Abstract
Ranolazine, a newly introduced, FDA-approved antianginal agent, has more recently been shown to have additional beneficial antiarrhythmic actions attributed to its inhibitory effect on both peak and late sodium current. The first clinical evidence of ranolazine’s antiarrhythmic efficacy has been provided by the MERLIN-TIMI 36 trial, which showed that ranolazine may suppress both supraventricular and ventricular arrhythmias in patients with non-ST-segment elevation acute coronary syndrome. An interesting observation of available studies is that ranolazine seems to be more effective in pathological conditions, such as heart failure, ischemia, tachyarrhythmias or long QT3 syndrome, and has little effect on normal myocytes. Importantly, the drug may have an antiarrhythmic effect without causing proarrhythmia. The mechanisms involved in the antiarrhythmic action of ranolazine, experimental and clinical data for its antiarrhythmic efficacy in suppressing atrial fibrillation and ventricular tachyarrhythmias, are herein reviewed. Current data from small randomized trials indicate that further larger randomized controlled trials are needed that will examine the antiarrhythmic effects of ranolazine and its potential use in patients with arrhythmias.
Keywords: Antiarrhythmic agents, atrial fibrillation, late sodium current, myocardial ischemia, proarrhythmia, ranolazine, ventricular fibrillation, ventricular tachycardia.
Cardiovascular & Hematological Agents in Medicinal Chemistry
Title:Ranolazine and its Antiarrhythmic Actions
Volume: 13 Issue: 1
Author(s): Kali Polytarchou and Antonis S. Manolis
Affiliation:
Keywords: Antiarrhythmic agents, atrial fibrillation, late sodium current, myocardial ischemia, proarrhythmia, ranolazine, ventricular fibrillation, ventricular tachycardia.
Abstract: Ranolazine, a newly introduced, FDA-approved antianginal agent, has more recently been shown to have additional beneficial antiarrhythmic actions attributed to its inhibitory effect on both peak and late sodium current. The first clinical evidence of ranolazine’s antiarrhythmic efficacy has been provided by the MERLIN-TIMI 36 trial, which showed that ranolazine may suppress both supraventricular and ventricular arrhythmias in patients with non-ST-segment elevation acute coronary syndrome. An interesting observation of available studies is that ranolazine seems to be more effective in pathological conditions, such as heart failure, ischemia, tachyarrhythmias or long QT3 syndrome, and has little effect on normal myocytes. Importantly, the drug may have an antiarrhythmic effect without causing proarrhythmia. The mechanisms involved in the antiarrhythmic action of ranolazine, experimental and clinical data for its antiarrhythmic efficacy in suppressing atrial fibrillation and ventricular tachyarrhythmias, are herein reviewed. Current data from small randomized trials indicate that further larger randomized controlled trials are needed that will examine the antiarrhythmic effects of ranolazine and its potential use in patients with arrhythmias.
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Cite this article as:
Polytarchou Kali and Manolis S. Antonis, Ranolazine and its Antiarrhythmic Actions, Cardiovascular & Hematological Agents in Medicinal Chemistry 2015; 13 (1) . https://dx.doi.org/10.2174/187152571301150730113903
DOI https://dx.doi.org/10.2174/187152571301150730113903 |
Print ISSN 1871-5257 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6182 |
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