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  1. Article ; Online: Atrial Fibrillation Induced by Anticancer Drugs and Underling Mechanisms.

    Burashnikov, Alexander

    Journal of cardiovascular pharmacology

    2022  Volume 80, Issue 4, Page(s) 540–546

    Abstract: Abstract: Cancer therapy has made major progress in the past several decades, but treatments are often accompanied by significant side effects. Arrhythmias are a widespread complication of some antineoplastic drugs, with atrial fibrillation (AF) being ... ...

    Abstract Abstract: Cancer therapy has made major progress in the past several decades, but treatments are often accompanied by significant side effects. Arrhythmias are a widespread complication of some antineoplastic drugs, with atrial fibrillation (AF) being the most often encountered drug-associated arrhythmia. Preexisting AF risk factors are commonly present in cancer patients who develop drug-associated AF, and active cancer itself may cause or promote AF. Although anticancer drugs may induce AF in cancer patients without AF risk factors, it appears that most drug-associated AF develop when cancer drugs add or aggravate precancer-existing and/or cancer-related pro-AF factors/alterations, additively or synergistically producing AF. Abnormalities in intracellular calcium activity seem to be involved in the generation of anticancer drug-induced AF. In cancer survivors with cancer therapy-induced cardiomyopathy, AF often occurs, with most of the arrhythmias likely to develop secondary to the cardiomyopathy. AF may lead to modification or even cessation of cancer therapy. The management of AF in patients with cancer is currently conducted largely based on pragmatic assumptions. This review briefly discusses AF caused by anticancer drugs and the underlying mechanisms.
    MeSH term(s) Anti-Arrhythmia Agents/pharmacology ; Antineoplastic Agents/adverse effects ; Atrial Fibrillation/chemically induced ; Atrial Fibrillation/diagnosis ; Atrial Fibrillation/drug therapy ; Calcium ; Drug-Related Side Effects and Adverse Reactions ; Humans
    Chemical Substances Anti-Arrhythmia Agents ; Antineoplastic Agents ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-10-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 391970-5
    ISSN 1533-4023 ; 0160-2446
    ISSN (online) 1533-4023
    ISSN 0160-2446
    DOI 10.1097/FJC.0000000000001182
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Depolarization of the atrial resting membrane potential as an approach to enhance the anti-atrial fibrillation efficacy of sodium channel blockers.

    Burashnikov, Alexander

    Heart rhythm

    2021  Volume 18, Issue 7, Page(s) 1221–1222

    MeSH term(s) Atrial Fibrillation/drug therapy ; Heart Atria ; Humans ; Membrane Potentials ; Sodium Channel Blockers/pharmacology ; Sodium Channel Blockers/therapeutic use
    Chemical Substances Sodium Channel Blockers
    Language English
    Publishing date 2021-03-27
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2021.03.039
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Investigational Anti-Atrial Fibrillation Pharmacology and Mechanisms by Which Antiarrhythmics Terminate the Arrhythmia: Where Are We in 2020?

    Burashnikov, Alexander

    Journal of cardiovascular pharmacology

    2020  Volume 76, Issue 5, Page(s) 492–505

    Abstract: Antiarrhythmic drugs remain the mainstay therapy for patients with atrial fibrillation (AF). A major disadvantage of the currently available anti-AF agents is the risk of induction of ventricular proarrhythmias. Aiming to reduce this risk, several atrial- ...

