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Thematische Bibliographien / Antiarrhythmic effect / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Antiarrhythmic effect“

Autor: Grafiati

Veröffentlicht am 29. Juni 2021

Zuletzt aktualisiert am 13. Februar 2022

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1

Calvert, Clay A., and John Brown. "Influence of Antiarrhythmia Therapy on Survival Times of 19 Clinically Healthy Doberman Pinschers With Dilated Cardiomyopathy That Experienced Syncope, Ventricular Tachycardia, and Sudden Death (1985–1998)." Journal of the American Animal Hospital Association 40, no. 1 (2004): 24–28. http://dx.doi.org/10.5326/0400024.

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Overtly healthy Doberman pinschers, having moderate to severe myocardial failure secondary to dilated cardiomyopathy, which experienced ventricular tachycardia, syncope or collapse, and sudden death were studied to determine the effect of antiarrhythmic medication on their clinical outcome. Antiarrhythmia drug therapy may have retarded sudden death in 13 treated dogs compared to the six dogs not administered antiarrhythmia drugs.

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2

Mont, Lluís. "Antiarrhythmic Effect of Cardiac Resynchronization." Revista Española de Cardiología (English Edition) 58, no. 10 (2005): 1139–41. http://dx.doi.org/10.1016/s1885-5857(06)60390-3.

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3

Pandya, Bejal, and Pier D. Lambiase. "An avoidable antiarrhythmic side effect." British Journal of Hospital Medicine 67, Sup1 (2006): M14—M15. http://dx.doi.org/10.12968/hmed.2006.67.sup1.20338.

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4

Madakasira, Sudhakar. "Cardiac antiarrhythmic effect of nortriptyline." General Hospital Psychiatry 8, no. 2 (1986): 123–25. http://dx.doi.org/10.1016/0163-8343(86)90098-8.

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5

Rusinova, Radda, Roger E. Koeppe, and Olaf S. Andersen. "A general mechanism for drug promiscuity: Studies with amiodarone and other antiarrhythmics." Journal of General Physiology 146, no. 6 (2015): 463–75. http://dx.doi.org/10.1085/jgp.201511470.

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Amiodarone is a widely prescribed antiarrhythmic drug used to treat the most prevalent type of arrhythmia, atrial fibrillation (AF). At therapeutic concentrations, amiodarone alters the function of many diverse membrane proteins, which results in complex therapeutic and toxicity profiles. Other antiarrhythmics, such as dronedarone, similarly alter the function of multiple membrane proteins, suggesting that a multipronged mechanism may be beneficial for treating AF, but raising questions about how these antiarrhythmics regulate a diverse range of membrane proteins at similar concentrations. One possible mechanism is that these molecules regulate membrane protein function by altering the common environment provided by the host lipid bilayer. We took advantage of the gramicidin (gA) channels’ sensitivity to changes in bilayer properties to determine whether commonly used antiarrhythmics—amiodarone, dronedarone, propranolol, and pindolol, whose pharmacological modes of action range from multi-target to specific—perturb lipid bilayer properties at therapeutic concentrations. Using a gA-based fluorescence assay, we found that amiodarone and dronedarone are potent bilayer modifiers at therapeutic concentrations; propranolol alters bilayer properties only at supratherapeutic concentration, and pindolol has little effect. Using single-channel electrophysiology, we found that amiodarone and dronedarone, but not propranolol or pindolol, increase bilayer elasticity. The overlap between therapeutic and bilayer-altering concentrations, which is observed also using plasma membrane–like lipid mixtures, underscores the need to explore the role of the bilayer in therapeutic as well as toxic effects of antiarrhythmic agents.

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Martinez-Hernandez, E., and L. A. Blatter. "Effect of carvedilol on atrial excitation-contraction coupling, Ca2+ release, and arrhythmogenicity." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 5 (2020): H1245—H1255. http://dx.doi.org/10.1152/ajpheart.00650.2019.

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Here we show that the clinically widely used β-blocker carvedilol has profound effects on Ca2+ signaling and ion currents, but also antiarrhythmic effects in adult atrial myocytes. Carvedilol inhibits sodium and calcium currents and leads to failure of ECC but also prevents spontaneous Ca2+ release from cellular sarcoplasmic reticulum (SR) Ca2+ stores in form of arrhythmogenic Ca2+ waves. The antiarrhythmic effect occurs by carvedilol acting directly on the SR ryanodine receptor Ca2+ release channel.

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Frustaci, Andrea, Marina Caldarulo, Valerio di Rienzo, Matteo A. Russo, and Nicola Gentiloni. "Antiarrhythmic Effect of H-2 Antihistamines." Chest 99, no. 1 (1991): 262–63. http://dx.doi.org/10.1378/chest.99.1.262.

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8

HAYAKAWA, KOICHI. "Evaluation of drug effect of antiarrhythmic agents. a. Guideline of evaluation of effect of antiarrhythmic agents." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 17, no. 2 (1986): 413–14. http://dx.doi.org/10.3999/jscpt.17.413.

