Julián Villacastín
Cardiovascular Institute of the South
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Publication
Featured researches published by Julián Villacastín.
Journal of Cardiovascular Electrophysiology | 2011
David Tamborero; Barbara Vidal; José María Tolosana; Marta Sitges; Antonio Berruezo; Etelvino Silva; Mángeles Castel; Mariona Matas; Elena Arbelo; José Ríos; Julián Villacastín; Josep Brugada; Lluis Mont
Electrocardiographic VV Optimization.u2002Introduction: Echocardiographic optimization of the VV interval may improve CRT response, but it is time‐consuming and not routinely performed. The aim of this study was to compare the response to cardiac resynchronization therapy (CRT) when the interventricular pacing (VV) interval was optimized by Tissue Doppler Imaging (TDI) to CRT response when it was optimized following QRS width criteria.
Medical & Biological Engineering & Computing | 2009
Raquel Cervigón; Javier Moreno; César Sánchez Sánchez; Richard B. Reilly; Julián Villacastín; José Millet; Francisco Castells
The effect of conventional i.v. anaesthetic agents on atrial fibrillation (AF) dynamics has not been fully addressed. We aim to evaluate whether the most frequently used intravenous anaesthetic agent, propofol, modifies AF organization parameters. Multiple and simultaneous intraatrial bipolar recordings from 27 patients in AF were analyzed before and after infusing a propofol bolus. Signal organization parameters were determined using time and frequency domain analysis. Non-linear analysis was also performed to determine signal entropy. Linear analysis showed that AF becomes more organized in right atrial recordings after infusing propofol, increasing interelectrode correlation (difference of 0.017 ±xa00.005), with the contrary effect on the left atrial dipoles (difference of −0.015 ±xa00.009, pxa0=xa00.008). Entropy analysis showed similar findings, achieving a statistical significance of pxa0=xa00.001 with Shannon Entropy.
Journal of Cardiovascular Electrophysiology | 2010
Nicasio Pérez-Castellano; Julián Villacastín; Jorge Salinas; Mercedes Vega; Javier Moreno; Manuel Doblado; Eduardo Ruiz; Carlos Macaya
Epicardial Connections Between PVs and the LA.u2002Introduction: Some observations support the existence of epicardial connections (ECs) between ipsilateral pulmonary veins (vein to vein ECs [VVECs]), and we have observed venoatrial ECs inserted at distance from the pulmonary vein ostium (vein to atrium ECs [VAECs]). Our aim was to determine the prevalence of ECs and their relevance for pulmonary vein isolation.
Journal of Cardiovascular Electrophysiology | 2006
Nicasio Pérez-Castellano; Julián Villacastín; Paloma Aragoncillo; Panayotis Fantidis; Manel Sabaté; María Jesús García-Torrent; Carlos Alberto Vanegas Prieto; José María Corral; Javier Moreno; Antonio Fernández-Ortiz; Eliseo Vano; Carlos Macaya
Introduction: Atrial fibrillation (AF) may be triggered by ectopic beats originating in sleeves of atrial myocardium entering the pulmonary veins (PVs). PV isolation by means of circumferential ostial or atrial radiofrequency ablation is an effective but also a difficult and long procedure, requiring extensive applications that can have serious potential complications. Our objective was to examine pathological effects of PV β‐radiation, particularly the ability to destroy PV myocardial sleeves without inducing PV stenosis and other unwanted effects, in order to establish its potential feasibility for the treatment of AF.
