Agustín Pastor

Incidence and Clinical Significance of Multiple Consecutive, Appropriate, High-Energy Discharges in Patients With Implanted Cardioverter-Defibrillators

BACKGROUND Some patients with an automatic implantable cardioverter-defibrillator (ICD) suffer multiple appropriate, consecutive, high-energy discharges (MCDs) during follow-up. Such events might represent resistant ventricular arrhythmias and might have prognostic significance. METHODS AND RESULTS Eighty consecutive patients with an ICD were followed up for up to 82 months (mean, 21 +/- 19 months). Thirty-eight patients had survived an out-of-hospital cardiac arrest and 42 had recurrent ventricular tachycardia. During follow-up, 16 patients had MCD (group A), 26 patients had episodes of single appropriate discharges (group B), and 38 patients had no appropriate discharges (group C). Group A patients had worse functional status (P = .001), lower left ventricular ejection fractions (LVEFs) (P = .001), and lower survival rates (log rank, P = .003) than the remaining two groups of patients. Cox analysis showed LVEF (P = .001) to be an independent predictor of MCD. Independent predictors of death or heart transplant were MCD (P = .001), female sex (P = .001), age (P = .001), history of cardiac arrest (P = .003), and functional status (P = .003). The only independent predictor of total mortality was female sex (P = .002). Independent predictors of cardiac death were MCD (P = .007) and female sex (P = .018). Independent predictors of arrhythmic death were age (P = .001), female sex (P = .02), and MCD (P = .023). CONCLUSIONS In patients with an ICD, the development of MCD is an independent predictor of cardiac and arrhythmic mortality. If this finding is confirmed in larger studies, it may help to identify patients in whom other therapeutic alternatives, ie, heart transplantation, should be considered during follow-up after ICD implantation.

Atypical flutter: a review.

Understanding of typical flutter circuits led the way to the study of other forms of macroreentrant tachycardias of the atria, and to their treatment by catheter ablation. It has become evident that the ECG classification of atrial flutter and atrial tachycardia by a rate cutoff and the presence or absence of isoelectric baselines between atrial deflections is not a valid indicator of tachycardia mechanism. Macroreentrant circuits where activation rotates around large obstacles are the most common arrhythmias found in patients with atypical forms of flutter or atrial tachycardia, especially after surgery for congenital heart disease, however, focal mechanisms can also be found. Large areas of low voltage electrograms, suggestive of severe myocardial damage (fibrosis or infiltration) can be found in many atypical macroreentrant tachycardias at the center of the circuit. Many of these circuits can be mapped precisely, critical isthmuses can be defined, and effective catheter ablation can be performed. The need to match activation maps with anatomy precisely, makes computer assisted, anatomically precise mapping a useful tool. Entrainment techniques have to be used sparingly to avoid tachycardia interruption. In complex cases, ablation can be done in sinus rhythm, after definition of conducting channels between low voltage areas and scars or anatomic obstacles. Long‐term prognosis is uncertain and depends on the underlying pathology. (PACE 2003; 26:2157–2169)

Atrial activation mapping in sinus rhythm in the clinical electrophysiology laboratory: observations during Bachmann's bundle block.

Introduction: The high posterolateral right atrium (RA) is considered the “sinus node area,” but we lack information on endocardial atrial activation in sinus rhythm. We studied RA and left atrial (LA) endocardial activation in the electrophysiology laboratory.

Identification of concealed posteroseptal Kent pathways by comparison of ventriculoatrial intervals from apical and posterobasal right ventricular sites.

BACKGROUND The differential diagnosis of supraventricular tachycardia with concentric atrial activation usually requires the inducibility of sustained tachycardia and needs a complex and time-consuming electrophysiological evaluation. To develop a simple test to establish if ventriculoatrial conduction uses a posteroseptal accessory pathway or the normal conduction system, we compared the ventriculoatrial intervals during right ventricular pacing from apical and posterobasal sites. METHODS AND RESULTS Continuous pacing was performed from an apical and a posterobasal right ventricular site in 34 patients with retrograde conduction over the normal conduction system (group A) and in 22 patients with conduction over a posteroseptal accessory pathway (group B). During apical pacing, ventriculoatrial intervals in group A (176 +/- 40 milliseconds) were not significantly different than those in group B (197 +/- 47 milliseconds, P = NS). During posterobasal pacing, group B patients had significantly shorter ventriculoatrial intervals than group A patients (158 +/- 46 versus 197 +/- 39 milliseconds, P < .01). The difference between the ventriculoatrial interval obtained during apical pacing and that obtained during posterobasal pacing (ventriculoatrial index) discriminated between the two groups without overlapping: It was positive in all group B patients (39 +/- 19; range, +10 to +70 milliseconds) and negative in all except two group A patients (-21 +/- 13; range, -50 to +5 milliseconds; P < .001). CONCLUSIONS This ventriculoatrial index can identify accurately and in the absence of tachycardia whether concentric retrograde conduction is proceeding over a posteroseptal accessory pathway or over the normal conduction system.

