Comparison of Antiarrhythmic and Electrophysiologic Effects of Diltiazem and Its Analogue Siratiazem

Mo, Guc; Boachie-Ansah, G; Ka, Kane; Wadsworth, RM

doi:10.1097/00005344-199311000-00002

Cited by 14 publications

(4 citation statements)

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“…Therefore, several groups of natural and synthetic pharmacological agents could significantly diminish and/or suppress the incidence of reperfusion-induced arrhythmias. Thus, beta adrenergic receptor blockers (Manning and Hearse, 1984;Lujan et al, 2007;Kloner et al, 2011), calcium channel antagonists (Guc et al, 1993;Podesser et al, 1995;Kato et al, 2004;Bukhari et al, 2018), spin traps (Hearse and Tosaki, 1987;Tosaki et al, 1993a;Zuo et al, 2009;Pisarenko et al, 2019), and natural plants or their extracts (Tosaki et al, 1996;Shen et al, 1998;Broskova et al, 2013;Sedighi et al, 2018;Zhang et al, 2019b) alone, or in their combinations can significantly reduce the severity of ischemia/reperfusion-induced arrhythmias. Several natural products originated from plants, fruits, and/or vegetables showing antiarrhythmic activity by reducing the incidence of reperfusion-induced arrhythmias and preserving myocardial function, include mainly polyphenol and flavonoid molecular structures (Hung et al, 2000;Pataki et al, 2002;Bak et al, 2006;Broskova et al, 2013;Ma et al, 2014;Woodman et al, 2018;Kaya et al, 2019).…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

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This review is focusing on the understanding of various factors and components governing and controlling the occurrence of ventricular arrhythmias including (i) the role of various ion channel-related changes in the action potential (AP), (ii) electrocardiograms (ECGs), (iii) some important arrhythmogenic mediators of reperfusion, and pharmacological approaches to their attenuation. The transmembrane potential in myocardial cells is depending on the cellular concentrations of several ions including sodium, calcium, and potassium on both sides of the cell membrane and active or inactive stages of ion channels. The movements of Na + , K + , and Ca 2+ via cell membranes produce various currents that provoke AP, determining the cardiac cycle and heart function. A specific channel has its own type of gate, and it is opening and closing under specific transmembrane voltage, ionic, or metabolic conditions. APs of sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells determine the pacemaker activity (depolarization phase 4) of the heart, leading to the surface manifestation, registration, and evaluation of ECG waves in both animal models and humans. AP and ECG changes are key factors in arrhythmogenesis, and the analysis of these changes serve for the clarification of the mechanisms of antiarrhythmic drugs. The classification of antiarrhythmic drugs may be based on their electrophysiological properties emphasizing the connection between basic electrophysiological activities and antiarrhythmic properties. The review also summarizes some important mechanisms of ventricular arrhythmias in the ischemic/ reperfused myocardium and permits an assessment of antiarrhythmic potential of drugs used for pharmacotherapy under experimental and clinical conditions.

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Section: Reactive Oxygen Speciesmentioning

confidence: 99%

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

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“…In depolarized ovine coronary artery rings potassium-stimulated calcium uptake was also inhibited by siratiazem and diltiazem with similar potencies [30]. Siratiazem dose-dependently (1-10 µM) reduced APA, V max , APD 50 and APD 90 values of ovine Purkinje fibers without affecting resting membrane potential (RMP) [115].…”

Section: Siratiazem (Lr-a113)mentioning

confidence: 92%

“…Inhibitions of I Na and I NCX have already been mentioned above to reduce the calcium overload and its arrhythmogenic consequences. Sodium channel inhibition was observed with many CCAs although in most cases only indirect, maximal rate of depolarization (V max ) measurements are available (for verapamil [113], for diltiazem [114], for siratiazem [115], for semotiadil [116], for levosemotiadil [117], for KT-362 [118], for mibefradil [119], for AH-1058 [38] and for bepridil [33]). Potassium channels were also reduced by some nonselective CCAs.…”

Section: Potential Mechanisms Behind the Antiarrhythmic Actions Of Ccasmentioning

confidence: 99%

See 1 more Smart Citation

Class IV Antiarrhythmic Agents: New Compounds Using an Old Strategy

Szentandrássy

Nagy²,

Hegyi³

et al. 2014

CPD

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Cardiac arrhythmias are a major cause of morbidity and mortality in the industrialized world. Among their treatment regimens one can find the calcium channel antagonists (CCAs), the class IV agents. In the cardiovascular system Land T-type calcium channels are found on vascular smooth muscle cells and cardiac myocytes with well defined physiological roles. Inhibition of calcium channels by CCAs has widely been used in clinical practice for several decades. Cardiovascular disorders are one of the many fields of medicine in which CCAs are used for various reasons and conditions. The three main indications of them are hypertension, angina and various cardiac arrhythmias. The most important classes of CCAs are dihydropyridines, phenylalkylamines and benzothiazepines but some newer compounds do not fall into any of these major classes. Dihydropyridines are not used in the antiarrhythmic therapy but are good vasodilators and antianginal agents. In contrast, phenylalkylamines and benzothiazepines exert cardiac actions in vivo and therefore these are one choice of antiarrhythmic drugs. This review focuses on phenylalkylamines, benzothiazepines and on new drugs with potential antiarrhythmic action in the heart as well as the mechanisms how calcium channels antagonism can lead to an antiarrhythmic action.

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