[Pathophysiologic principles of ventricular late potentials--mechanisms].
The majority of sustained ventricular tachycardias are caused by a reentry mechanism. Conditions prerequisite to a reentry circuit are electrophysiological changes, namely conduction delay and block which are incurred by virtue of changes in the myocardial tissue due to scarring, ischemia or fatty infiltration and result in an abnormal action potential, increased intracellular resistance and reduction in intercellular coupling (intercalated discs). Additionally, the principle of anisotropy, that is, the varying velocity of conduction parallel and perpendicular to the fiber axis (increased axial resistance) can also be responsible for circling movement. A further factor predisposing to ventricular tachyarrhythmias is the heterogeneity of repolarization. Delayed and inhomogeneous spread of conduction in morphologically altered tissue can be detected invasively as delayed and fragmented electrograms during sinus rhythm and induced ventricular tachycardia and noninvasively as high-frequency signals which begin in the terminal portion of the QRS complex and can extend far into the ST segment. In a study on our service, electrograms from post-infarct patients with sustained ventricular tachycardia were compared with those without ventricular arrhythmias. In patients with ventricular tachycardia there was markedly delayed activation (greater than 100 ms after begin of the QRS complex, mean 137 ms) over the infarct area. In patients with ventricular arrhythmias, three electrogram types could be differentiated: 1. a delayed singular deflection at the end of the QRS complex (late potential); 2. a diminished amplitude of the electrogram as well as fragmentation into many single deflections for a duration of more than 100 ms; 3. two deflections clearly distinguishable from each other. All three electrogram types represent a different extent of delayed conduction. With one singular late potential there is homogeneous conduction delay throughout the entire region of tissue under the electrode; with fragmentation there is desynchronization of the spread of conduction; with double potentials there are structures of two different velocities of conduction next to or above each other. In almost all patients with ventricular tachycardias fragmented electrograms could be registered in a circumscribed region, in more than one-half there were double potentials. The areas from which abnormal electrograms could be registered were significantly larger in patients with ventricular tachycardias than in those without tachycardia.(ABSTRACT TRUNCATED AT 400 WORDS)
D001283:Atrioventricular Node / Q000503:physiopathology; D004562:Electrocardiography; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology*; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000503:physiopathology*; D013617:Tachycardia, Supraventricular / Q000503:physiopathology*
Pathophysiologische Grundlagen ventrikulärer Spätpotentiale--Mechanismen.