Gunter Breithardt – författare

In this book, well-known physicians, Bocker, Eckardt and Breithardt have put together a succinct and focused book that compliments the CATA Series well. Implantation of defibrillators has evolved dramatically since its introduction by Mirowski in 1980. Technological improvements in devices and leads included a gradual reduction in the size of the device, the introduction of the endocardial approach in 1988, the biphasic waveform and antitachycardia pacing in 1991, pectoral implantation in 1995, inclusion of DDD pacing in 1996 and the delivery of atrial therapies in 1998.

Since the first implantation, a huge body of information on the impact of implantable cardioverter defibrillators (ICD) on prognosis has become available, first as observational studies and later as prospective randomized trials. At the present time, there is a large evidence base from the several ICD trials, although it was not always certain that such a large body of ICD evidence would accumulate.

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.

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.

The exact mechanism of a cardiac arrhythmia becomes fundamentally important when treatment can be directed specifically toward that mechanism. Advances in body surface electrograms and mapping techniques have allowed the causes of ventricular tachyarrhythmias to be pinpointed, thus suggesting viable targets for ablation therapy. However, substantial anatomical and electrophysiological knowledge and catheter-handling skills on the part of the physician are prerequisites for successful ablative technique. Catheter Ablation of Ventricular Tachycardia in Patients with Structural Heart Disease is an in-depth review of this still-expanding subject, presenting both updated information from the current literature and the personal experiences of the authors. The purpose of this book is to provide a comprehensive description of radiofrequency catheter ablation of ventricular tachycardia from history, basic concepts and pathophysiology of radiofrequency lesion formation, to clinical applications and outcomes of these techniques in various subsets of patients with ventricular tachycardia and underlying structural heart disease. Its 128 pages offer a succinct yet comprehensive exchange of information relative to this still-experimental and important field.This book will benefit readers including clinical electrophysiologists, cardiologists, allied industry, and other health care providers who work with patients suffering from ventricular tachycardia.