Ventricular fusion during resetting and entrainment of orthodromic supraventricular tachycardia involving septal accessory pathways. Implications for the differential diagnosis with atrioventricular nodal reentry.

BackgroundVentricular fusion during transient entrainment of orthodromic atrioventricular reciprocating tachycardias (OAVRT) was originally found to be absent and recently observed only with left ventricular stimulation. However, previous studies were restricted to cases with a left free wall accessory pathway. The hypothesis of the present study was that fusion is likely during resetting and entrainment of OAVRT with right ventricular stimulation if the accessory pathway is septally located, since its insertion is relatively close to the stimulation site. This phenomenon can help in the differential diagnosis with atrioventricular nodal reentry (AVNR). Methods and ResultsWe performed programmed right ventricular stimulation during regular inducible supraventricular tachycardia with concentric atrial activation in 44 patients- 20 with OAVRT and 24 with AVNR Fusion in the ECG morphology of extrastimuli producing resetting was observed in 19 of 19 OAVRT but in 0 of 11 AVNR reset (P<.001). Transient entrainment was demonstrated in all 31 cases undergoing rapid ventricular pacing (14 OAVRT and 17 AVNR). Entrainment with fusion occurred in 13 of 14 OAVRT and in 0 of 17 AVNR (P<.001). Fusion was critically dependent on the coupling intervals or pacing rates, sometimes having a narrow window for its observation. ConclusionsThe relative proximity (conduction time) among pacing site, site of entrance to a reentrant circuit, and site of exit from the circuit to the paced chamber are critical for the occurrence of fusion during resetting and/or entrainment. The presence or absence of fusion during these phenomena can help in the differential diagnosis of certain supraventricular tachycardias.

Severe mitral regurgitation with right ventricular pacing, successfully treated with left ventricular pacing.

NÚNEZ, A., et al.: Severe Mitral Regurgitation with Right Ventricular Pacing, Successfully Treated with Left Ventricular Pacing. A case of severe mitral regurgitation with refractory heart failure, after atrioventricular junction ablation and pacemaker implant, was solved with left ventricular pacing. Mitral regurgitation was related to a change in segmental left ventricular motion during right ventricular pacing.

Atrial Flutter: an Update

Invasive electrophysiologic studies have changed the clinical outlook for patients with atrial flutter. Recognition of the reentrant circuit responsible for typical atrial flutter has led to the development of catheter ablation techniques that can prevent recurrence in >90% of cases. In addition, general understanding of atrial tachycardias has changed radically, such that ECG-based classifications are now obsolete. Atypical reentrant circuits associated with surgical scars or fibrotic areas in either atrium, which are indistinguishable from focal tachycardias on ECG, have been identified. These circuits also seem amenable to treatment by ablation. Recently, a new type of reentrant tachycardia that could be problematic in the future has emerged in patients who have undergone extensive left atrial ablation for the treatment of atrial fibrillation. These atypical circuits can be characterized using the mapping and entrainment techniques initially developed for typical flutter. In these cases, electroanatomical mapping, involving the construction of a virtual anatomical model of the atria, is extremely helpful. Despite the success of ablation, long-term prognosis is frequently overshadowed by the appearance of atrial fibrillation, which suggests that flutter and fibrillation share a common arrhythmogenic origin that is not modified by cavotricuspid isthmus ablation. In contrast with our clear electrophysiologic understanding of atrial flutter, little is known about the natural history of the condition because the literature has traditionally grouped patients with flutter and fibrillation together. Consequently, the complex relationship between the two arrhythmias has still to be clearly delineated. Primary prevention and preventing the development of atrial fibrillation after ablation remain outstanding clinical challenges.

The Importance of Antitachycardia Pacing for Patients Presenting with Ventricular Tachycardia

The initial experience from electrophysiological studies showed that pacing induced termination of ventricular tachycardias is usually possible but requires a critical pacing sequence. Studies on the resetting phenomenon showed, in most instances of failure of termination, that the “limiting factor” to produce ventricular tachycardia termination is usually failure to produce block within the circuit rather than failure to access or interact with the ventricular tachycardia origin. The resetting response is related to tachycardia termination in a number of ways. Of note is that a steeply increasing resetting pattern usually predicts tachycardia termination. Between 50% and 90% of induced ventricular tachycardias will be terminated by trains of rapid ventricular pacing. The analysis of the pacing rate necessary for termination shows that it varies widely. Paced cycle lengths of < 80% of tachycardia cycle length are necessary in at least 20% of tachycardias. In contrast, the incidence of acceleration is closely related to the paced cycle length: it is negligible with paced cycle lengths over 80% of tachycardia cycle length and increases to 36% with paced cycle lengths below 76% of tachycardia cycle length. Present information about efficacy of antitachycardia pacing in spontaneous tachycardias suggests that it is extremely effective, with over 90% success. However, it is likely that these data correspond to a selected group of tachycardias.

