0034: Preexcitation syndrome and atrioventricular nodal reentrant tachycardia: coincidence or not?

BackgroundReciprocating tachycardia which occurs in patients with a preexcitation syndrome (PS) generally is directly related to the presence of the accessory pathway (AP) and is called atrioventricular re-entrant tachycardia (AVRT). The purpose of the study was to evaluate the incidence of re-entrant tachycardia of other nature among patients with a PS.Methods785 patients with paroxysmal tachycardia were admitted AP ablation, 294 patients with a concealed AP (group I) and 491 patients with a Wolff-Parkinson-White syndrome (WPW) (group II). Programmed atrial stimulation was performed in the control state and if necessary after isoproterenol to induce the clinical tachycardia and determine its mechanism.ResultsAVRT was induced in 760 patients (97%), 282 of group I (96%)and 478 of group II (97%) (NS). Atrioventricular nodal re-entrant tachycardia (AVNRT) was induced in 13 group I patients (4.6%) and 12 group II patients(2.5%) (NS; 0.11). In 9 group I patients (3%) and in 4 group II patients (1%) (p<0.015), both AVRT and AVNRT were induced. In patients with only induced AVNRT, slow pathway ablation was performed and accessory pathway was respected because there was no inducible tachycardia using AP and the conduction over AP was poor. These patients remained free of symptoms after ablation of AV node slow pathway. Among this population 3 families were identified as having either AVRT or AVNRT.ConclusionsIn patients with concealed or patent accessory pathway and complaining of paroxysmal tachycardia, a careful evaluation of the mechanism of tachycardia is required before ablation. Patients with concealed conduction over an AP have more frequently an association of AVRT and AVNRT than patients with a patent preexcitation syndrome. Rarely AVNRT can be the only mechanism of symptoms

AGE AND GENDER-RELATED SYMPTOMS RECURRENCE AFTER AV NODE RE-ENTRANT TACHYCARDIA

International audienc

190: In how many patients with Wolff-Parkinson-White syndrome-related adverse presentation isoproterenol infusion was required to reproduce the arrhythmia?

Electrophysiological study is the main method for the detection of patients with a Wolff-Parkinson-White syndrome (WPW) at risk of adverse presentation (resuscitated ventricular fibrillation (VF), documented life-threatening arrhythmia): the protocol is debated. The purpose of the study was to look in how many patients with WPW-related adverse presentation, atrial fibrillation (AF) or atrial tachycardia with the shortest RR cycle length (CL) with 1/1 conduction over accessory pathway (AP)<250msec was induced in control state (CS) and when isoproterenol was required.Methods63 patients, mean age 38±18, were referred for WPW-related adverse presentation (VF 6, other 56). EPS included in CS atrial pacing and measurement of the shortest CL with 1/1 conduction over AP and programmed stimulation with 1 and 2 extrastimuli. AP effective refractory period (ERP) was determined. In absence of induction of a tachycardia with a CL <250msec, isoproterenol (0.02 to 1μg. min-1) was infused to increase sinus rate to 130bpm; the protocol was repeated.ResultsMean shortest CL conducted over AP was 223±30msec in CS, 192±25msec after isoproterenol. APERP was 225±29msec in CS, 191±19msec after isoproterenol. Atrioventricular orthodromic tachycardia (AVRT) was induced in 34 patients (54%), antidromic tachycardia (ATD) in 13 (21%), AF in 43 (68%). Criteria for a malignant form (induction of AF or ATD with a shortest CL <250mesc) were noted in 42 patients (67%) in CS and were obtained after isoproterenol in remaining 21 patients (33%). Among these patients, 12 had inducible tachycardia in CS (AVRT (n=6), ATD (n=3), AF (n=3) but the shortest CL was >240msec. A tachycardia was only induced after isoproterenol in 9 patients (14%).ConclusionsInfusion of isoproterenol should be systematic when WPW is evaluated. EPS performed only in CS missed at least 14% of patients at risk of life-threatening arrhythmias who had no inducible supraventricular tachyarrhythmia and 33% of patients with a WPW without the classical criteria for a malignant form. Isoproterenol increased the sensitivity of EPS for the detection of malignant form from 67 to 100%

