanent AF. Conclusions— Upregulation of atrial NADPH oxidases is an early but transient event in the natural history of AF. Changes in the sources of reactive oxygen species with atrial remodeling may explain why statins are effective in the primary prevention of AF but not in its management.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.111.029223
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
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  • 7
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    Transmural Conduction Is the Predominant Mechanism of Breakthrough During Atrial Fibrillation : Evidence From Simultaneous Endo-Epicardial High-Density Activation Mapping
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Circulation: Arrhythmia and Electrophysiology Vol. 6, No. 2 ( 2013-04), p. 334-341
    Details
    In: Circulation: Arrhythmia and Electrophysiology, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 2 ( 2013-04), p. 334-341
    Abstract: Endo-epicardial dissociation (EED) of electric activations resulting in transmural conduction of fibrillation waves (breakthroughs) has been postulated to contribute to the complexity of the substrate of atrial fibrillation (AF). The aim of this study was to elucidate the correlation between EED and incidence of breakthrough and to test the plausibility of transmural conduction versus ectopic focal discharges as sources of breakthrough. Methods and Results— We analyzed high-resolution simultaneous endo-epicardial in vivo mapping data recorded in left atrial free walls of goats with acute AF, 3 weeks and 6 months of AF (all n=7). Waves were analyzed for number, size, and width and categorized according to their origin outside (peripheral wave) or within the mapping area (breakthrough). Breakthrough incidence was lowest (2.1±1.0%) in acute AF, higher (11.4±6.1%) after 3 weeks ( P 〈 0.01 versus acute AF) and highest (14.2±3.8%) after 6 months AF ( P 〈 0.001 versus acute AF) and similar in the epicardium and endocardium. Most of the breakthroughs (86%; n=564) could be explained by transmural conduction, whereas only 13% (n=85) could be explained by ectopic focal discharges. Transmural microreentry did not play a role as source of breakthrough. Conclusions— This is the first study to present simultaneous endo-epicardial in vivo mapping data at sites of breakthrough events. Breakthrough incidence and degree of EED increased with increasing AF substrate complexity. In goat left atrial free walls, most of the breakthroughs can be explained by transmural conduction, whereas ectopic focal discharges play a limited role as source of breakthrough.
    Type of Medium: Online Resource
    ISSN: 1941-3149 , 1941-3084
    URL: Article
    DOI: 10.1161/CIRCEP.113.000342
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
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  • 8
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    Abstract 2169: Chronic Intra-cardiac Parasympathetic AV-node Pacing In Goats With Chronic AF To Control Ventricular Rate
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Abstract: INTRODUCTION Drug therapy to reduce the ventricular rate during atrial fibrillation (AF) is effective in only 50% of the patients and limited by side effects. Currently available pacing algorithms are even less effective. The aim of this study was to test the feasibility of chronic AV-Node Inhibition (AVNI) by intra-cardiac parasympathetic nerve stimulation. Our ultimate goal is to develop a pacemaker device with a feature to inhibit AV node function to decrease ventricular rate during AF. METHODS Leads were implanted in the right atrial appendage and right ventricular apex and connected to a pacemaker for AF induction. In addition, an atrial lead (’AVNI lead’) connected to an implantable high frequency neurostimulator was implanted at a site with a strong prolongation of the PQ-time. Immediately after implantation optimal settings, optimal location, acute effects of AVNI on ventricular rate and the possible pro-arrhythmic effects of AVNI were assessed. The ’safety window’ for AVNI was defined as the difference between the output at the AVNI lead that produced atrial capture and the output that produced AVNI. One week after implantation, AF was maintained for one week by burst pacing via the lead in the right atrial appendage. After this 2 week period, the chronic effects of AVNI were assessed weekly for periods ranging from 3 weeks to 7 months. RESULTS In total, 5 goats were studied . The optimal location for AVNI was located at the junction of the coronary sinus and inferior vena cava. Optimal AVNI was found at a stimulation frequency of 30Hz and pulse width of 180 μs in each animal. During the implant procedure “a safety window” appeared to be present. However, it became smaller after a longer period of AVNS. The acute effect of AVNI (averaged over the experiments) was a prolongation of the median R-R interval of 37 % (SD = 21%), which was not significantly different from the chronic effect at the end of the study (average = 32% (SD = 18%). CONCLUSIONS Chronic intra-cardiac AV-node inhibition to reduce the ventricular rate during AF is feasible. Atrial pro-arrhythmic effects can be avoided by optimization of the stimulus parameters and location.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_680-c
