Modificaciones de la fibrilación ventricular y de la capacidad de captura inducidas por una lesión lineal con radiofrecuencia / Modifications in ventricular fibrillation and capture capacity induced by a linear radiofrequency lesion

Introducción y objetivos. Analizar los efectos, en la fibrilación ventricular y en la capacidad de capturar al miocardio mediante estimulación a frecuencias rápidas, de una lesión lineal producida con radiofrecuencia. Métodos. En 22 corazones de conejo aislados y perfundidos, se utilizaron electrodos múltiples epicárdicos para registrar la fibrilación ventricular. Se analizaron los mapas de activación al aplicar trenes de estímulos a tres frecuencias distintas, cercanas a las de la arritmia, en tres situaciones: a) basalmente; b) tras producir con radiofrecuencia una lesión en la pared libre del ventrículo izquierdo (longitud, 10±1mm), y c) tras ampliar su extensión (longitud, 23±2mm). Resultados. Tras la lesión, se observó una disminución de la regularidad de las señales registradas y variaciones significativas en la dirección de los frentes de activación. Con la lesión ampliada, se incrementaron ligeramente los episodios con al menos tres capturas consecutivas al estimular con ciclos un 10% más largos que los de la arritmia (basal, 0,6±0,7; lesión inicial, 1±1, diferencias no significativas; lesión ampliada, 3±2,8; p<0,001), mientras que se redujeron los obtenidos al estimular con ciclos un 10% más cortos que los de la arritmia. Conclusiones. La lesión efectuada con radiofrecuencia aumenta la heterogeneidad de la activación miocárdica durante la fibrilación ventricular y modifica la llegada de los frentes de activación a las zonas adyacentes. La estimulación durante la fibrilación ventricular a frecuencias rápidas provoca capturas ocasionales durante al menos tres estímulos consecutivos. La lesión ampliada incrementa ligeramente la capacidad de captura al utilizar ciclos ligeramente más largos que los de la fibrilación ventricular (AU)

Introduction and objectives. An analysis was made of the effects of a radiofrequency-induced linear lesion during ventricular fibrillation and the capacity to capture myocardium through high-frequency pacing. Methods. Using multiple epicardial electrodes, ventricular fibrillation was recorded in 22 isolated perfused rabbit hearts, analyzing the activation maps upon applying trains of stimuli at 3 different frequencies close to that of the arrhythmia: a) at baseline; b) after radio-frequency ablation to induce a lesion of the left ventricular free wall (length=10 [1]mm), and c) after lengthening the lesion (length=23 [2]mm). Results. Following lesion induction, the regularity of the recorded signals decreased and significant variations in the direction of the activation fronts were observed. On lengthening the lesion, there was a slight increase in the episodes with at least 3 consecutive captures when pacing at cycles 10% longer than the arrhythmia (baseline: 0.6 [0.7]; initial lesion: 1 [1] no significant differences; lengthened lesion: 3 [2.8]; P<.001), while a decrease was observed in those obtained upon pacing at cycles 10% shorter than the arrhythmia. Conclusions. The radio-frequency -induced lesion increases the heterogeneity of myocardial activation during ventricular fibrillation and modifies arrival of the activation fronts in the adjacent zones. High-frequency pacing during ventricular fibrillation produces occasional captures during at least 3 consecutive stimuli. The lengthened lesion in turn slightly increases capture capacity when using cycles slightly longer than the arrhythmia (AU)

[Experimental study of laser ablation on lethal arrhythmias--features and effectiveness of epicardial mapping].

To find the exact location of the ventricular arrhythmogenic myocardium, we mapped activation times of local epicardial electrograms (ATLE: 16 bipolar electrodes, 2 x 2 cm2) aided by an on-line computer and guided laser ablation of lethal ventricular arrhythmias induced by aconitine. Thirty-six tests involved 12 dog hearts. Nd:YAG laser application converted ventricular tachycardias and fibrillation to sinus rhythm in all tests. Epicardial mapping results showed: Taking ECG lead II as reference, the differences among all ATLE were within 15ms, and there was no obvious conduct slow zone before drugging and after resuming sinus rhythm, even though 298 +/- 157 mm2 photocoagulation areas (n = 36) resulted from laser irradiation; During VT, the majority of ATLE were preexcited from 90 to 30 ms, and more than one breakthrough point existed, with one predominating; ATLE changed significantly after laser. The ectopic foci were located exactly by using ATLE for laser treatment.

[Laser therapy and death caused by arrhythmia in ischemic heart disease]. / Lazeroterapiia i aritmicheskaia smert' pri ishemicheskoi bolezni serdtsa.

The paper presents a new treatment of myocardial infarction which proved its high antiarrhythmic effectiveness in 300 MI patients followed up for 2 years. The method implies endogenous radiation of blood by He-Ne laser. Holter monitoring revealed that such radiation in the acute MI period promoted the arrest of high-grade ventricular arrhythmia more efficiency than lidocaine++ and prevented primary ventricular fibrillation. The 2-year follow-up provides evidence for a significant reduction in the occurrence of high-grade and lethal outcomes which decreased by half. In view of high occurrence of high-grade extrasystole in most decreased control subjects, this may be attributed to less frequent arrhythmic deaths. Lethal outcomes in laser therapy were reported in persistent cardiac failure, repeat myocardial damage and in presenile and senile patients.