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9

Wang, Jie, Jun Li, and Bo Feng. "Shen Song Yang Xin Capsule Combined with Antiarrhythmic Drugs, a New Integrative Medicine Therapy, for the Treatment of Frequent Premature Ventricular Contractions (FPVC): A Meta-Analysis of Randomized Controlled Trials." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/976713.

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Objective. To evaluate the beneficial and adverse effects of Shen Song Yang Xin Capsule (SSYX Capsule) combined with antiarrhythmic drugs for the treatment of frequent premature ventricular contractions (FPVC).Methods. Seven electronic databases were searched to retrieve any potential randomized controlled trials (RCTs) designed to evaluate the clinical efficacy of SSYX Capsule combined with Antiarrhythmic Drugs for FPVC reported in any language, with total effect for FPVC and number of ventricular premature contraction as the main outcome measure. The methodological quality of the included studies was assessed using criteria from the Cochrane Handbook for Systematic Review of Interventions, Version 5.1.0, and analysed using RevMan 5.1.0 software.Results. Sixteen RCTs of SSYX Capsule were included. The methodological quality of the trials was generally evaluated as low. The results of meta-analysis showed that SSYX Capsule combined with antiarrhythmic drugs was more effective in total effect for FPVC and number of ventricular premature contraction compared with Antiarrhythmic Drugs in patients with FPVC or FPVC complicated by other diseases. Ten of the trials reported adverse events, indicating that the safety of SSYX Capsule is still uncertain.Conclusions. There is some but weak evidence about SSYX Capsule combined with antiarrhythmic drugs appearing to be more effective in total effect for FPVC and number of ventricular premature contraction in patients with FPVC and its complications.

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Mirzoyan, Ruben S., Antonina I. Turilova, Tamara S. Gan’shina, et al. "New Antiarrhythmic Agent to Stabilize Functional Activity of Rat Heart Sinus Node Cardiomyocytes." Research Results in Pharmacology 6, no. 4 (2020): 19–27. http://dx.doi.org/10.3897/rrpharmacology.6.58520.

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Introduction: The aim of this study was to explore the antiarrhythmic activity of the new antiarrhythmic drug, succinic acid ester of 5-hydroxyadamantane-2-one (ADK-1110) and its effect on the functional activity of rat heart sinus node. Materials and methods: Experiments were performed on 80 non-linear white awake male rats weighing 200 g, using calcium chloride and aconitine arrhythmia models. The ECG was recorded from all the animals in the II standard lead before the start of the experiment. The effect of ADK-1110 on the electrical activity characteristics of rat heart sinus node pacemakers in vitro was studied on 26 outbred Wistar rats of both sexes with a body weight of 160 to 200 g, using the microelectrode technique. Results and discussion: The compound significantly exceeds the known reference drugs in terms of the antiarrhythmic index. The agent also surpasses our previously proposed adamantane derivative ADK-1100 on calcium chloride model and is not inferior to the aconitine one. The electrophysiological analysis of the sinus node pacemaker cardiomyocytes characteristics in vitro under the influence of ADK-1110 revealed that the compound expands the area occupied by true pacemakers. Discussion: The obtained data indicate the presence of properties of antiarrhythmics of classes I, III, and IV in ADK-1110. The indicated functional remodeling stabilizes the functional activity of the central part of the sinus node. Conclusion: ADK-1110 stabilizes the functional activity of the central part of the sinus node. ADK-1110 also has a cerebrovascular anti-ischemic property.

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Hernandez-Cascales, Jesús. "Resveratrol enhances the inotropic effect but inhibits the proarrhythmic effect of sympathomimetic agents in rat myocardium." PeerJ 5 (March 30, 2017): e3113. http://dx.doi.org/10.7717/peerj.3113.

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BackgroundResveratrol is a cardioprotective agent with known antiarrhythmic effects that has recently been shown to inhibit phosphodiesterase (PDE) enzyme activity. Thus, it is possible that resveratrol increases the inotropic effect of sympathomimetic agents, as PDE inhibitors do but, unlike other PDE inhibitors, its effect may not be accompanied by proarrhythmia due to its antiarrhythmic action. This work is aimed to test this hypothesis.MethodsThis is an “in vitro” concentration-response relationship study. The effects of noradrenaline, tyramine and isoproterenol, alone or in combination with either resveratrol or with the typical PDE inhibitor 3-isobutylmethylxantine (IBMX), were studied in electrically driven strips of right ventricle or in the spontaneously beating free wall of the right ventricle of rat heart in order to investigate inotropic or proarrhythmic effects respectively. Also, the effects of resveratrol or IBMX on the sinoatrial node rate were examined in the isolated right atria of rat heart.ResultsResveratrol (10 µM and 100 µM) produces a leftward shift in the concentration-response curves for the contractile effects of noradrenaline, tyramine or isoproterenol and reduces the –log EC50values of these three agents. IBMX produces similar effects. The spontaneous ventricular beating rate was increased by all three compounds, an effect that was further enhanced by the addition of IBMX. In contrast, resveratrol (100 µM) abolished the effects of these sympathomimetic agents on the ventricular rate. Resveratrol (1–100 µM) had no effect on the sinoatrial node rate, while IBMX produce a concentration dependent sinoatrial tachycardia.DiscussionTaken together, the finding, indicate that resveratrol, like the PDE inhibitor IBMX enhances the contractile effects of sympathomimetic agents but, in contrast to IBMX, it does not enhance their proarrhythmic effect or produce sinoatrial tachycardia. This is most probably consequence of the antiarrhythmic effect of resveratrol which protect against the proarrhythmic effects resulting from PDE inhibition.