Pacing and Clinical Electrophysiology | 2004
Nicasio Pérez-Castellano; Jesús Almendral; Julián Villacastín; Angel Arenal; Sergio Gonzalez; Javier Moreno; Ricardo Morales; Carlos Macaya
Some experiences support the use of atrial paced activation sequence mapping, but there is no systematic study assessing its spatial resolution, reproducibility, and influence of pacing parameters. The aim of this study was to evaluate these issues by using a 24‐pole catheter positioned at the atrial aspect of the tricuspid and mitral annuli in 15 patients. Bipolar pacing was performed at two sites (right and left atria), 2 cycle lengths (300 and 500 ms) and two outputs (twice and tenfold the late diastolic threshold voltage for 2‐ms pulses). The elapsed time between the atrial activation at the two dipoles adjacent to the pacing dipole (activation time [AT]) was measured during each pacing sequence. Changes in cycle length did not modify the AT. The increase in voltage slightly modified the AT (maximum −2 ms at the RA; 95% CI −3 to −1 ms) due to a greater shortening of the conduction time to the dipole located next to the anode. The 95% limits of the intraobserver and interobserver agreements in the AT measurement were −2 to 3 ms and −3 to 3 ms, respectively. The spatial resolution was studied in ten patients by measuring the AT during pacing from each dipole of a 20‐pole catheter with a 1‐3‐1 mm interelectrode distance. The mean AT change was 10 ± 4 ms per 6 mm of pacing site displacement (95% CI 8–11 ms, range 2.5–20 ms). In conclusion, paced atrial activation sequence analysis is reproducible, accurate, and relatively independent of pacing parameters. (PACE 2004; 27:651–656)
Journal of Cardiovascular Electrophysiology | 2006
Jorge Salinas; Nicasio Pérez-Castellano; Rodrigo Isa; Julián Villacastín
Figure 1. Upper panel: Sinus node inhibition during ventricular pacing in the absence of VA conduction. At the end of pacing, there is suprahisian AV block of one atrial beat (asterisk), which can be better appreciated at the bottom panel. This observation was reproducible and indicates that cardioinhibitory effects of ventricular pacing were also elicited on the AV node. A = atrial beat; P = ventricular paced beat. electrophysiologic study showed normal corrected sinus node recovery time (350 msec), normal sinoatrial conduction time (105 msec), and dual antegrade nodal pathways. The AV node Wenckebach block cycle length was 380 msec. There was neither inducible tachycardia nor VA conduction. Surprisingly, a sustained sinus node inhibition was observed during ventricular pacing at 600 msec cycle length. Suprahisian AV block was also observed once ventricular pacing was stopped (Fig. 1). What is the mechanism responsible for this phenomenon?
Archives of Cardiovascular Diseases Supplements | 2015
Serge Boveda; Pascal Defaye; Javier Moreno; B. Stancak; Julián Villacastín; Arnaud Lazarus; J. Sipoetz; J. Seara Garcia; Anne Rousseau; Martin Stockburger
Introduction Several studies have shown that unnecessary right ventricular pacing (Vp) has detrimental effects. The ANSWER study evaluated whether minimization of Vp improves clinical outcome compared to standard DDD pacing in patients (pts) referred for dual chamber pacemaker implantation. Methods ANSWER is a randomized, long term follow-up, multicenter, international trial comparing SafeR, a mode designed to minimize Vp by promoting intrinsic conduction, to standard DDD (AV delay left to physician’s discretion). Pts enrolled suffered from sinus node disease (SND), intermittent AV block (AVB) or allegedly permanent AVB. All pts were programmed in SafeR at implant. 1 month after implant, pts were randomized 1:1 to either SafeR or DDD. All adverse events were blindly adjudicated by a Clinical Event Committee. Secondary endpoints, presented here, included a composite of cardiac deaths and HF hospitalizations and cardiovascular (CV) hospitalizations, at 3 years. Treatment groups were compared based on an intention-totreat principle. Results 650 pts were enrolled in 43 centers in 7 countries (72.4±11.2 years, 55.2% males, 52.0% SND, 41.8% intermittent AVB and 6.2% permanent AVB) and implanted with a dual chamber pacemaker. 632 pts were randomized (314 in SafeR and 318 in DDD). Median%Vp was 11.5% in SafeR vs. 93.6% in DDD (p Conclusion As compared to DDD, the SafeR pacing mode significantly increased the time to cardiac death or first HF hospitalization, the time to first CV hospitalization and significantly reduced the duration of hospitalizations for any CV reason. Download : Download full-size image Abstract 0184 - Figure: Kaplan Meier curve of CV hospitalizations
Heart Rhythm | 2005
Nicasio Pérez-Castellano; Julián Villacastín; Javier Moreno; Aníbal Rodríguez; Mauricio Moreno; Asunción Conde; Ricardo Morales; Carlos Macaya
International Journal of Cardiology | 2007
Sergio Alonso-Orgaz; José J. Zamorano-León; § Miguel Fernández-Arquero; Julián Villacastín; Nicasio Perez-Castellanos; María Jesús García-Torrent; Carlos Macaya; Antonio López Farré
/data/revues/18786480/v7i1/S1878648015715600/ | 2015
Serge Boveda; Pascal Defaye; Javier Moreno; B. Stancak; Julián Villacastín; Arnaud Lazarus; J. Sipoetz; J. Seara Garcia; Anne Rousseau; Martin Stockburger