Showing papers by "Paulus Kirchhof published in 2000"
TL;DR: The electrophysiologic changes after ventricular dilatation to a degree that increases left ventricular pressure in a clinically relevant range can be influenced by the stretch-activated channel blocker streptomycin but not by specific calcium channel block, which may have clinically important implications for the development of new antiarrhythmic drugs.
Abstract: The exact mechanism of mechano-electrical feedback and stretch-induced arrhythmias is unknown, but the role of stretch-activated ion channels and specific calcium channels has been proposed. The aim of the present study was to test the hypothesis that stretch-activated ion channels and not calcium channels contribute to stretch-related alterations of repolarization and that these effects can be neutralized by stretch-activated channel block. We studied the interaction of acute ventricular dilatation and the stretch-activated channel blocker streptomycin and the specific calcium channel blocker verapamil in an isolated retrogradely perfused rabbit heart model in which the left ventricular size is modified by abruptly changing the volume of a fluid-filled balloon placed in the left ventricle. Acute ventricular dilatation led to a rate-dependent decrease in repolarization. The mean effective refractory period (ERP) and monophasic action potential duration (MAP90) for cycle lengths between 300 and 1,000 ms decreased from 174.2+/-9 ms and 178.9+/-7 ms to 161.6+/-11 ms and 169.7+/-5 ms, respectively. Streptomycin (80 microM) inhibited this stretch-related shortening of repolarization (ERP: 175.4+/-8 ms; MAP90: 179.7+/-8 ms, p < 0.05) but had almost no effect on already dilated ventricles. Counteraction of the observed electrophysiologic changes could only be achieved by increasing the streptomycin concentration to 200 microM. Streptomycin nearly completely suppressed stretch-related ectopic ventricular complexes. In contrast, verapamil (1 microM) had no effect on stretch-related changes in repolarization and stretch-induced arrhythmias. The present study indirectly implicates stretch-activated ion channels in the genesis of stretch-related changes in repolarization and arrhythmias. The electrophysiologic changes after ventricular dilatation to a degree that increases left ventricular pressure in a clinically relevant range can be influenced by the stretch-activated channel blocker streptomycin but not by specific calcium channel block. This may have clinically important implications for the development of new antiarrhythmic drugs.
38 citations
TL;DR: This is the first reported case of “atrial torsades de pointes” in a patient with long QT syndrome and a history of palpitations, and a new action potential reproducibly emerged from these afterdepolarizations.
Abstract: Atrial Torsades de Pointes. A patient with long QT syndrome and a history of palpitations underwent electrophysiologic study. Runs of polymorphic self-terminating atrial tachyarrhythmias were easily induced and occurred spontaneously several times. Atrial monophasic action potential (MAP) durations were prolonged at short pacing cycle lengths. Premature high right atrial extrastimuli prolonged MAP duration in the low right atrium, resulting in an inverse electrical restitution curve, and increased dispersion of repolarization. MAP morphology showed gradually increasing early afterdepolarizations. When the arrhythmia was initiated, a new action potential reproducibly emerged from these afterdepolarizations. To the knowledge of the authors, this is the first reported case of “atrial torsades de pointes” in a patient.
32 citations
TL;DR: The understanding of the structure, function and mechanisms of the regulation of ion channels as well as their contribution to the pathogenesis of caridac arrhythmias has substantially increased and it is likely to assume that, in the future, they will increasingly influeince the diagnosis and treatment of arrh rhythmias.
Abstract: Die moderne Krankheitsursachenforschung wird in wachsendem Ausmas von den technischen Moglichkeiten der molekularen Biologie und Genetik bestimmt. Auch die Rhythmologie ist von dieser Entwicklung nicht unbeeinflusst geblieben. Ganz im Vordergrund des aktuellen Interesses stehen die Ionenkanale. Die Verfugbarkeit neuer molekulargenetischer Techniken hat dazu gefuhrt, dass wir heute den Aufbau, die Funktion und die Regulationsmechanismen von Ionenkanalen und ihre Bedeutung fur die Arrhythmogenese viel besser verstehen als noch vor wenigen Jahren. Die in den letzten Jahren gewonnenen Erkenntnisse sind jedoch nicht nur hinsichtlich der Mechanismen und der Pathogenese von Rhythmusstorungen von Interesse. Es ist anzunehmen, dass sie in den nachsten Jahren in zunehmend starkerem Mase auch die Diagnostik bei Herzrhythmusstorungen und unser therapeutisches Handeln beeinflussen werden.
3 citations
TL;DR: A 31-year-old woman underwent an electrophysiologic procedure because of paroxystnal palpitations occurring since childhood and found the atrial activation sequence was idetuical during both tachycardias and during ventricular pacing in sinus rhythm.
Abstract: A 31-year-old woman underwent an electrophysiologic procedure because of paroxystnal palpitations occurring since childhood. The baseline ECG was unremarkable. Sinus cycle length was 1,070 msec, and ihe AH and HV intervals were 85 and 35 msec, respectively. During programmed atrial and ventricular stimulation, two regulai' tachycardias were induced reproducibly with one premature stimulus: a nanow QRS cotiiplex tachycardia with a cycle length of 420 tnsec, and a wide QRS complex tachycardia with lett bundle branch block (LBBB) morphology and a cycle length of 385 msec (Fig. 1). Intracardiac recordings (Fig. 2) revealed 1:1 AV associatioti and eccentric atrial activation in both tachycardias. The atrial activation sequence was idetuical during both tachycardias and during ventricular pacing in sinus rhythm. A critically timed premature stimulus in the right atrial appendage reproducibly converted the wide QRS cotnplex tachycardia to the natrow QRS complex tachycardia (Fig. 2). What are the mechanistns of the tachycardias? What is the mechanism responsible for the change in QRS tnorphology and cycle length?