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Sugiyama, Atsushi, Yi-xue Xue, Atsushi Hagihara, Masaki Saitoh, and Keitaro Hashimoto. "Characterization of Magnesium Sulfate as an Antiarrhythmic Agent." Journal of Cardiovascular Pharmacology and Therapeutics 1, no. 3 (1996): 243–54. http://dx.doi.org/10.1177/107424849600100308.

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Background Recently, intravenous magnesium therapy has been used for the treatment of ventricular arrhythmias, but data to establish a causal link between the electrophysiological properties and the antiarrhythmic actions are lacking. Methods and Results The acute antiarrhythmic effect of magnesium sulfate was assessed using epinephrine-, digitalis-, and coronary ligation-induced canine ventricular arrhythmia models. The intravenous administration of magnesium sulfate (100 mg/kg) reduced the incidence of the ventricular arrhythmias of all models. The antiarrhythmic effect on the epinephrine-induced arrhythmia was potent and long-lasting, while those on the other arrhythmia models were weak and transient. The direct cardiovascular effects were assessed using the canine isolated, blood-perfused sinus node, papillary muscle, and atrioventricular node preparations. The intracoronary administration of magnesium sulfate (0.1–30 mg) suppressed sinoatrial automaticity and ventricular contraction, while it increased atrio-His and His-ventricular conduction time, coronary blood flow, and the duration of monophasic action potential in a dose-dependent manner. The effects on His-ventricular conduction and monophasic action potential duration were less potent compared with the other cardiovascular effects. Conclusion These results suggest that magnesium sulfate possesses multiple electrophysiological properties and that the effects related to the calcium channel inhibition may be the most relevant for the antiarrhythmic actions.

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13

Choi, Suck Koo, Yeong Ho Choi, and Won Sang Yoo. "Antiarrhythmic Effect of Amiodarone on Ventricular Arrhythmias." Korean Circulation Journal 17, no. 3 (1987): 585. http://dx.doi.org/10.4070/kcj.1987.17.3.585.

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14

Alvarez, Julio L., Lourdes Rubio, Gabino Garrido, and Guy Vassort. "Prajmalium, an Antiarrhythmic with Positive Inotropic Effect." Journal of Cardiovascular Pharmacology 20, no. 1 (1992): 43–49. http://dx.doi.org/10.1097/00005344-199207000-00007.

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15

Alvarez, Julio L., Lourdes Rubio, Gabino Garrido, and Guy Vassort. "Prajmalium, an Antiarrhythmic with Positive Inotropic Effect." Journal of Cardiovascular Pharmacology 20, no. 1 (1992): 43–49. http://dx.doi.org/10.1097/00005344-199220010-00007.

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16

Varró, András, Ilona Bódi, and George Rabloczky. "Antiarrhythmic effect of desethylamiodarone in conscious rats." Journal of Pharmacy and Pharmacology 39, no. 6 (1987): 483–84. http://dx.doi.org/10.1111/j.2042-7158.1987.tb03426.x.

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17

Maslov, L. N., Yu B. Lishmanov, L. A. Maimesculova, and E. A. Krasnov. "A mechanism of antiarrhythmic effect ofRhodiola Rosea." Bulletin of Experimental Biology and Medicine 125, no. 4 (1998): 374–76. http://dx.doi.org/10.1007/bf02499162.

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18

Balashov, V. P., E. A. Sosunov, L. A. Balykova, and L. N. Sernov. "Some mechanisms of antiarrhythmic effect of phosphoenolpyruvate." Bulletin of Experimental Biology and Medicine 128, no. 4 (1999): 1015–17. http://dx.doi.org/10.1007/bf02433193.

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19

Balashov, V. P., D. S. Blinov, V. N. Kazachenko, M. E. Astashev, and O. G. Agenosova. "Membrane Mechanisms of Antiarrhythmic Effect of Quaternidine." Bulletin of Experimental Biology and Medicine 139, no. 6 (2005): 688–91. http://dx.doi.org/10.1007/s10517-005-0379-y.

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20

HASHIMOTO, Keitaro, Kentaro AKIYAMA, and Harumi MITSUHASHI. "Antiarrhythmic Effect of a New Class 1 Antiarrhythmic Drug, Nicainoprol, on Canine Ventricular Arrhythmias." Japanese Journal of Pharmacology 49, no. 2 (1989): 245–54. http://dx.doi.org/10.1016/s0021-5198(19)43074-6.

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HASHIMOTO, Keitaro, Kentaro AKIYAMA, and Harumi MITSUHASHI. "Antiarrhythmic effect of a new class 1 antiarrhythmic drug, nicainoprol, on canine ventricular arrhythmias." Japanese Journal of Pharmacology 49, no. 2 (1989): 245–54. http://dx.doi.org/10.1254/jjp.49.245.

