RESUMEN
Biventricular pacing for cardiac resynchronization is a promising therapy for symptomatic improvement in selected patients with underlying severe congestive heart failure. ICD treatment has been shown to prolong life in patients with life threatening ventricular tachyarrhythmias, but it does not improve quality of life. This review discusses current experience with ICD's incorporating biventricular pacing.
Asunto(s)
Desfibriladores Implantables , Insuficiencia Cardíaca/terapia , Ventrículos Cardíacos/cirugía , Marcapaso Artificial , Arritmias Cardíacas/complicaciones , Insuficiencia Cardíaca/etiología , HumanosRESUMEN
The lack of specificity in the detection of ventricular tachyarrhythmias remains a major clinical problem in the therapy with ICDs. The stability criterion has been shown to be useful in discriminating ventricular tachyarrhythmias characterized by a small variation in cycle lengths from AF with rapid ventricular response presenting a higher degree of variability of RR intervals. But RR variability decreases with increasing heart rate during AF. Therefore, the aim of the study was to determine if the sensitivity and specificity of the STABILITY algorithm for spontaneous tachyarrhythmias is related to ventricular rate. Forty-two patients who had received an ICD (CPI Ventak Mini I, II, III or Ventak AV) were enrolled in the study. Two hundred ninety-eight episodes of AF with rapid ventricular response and 817 episodes of ventricular tachyarrhythmias were analyzed. Sensitivity and specificity in the detection of ventricular tachyarrhythmias were calculated at different heart rates. When a stability value of 30 ms was programmed the result was a sensitivity of 82.7% and a specificity of 91.4% in the detection of slow ventricular tachyarrhythmias (heart rate < 150 beats/min). When faster ventricular tachyarrhythmias with rates between 150 and 169 beats/min (170-189 beats/min) were analyzed, a stability value of 30 ms provided a sensitivity of 94.5% (94.7%) and a specificity of 76.5% (54.0%). For arrhythmia episodes > or = 190 beats/min, the same stability value resulted in a sensitivity of 78.2% and a specificity of 41.0%. Even when other stability values were taken into consideration, no acceptable sensitivity/specificity values could be obtained in this subgroup. RR variability decreases with increasing heart rate during AF while RR variability remains almost constant at different cycle lengths during ventricular tachyarrhythmias. Thus, acceptable performance of the STABILITY algorithm appears to be limited to ventricular rate zones < 170 beats/min.
Asunto(s)
Algoritmos , Fibrilación Atrial/diagnóstico , Desfibriladores Implantables , Electrocardiografía/instrumentación , Taquicardia Ventricular/diagnóstico , Fibrilación Ventricular/diagnóstico , Anciano , Fibrilación Atrial/fisiopatología , Fibrilación Atrial/terapia , Diseño de Equipo , Femenino , Estudios de Seguimiento , Frecuencia Cardíaca/fisiología , Humanos , Masculino , Persona de Mediana Edad , Sensibilidad y Especificidad , Programas Informáticos , Taquicardia Ventricular/fisiopatología , Taquicardia Ventricular/terapia , Resultado del Tratamiento , Fibrilación Ventricular/fisiopatología , Fibrilación Ventricular/terapiaRESUMEN
1. The class III antiarrhythmic azimilide has previously been shown to inhibit I(Ks) and I(Kr) in guinea-pig cardiac myocytes and I(Ks) (minK) channels expressed in Xenopus oocytes. Because HERG channels underly the conductance I(Kr), in human heart, the effects of azimilide on HERG channels expressed in Xenopus oocytes were the focus of the present study. 2. In contrast to other well characterized HERG channel blockers, azimilide blockade was reverse use-dependent, i.e., the relative block and apparent affinity of azimilide decreased with an increase in channel activation frequency. Azimilide blocked HERG channels at 0.1 and 1 Hz with IC50s of 1.4 microM and 5.2 microM respectively. 3. In an envelope of tail test, HERG channel blockade increased with increasing channel activation, indicating binding of azimilide to open channels. 4. Azimilide blockade of HERG channels expressed in Xenopus oocytes and I(Kr) in mouse AT-1 cells was decreased under conditions of high [K+]e, whereas block of slowly activating I(Ks) channels was not affected by changes in [K+]e. 5. In summary, azimilide is a blocker of cardiac delayed rectifier channels, I(Ks) and HERG. Because of the distinct effects of stimulation frequency and [K+]e on azimilide block of I(Kr) and I(Ks) channels, we conclude that the relative contribution of block of each of these cardiac delayed rectifier channels depends on heart frequency. [K+]e and regulatory status of the respective channels.