RESUMEN
Current radiofrequency (RF) ablation technology is limited by small lesion size. To enhance the size of RF-induced left ventricular (LV) endocardial lesions, we evaluated the effects of an enlarged distal electrode tip and increased RF power on lesion volume. Steerable electrode catheters with distal electrode tips of 4 to 12 mm were studied in anesthetized dogs at power settings of 20 to 100 W. Temperature was continuously monitored from a thermistor located at the tip of the catheter. RF energy (500 kHz, unmodulated) was applied between the tip of the catheter and a large skin electrode at four separate LV sites in each animal. Hearts were excised, frozen, sectioned, and stained with nitroblue tetrazolium. Lesion area was planimetered and volume was calculated. Lesion volume increased with increasing electrode size and delivered power. However, a rise in impedance limited maximal lesion size at higher power with each electrode. Maximal lesion size with an 8 mm tip was approximately twice the size of the maximal lesion with a 4 mm tip (914 +/- 362 mm3 vs 460 +/- 150 mm3, p < 0.01). Minimal lesions were seen with large tip electrodes at power < 40 W because of low tip temperature (< 55 degrees C). Average tip temperature correlated with measured lesion volume (r = 0.7). Ventricular fibrillation occurred in approximately one half of the animals studied, and was associated with larger lesion volume (p < 0.01). Catheter ablation of ventricular tachycardia may be enhanced by this technology.
Asunto(s)
Ablación por Catéter/instrumentación , Miocardio/patología , Taquicardia Ventricular/cirugía , Animales , Ablación por Catéter/efectos adversos , Perros , Impedancia Eléctrica , Electrodos , Endocardio/patología , Femenino , Masculino , Temperatura , Fibrilación Ventricular/etiologíaRESUMEN
Late potentials arise from areas of slowly depolarizing myocardium and may represent the substrate for sustained VTs. Because they may be recorded from the body surface using signal-averaging techniques, they represent a noninvasive marker for potential malignant ventricular arrhythmias. The effects of antiarrhythmic drugs on the SAECG and late potentials are reviewed in this article. Unfortunately, there is no SAECG parameter (either total QRS, late potential, or frequency content) that appears to be useful in predicting drug efficacy. However, there are type-specific changes in global ventricular activation that can be quantified by the SAECG. These changes may be useful in categorizing the effects of new type I antiarrhythmic drugs. The effects of antiarrhythmic drugs on tachycardia cycle length are complex and probably represent combined effects of the drug on conduction and refractoriness. Such changes cannot be reliably categorized by the SAECG. Medical therapy of sustained VTs cannot be guided by the SAECG.
Asunto(s)
Antiarrítmicos/uso terapéutico , Arritmias Cardíacas/tratamiento farmacológico , Electrocardiografía/efectos de los fármacos , Animales , Arritmias Cardíacas/diagnóstico , HumanosRESUMEN
BACKGROUND: Type I antiarrhythmic drugs block the cardiac sodium channel in a use-dependent fashion. This use-dependent behavior causes increased drug binding and consequently increased sodium channel blockade at faster stimulation rates. Importantly, the kinetics of drug association and dissociation from the sodium channel differ for each type I antiarrhythmic drug. METHODS AND RESULTS: Thirty-five patients receiving type I antiarrhythmic drugs for the treatment of sustained monomorphic ventricular tachycardia (VT) were studied before and after drug therapy. A total of 41 drug studies were performed (lidocaine, n = 10; procainamide, n = 16; flecainide, n = 15). Sustained monomorphic VT of an identical electrocardiographic morphology was induced during the control and follow-up drug studies. During the control study, there was no significant change in the VT cycle length over time. Compared with control, significant prolongation of the onset VT cycle length was observed after treatment with procainamide and flecainide (increase of 52 +/- 24 and 80 +/- 49 msec, respectively) but not after treatment with lidocaine (increase of 8 +/- 37 msec). Additional drug-induced prolongation of the VT cycle length occurred during a 40-second observation period. This secondary "use-dependent" cycle length prolongation contributed significantly to the steady-state VT cycle length during treatment with flecainide (increase of 82 +/- 34 msec; p < 0.0001). Although a use-dependent increase in VT cycle length was observed with procainamide and lidocaine, the increase was not statistically significant (increase of 12 +/- 15 and 8 +/- 8 msec, respectively). The estimated time constants for the onset of use-dependent VT cycle length prolongation were distinctly different for the three drugs. Flecainide's prolongation of the VT cycle length occurred slowly, with an estimated time constant of 12.5 +/- 5.0 seconds. In contrast, the time course of VT cycle length prolongation was rapid during treatment with lidocaine and intermediate during treatment with procainamide (time constants of 0.52 +/- 0.51 and 4.0 +/- 1.3 seconds, respectively). CONCLUSIONS: Use-dependent prolongation of VT cycle length during treatment with type I antiarrhythmic drugs was observed in humans. This effect was clinically significant during treatment with flecainide (i.e., the use-dependent slowing of the heart rate improved the hemodynamic tolerance of the arrhythmia). Finally, the estimated time constants for the use-dependent prolongation of VT cycle length by the three test drugs are similar to their reported in vitro time constants for use-dependent sodium channel blockade.
