Irene Valverde

Electrodo de desfibrilación Sprint Fidelis: experiencia de nueve centros en España

INTRODUCTION AND OBJECTIVES Sprint Fidelis defibrillation leads are prone to early failure. Most of the reported series come from a single institution. This paper describes the clinical experience in nine Spanish hospitals. METHODS Clinical, implant, and follow-up data of all patients with a Sprint Fidelis lead were analyzed. All cases of lead failure were identified, medium-term lead survival was calculated, and possible predictors for lead failure were determined. RESULTS In total, 378 leads in 376 patients were studied. The mean age (male 85.7%) was 64.9 ± 13.6 years. The majority of patients (59.8%) had ischemic heart disease. Mean left ventricular ejection fraction was 33.4% ± 14.5%. Left subclavian vein puncture was used in 74.8%. During a mean follow-up of 30.9 ± 14 months, 16 lead failures have occurred, with a lead survival of 96.1% at 36 months after implantation. Eleven of 16 lead failures were caused by failure of pace/sense conductors, 3 by defects in the high-voltage conductor, and 2 by defects in both types of conductors. A less depressed left ventricular ejection fraction was associated with an increased probability of lead failure (42.4% ± 16% vs. 33% ± 14.3%; P =.011). Three hospitals presented a rate of lead failure higher than 10%; the rate was less than 5% in the remaining 6 hospitals. CONCLUSIONS In this multicenter series of 378 leads, the 3-year estimated survival was higher than that reported in prior series. Clinical presentation of lead failures was similar to that reported previously. Left ventricular ejection fraction and hospital of implantation were variables associated to lead failure.

Holter implantable y síncope vasovagal: ¿herramienta diagnóstica con efecto terapéutico?

El síncope vasovagal o neurocardiogénico es la forma más habitual de síncope reflejo. En este caso, el mecanismo final del síncope es el fracaso súbito del sistema nervioso autónomo para mantener las mínimas presión arterial y frecuencia cardiaca para una adecuada perfusión cerebral. El pronóstico de los pacientes con síncope vasovagal es habitualmente favorable, pero un subgrupo de ellos presenta episodios acompañados de bradicardia severa e incluso asistolia que frecuentemente no se preceden de síntomas prodrómicos. A esta variedad de síncope vasovagal se la denomina maligna, ya que puede conllevar importante morbilidad. El posible papel de la estimulación cardiaca para prevenir el desarrollo de los episodios sincopales, al evitar las pausas ventriculares prolongadas, no está bien definido, debido a los resultados contradictorios obtenidos de los principales estudios realizados en este campo. Algunos autores opinan que parte del beneficio observado en algunos estudios con la estimulación permanente pudiera deberse a un efecto placebo, aunque persiste la controversia. Presentamos el caso de una mujer de 38 años, remitida para implante de un Holter insertable o registrador de eventos electrocardiográficos (Reveal Plus, Medtronic Ibérica SA) por historia de síncopes recurrentes y diagnóstico establecido de síncope vasovagal maligno. La paciente fue diagnosticada de un bocio normofuncionante, se dedicaba a labores domésticas y no tomaba ninguna medicación. El electrocardiograma basal era normal y no había datos de cardiopatía estructural. Desde hacía más de 5 años, presentaba episodios súbitos de pérdida de conocimiento y tono postural, con recuperación espontánea sin secuelas en varios minutos, sin pródromos, aunque en algunos episodios refería náuseas. No existían factores desencadenantes de los eventos, y en los últimos meses los síncopes eran semanales e incluso diarios. Dos años antes se realizó una prueba de mesa basculante, con resultado positivo y respuesta 2B, cardioinhibitoria con asistolia, obtenida en el tercer minuto de la fase de basculación sin nitroglicerina, con un período de asistolia de 13 s. Ante los hallazgos descritos, con un mecanismo neuromediado, respuesta cardioinhibitoria severa y la ausencia de efecto de medidas fármacológicas o de hiperhidratación, así como la escasez de pródromos, se le planteó la posibilidad de la terapia con estimulación cardiaca. Antes de ello, se solicitó que se le implantara un Holter para corroborar reproduciblemente los hallazgos de la mesa basculante e intentar así aumentar la probabilidad de eficacia de la estimulación permanente. El implante del dispositivo se realizó sin incidencias, y al alta se le recomendó continuar su vida habitual. Se hicieron seguimientos clínicos periódicos y de interrogación del dispositivo y, tras 1 año de seguimiento, la paciente no ha presentado ningún episodio sincopal ni se han objetivado hallazgos específicos en las consultas al dispositivo. La enferma ha continuaCartas al Editor

Atrioventricular Nodal Tachycardia in a Patient with Anomalous Inferior Vena Cava with Azygos Continuation and Persistent Left Superior Vena Cava

A 39‐year‐old female patient was referred for ablation of recurrent episodes of atrioventricular nodal reentrant tachycardia. A combination of an anomalous inferior vena cava with azygos continuation and a persistent left superior vena cava was discovered. A nonfluoroscopic navigation system was very useful for catheter ablation of the tachycardia in this unusual case of anomalous venous system of the heart.

A single implantable cardioverter-defibrillator shock unmasking an electrical storm of 389 ventricular tachycardia episodes triggering device therapies

We describe the case of a patient with ischemic cardiomyopathy who presented the first implantable cardioverter-defibrillator (ICD) shock approximately 5 months after implantation. Device interrogation surprisingly revealed the occurrence of 389 ventricular tachyarrhythmia episodes terminated by asymptomatic antitachycardia pacing (ATP) except for the episode requiring shock. The present case of electrical storm highlights how contemporary tiered ATP schemes constitute a valuable but underused form of termination for ventricular tachyarrhythmias in ICD patients, reducing the number of painful shocks and their adverse consequences.

