Is the Measurement of Accessory Pathway Refractory Period Reproducible?

AbstractIntroductionShort accessory pathway (AP) effective refractory period (ERP) is one of the risk factors in Wolff-Parkinson-White syndrome (WPW). The purpose of study was to evaluate the reproducibility of APERP measurement during a same electrophysiological study (EPS).MethodsEPS consisted of 2 APERP measurements performed prospectively in 77 patients for a WPW in control state (CS) at a cycle length of 400ms (n=76) and after isoproterenol (n=56).ResultsIn CS, 18 patients (24 %) had the same APERP at both measurements; 41 (54.6 %) had differences from 10 to 40ms, 17 (22.4 %) had differences >40ms. Among 45 patients with initial APERP>240ms, 7 had an APERP≤240ms at 2nd study. Among 31 patients with initial APERP≤240ms, 5 had an APERP>240ms at 2nd study. Pearson’s productmoment correlation was 0.75. After isoproterenol, 5 patients (9 %) had the same APERPs; 37 (66 %) had differences from 10 to 40ms and 14 had differences >40ms. Among 38 patients with initial APERP>200ms, 12 had an AP ERP≤200ms at 2nd study. Among 18 patients with initial APERP≤200ms, 10 had still APERP≤200ms at 2nd study. Pearson’s productmoment correlation was 0.54.ConclusionsThere are important variations of APERPs during EPS mainly after isoproterenol infusion. Therefore the values of APERPs should be interpreted cautiously

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

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Factors Likely to Affect the Long-term Results of Ventricular Stimulation After Myocardial Infarction

Background: The results of programmed ventricular stimulation (PVS) may change after myocardial infarction (MI). The objective was to study the factors that could predict the results of a second PVS.Methods: Left ventricular ejection fraction (LVEF) and QRS duration were determined and PVS performed within 3 to 14 years of one another (mean 7.5±5) in 50 patients studied systematically between 1 and 3 months after acute MI.Results: QRS duration increased from 120±23 ms to 132±29 (p 0.04). LVEF did not decrease significantly (36±12 % vs 37±13 %). Ventricular tachycardia with cycle length (CL) > 220ms (VT) was induced in 11 patients at PVS 1, who had inducible VT with a CL > 220 ms (8) or < 220 ms (ventricular flutter, VFl) (3) at PVS 2. VFl or fibrillation (VF) was induced in 14 patients at PVS 1 and remained inducible in 5; 5 patients had inducible VT and 4 had a negative 2nd PVS. 2. 25 patients had initially negative PVS; 7 had secondarily inducible VT, 4 a VFl/VF, 14 a negative PVS. Changes of PVS were related to initially increasing QRS duration and secondarily changes in LVEF and revascularization but not to the number of extrastimuli required to induce VFl.Conclusions: In patients without induced VT at first study, changes of PVS are possible during the life. Patients with initially long QRS duration and those who developed decreased LVEF are more at risk to have inducible monomorphic VT at 2nd study, than other patients

What is The Utility of Electrophysiological Study in Elderly Patients with Syncope and Heart Disease?

Background: Syncope in elderly patients with heart disease is a growing problem. Its aetiological diagnosis is often difficult. We intended to investigate the value of the electrophysiological study (EPS) in old patients with syncope and heart disease. Methods: EPS was performed in 182 consecutive patients with syncope and heart disease, among whom 62 patients were ≥75 years old and 120 patients <75. Results: Left ventricular ejection fraction was 43.9±11.7% in patients ≥75 and 41.1±12.6% in patients <75. During EPS, induced sustained ventricular arrhythmias were as frequent in both groups (27.4% in patients ≥75 versus 27.5% in patients <75, p=0.99) whereas AV conduction abnormalities were more frequent in older patients (37.1% in patients ≥75 versus 18.3% in patients<75, p<0.005). Syncope remained unexplained in 35.5% of patients ≥75 and in 51.7% of patients <75 (p<0.04). ICD was more likely to be implanted in younger patients than in patients ≥75 years (37.5% vs 21% respectively, p<0.009). During a mean follow-up period of 3.3±3 years, the 4-year-survival rate was 66.9±6.8 % in patients ≥75 and 75.9±6.2 % in patients <75 years. The main cause of death was heart failure in both groups. The factors related to a worse outcome in a multivariate analysis were low LVEF and higher age. Conclusion: Complete EPS allows the identification of treatable causes in a high proportion of elderly patients with syncope and heart disease. Yet, the prognosis of these patients is mainly related to LVEF and age

Is Ablation of Atrial Flutter Always Safe?

International audienceBackground: Radiofrequency ablation of typical atrial flutter is largely used and is considered as safe. The purpose of the study was to evaluate the prevalence and the causes of severe adverse event (AE) following atrial flutter ablation.Methods: Ablation of typical flutter was performed by conventional method with an 8-mm-tip electrode catheter, a maximum power of 70 W, and a maximum target temperature of 70° for 60 seconds in 883 patients, (685 males and 198 females aged from 18 to 93 years [64 ± 11.5]; 664 had heart disease [HD]).Results: AE occurred in 44 patients (5%). AE was life threatening in 14 patients: poorly tolerated bradycardia (transient complete atrioventricular block [AVB] or sinus bradycardia [SB] <40 beats per minute) associated with cardiac shock and acute renal failure in five patients, tamponade (n = 1), bleeding leading to death (n = 1), various AE-related deaths (n = 2), ventricular tachycardia-related death (n = 1), definitive complete AVB (n = 3), and right coronary artery occlusion-related complete AVB (n = 1). Less serious AE occurred in 30 patients: transitory major SB or second- or third-degree AVB (n = 23), bleeding (n = 4), transient ischemic attack (n = 1), and various AE (n = 2). Most of the bradycardia was related to β-blockers or other antiarrhythmic drugs used to slow atrial flutter. Factors of AE were female gender (36% vs 22%, P < 0.02) and the presence of ischemic (P < 0.03) or valvular HD (P < 0.01).Conclusions: AE following atrial flutter ablation occurred in 5% of patients. Most of them are avoidable by control of anticoagulants and arrest of rate-control drugs used to slow the rate of atrial flutter