    Abstract Antiarrhythmic drugs remain the mainstay therapy for patients with atrial fibrillation (AF). A major disadvantage of the currently available anti-AF agents is the risk of induction of ventricular proarrhythmias. Aiming to reduce this risk, several atrial-specific or -selective ion channel block approaches have been introduced for AF suppression, but only the atrial-selective inhibition of the sodium channel has been demonstrated to be valid in both experimental and clinical studies. Among the other pharmacological anti-AF approaches, "upstream therapy" has been prominent but largely disappointing, and pulmonary delivery of anti-AF drugs seems to be promising. Major contradictions exist in the literature about the electrophysiological mechanisms of AF (ie, reentry or focal?) and the mechanisms by which anti-AF drugs terminate AF, making the search for novel anti-AF approaches largely empirical. Drug-induced termination of AF may or may not be associated with prolongation of the atrial effective refractory period. Anti-AF drug research has been largely based on the "suppress reentry" ideology; however, results of the AF mapping studies increasingly indicate that nonreentrant mechanism(s) plays an important role in the maintenance of AF. Also, the analysis of anti-AF drug-induced electrophysiological alterations during AF, conducted in the current study, leans toward the focal source as the prime mechanism of AF maintenance. More effort should be placed on the investigation of pharmacological suppression of the focal mechanisms.
    MeSH term(s) Action Potentials/drug effects ; Animals ; Anti-Arrhythmia Agents/pharmacology ; Atrial Fibrillation/diagnosis ; Atrial Fibrillation/drug therapy ; Atrial Fibrillation/physiopathology ; Heart Conduction System/drug effects ; Heart Conduction System/physiopathology ; Heart Rate/drug effects ; Humans ; Potassium Channel Blockers/pharmacology ; Refractory Period, Electrophysiological/drug effects ; Sodium Channel Blockers/pharmacology
    Chemical Substances Anti-Arrhythmia Agents ; Potassium Channel Blockers ; Sodium Channel Blockers
    Language English
    Publishing date 2020-11-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 391970-5
    ISSN 1533-4023 ; 0160-2446
    ISSN (online) 1533-4023
    ISSN 0160-2446
    DOI 10.1097/FJC.0000000000000892
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mild elevation of extracellular potassium greatly potentiates the effect of sodium channel block to cardiovert atrial fibrillation: The Lankenau approach.

    Burashnikov, Alexander / Antzelevitch, Charles

    Heart rhythm

    2023  Volume 20, Issue 9, Page(s) 1257–1264

    Abstract: Background: Cardioversion of atrial fibrillation (AF) is a common clinical necessity, and there is a need for more effective and safe options for acute cardioversion of AF.: Objective: The purpose of this study was to test the hypothesis that the ... ...

    Abstract Background: Cardioversion of atrial fibrillation (AF) is a common clinical necessity, and there is a need for more effective and safe options for acute cardioversion of AF.
    Objective: The purpose of this study was to test the hypothesis that the efficacy and time course of AF cardioversion by sodium channel current (I
    Methods: Using a canine acetylcholine (ACh)-mediated AF model (isolated coronary-perfused right atrial preparations with a rim of right ventricle), we evaluated the ability of flecainide to suppress AF in the presence of [K
    Results: At [K
    Conclusion: Our findings suggest that a combination of I
    MeSH term(s) Animals ; Dogs ; Atrial Fibrillation ; Flecainide/pharmacology ; Anti-Arrhythmia Agents/pharmacology ; Anti-Arrhythmia Agents/therapeutic use ; Heart Atria ; Sodium Channels
    Chemical Substances Flecainide (K94FTS1806) ; Anti-Arrhythmia Agents ; Sodium Channels
    Language English
    Publishing date 2023-05-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2023.05.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Late INa Inhibition as an Antiarrhythmic Strategy.

    Burashnikov, Alexander

    Journal of cardiovascular pharmacology

    2017  Volume 70, Issue 3, Page(s) 159–167

    Abstract: Late sodium channel current (late INa) is considered to be an antiarrhythmic target. The prime antiarrhythmic mechanisms of late INa inhibition have been suggested to be (1) suppression of intracellular calcium [Cai]-mediated rhythmic activity (through ... ...

