Functional mapping to reveal slow conduction and substrate progression in atrial fibrillation.

AIMS: The aim of our study was to analyse the response to short-coupled atrial extrastimuli to identify areas of hidden slow conduction (HSC) and their relationship with the atrial fibrillation (AF) phenotype. METHODS AND RESULTS: Twenty consecutive patients with paroxysmal AF and persistent AF (10:10) underwent the first pulmonary vein isolation procedure. Triple short-coupled extrastimuli were delivered in sinus rhythm (SR), and the evoked response was analysed: sites exhibiting double or highly fragmented electrograms (EGM) were defined as positive for HSC (HSC+). The delta of the duration of the bipolar EGM was analysed, and bipolar EGM duration maps were built. High-density maps were acquired using a multipolar catheter during AF, SR, and paced rhythm. Spatial co-localization of HSC+ and complex fractionated atrial EGMs (CFAE) during AF was evaluated. Persistent AF showed a higher number and percentage of HSC+ than paroxysmal AF (13.9% vs. 3.3%, P < 0.001). The delta of EGM duration was 53 ± 22 ms for HSC+ compared with 13 ± 11 (10) ms in sites with negative HSC (HSC-) (P < 0.001). The number and density of HSC+ were lower than CFAE during AF (19 vs. 56 per map, P < 0.001). The reproducibility and distribution of HSC+ in repeated maps were superior to CFAE (P = 0.19 vs. P < 0.001). Sites with negative and positive responses showed a similar bipolar voltage in the preceding sinus beat (1.65 ± 1.34 and 1.48 ± 1.47 mV, P = 0.12). CONCLUSION: Functional mapping identifies more discrete and reproducible abnormal substrates than mapping during AF. The HSC+ sites in response to triple extrastimuli are more frequent in persistent AF than in paroxysmal AF.

[External and internal electrical cardioversion: comparative, prospective evaluation of cell damage by means of troponin I]. / Cardioversión eléctrica externa y sistemas de cardioversión interna: evaluación prospectiva y comparativa del daño celular con troponina I.

INTRODUCTION AND OBJECTIVES: In this study we measured the concentrations of cardiac troponin I (cTnI) and several biochemical markers of myocardial damage after elective external cardioversion or internal cardioversion by specific catheters or automatic defibrillators. MATERIAL AND METHODS: Biochemical markers were analyzed prospectively for 30 consecutive patients after electrical cardioversion. Concentrations of cTnI, myoglobin, creatine kinase (CK), CK-MB and the MB/CK ratio were determined in samples before cardioversion and 2, 8 and 24 h later. The shock energy ranged from 50 to 360 joules (235 106 joules) in external cardioversions and from 3 to 37 joules (15 8 joules) in internal cardioversions. RESULTS: We detected abnormal concentrations of CK, myoglobin, CK-MB and MB/CK in 33% of the patients after external cardioversion. The concentrations of cTnI remained within normal limits at all times, with no elevations detected. Whereas no abnormal concentration of any biochemical marker was detected in any patient who required internal cardioversion for atrial fibrillation, two patients who underwent external cardioversion from an automatic defibrillator did have abnormal concentrations of CK-MB, myoglobin, and even of cTnI. CONCLUSIONS: The concentration of cTnI remained below the detection limit after external cardioversion, even though the other more non-specific markers changed. No enzyme alteration was detected in patients who underwent internal cardioversion of atrial fibrillation.

Cardioversión eléctrica externa y sistemas de cardioversión interna: evaluación prospectiva y comparativa del daño celular con troponina I / External and internal electrical cardioversion: comparative, prospective evaluation of cell Damage by means of troponin I

Introducción y objetivos. En este estudio evaluamos las concentraciones de troponina I cardíaca (cTnI) y distintos marcadores de lesión miocárdica tras cardioversión externa electiva o interna a través de catéteres específicos o de desfibrilador automático. Material y métodos. Analizamos prospectiva y consecutivamente los datos de 30 pacientes tras cardioversión eléctrica. Se determinaron concentraciones de cTnI, mioglobina, creatincinasa (CK), CK-MB-masa e índice MB/CK en muestras precardioversión, y a las 2, 8 y 24 h poscardioversión. La energía de choque estuvo comprendida entre 50 y 360 J (235 ñ 106 J) en cardioversiones externas, y entre 3 y 37 J (15 ñ 8 J) en cardioversiones internas. Resultados. Tras las cardioversiones externas se detectaron valores anormales de CK en el 33 por ciento de los pacientes, así como de mioglobina, CK-MB e índex. Las concentraciones de cTnI permanecieron en todo momento dentro de límites normales, sin detectarse elevaciones patológicas en ninguno de los pacientes. A diferencia de las cardioversiones externas, tras las internas, en los pacientes que la precisaron por fibrilación auricular, no se detectaron valores patológicos de ningún marcador bioquímico. Por el contrario, sí encontramos concentraciones patológicas de CK-MB-masa y mioglobina, e incluso de cTnI en dos de los pacientes que recibieron cardioversión interna a través de un desfibrilador automático. Conclusiones. La concentración de cTnI se mantuvo en valores indetectables tras la cardioversión externa, aunque el resto de los marcadores más inespecíficos se modificaran. En el grupo de cardioversión interna por fibrilación auricular no se detectó ningún movimiento enzimático (AU)