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22

Diez, Emiliano, Jose Sánchez, Natalia Prado, et al. "Ischemic Postconditioning Reduces Reperfusion Arrhythmias by Adenosine Receptors and Protein Kinase C Activation but Is Independent of KATP Channels or Connexin 43." International Journal of Molecular Sciences 20, no. 23 (2019): 5927. http://dx.doi.org/10.3390/ijms20235927.

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Ischemic postconditioning (IPoC) reduces reperfusion arrhythmias but the antiarrhythmic mechanisms remain unknown. The aim of this study was to analyze IPoC electrophysiological effects and the role played by adenosine A1, A2A and A3 receptors, protein kinase C, ATP-dependent potassium (KATP) channels, and connexin 43. IPoC reduced reperfusion arrhythmias (mainly sustained ventricular fibrillation) in isolated rat hearts, an effect associated with a transient delay in epicardial electrical activation, and with action potential shortening. Electrical impedance measurements and Lucifer-Yellow diffusion assays agreed with such activation delay. However, this delay persisted during IPoC in isolated mouse hearts in which connexin 43 was replaced by connexin 32 and in mice with conditional deletion of connexin 43. Adenosine A1, A2A and A3 receptor blockade antagonized the antiarrhythmic effect of IPoC and the associated action potential shortening, whereas exogenous adenosine reduced reperfusion arrhythmias and shortened action potential duration. Protein kinase C inhibition by chelerythrine abolished the protective effect of IPoC but did not modify the effects on action potential duration. On the other hand, glibenclamide, a KATP inhibitor, antagonized the action potential shortening but did not interfere with the antiarrhythmic effect. The antiarrhythmic mechanisms of IPoC involve adenosine receptor activation and are associated with action potential shortening. However, this action potential shortening is not essential for protection, as it persisted during protein kinase C inhibition, a maneuver that abolished IPoC protection. Furthermore, glibenclamide induced the opposite effects. In addition, IPoC delays electrical activation and electrical impedance recovery during reperfusion, but these effects are independent of connexin 43.

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Parasuraman, Subramani, Ramasamy Raveendran, and Raja J. Selvaraj. "Effects of Cleistanthins A and B on Blood Pressure and Electrocardiogram in Wistar Rats." Zeitschrift für Naturforschung C 66, no. 11-12 (2011): 581–87. http://dx.doi.org/10.1515/znc-2011-11-1207.

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We have studied the effects of cleistanthin A and cleistanthin B, phytoconstituents isolated from the leaves of Cleistanthus collinus Roxb. (Euphorbiaceae), on blood pressure, electrocardiogram, and barium chloride-induced arrhythmia in Wistar rats. The two compounds were isolated by column chromatography and their identity was confirmed spectroscopically. A healthy, male Wistar rat was used to record the invasive blood pressure and electrocardiograph. The antiarrhythmic effects of cleistanthins A and B were studied using the barium chloride model. Both cleistanthin A and cleistanthin B showed a dosedependent hypotensive effect. Both compounds reduced the mean blood pressure significantly although the dose required for the effect was higher in the case of cleistanthin B. In the electrocardiogram, cleistanthins A and B significantly altered the electrical activity of the heart, the changes were transient and of no further consequence. Intravenous injection of 64 μg or more of cleistanthins A and B caused a sudden respiratory depression without affecting the electrocardiogram. Cleistanthins A and B did not display any antiarrhythmic effect against barium chloride-induced arrhythmia. In conclusion, both cleistanthin A and cleistanthin B exert a hypotensive effect and have no antiarrhythmic effect against barium chloride-induced arrhythmia in Wistar rats

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Boukhabza, Maroua, Jaouad El Hilaly, Nourdine Attiya, et al. "In SilicoEvaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies." Computational and Mathematical Methods in Medicine 2016 (2016): 1–17. http://dx.doi.org/10.1155/2016/7861653.

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Ion channels are transmembrane proteins that allow the passage of ions according to the direction of their electrochemical gradients. Mutations in more than 30 genes encoding ion channels have been associated with an increasingly wide range of inherited cardiac arrhythmias. In this line, ion channels become one of the most important molecular targets for several classes of drugs, including antiarrhythmics. Nevertheless, antiarrhythmic drugs are usually accompanied by some serious side effects. Thus, developing new approaches could offer added values to prevent and treat the episodes of arrhythmia. In this sense, green tea catechins seem to be a promising alternative because of the significant effect of Epigallocatechin-3-Gallate (E3G) on the electrocardiographic wave forms of guinea pig hearts. Thus, the aim of this study was to evaluate the benefits-risks balance of E3G consumption in the setting of ion channel mutations linked with aberrant cardiac excitability phenotypes. Two gain-of-function mutations,Nav1.5-p.R222Q andNav1.5-p.I141V, which are linked with cardiac hyperexcitability phenotypes were studied. Computer simulations of action potentials (APs) show that 30 μM E3G reduces and suppresses AP abnormalities characteristics of these phenotypes. These results suggest that E3G may have a beneficial effect in the setting of cardiac sodium channelopathies displaying a hyperexcitability phenotype.

