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Antiarrhythmic Drugs - Mechanisms of Antiarrhythmic and Proarrhythmic Actions (Paperback, Softcover reprint of the original 1st... Antiarrhythmic Drugs - Mechanisms of Antiarrhythmic and Proarrhythmic Actions (Paperback, Softcover reprint of the original 1st ed. 1995)
Gunter Breithardt; Edited by (associates) W. Haverkamp, G. Hindricks; Edited by Martin Borggrefe, John A. Camm, …
R2,826 Discovery Miles 28 260 Ships in 10 - 15 working days

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."

Herzrhythmusstoerungen Bei Myokardischamie Und Myokardnekrose - Pathophysiologische Grundlagen, Therapeutische... Herzrhythmusstoerungen Bei Myokardischamie Und Myokardnekrose - Pathophysiologische Grundlagen, Therapeutische Beeinflussbarkeit Und Aspekte Der Pravention (German, Paperback, Softcover Reprint of the Original 1st 1989 ed.)
B. Frenking; H. Gulker; Contributions by W. Haverkamp, G. Hindricks, J. Thale
R1,593 Discovery Miles 15 930 Ships in 10 - 15 working days

Der ploetzliche Herztod ist die haufigste Einzeltodesursache in den europaischen und nordamerikanischen Industriestaaten. Die Gesamtzahl der Todesfalle wird auf 20 bis 30 pro Woche und 1 000000 Einwohner, somit auf 600000-1000000 pro Jahr geschatzt. Die Mehrzahl der Todesfalle betrifft Manner im Alter von 20 bis 65 Jahren (394, 459, 508). Als wichtigste unmittelbare Todesursache wurde bereits 1917 von Hering das primare Kammerflimmern erkannt (257). Andere Ursachen wie akute AV-Blockierungen mit UEbergang in Herzstillstand oder akuter kardiogener Schock sind vergleichsweise selten (208, 288, 459, 489). Die toedlichen Rhythmusstoerungen treten oft ohne Wamsymptome auf. 30-70 % der Todesfalle ereignen sich innerhalb der ersten Stunde, bis zu 90 % innerhalb der ersten beiden Stunden nach Ausbildung einer akuten kardiologischen Symptomatik (Abb. 1) ____________________________ 8 ______________________________ 6 % ________________________________,4 __________________________ 2 o 2 3 456 7 8 Stunden nach Beginn der Symptomatik Abb. 1. Zeitliches Auftreten von Kammerflimmern in den ersten 72 Stunden nach Beginn der Symptomatik eines akuten Myokardinfarktes (Ordinate: Patienteninitialen, Abzisse: Zeitachse). 1 (25,209,312, 361, 489). Grunderkrankung ist in 60-70 % der Falle eine stenosierende Koronararteriensklerose, zu ca. 30% finden sich akute Koronarthrombosen bzw. frische Myokardnekrosen (101, 390).

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