Delta of the local ventriculo-atrial intervals at the septal location to differentiate tachycardia using septal accessory pathways from atypical atrioventricular nodal re-entry

Aims Tachycardia mediated by septal accessory pathways (AP) and atypical atrioventricular nodal re-entry (AVNRT) require careful electrophysiologic evaluation for differential diagnosis. We aim to describe the differential behaviour of local ventriculo-atrial (VA) intervals which predicts the tachycardia mechanism. Methods and results The local VA intervals at the para-Hisian septum were measured under three different situations: (i) tachycardia; (ii) sustained entrainment from the right ventricular apex (RVA); and (iii) continuous pacing from the RVA during sinus rhythm. Differences were computed as follows: Δ-VAentr = VA during entrainment - VA during tachycardia; and Δ-VApac = VA while pacing during sinus rhythm - VA during tachycardia. In contrast to AVNRT, we hypothesized that an invariable retrograde conduction through the septal AP will keep the result of the subtractions close to 0 ms in cases of ortodromic atrioventricular re-entrant tachycardia (AVRT). We analysed 55 atypical AVNRT (45% posterior type) and 82 AVRT (10 anteroseptal, 18 para-Hisian, 12 mid-septal, and 42 posteroseptal). Δ-VAentr was longer for AVNRT (98.5 ± 40.3 ms) compared with septal AP (-5.7 ± 19.3 ms; P < 0.001). A value of 50 ms showed 98.7% sensitivity and 92% specificity (AUC 0.99; 95% CI 0.98-1). According to physiological criteria, a negative Δ-VAentr remains unobserved in the case of AVNRT (positive predictive value 100% for septal AP). Δ-VApac was also longer for AVNRT (66.5 ± 14.6 ms) compared with septal AP (-9.7 ± 3.3 ms; P < 0.001). A value of 50 ms showed 100% sensitivity and 74% specificity (AUC 0.86; 95% CI 0.76-0.93). Conclusions Delta of the local VA intervals enables distinction between atypical AVNRT and AVRT mediated by septal AP.

The implantable holter monitor and vasovagal syncope: a diagnostic tool with a therapeutic effect?

Vasovagal or neurocardiogenic syncope is the most common form of reflex syncope. In this case, the final syncope mechanism is the sudden shut-down of the autonomic nervous system to maintain the minimum blood pressure and heart rate for proper cerebral perfusion. The prognostic outlook for patients with vasovagal syncope is usually favourable, but a patient subgroup presents episodes that are accompanied by severe bradycardia and even asystole, which are often not preceded by prodromic symptoms. This variety is called malignant vasovagal syncope, as it has a significant morbidity rate. The possible role of cardiac stimulation in preventing the development of syncopal episodes by avoiding long ventricular pauses is not well defined, due to contradictory results having been obtained from the first studies elaborated in this field. Some authors believe that some of the benefits observed in studies of permanent cardiac stimulation could have been due to the placebo effect, but the debate continues. We present the case of a 38-year-old woman admitted for the implantation of an insertable Holter or cardiac event recorder (Reveal Plus, Medtronic Ibérica SA) due to a history of recurring syncopic events and the established diagnosis of malignant vasovagal syncope. The patient was diagnosed with a non-toxic goitre, she worked as a domestic assistant and was not taking any medications. The basal electrocardiogram was normal and there was no indication of structural heart disease. For more than 5 years, she had experienced sudden losses of consciousness and postural tone, with spontaneous recovery without after-effects in several minutes, and without prodromes, although with some episodes she experienced nausea. There were no trigger factors for the events, and in recent months the syncopes had occurred weekly or even daily. Two years previously, she underwent a tilt table test, with a positive result, and type 2B, cardio-inhibitory with asystole was confirmed, in the third minute of the tilt phase without nitroglycerine, by an asystolic period of 13s. Given the findings described, with a neuromediated mechanism, severe cardio-inhibitory response, and the non-response to medication or hyper-hydration, as well as the lack of prodromes, she was presented with the possibility of cardiac stimulation therapy. Given this choice, she asked to have an insertable Holter implanted to corroborate the findings from the tilt table and also to increase the effectiveness probability of permanent stimulation. The implantation of the device was uneventful, and when she was discharged, she was recommended to live her life normally. Periodic clinical sessions for follow-up and checking the device were established, and after 1 year under observation, the patient has not experienced any syncopal episodes, nor have there been any specific findings in the device readings. The patient has been living normally and at this time no medication has been prescribed. The possibility that the beneficial effect to some patients with cardio-inhibitory vasovagal syncope, through the implantation of a pacemaker, is at least partly due to the placebo effect is magnificently illustrated in the present case. It is evident that the implanted device has no physical Letters to the Editor

Atrial Overdrive Pacing Inducing QRS Complexes of Varying Duration in a Patient with Recurrent Syncope. What is the Mechanism

A 52-year-old man was admitted in our institution with cranial traumatism due to a syncopal episode that occurred while he was walking. Several weeks before, one other event with identical features occurred. The patient did not experience any prodromal symptoms before the episodes. Baseline electrocardiogram (EKG), physical examination, transthoracic echocardiogram, and neurological investigation were all normal. No episodes of cardiac rhythm disturbance were noted on telemetry, and infrequent brief episodes of asymptomatic intermittent left bundle branch block in sinus rhythm were observed. The patient underwent electrophysiologic testing. Conduction intervals were normal, with baseline sinus cycle length, atrial-His (AH), and His-ventricular (HV) intervals of 1012, 68, and 51 ms, respectively. During atrial overdrive pacing at a cycle length of 420 ms, the following EKG was recorded (Fig. 1). What is the mechanism for the progressive widening of QRS complexes and for the normal narrow QRS complexes observed in the 13 and 18 atrial-paced beats?