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Sergeevichev, David, Vladislav Fomenko, Artem Strelnikov, et al. "Botulinum Toxin-Chitosan Nanoparticles Prevent Arrhythmia in Experimental Rat Models." Marine Drugs 18, no. 8 (2020): 410. http://dx.doi.org/10.3390/md18080410.

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Several experimental studies have recently demonstrated that temporary autonomic block using botulinum toxin (BoNT/A1) might be a novel option for the treatment of atrial fibrillation. However, the assessment of antiarrhythmic properties of BoNT has so far been limited, relying exclusively on vagal stimulation and rapid atrial pacing models. The present study examined the antiarrhythmic effect of specially formulated BoNT/A1-chitosan nanoparticles (BTN) in calcium chloride-, barium chloride- and electrically induced arrhythmia rat models. BTN enhanced the effect of BoNT/A1. Subepicardial injection of BTN resulted in a significant antiarrhythmic effect in investigated rat models. BTN formulation antagonizes arrhythmia induced by the activation of Ca, K and Na channels.

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Khamroev, Tolmas Tolibovich, Zafar Isomiddinovich Sanoev, Ibrokhim To’ychievich Abdinazarov, Sukhrob Davlatyor O’gli Rakhimboev, and Sokhib Zamon O’gli Rashidov. "Study Of The General Pharmacological Properties Of A New Antiarrhythmic N-Deacetyllappaconitine With Oral Administration." American Journal of Medical Sciences and Pharmaceutical Research 03, no. 03 (2021): 60–64. http://dx.doi.org/10.37547/tajmspr/volume03issue03-08.

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The aim of the present study was to study a new antiarrhythmic effect of N-deacetyllappaconitine on the general pharmacological irritant effect on the skin, when applied to the conjunctival sac of the eye, mucosal hyperemia and lacrimation, cumulative, allergenic and diuretic effects. At the same time, it does not cause changes, which makes it more secure.

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Tatarsky, B. A., and N. V. Kazyonnova. "Safety and interaction of direct oral anticoagulants with antiarrhythmic drugs." Russian Journal of Cardiology 26, no. 7 (2021): 4482. http://dx.doi.org/10.15829/1560-4071-2021-4482.

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The use of direct oral anticoagulants minimized the risks associated with vitamin K antagonist (warfarin) therapy. Currently, direct oral anticoagulants have priority over warfarin for the prevention of thromboembolic events in patients with atrial fibrillation and a number of other conditions requiring anticoagulant therapy. Direct oral anticoagulants along with antiarrhythmic therapy are the accepted strategy for atrial fibrillation treatment. At the same time, the effect of drug-drug interactions (DDI) between direct oral anticoagulants and antiarrhythmic drugs, which have common points of metabolic application, has not been fully elucidated. In order to provide effective and safe anticoagulant and antiarrhythmic therapy in patients with AF, it is important to understand the mechanisms and severity of DDI of direct oral anticoagulants and antiarrhythmic agents. This review discusses the issues of DDI of direct oral anticoagulants and antiarrhythmic drugs used to treat atrial fibrillation.

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Dunnington, CS. "Sotalol hydrochloride (Betapace): a new antiarrhythmic drug." American Journal of Critical Care 2, no. 5 (1993): 397–406. http://dx.doi.org/10.4037/ajcc1993.2.5.397.

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Sotalol hydrochloride (Betapace), recently released by the Food and Drug Administration for general use, is used to treat a variety of ventricular and supraventricular tachyarrhythmias. The drug's dominant action is the result of combined nonselective beta-adrenergic antagonism (Class II effect) and monophasic action potential duration prolongation in all cardiac tissues (Class III effect). It causes less left ventricular depression than propranolol and has a low incidence of toxicity. It is a useful addition to the antiarrhythmic drug armamentarium. This article reviews the drug's pharmacokinetic, pharmacodynamic and electrophysiologic properties, clinical uses and potential side effects. Reports on the drug's use as an antianginal and antihypertensive agent are also discussed.

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Yoon, Namsik, Seo Na Hong, Ki Hong Lee, et al. "ANTIARRHYTHMIC EFFECT OF ARTEMISININ IN BRUGADA SYNDROME MODEL." Journal of the American College of Cardiology 71, no. 11 (2018): A424. http://dx.doi.org/10.1016/s0735-1097(18)30965-3.

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Kurita, Takashi, Tohru Ohe, Yuichi Katagiri, et al. "Clinical investigation of proarrhythmic effect with antiarrhythmic agents." Japanese Journal of Electrocardiology 13, no. 1 (1993): 48–60. http://dx.doi.org/10.5105/jse.13.48.

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Kiss, Attila, László Juhász, Ildikó Huliák⁎, Péter Ferdinady⁎, and Ágnes Végh. "Peroxynitrite induces an antiarrhythmic effect in anaesthetised dogs." Journal of Molecular and Cellular Cardiology 42, no. 6 (2007): S9—S10. http://dx.doi.org/10.1016/j.yjmcc.2007.03.027.