Perfil clínico de los pacientes con fibrilación auricular persistente remitidos a cardioversión: Registro sobre la cardioversión en España (REVERSE)

Los objetivos fueron conocer el manejo y las caracteristicas clinicas de los pacientes remitidos a cardioversion en Espana y compararlos con los de los estudios AFFIRM y RACE. Se registro prospectiva y consecutivamente a 1.515 pacientes con fibrilacion auricular persistente remitidos a cardioversion en 96 hospitales espanoles. La mitad recibia tratamiento con antiarritmicos de los grupos I o III de Vaughan-Williams. La estrategia de anticoagulacion con dicumarinicos 3-4 semanas antes y despues de la cardioversion fue la mas utilizada. Nuestros pacientes eran mas jovenes que los de AFFIRM y RACE. Respecto al AFFIRM, tenian menor prevalencia de embolias previas, cardiopatia isquemica, hipertension, diabetes y disfuncion sistolica. Respecto al RACE, tenian menor prevalencia de cardiopatia isquemica y embolias previas, pero algo mayor de hipertension y diabetes. Concluimos que los pacientes remitidos a cardioversion en Espana tienen un perfil de menor riesgo cardiovascular que los del AFFIRM y aparentemente menor que los del RACE.

Taquicardia ventricular como manifestación clínica inicial de feocromocitoma

El feocromocitoma se presenta clínicamente con cefalea, sudoración y palpitaciones asociadas a hipertensión, insuficiencia cardiaca y arritmias debidas a la secreción de catecolaminas. La presencia de taquicardia ventricular (TV) sostenida se ha descrito de manera excepcional. Describimos un caso de feocromocitoma que se manifestó con TV monomorfa, sostenida e incesante. Mujer de 74 años, diabética e hipertensa en tratamiento, con episodios de dolor de espalda, palpitaciones y disnea desde 5 meses antes, que acude a urgencias durante un episodio. La presión arterial era 130/65 mmHg, la troponina T de 0,30 ng/ml (normal < 0,01), y la creatincinasa y la mioglobina normales. El electrocardiograma basal era normal (fig. 1), pero durante el seguimiento presentó salvas sostenidas e incesantes de taquicardia regular con un complejo QRS de 0,11 s a 180 lat/min, patrón de bloqueo de rama derecha y eje inferior, y disociación auriculoventricular (fig. 2), que reproducían la sintomatología. La ecocardiografía mostró hipertrofia concéntrica ventricular izquierda con función sistólica normal y la coronariografía fue normal. El patrón típico de origen fascicular izquierdo llevó a administrar verapamilo intravenoso y oral, lo cual estabilizó el ritmo sinusal. Durante la monitorización efectuada en el ingreso se observaron episodios de taquicardia auricular con un complejo QRS estrecho, con frecuencias cardiacas alrededor de 150 lat/min y taquicardia sinusal persistente. Un cuadro sincopal se asoció con una presión arterial sistólica de 240 mmHg, que en pocos minutos descendió a 70 mmHg sin tratamiento. Las concentraciones de hormona tiroidea y TSH fueron normales, pero el contenido de metanefrinas en la orina era elevado. Una tomografía computarizada puso de manifiesto una masa suprarrenal derecha de 6 cm de diámetro y la gammagrafía con metayodobencilguanidina demostró captación por la masa. El tratamiento con fenoxibenzamina y atenolol estabilizó la presión arterial y previno las recurrencias de taquicardia ventricular y auricular. Se realizó una suprarrenalectomía unilateral, confirmándose mediante histología el diagnóstico de feocromocitoma. Tras la cirugía se controló la hipertensión y se normalizaron las concentraciones de metanefrinas en orina. Dos años después de la cirugía la paciente permanece asintomática, sin recurrencia arrítmica y normotensa. Las manifestaciones cardiológicas más comunes del feocromocitoma son la insuficiencia cardiaca y la miocarditis o miocardiopatía dilatada. La TV ha sido descrita de forma anecdótica y no hay datos sobre el mecanismo de estas taquicardias, aunque en algún caso se ha descrito torsade de pointes en relación con un intervalo QT largo. En nuestro caso, el intervalo QTc era normal y el patrón de la taquicardia indicaba un origen fascicular, pero la asociación con taquicardias auriculares señalaba un factor arritmogénico sistémico. Los valores elevados de catecolaminas podrían ser