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      Electrophysiological Actions of Calcium Antagonists in the Heart

      ,

      Cardiology

      S. Karger AG

      Ca antagonists, Electrophysiology, His bundle electrography, Autonomic blockade

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          Abstract

          Electrophysiological studies have shown that Ca antagonists affect only cardiac structures in which impulse propagation is mediated by the slow channel, i.e., mainly the sinoatrial and atrioventricular nodes. In addition they may depress abnormal slow conduction in diseased fibers. Ca antagonists do not represent a homogeneous group as different compounds seem to have different electrophysiological actions. In man, Ca antagonists normally have no significant effect on sinus node function. However, in patients with sinus node dysfunction, the same drugs may induce dangerous brady-cardia or sinoatrial block. These different effects seem to be at least in part due to the different responsiveness of the normal and diseased sinus node to changes in autonomic tone via the baroreceptor reflex. In the A-V node, conduction and refractoriness are prolonged by each Ca antagonist to a different degree. In this regard, D 600 and verapamil have a very strong effect, whereas nifedipine in normal doses does not influence A-V nodal conductivity, and tiapamil and diltiazem have an intermediate position between these extremes. The results may have clinical relevance for antiarrhythmic therapy with Ca antagonists. In addition, they can help to avoid dangerous side effects in patients with disease of the sinus or A-V node.

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          Author and article information

          Journal
          CRD
          Cardiology
          10.1159/issn.0008-6312
          Cardiology
          S. Karger AG
          978-3-8055-3588-5
          978-3-318-01756-4
          0008-6312
          1421-9751
          1982
          1982
          07 November 2008
          : 69
          : Suppl 1
          : 105-116
          Affiliations
          Medical Department III, University of Tübingen and Medical Department B, University of Düsseldorf, FRG
          Article
          173544 Cardiology 1982;69:105–116
          10.1159/000173544
          © 1982 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
          Pages: 12
          Categories
          Electrophysiological Property

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