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Manoach, Mordechai, and Narcis Tribulova. "Sotalol: The Mechanism of Its Antiarrhythmic-Defibrillating Effect." Cardiovascular Drug Reviews 19, no. 2 (2006): 172–82. http://dx.doi.org/10.1111/j.1527-3466.2001.tb00062.x.

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KATO, Rinya, Iwao SOTOBATA, Mitsuhiro YOKOTA, et al. "The pharmacokinetics and antiarrhythmic effect of oral cibenzoline." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 20, no. 2 (1989): 363–72. http://dx.doi.org/10.3999/jscpt.20.363.

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Giardina, Elsa-Grace V., Khether Raby, Alan L. Saroff, and May Louie-Chu. "Antiarrhythmic Effect of Lorcainide in Patients Taking Digoxin." Journal of Clinical Pharmacology 27, no. 5 (1987): 378–83. http://dx.doi.org/10.1002/j.1552-4604.1987.tb03034.x.

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McMurray, John, Lars Køber, Michele Robertson, et al. "Antiarrhythmic effect of carvedilol after acute myocardial infarction." Journal of the American College of Cardiology 45, no. 4 (2005): 525–30. http://dx.doi.org/10.1016/j.jacc.2004.09.076.

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Fauchier, Laurent, Bertrand Pierre, Axel de Labriolle, Caroline Grimard, Noura Zannad, and Dominique Babuty. "Antiarrhythmic Effect of Statin Therapy and Atrial Fibrillation." Journal of the American College of Cardiology 51, no. 8 (2008): 828–35. http://dx.doi.org/10.1016/j.jacc.2007.09.063.

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37

Lishmanov, Yu B., E. V. Uskina, L. N. Maslov, and A. V. Krylatov. "Opiatergic mechanisms of the antiarrhythmic effect of adaptation." Bulletin of Experimental Biology and Medicine 122, no. 3 (1996): 892–94. http://dx.doi.org/10.1007/bf02446573.

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38

Lishmanov, Yu B., L. V. Maslova, L. N. Maslov, and E. N. Dan'shina. "Antiarrhythmic effect ofRodiola rosea and its possible mechanism." Bulletin of Experimental Biology and Medicine 116, no. 2 (1993): 974–76. http://dx.doi.org/10.1007/bf00786074.

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39

Mikhailova, S. D., G. I. Storozhakov, S. Yu Gukova, and T. M. Semushkina. "Mechanism of the antiarrhythmic effect of laser irradiation." Bulletin of Experimental Biology and Medicine 113, no. 5 (1992): 612–15. http://dx.doi.org/10.1007/bf00783735.

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40

Paterson, D. J. "Antiarrhythmic mechanisms during exercise." Journal of Applied Physiology 80, no. 6 (1996): 1853–62. http://dx.doi.org/10.1152/jappl.1996.80.6.1853.

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Exercise disturbs cardiac sympathovagal and ionic balance. In arterial blood, vigorous exercise can double plasma K(+), decrease pH by 0.4 unit, and raise catecholamines 15-fold. If any of these changes are experienced at rest, there is an increased risk of arrhythmia and cardiac arrest, yet in exercise they are usually tolerated. How the heart is protected from the chemical stress caused by exercise is not fully understood but may be related to a collective antiarrhythmic effect of these chemical changes, so when they combine there is a mutual antagonism. Catecholamines can offset the harmful cardiac effects of hyperkalemia and acidosis in isolated hearts and whole hearts in vivo and improve action-potential characteristics in K(+)-depolarized ventricular myocytes. This results from an increase in the inward Ca2(+) current that is modulated by both adrenergic and nonadrenergic hormones. Conversely, hyperkalemia can reduce or abolish the incidence of norepinephrine-induced arrhythmias. The efficacy of the mutual antagonism is reduced when the combination of acidosis, hyperkalemia, and high levels of norepinephrine are superimposed on a heart with regional ischemia or a small infarct. However, the heart may be at greatest risk in the postexercise period when plasma K(+) is low and the adrenergic tone is high. Little is known about this period, but abnormal regulation of electrolyte and cardiac sympathovagal balance may increase the incidence of arrhythmia, especially if there is underlying ischemia. Although regular physical activity can reduce the incidence of sudden cardiac death, recent epidemiological studies show that vigorous exercise can trigger myocardial infarction and sudden cardiac death, especially in habitually sedentary subjects with coronary artery disease. This may be partly related to disruption of the normal protective mechanism that allows the heart to cope with the chemical stress caused by exercise.

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41

Provenier, Frank, and Steven Droogmans. "Atrial Fibrillation and Flecainide – Safety, Effectiveness and Quality of Life Outcomes." European Cardiology Review 6, no. 3 (2010): 44. http://dx.doi.org/10.15420/ecr.2010.6.3.44.