Asunto(s)
Antiarrítmicos/uso terapéutico , Flecainida/uso terapéutico , Lidocaína/uso terapéutico , Procainamida/uso terapéutico , Taquicardia Ventricular/tratamiento farmacológico , Adulto , Anciano , Electrocardiografía , Femenino , Humanos , Masculino , Persona de Mediana Edad , Taquicardia Ventricular/fisiopatología , Factores de TiempoRESUMEN
BACKGROUND: Concealed retrograde activation has been proposed as a mechanism for antegrade conduction block in the bundle branches and atrioventricular accessory pathways. We studied this hypothesis (linking) in 10 patients with the Wolff-Parkinson-White syndrome in whom antegrade preexcitation could be persistently blocked by overdrive atrial pacing. METHODS AND RESULTS: An atrial pacing protocol, with a decremental ramp followed by an incremental ramp, defined a range of atrial paced cycle lengths (linking window) associated with both persistent conduction and block in the accessory pathway. Within the limits of the linking window, the ability of an atrial impulse to conduct over the accessory pathway was dependent on the preceding state (i.e., conduction or block). The observed linking window ranged from 70 to 290 msec (mean, 185 +/- 68 msec) and closely approximated the measured delay in retrograde activation of the accessory pathway during persistent antegrade block. The mean antegrade effective refractory period of the accessory pathways was long (486 +/- 156 msec), and in each case, it exceeded the antegrade refractory period of the normal atrioventricular pathway. Critically timed premature ventricular extrastimuli, delivered while linking was maintained in the accessory pathway, were able to interrupt the linking and restore antegrade accessory pathway conduction. CONCLUSIONS: These observations suggest that accessory pathway linking is associated with bidirectional block in the accessory pathway. The ability to initiate linking (and the stability of the phenomenon) depends on a critical relation between antegrade accessory pathway refractoriness and the magnitude of retrograde accessory pathway activation delay.
Asunto(s)
Bloqueo de Rama/fisiopatología , Estimulación Cardíaca Artificial , Sistema de Conducción Cardíaco/fisiopatología , Síndrome de Wolff-Parkinson-White/fisiopatología , Adulto , Nodo Atrioventricular/fisiopatología , Bloqueo de Rama/etiología , Cateterismo Cardíaco , Complejos Cardíacos Prematuros/etiología , Electrocardiografía/métodos , Electrofisiología , Femenino , Humanos , MasculinoRESUMEN
The effects of atrial pacing on the signal-averaged electrocardiogram were studied in 14 patients with remote myocardial infarction and a history of cardiac arrest or sustained ventricular tachycardia (group I) and in 13 patients with coronary artery disease and no history of sustained ventricular tachyarrhythmia (group II). Recordings of the signal-averaged electrocardiogram were obtained at control and during atrial pacing at rates of 80, 100, and 120 beats/min. All patients had recordings analyzed from at least two paced rates. At control, the mean high frequency total duration of the QRS complex (HFTD) was significantly longer in group I versus group II patients (123 +/- 5.6 versus 111 +/- 3.5 msec, p less than 0.05). Although the duration of the QRS signal under 40 microV (D40) was higher in group I versus group II patients (42 +/- 4.7 versus 32.4 +/- 3.5 msec) and the root mean square amplitude of the terminal 40 msec QRS (RMSA) was lower in the group I patients (27 +/- 7.5 versus 38.1 +/- 8.8 microV), these differences did not achieve statistical significance. There was no effect of atrial pacing on the measured signal-averaged parameters of HFTD, D40, and RMSA. Although there was a difference between group I and group II at each paced rate analyzed, atrial pacing did not help to further stratify the groups. In patients with coronary artery disease, atrial pacing is not a useful method of stratifying high-risk patients. Changes in serial signal-averaged electrocardiograms from the same patient are not due to heart rate variability.