    Abstract Late sodium channel current (late INa) is considered to be an antiarrhythmic target. The prime antiarrhythmic mechanisms of late INa inhibition have been suggested to be (1) suppression of intracellular calcium [Cai]-mediated rhythmic activity (through reduction in Cai secondary to the decrease in intracellular sodium [Nai]) and (2) normalization of repolarization. Endogenous late INa is a small current and acceleration of the heart rate decreases late INa density. Late INa influx may significantly contribute to Nai loading, but it seems to largely occur under the combined conditions of augmented late INa density, bradycardia, and prolonged repolarization. At the same time, the relative contribution of late INa (including endogenous) in any type of prolonged cardiac repolarization is critical. Sodium channel blockers inhibit both late INa and peak INa, and a specific block of late INa might be achieved at slow and normal but seems not at rapid activation rates, at which peak INa, a much greater current, is also likely to be inhibited. The antiarrhythmic potential of a specific inhibition of late INa seems to best fit for, or may be limited to, the prevention of arrhythmias associated with prolonged repolarization, but it seems to be applicable to all types of arrhythmic abnormalities with elongated cardiac repolarization.
    Language English
    Publishing date 2017-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 391970-5
    ISSN 1533-4023 ; 0160-2446
    ISSN (online) 1533-4023
    ISSN 0160-2446
    DOI 10.1097/FJC.0000000000000510
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Cardiovascular Complications of Anticancer Therapy: A Developing Storm in Medicine.

    Burashnikov, Alexander / Abbate, Antonio / Booz, George W

    Journal of cardiovascular pharmacology

    2022  Volume 80, Issue 4, Page(s) 491–492

    MeSH term(s) Heart Diseases ; Humans
    Language English
    Publishing date 2022-10-01
    Publishing country United States
    Document type Editorial
    ZDB-ID 391970-5
    ISSN 1533-4023 ; 0160-2446
    ISSN (online) 1533-4023
    ISSN 0160-2446
    DOI 10.1097/FJC.0000000000001355
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Effect of Flecainide and Ibutilide Alone and in Combination to Terminate and Prevent Recurrence of Atrial Fibrillation.

    Burashnikov, Alexander / Di Diego, José M / Patocskai, Bence / Echt, Debra S / Belardinelli, Luiz / Antzelevitch, Charles

    Circulation. Arrhythmia and electrophysiology

    2023  Volume 17, Issue 1, Page(s) e012454

    Abstract: Background: There is a need for improved approaches to rhythm control therapy of atrial fibrillation (AF).: Methods: The effectiveness of flecainide (1.5 µmol/L) and ibutilide (20 nmol/L), alone and in combination, to cardiovert and prevent AF ... ...

    Abstract Background: There is a need for improved approaches to rhythm control therapy of atrial fibrillation (AF).
    Methods: The effectiveness of flecainide (1.5 µmol/L) and ibutilide (20 nmol/L), alone and in combination, to cardiovert and prevent AF recurrence was studied in canine-isolated coronary-perfused right atrioventricular preparations. We also examined the safety of the combination of flecainide (1.5 µmol/L) and ibutilide (50 nmol/L) using canine left ventricular wedge preparations.
    Results: Sustained AF (>1 hour) was inducible in 100%, 60%, 20%, and 0% of atria in the presence of acetylcholine alone, acetylcholine+ibutilide, acetylcholine+flecainide, and acetylcholine+ibutilide+flecainide, respectively. When used alone, flecainide and ibutilide cardioverted sustained AF in 40% and 20% of atria, respectively, but in 100% of atria when used in combination. Ibutilide prolonged atrial and ventricular effective refractory period by 15% and 8%, respectively, at a cycle length of 500 ms (
    Conclusions: In our experimental model, a combination of flecainide and ibutilide significantly improves cardioversion and prevents the recurrence of AF compared with monotherapies with little to no risk for the development of long-QT-mediated ventricular proarrhythmia.
    MeSH term(s) Animals ; Dogs ; Flecainide/therapeutic use ; Atrial Fibrillation/drug therapy ; Atrial Fibrillation/prevention & control ; Anti-Arrhythmia Agents/pharmacology ; Anti-Arrhythmia Agents/therapeutic use ; Acetylcholine ; Long QT Syndrome/drug therapy ; Sulfonamides
    Chemical Substances Flecainide (K94FTS1806) ; Anti-Arrhythmia Agents ; ibutilide (2436VX1U9B) ; Acetylcholine (N9YNS0M02X) ; Sulfonamides
    Language English
    Publishing date 2023-12-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2426129-4
    ISSN 1941-3084 ; 1941-3149
    ISSN (online) 1941-3084
    ISSN 1941-3149
    DOI 10.1161/CIRCEP.123.012454
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Is extensive atrial fibrosis in the setting of heart failure associated with a reduced atrial fibrillation burden?

