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      Interactions of Esmolol and Adenosine in Atrioventricular Nodal-Dependent Supraventricular Tachycardia: Implication for the Cellular Mechanisms of Adenosine

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          Abstract

          Introduction: Cellular mechanisms of adenosine include a direct effect on the activation of the adenosine-sensitive potassium current (I<sub>K,Ado</sub>) and an indirect effect on antagonism of catecholamine-stimulated adenylate cyclase activity. However, previous studies evaluating the influence of catecholamine activity on the electrophysiologic effects of adenosine have yielded conflicting results. We tested the hypotheses that if adenosine exerts its atrioventricular (AV) nodal blocking effects directly by activating the I<sub>K,Ado</sub> potassium current, rather than indirectly by reversing the catecholamine effects, then pretreatment with β-adrenergic blockade would not potentiate the effects of adenosine in terminating AV nodal-dependent supraventricular tachycardia (SVT). Methods and Results: During sustained AV nodal reentrant tachycardia (AVNRT) or AV reentrant tachycardia (AVRT) in 28 patients, adenosine was rapidly injected in incremental doses of 1.5, 3, 6, 9, 12 and 18 mg to determine the lowest effective dose required for tachycardia termination before and immediately after the end of esmolol infusion. Esmolol infusion was started with loading doses of 500 µg/kg/min for 1 min and 150 µg/kg/min for 4 min, followed by a maintenance infusion of 50–100 µg/kg/min. Esmolol infusion was continued until the tachycardia was terminated or the maximal dose of 100 mg was reached. Adenosine was effective in terminating SVT in all 28 patients with a mean lowest effective dose of 96 ± 54 µg/kg before esmolol. During esmolol infusion, tachycardia was reproducibly terminated in 8 patients (6 with AVNRT, 2 with AVRT) with a mean dose of 67 ± 23 mg. In the other 20 patients with persistent tachycardia after 100 mg of esmolol infusion, the lowest effective dose of adenosine could be determined in 19 patients. In the remaining patient with AVRT, the maximal dose of adenosine (18 mg) was unable to terminate the tachycardia immediately after the end of esmolol infusion. In these 19 patients, esmolol infusion caused significant lengthening of the tachycardia cycle length from 338 ± 36 to 372 ± 51 ms (p < 0.0001) and reduction of the mean arterial blood pressure from 96 ± 15 to 88 ± 18 mm Hg (p = 0.034). Compared to the dosage that was determined before esmolol infusion, the lowest effective dose of adenosine remained the same in 13 patients after the end of esmolol infusion, whereas the dose increased in 5 and decreased in 1 patient. The mean lowest effective dose of adenosine was not significantly different before (98 ± 54 µg/kg) and immediately after (115 ± 56 µg/kg) the end of esmolol infusion (p = 0.054). Conclusions: Intravenous esmolol infusion (up to 100 mg total dose) usually fails to terminate AV nodal-dependent SVT. In the esmolol-resistant tachycardia, esmolol pretreatment does not produce a positive synergistic effect on the efficacy of adenosine-induced termination of SVT. Therefore, in this tachycardia adenosine may exert its effects on AV nodal conduction directly by activation of the I<sub>K,Ado</sub> potassium current, rather than by antagonizing the β-adrenergic system.

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          Author and article information

          Journal
          CRD
          Cardiology
          10.1159/issn.0008-6312
          Cardiology
          S. Karger AG
          0008-6312
          1421-9751
          2002
          June 2002
          12 June 2002
          : 97
          : 3
          : 138-146
          Affiliations
          Division of Cardiology, Department of Medicine, China Medical College Hospital, Taichung, Taiwan, ROC
          Article
          63330 Cardiology 2002;97:138–146
          10.1159/000063330
          12077566
          © 2002 S. Karger AG, Basel

          Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

          Page count
          Figures: 3, Tables: 2, References: 26, Pages: 9
          Categories
          Arrhythmias, Electrophysiology, and Electrocardiography

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