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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  • 9
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    Abstract 3491: Endo-Epicardial Dissociation of Electrical Activity Increases During the Development of the Substrate for Atrial Fibrillation in the Goat
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Abstract: Background: The high incidence of transmural conduction of fibrillation waves (breakthroughs) in a complex substrate for atrial fibrillation (AF) implies the presence of electrical dissociation between the subepicardial layer (Epi) and the endocardial bundle network (Endo). The presence of this Endo/Epi dissociation (EED) in remodeled atria and its role in the progressive stabilization of AF over time has not been studied yet. Methods: We developed a mapping tool for synchronous Endo/Epi mapping (spatial resolution 1.6mm) with 90 exactly opposing electrode pairs (open chest experiment). We included 3 groups of goats: C = Control (acute AF induced by 50Hz burst pacing, n=7), 3wk = 3weeks AF (n=7) and 6mo = 6months AF (n=7). Dissociated activity was postulated when either activation times differed by more than 12ms vertically or 8ms horizontally (indicating a local conduction velocity 〈 20cm/s) or local direction of propagation between Endo and Epi differed by more than 90 degrees. To monitor AF stability, repetitive in-vivo cardioversion experiments with class 1C drugs were performed in 6 of the 6mo goats at 2,6,10 and 14wk AF. Results: Applying the time criterion, EED increased from 15±4% (C) to 22±11% (3wk) and 35±13% (6mo, p=0.002 vs. C). Also the differences in the direction of propagation significantly contributed to EED. Using the combined criterion, EED increased from 38±5% (C) to 46±10% (3wk) and 53±11% (6mo, p=0.007 vs. C). Dissociation within the epicardial and the endocardial layer (time criterion) increased to a comparable extent (19±8% vs. 27±14% vs. 37± 7%, p 〈 0.001 C vs. 6mo). Mean Endo/Epi activation time differences were close to 0ms in all three groups (−1.0±15ms vs. −0.8±16ms vs. −0.3±20ms), ruling out preferential conduction from Endo to Epi or vice versa. Success rate of cardioversion experiments decreased from 83% (2w) to 33% (6wk) to 16% (10wk) to 0% (14wk) indicating increasing stability of AF over time. Conclusion: During AF, pronounced EED occurs. EED (like dissociation within Endo and Epi) increases over time, contributing to the progressive stabilization of AF. Enhanced EED might explain the high incidence of transmural conduction (breakthroughs) in a complex substrate for AF.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_435
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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  • 10
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    Alterations in Atrial Electrophysiology and Tissue Structure in a Canine Model of Chronic Atrial Dilatation Due to Mitral Regurgitation
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Circulation Vol. 107, No. 20 ( 2003-05-27), p. 2615-2622
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 107, No. 20 ( 2003-05-27), p. 2615-2622
    Abstract: Background— Clinically, chronic atrial dilatation is associated with an increased incidence of atrial fibrillation (AF), but the underlying mechanism is not clear. We have investigated atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation (MR). Methods and Results— Thirteen control and 19 MR dogs (1 month after partial mitral valve avulsion) were studied. Dogs in the MR group were monitored using echocardiography and Holter recording. In open-chest follow-up experiments, electrode arrays were placed on the atria to investigate conduction patterns, effective refractory periods, and inducibility of AF. Alterations in tissue structure and ultrastructure were assessed in atrial tissue samples. At follow-up, left atrial length in MR dogs was 4.09±0.45 cm, compared with 3.25±0.28 at baseline ( P 〈 0.01), corresponding to a volume of 205±61% of baseline. At follow-up, no differences in atrial conduction pattern and conduction velocities were noted between control and MR dogs. Effective refractory periods were increased homogeneously throughout the left and right atrium. Sustained AF ( 〉 1 hour) was inducible in 10 of 19 MR dogs and none of 13 control dogs ( P 〈 0.01). In the dilated MR left atrium, areas of increased interstitial fibrosis and chronic inflammation were accompanied by increased glycogen ultrastructurally. Conclusions— Chronic atrial dilatation in the absence of overt heart failure leads to an increased vulnerability to AF that is not based on a decrease in wavelength.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000066915.15187.51
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
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