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Journal articles on the topic 'Antiarrhythmic effect'

Author: Grafiati

Published: 29 June 2021

Last updated: 29 July 2025

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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

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

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3

Rudakova, I. P., and O. V. Gashkova. "Assessment of impact of a new derivative 2-(diethylamino)-N-(o-toluyl) acetamide, manifesting antiarrhythmic effect in heart rhythm disorders of peripheral origin, on cardiovascular system." Perm Medical Journal 39, no. 4 (2022): 58–64. http://dx.doi.org/10.17816/pmj39458-64.

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Objective. To study the effect of a new derivative of arylamides of aminocarboxylic acids, which has a high antiarrhythmic activity on the state of the cardiovascular system. Materials and methods. To study the antiarrhythmic activity of the compound, the experiment was carried out on a model of arrhythmia caused by intravenous administration of aconitine. The effect was evaluated by its ability to prevent the occurrence of arrhythmia or to prolong the survival time of animals. In addition, an analysis of the electrocardiogram of awake rats and rabbits was carried out. The test compound

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4

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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5

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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6

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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7

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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8

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 st

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9

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 pacemaker

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10

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. https://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 pacemaker

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11

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-in

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12

Murai, Kyosuke, Amir Vasigh, Tamás Alexy, Kálmán Tóth, and László Czopf. "The Role of Ranolazine in the Treatment of Ventricular Tachycardia and Atrial Fibrillation: A Narrative Review of the Clinical Evidence." Biomedicines 12, no. 8 (2024): 1669. http://dx.doi.org/10.3390/biomedicines12081669.

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Cardiac arrhythmias are among the leading causes of morbidity and mortality worldwide. While antiarrhythmic drugs traditionally represent the first-line management strategy, their use is often limited by profound proarrhythmic effects. Several studies, including randomized control trials (RCTs), have demonstrated the antiarrhythmic efficacy of ranolazine, which is registered as an antianginal agent, while also establishing its safety profile. This review compiles clinical evidence investigating the antiarrhythmic properties of ranolazine, focusing primarily on ventricular tachycardia (VT) and

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13

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 di

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14

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

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15

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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16

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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17

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 injec

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18

Lustyk, Klaudia, Kinga Sałaciak, Agata Siwek та ін. "The Antiarrhythmic and Hypotensive Effects of S-61 and S-73, the Pyrrolidin-2-one Derivatives with α1-Adrenolytic Properties". International Journal of Molecular Sciences 23, № 18 (2022): 10381. http://dx.doi.org/10.3390/ijms231810381.

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Heart rhythm abnormalities are a cause of many deaths worldwide. Unfortunately, the available antiarrhythmic drugs show limited efficacy and proarrhythmic potential. Thus, efforts should be made to search for new, more effective, and safer pharmacotherapies. Several studies suggested that blocking the α1-adrenoceptors could restore normal heart rhythm in arrhythmia. In this study, we aimed to assess the antiarrhythmic potential of S-61 and S-73, two novel pyrrolidin-2-one derivatives with high affinity for α1-adrenergic receptors. First, using radioligand binding studies, we demonstrated that

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19

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 wi

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20

Namekata, Iyuki, Maika Seki, Taro Saito, Ryosuke Odaka, Shogo Hamaguchi, and Hikaru Tanaka. "Automaticity of the Pulmonary Vein Myocardium and the Effect of Class I Antiarrhythmic Drugs." International Journal of Molecular Sciences 25, no. 22 (2024): 12367. http://dx.doi.org/10.3390/ijms252212367.

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The pulmonary vein wall contains a myocardial layer whose ectopic automaticity is the major cause of atrial fibrillation. This review summarizes the results obtained in isolated pulmonary vein myocardium from small experimental animals, focusing on the studies with the guinea pig. The diversity in the action potential waveform reflects the difference in the repolarizing potassium channel currents involved. The diastolic depolarization, the trigger of automatic action potentials, is caused by multiple membrane currents, including the Na+-Ca2+ exchanger current and late INa. The action potential

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21

Ivković, Branka, Dragan Opačić, Boris Džudović, Milkica Crevar, and Ljiljana Gojković-Bukarica. "Antiarrhythmic effects of newly developed propafenone derivatives." Arhiv za farmaciju 72, no. 4 (2022): 392–412. http://dx.doi.org/10.5937/arhfarm72-37114.

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It is well known that the presence of different chemical groups in drug molecules influences their pharmacological properties. The aim of our study is to investigate whether newly synthesized derivatives of propafenone, with changes in benzyl moiety, have a different effect upon arrhythmia, compared to propafenone. 5OCl-PF and 5OF-PF are derivatives of propafenone with -Cl or -F substituent on the ortho position of the benzyl moiety. For verification of their antiarrhythmic effect, we used an in vivo rat model of aconitine-induced arrhythmia. 5OCl-PF speeded the appearance of supraventricular

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22

Oknińska, Marta, Aleksandra Paterek, Zuzanna Zambrowska, Urszula Mackiewicz, and Michał Mączewski. "Effect of Ivabradine on Cardiac Ventricular Arrhythmias: Friend or Foe?" Journal of Clinical Medicine 10, no. 20 (2021): 4732. http://dx.doi.org/10.3390/jcm10204732.