    Burashnikov, Alexander / Antzelevitch, Charles

    Pacing and clinical electrophysiology : PACE

    2018  Volume 41, Issue 10, Page(s) 1289–1297

    Abstract: Atrial fibrillation (AF) affects 10-50% of patients with chronic heart failure (HF) and is associated with poor long-term prognosis. AF is commonly associated with atrial structural remodeling (ASR), principally characterized by atrial dilatation and ... ...

    Abstract Atrial fibrillation (AF) affects 10-50% of patients with chronic heart failure (HF) and is associated with poor long-term prognosis. AF is commonly associated with atrial structural remodeling (ASR), principally characterized by atrial dilatation and fibrosis. However, the occurrence of AF in the full spectrum of ASR encountered in patients with HF is poorly defined. Experimental studies have presented evidence that extensive ASR can be accompanied with a reduced burden of AF, secondary to a prominent depression of atrial excitability. This reduction in AF burden is associated with severe atrial fibrosis rather than with dilatation. Clinical studies of patients with HF point to the possibility that advanced ASR is associated with a less frequent AF occurrence than moderate ASR. Our goal in this review is to introduce the hypothesis that AF is less likely to occur in severe versus moderate atrial ASR in the setting of HF and that it is severe atrial fibrosis-associated depression of atrial excitability that reduces AF burden.
    MeSH term(s) Animals ; Atrial Fibrillation/physiopathology ; Endomyocardial Fibrosis/physiopathology ; Heart Atria/physiopathology ; Heart Failure/physiopathology ; Humans
    Language English
    Publishing date 2018-09-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 424437-0
    ISSN 1540-8159 ; 0147-8389
    ISSN (online) 1540-8159
    ISSN 0147-8389
    DOI 10.1111/pace.13474
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Effectiveness of Late

    Burashnikov, Alexander / Antzelevitch, Charles

    Circulation. Arrhythmia and electrophysiology

    2017  Volume 10, Issue 3

    MeSH term(s) Animals ; Heart Ventricles ; Rabbits ; Sodium ; Sodium Channel Blockers ; Ventricular Fibrillation
    Chemical Substances Sodium Channel Blockers ; Sodium (9NEZ333N27)
    Language English
    Publishing date 2017-03-17
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2426129-4
    ISSN 1941-3084 ; 1941-3149
    ISSN (online) 1941-3084
    ISSN 1941-3149
    DOI 10.1161/CIRCEP.117.005111
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Are there atrial selective/predominant targets for "upstream" atrial fibrillation therapy?

    Burashnikov, Alexander

    Heart rhythm

    2008  Volume 5, Issue 9, Page(s) 1294–1295

    MeSH term(s) Atrial Fibrillation/genetics ; Cardiac Pacing, Artificial ; Cellular Structures ; GTP Phosphohydrolases/genetics ; Humans ; Inflammation/genetics ; Janus Kinase 2/metabolism ; Janus Kinases/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; STAT1 Transcription Factor/genetics ; STAT3 Transcription Factor/genetics ; Signal Transduction ; Transcriptional Activation ; Translocation, Genetic ; rac1 GTP-Binding Protein/metabolism
    Chemical Substances STAT1 Transcription Factor ; STAT1 protein, human ; STAT3 Transcription Factor ; STAT3 protein, human ; Janus Kinase 2 (EC 2.7.10.2) ; Janus Kinases (EC 2.7.10.2) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; GTP Phosphohydrolases (EC 3.6.1.-) ; rac1 GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2008-09
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2008.06.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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