Antiarrhythmic Drugs

1. Front Matter

   Pages I-XII

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2. Basic Mechanisms of Antiarrhythmic Drug Action

   1. Front Matter

      Pages 1-1

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   2. Sodium Channel Blockade as an Antiarrhythmic Mechanism

      • A. O. Grant

      Pages 3-22

   3. Pharmacology of T and L Type Ca2+ Channels in Cardiac Tissue

      • P. A. Boyden, G.-N. Tseng

      Pages 23-34

   4. Molecular Biology and Ion Channel Biophysics: Their Role in Rational Pharmacological Antiarrhythmic Therapy

      • T. J. Colatsky

      Pages 35-56

   5. Selective Pharmacological Modification of Repolarizing Currents: Antiarrhythmic and Proarrhythmic Actions of Agents that Influence Repolarization in the Heart

      • C. Antzelevitch, J. M. Di Diego, S. Sicouri, A. Lukas

      Pages 57-80

   6. A Shift from Class I to Class III Drugs in the Medical Treatment of Arrhythmias: Wishful Thinking?

      • E. Carmeliet

      Pages 81-91

   7. Use Dependence and Reverse Use Dependence of Antiarrhythmic Agents: Pro- and Antiarrhythmic Actions

      • L. M. Hondeghem

      Pages 92-105

3. Modulation of Antiarrhythmic Drug Action by Disease and Injury

   1. Front Matter

      Pages 107-107

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   2. Interaction of Transient Ischemia with Antiarrhythmic Drugs

      • K. S. Ginsburg, M. F. Arnsdorf

      Pages 109-121

   3. Management of Patients with Sustained Ventricular Tachyarrhythmias: Different Clinical Studies, Different Patients

      • M. Borggrefe, W. Haverkamp, A. Martinez-Rubio, T. Wichter, G. Breithardt

      Pages 122-143

   4. Antiarrhythmic Drug Action: Modulation by Disease and Injury

      • G. Breithardt, W. Haverkamp, B. Rotman, S. Willems, G. Hindricks, M. Shenasa et al.

      Pages 144-170

4. Reentrant Excitation: Pharmacological Interactions

   1. Front Matter

      Pages 171-171

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   2. Pharmacological Modulation of Reentrant Excitation in Experimental Models

      • L. Boersma, J. Brugada, M. Allessie

      Pages 173-191

   3. Reentry in Clinical Arrhythmias: Mechanisms Responsible for Antiarrhythmic Drug Efficacy

      • D. J. Callans, M. E. Josephson

      Pages 192-204

5. Variability of the Arrhythmogenic Substrate: Drug Influences

   1. Front Matter

      Pages 205-205

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   2. Experimental Models for the Assessment of Antiarrhythmic and Proarrhythmic Drug Action: Traditional and Newer Models

      • S. C. Black, G. S. Friedrichs, B. R. Lucchesi

      Pages 207-239

   3. Influence of the Autonomic Nervous System on the Action of Antiarrhythmic Drugs

      • P. J. Schwartz, S. G. Priori, E. Vanoli, A. Zaza

      Pages 240-250

   4. Role of Drugs in Torsade de Pointes and Triggered Activity

      • W. Haverkamp, M. Hördt, R. Johna, H. Mertens, E. Schulze-Bahr, T. Wichter et al.

      Pages 251-289

   5. The Study of Pharmacokinetics and Pharmacodynamics as a Tool for Understanding Mechanisms of Antiarrhythmic Drug Action

      • D. M. Roden

      Pages 290-299

The past 10 years have seen a remarkable change in the approach to cardiac arrhythmias, from a position of confidence and a feeling of well-being about pharmacological treatment to a situation in which there is now marked uncertainty and general apprehension about the role of antiarrhythmic drugs. Until relatively recently the prevailing concept in antiarrhythmic therapy was that arrhythmias could be controlled by drugs which slowed conduction or suppressed automaticity, goals well served by the sodium channel-blocking drugs and glycosides. Drug re­ search was based largely on the development of agents mimicking those already available, but with greater efficacy, fewer side effects or a more favourable phar­ macokinetic profile. The CAST trial stands out as a landmark in the evolution of arrhytmia manage­ ment; rarely has a single trial had such a profound impact not only on clinical prac­ tice, but also on the whole approach of those involved in the research, development and regulation of antiarrhythmic drugs. The results of the CAST trial, designed to redress the shortcomings of earlier trials which had failed to demonstrate the anticipated improvement in mortality post-myocardial infarction with the use of class I agents, are well known. The CAST and CAST II showed an increase in mor­ tality associated with the active agent (encainide, flecainide or morizicine) com­ pared to placebo treatment. They firmly established the potential danger in the use of class I drugs.

• Drug action
• Interactions
• Ion channel biophysics
• arrhythmia
• drug
• drugs
• heart
• kinetics
• pharmacodynamics
• pharmacokinetics
• pharmacology
• sudden cardiac death

• Medizinische Klinik und Poliklinik, Innere Medizin C, Westfälische Wilhelms-Universität Münster, Münster, Germany

  Günter Breithardt, Wilhelm Haverkamp, Gerhard Hindricks

• Department of Cardiology and Angiology, Westfälische Wilhelms-Universität Münster, Münster, Germany

  Martin Borggrefe

• Dept. of Cardiological Sciences, St. George’s Hospital Medical School Cranmer Terrace, London, UK

  A. John Camm

• Department of Medicine, O’Connor Hospital, San Jose, USA

  Mohammad Shenasa

Policies and ethics