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Flecainide is a class IC antiarrhythmic agent indicated for patients with atrial fibrillation without any evidence of structural heart disease. This brief review of four recent studies on flecainide focuses on safety aspects, efficacy and the debate on impact on quality of life in this patient population. This article also briefly summarises data from the Cardiac Arrhythmia Suppression Trial (CAST) and the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study, which investigated the effect of antiarrhythmics such as flecainide on morbidity and mortality. When administered according to recommended guidelines, flecainide is safe and is not associated with increased mortality. It is effective for the treatment of atrial fibrillation, improving quality of life in these patients.

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42

Hashimoto, Keitaro, Kozo Watanabe, and Harumi Mitsuhashi. "Antiarrhythmic effect of a new class 1 antiarrhythmic drug, AN-132, on ventricular arrhythmias in beagles." Cardiovascular Drugs and Therapy 3, no. 5 (1989): 683–89. http://dx.doi.org/10.1007/bf01857620.

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43

Bernier, M., and D. J. Hearse. "Reperfusion-induced arrhythmias: mechanisms of protection by glucose and mannitol." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 5 (1988): H862—H870. http://dx.doi.org/10.1152/ajpheart.1988.254.5.h862.

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Isolated rat hearts (n = 15/group) were subjected to regional ischemia (10 min) and reperfusion (3 min). Mannitol (5, 11, 25, 50, 55, 61, or 75 mM included in the perfusate throughout) reduced reperfusion-induced sustained ventricular fibrillation (VF) from its control incidence of 93% (14/15) to 80, 80, 40, 27, 47, 80, and 80%, respectively. Addition of glucose (11 mM) potentiated this effect, VF now fell to 87, 47, 33, 7, 7, 7, 13, and 13%, respectively. However, 11 mM glucose alone exerted no antiarrhythmic effects. When hearts (n = 15/group) were perfused with identical osmotic loads of mannitol plus glucose (11 + 50, 50 + 11, 61 + 0, or 0 + 61 mM, respectively), very different antiarrhythmic effects were observed. When given throughout the experimental period, glucose alone (0, 11, 25, 50 or 61 mM) had no effect on the incidence of VF (93, 87, 47, 53, and 20%, respectively), but when glucose was added 2 min before reperfusion, improved protection was observed (VF: 93, 87, 40, 27, and 13%, respectively). Our results suggest that the osmotic and free-radical scavenging properties of hexoses are relatively unimportant in relation to their antiarrhythmic effects. The metabolic effects are complex, suggesting that low concentrations of glucose may be beneficial, whereas high concentrations may be detrimental.

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Lin, Yuanyuan, Junhu Li, Baozhong Zhu, et al. "Zacopride Exerts an Antiarrhythmic Effect by Specifically Stimulating the Cardiac Inward Rectifier Potassium Current in Rabbits: Exploration of a New Antiarrhythmic Strategy." Current Pharmaceutical Design 26, no. 44 (2020): 5746–54. http://dx.doi.org/10.2174/1381612826666200701135508.

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Background: Zacopride, a potent antagonist of 5-HT3 receptors and an agonist of 5-HT4 receptors, is a gastrointestinal prokinetic agent. In a previous study, we discovered that zacopride selectively stimulated the inward rectifier potassium current (IK1) in the rat and that agonizing IK1 prevented or eliminated aconitine-induced arrhythmias in rats. Objective: Our aims were to confirm that the antiarrhythmic effects of zacopride are mediated by selectively enhancing IK1 in rabbits. Methods: The effects of zacopride on the function of the main ion channels were investigated using a whole-cell patch-clamp technique in rabbits. Effects of zacopride on cardiac arrhythmias were also explored experimentally both in vivo and in vitro. Results: Zacopride moderately enhanced cardiac IK1 but had no apparent action on voltage-gated sodium current (INa), L- type calcium current (ICa-L), sodium-calcium exchange current (INa/Ca), transient outward potassium current (Ito), or delayed rectifier potassium current (IK) in rabbits. Zacopride also had a marked antiarrhythmic effect in vivo and in vitro. We proved that the resting membrane potential (RMP) was hyperpolarized in the presence of 1 μmol/L zacopride, and the action potential duration (APD) at 90% repolarization (APD90) was shortened by zacopride (0.1-10 μmol/L) in a concentration- dependent manner. Furthermore, zacopride at 1 μmol/L significantly decreased the incidence of drug-induced early afterdepolarization (EAD) in rabbit ventricular myocytes. Conclusion: Zacopride is a selective agonist of rabbit cardiac IK1 and that IK1 enhancement exerts potential antiarrhythmic effects.

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Dorian, Paul. "Antiarrhythmic Drug Therapy of Atrial Fibrillation: Focus on New Agents." Journal of Cardiovascular Pharmacology and Therapeutics 8, no. 1_suppl (2003): S27—S31. http://dx.doi.org/10.1177/107424840300800104.