Ciliary Neurotrophic Factor Protects Striatal Neurons against Excitotoxicity by Enhancing Glial Glutamate Uptake

Ciliary neurotrophic factor (CNTF) is a potent neuroprotective cytokine in different animal models of glutamate-induced excitotoxicity, although its action mechanisms are still poorly characterized. We tested the hypothesis that an increased function of glial glutamate transporters (GTs) could underlie CNTF-mediated neuroprotection. We show that neuronal loss induced by in vivo striatal injection of the excitotoxin quinolinic acid (QA) was significantly reduced (by ∼75%) in CNTF-treated animals. In striatal slices, acute QA application dramatically inhibited corticostriatal field potentials (FPs), whose recovery was significantly higher in CNTF rats compared to controls (∼40% vs. ∼7%), confirming an enhanced resistance to excitotoxicity. The GT inhibitor dl-threo-β-benzyloxyaspartate greatly reduced FP recovery in CNTF rats, supporting the role of GT in CNTF-mediated neuroprotection. Whole-cell patch-clamp recordings from striatal medium spiny neurons showed no alteration of basic properties of striatal glutamatergic transmission in CNTF animals, but the increased effect of a low-affinity competitive glutamate receptor antagonist (γ-d-glutamylglycine) also suggested an enhanced GT function. These data strongly support our hypothesis that CNTF is neuroprotective via an increased function of glial GTs, and further confirms the therapeutic potential of CNTF for the clinical treatment of progressive neurodegenerative diseases involving glutamate overflow

Estimulaçao dupla-câmara e miocardiopatias hipertróficas com obstruçao ventricular esquerda - Interesses e limites

Nas miocardiopatias obstrutivas (MCO), o gradiente sistólico intraventricular esquerdo é freqüentemente diminuído pela estimulaçao da ponta do ventrículo direito. Esta noçao, conhecida desde o fim dos anos 60, está novamente na ordem do dia, graças à estimulaçao dupla-câmara. Diante de uma MCO severa, resistente ao tratamento clínico, é recomendável efetuar uma exploraçao hemodinâmica, acoplada a uma estimulaçao AV seqüencial temporária. As variaçoes do gradiente intraventricular sao medidas pela ecocardiografia Doppler, sob estimulaçao ventricular, sincronizada pela onda P, variando-se o intervalo AV sob detecçao do átrio (P) e estimulaçao do ventrículo (V) chamado de intervalo PV. Se o gradiente cai de maneira significativa, podemos propor o implante de um marcapasso, na ausência de distúrbios da conduçao, com uma finalidade puramente hemodinâmica. O marcapasso dupla-câmara, é convenientemente selecionado e programado sob controle ecodopplercardiográfico, de forma a obter um gradiente mínimo à volume sistólico constante. Dentre 11 pacientes com MCO, 8 nao apresentavam distúrbios no sistema específico de conduçao cardíaco. Sete tiveram o gradiente significativamente diminuído sob estimulaçao ventricular direita. Seis foram submetidos a implante de MP, com o objetivo hemodinâmico. Três pacientes com distúrbios no sistema de conduçao receberam marcapassos sem exploraçao hemodinâmica prévia. A estimulaçao proporcionou melhora clínica e hemodinâmica, que se manteve após um seguimento médio de 13 meses. A única complicaçao foi o aparecimento de distúrbios do ritmo atrial, induzindo taquicardias mediadas pelo MP, quando o mesmo está mal programado ou mal protegido

Limitations of the isolated GP-STN network

An in vitro mouse slice preparation from control and MPTP-treated mice in which functional reciprocal GP-STN connectivity is maintained, does not produce oscillatory bursting or synchronous activity neuronal activity. Pharmacological interventions that produce bursting activity do so without concomitant neuronal synchrony, or a requirement for glutamate or GABA transmission. Pre-treatment with MPTP did not alter this behaviour. Thus, we have no evidence that the functionally connected, but isolated, GP — STN network can act as a pacemaker for synchronous correlated activity in the basal ganglia and must conclude that other inputs such as those from cortex and/or striatum are required