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Life-threatening ventricular arrhythmias, such as ventricular tachycardia and ventricular fibrillation remain an ongoing clinical problem and their prevention and treatment require optimization. Conventional antiarrhythmic drugs are associated with significant proarrhythmic effects that often outweigh their benefits. Another option, the implantable cardioverter defibrillator, though clearly the primary therapy for patients at high risk of ventricular arrhythmias, is costly, invasive, and requires regular monitoring. Thus there is a clear need for new antiarrhythmic treatment strategies. Ivabra

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23

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

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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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25

Zigmantaitė, Vilma, Eglė Jonušaitė, Ramunė Grigalevičiūtė, et al. "Evaluation of the Cardiac Electrophysiological and Haemodynamic Effects of Elsholtzia ciliata Essential Oil on Swine." Pharmaceuticals 15, no. 8 (2022): 982. http://dx.doi.org/10.3390/ph15080982.

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The demand for the development of novel medicines with few side effects and no proarrhythmic properties is increasing. Extensive research on herbal extracts has been conducted with the expectation that the compounds will exert precise effects without harmful side effects. Elsholtzia ciliata (Thunb.) Hyl. essential oil (EO) possesses antiarrhythmic properties similar to those of class 1B antiarrhythmics, such as prolonging myocardial activation of the QRS complex and shortening the QT interval. In this study, we determined the kinetic profile of EO phytocompounds and the effects of EO on heart

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26

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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27

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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28

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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29

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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30

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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31

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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32

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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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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34

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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35

van Bavel, Joanne J. A., Henriëtte D. M. Beekman, Agnieszka Smoczyńska, Marcel A. G. van der Heyden, and Marc A. Vos. "IKs Activator ML277 Mildly Affects Repolarization and Arrhythmic Outcome in the CAVB Dog Model." Biomedicines 11, no. 4 (2023): 1147. http://dx.doi.org/10.3390/biomedicines11041147.

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Long QT syndrome type 1 with affected IKs is associated with a high risk for developing Torsade de Pointes (TdP) arrhythmias and eventually sudden cardiac death. Therefore, it is of high interest to explore drugs that target IKs as antiarrhythmics. We examined the antiarrhythmic effect of IKs channel activator ML277 in the chronic atrioventricular block (CAVB) dog model. TdP arrhythmia sensitivity was tested in anesthetized mongrel dogs (n = 7) with CAVB in series: (1) induction experiment at 4 ± 2 weeks CAVB: TdP arrhythmias were induced with our standardized protocol using dofetilide (0.025

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Wang, Yu-Jie, Pei Tao, and Yan Wang. "Attenuated Structural Transformation of Aconitine during Sand Frying Process and Antiarrhythmic Effect of Its Converted Products." Evidence-Based Complementary and Alternative Medicine 2021 (October 25, 2021): 1–12. http://dx.doi.org/10.1155/2021/7243052.

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The transformation pathways of diterpenoid alkaloids have been clarified in the boiling and steaming process. Aconitine, a famous diterpenoid alkaloid, is successively transformed into benzoylaconine and aconine during the processes of boiling and steaming, but the transformation pathway remains to be determined in the sand frying process. The present study aims at investigating the transformation pathways of aconitine in the process of sand frying, as well as assessing the cardiotoxicity and antiarrhythmic activity of aconitine and its converted products. The parameters of temperature and tim

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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 ma

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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 arrhyth

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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 pharmacokin

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40

Turkyilmaz, Ismet Burcu. "Oxidative Brain Injury Induced by Amiodarone in Rats: Protective Effect of S‐Methyl Methionine Sulfonium Chloride." Acta Chimica Slovenica 70, no. 1 (2023): 131–38. http://dx.doi.org/10.17344/acsi.2022.7899.

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Amiodarone (AMD) is a powerful antiarrhythmic drug preferred for treatments of tachycardias. Brain can be affected negatively when some drugs are used, including antiarrhythmics. S-methyl methionine sulfonium chloride (MMSC) is a well-known sulfur containing substance and a novel powerful antioxidant. It was intended to investigate the protective effects of MMSC on amiodarone induced brain damage. Rats were divided to four groups as follows, control (given corn oil), MMSC (50 mg/kg per day), AMD (100 mg/kg per day), AMD (100 mg/kg per day) + MMSC (50 mg/kg per day). The brain glutathione and t

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Singh, Bramah N., Gregory Feld, and Koonlawee Nademanee. "Arrhythmia Control by Selective Lengthening of Cardiac Repolarization: Role of N-Acetylprocainamide, Active Metabolite of Procainamide." Angiology 37, no. 12 (1986): 930–38. http://dx.doi.org/10.1177/000331978603701202.

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In recent years, data has become available to support the concept that a selective lengthening of the cardiac action potential (a Class III antiarrhythmic action) by whatever mechanism with an attendant increase in the effective refractory period constitutes a distinct antiarrhythmic mechanism. Such an action is exemplified clinically by hypocalemia and hypothyroidism and pharmacologically by amiodarone, sotalol and bretylium, all of which have other associated features. The N-acetylation of procainamide leads to the pharmacologically active compound, N-acetylprocainamide (NAPA). The loss of p

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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 administ

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Yang, Wei, Wenping Wang, Song Cai, et al. "Synthesis and In Vivo Antiarrhythmic Activity Evaluation of Novel Scutellarein Analogues as Voltage-Gated Nav1.5 and Cav1.2 Channels Blockers." Molecules 28, no. 21 (2023): 7417. http://dx.doi.org/10.3390/molecules28217417.

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Malignant cardiac arrhythmias with high morbidity and mortality have posed a significant threat to our human health. Scutellarein, a metabolite of Scutellarin which is isolated from Scutellaria altissima L., presents excellent therapeutic effects on cardiovascular diseases and could further be metabolized into methylated forms. A series of 22 new scutellarein derivatives with hydroxyl-substitution based on the scutellarin metabolite in vivo was designed, synthesized via the conjugation of the scutellarein scaffold with pharmacophores of FDA-approved antiarrhythmic medications and evaluated for

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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

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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 incomplete

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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 L

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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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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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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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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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