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The precise mechanisms of clinical effect of antiarrhythmic agents and the ideal “molecular targets” against arrhythmias, in particular atrial fibrillation, are poorly understood. Current antiarrhythmic drug development, particularly for drugs expected to be active against atrial fibrillation, has focused on drugs with multiple ionic mechanisms of action, in particular on those that block multiple potassium channels. Investigation of antiarrhythmic agents is complicated by the diversity of animal-disease models studied, by the potential multiple mechanisms of arrhythmias, and by the incompletely understood relationships between risks and benefits of antiarrhythmic drug therapy. Furthermore, rhythm control strategies in large groups of patients with atrial fibrillation have failed to show substantial clinical benefit. Nevertheless, drugs that block multiple potassium channels and appear to have relatively little organ toxicity, such as tedisamil, may represent an important new avenue in the therapeutic approach to highly symptomatic arrhythmias such as atrial fibrillation.

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Kamiya, J., H. Banno, K. Yoshihara, M. Ishii, and T. Katakami. "Antiarrhythmic effect and haemodynamic properties of MS-551, a new class III antiarrhythmic agent, in anaesthetized dogs." European Journal of Pharmacology 183, no. 5 (1990): 1776–77. http://dx.doi.org/10.1016/0014-2999(90)92090-6.

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47

Dorian, Paul. "Antiarrhythmic Action ofβ-Blockers: Potential Mechanisms". Journal of Cardiovascular Pharmacology and Therapeutics 10, № 4_suppl (2005): S15—S22. http://dx.doi.org/10.1177/10742484050100i403.

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Sympathetic nervous system overactivity has been linked to ventricular tachyarrhythmias and sudden death. It has been hypothesized that the extent and nature of the arrhythmogenic effect of sympathetic stimulation depends on the underlying myocardial substrate, the mechanism of the arrhythmia, and the integrated effects of sympathetic stimulation in the particular individual circumstance. Multiple direct and indirect mechanisms of adrenergic action on the heart may benefit from the known antiarrhythmic actions of β-blocker therapy and other interventions that decrease sympathetic tone. The antiarrhythmic mechanism of β-blockade (and possibly α-blockade) will depend on the specific mechanism of the individual arrhythmia and will differ for those arrhythmias caused by tachycardia and ischemia, those caused by reentry and promoted by decreased conduction velocity and shortened refractoriness, and those caused by early or delayed afterdepolarizations, usually in the context of prolonged action potential duration. Antagonism of cardiac adrenergic activity by β-blockade in particular is the best-established drug therapy to prevent ventricular arrhythmias.

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Ramadeen, Andrew, and Paul Dorian. "How Are n-3 LCPUFAs Antiarrhythmic? A Reassessment of n-3 LCPUFAs in Cardiac Disease." Cardiology Research and Practice 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/746709.

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Long-chain n-3-polyunsaturated fatty acids (n-3 LCPUFAs), referring particularly to marine-derived eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been shown to be effective in treating arrhythmias in some clinical trials and animal studies. The mechanism for this effect of n-3 LCPUFAs is not well understood. Experimental studies and clinical trials published in the 1980s and 1990s suggested that n-3 LCPUFAs may be antiarrhythmic drugs, but more recent trials have not confirmed this. In this paper, we examine evidence for, and against, the direct antiarrhythmic action of n-3 LCPUFAs and suggest that antistructural remodeling effects of n-3 LCPUFAs may be more relevant in accounting for their clinical effects.

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Banach, Monika, Monika Rudkowska, Agata Sumara, and Kinga Borowicz-Reutt. "Amiodarone Enhances Anticonvulsive Effect of Oxcarbazepine and Pregabalin in the Mouse Maximal Electroshock Model." International Journal of Molecular Sciences 22, no. 3 (2021): 1041. http://dx.doi.org/10.3390/ijms22031041.

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Accumulating experimental studies show that antiarrhythmic and antiepileptic drugs share some molecular mechanisms of action and can interact with each other. In this study, the influence of amiodarone (a class III antiarrhythmic drug) on the antiseizure action of four second-generation antiepileptic drugs was evaluated in the maximal electroshock model in mice. Amiodarone, although ineffective in the electroconvulsive threshold test, significantly potentiated the antielectroshock activity of oxcarbazepine and pregabalin. Amiodarone, given alone or in combination with oxcarbazepine, lamotrigine, or topiramate, significantly disturbed long-term memory in the passive-avoidance task in mice. Brain concentrations of antiepileptic drugs were not affected by amiodarone. However, the brain concentration of amiodarone was significantly elevated by oxcarbazepine, topiramate, and pregabalin. Additionally, oxcarbazepine and pregabalin elevated the brain concentration of desethylamiodarone, the main metabolite of amiodarone. In conclusion, potentially beneficial action of amiodarone in epilepsy patients seems to be limited by neurotoxic effects of amiodarone. Although results of this study should still be confirmed in chronic protocols of treatment, special precautions are recommended in clinical conditions. Coadministration of amiodarone, even at low therapeutic doses, with antiepileptic drugs should be carefully monitored to exclude undesired effects related to accumulation of the antiarrhythmic drug and its main metabolite, desethylamiodarone.

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Airaksinen, K. E. Juhani, and Heikki V. Huikuri. "Antiarrhythmic Effect of Repeated Coronary Occlusion During Balloon Angioplasty." Journal of the American College of Cardiology 29, no. 5 (1997): 1035–38. http://dx.doi.org/10.1016/s0735-1097(97)00042-9.

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