Clinical course after radiofrequency ablation of type I atrial flutter. Identification of patients who risk atrial arrhythmia recurrences.
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Publications and source records attributed to B Brembilla-Perrot.
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The objectives of this study were to: (1) define the incidence of presyncope and/or syncope in patients with paroxysmal junctional tachycardias, (2) determine their causes, and (3) determine the outcome of symptoms. Syncope is a frequent problem and is often caused by paroxysmal tachycardia. The mechanism of hemodynamic instability is unknown. The population study consisted of 281 patients, consecutively recruited because they had paroxysmal tachycardia and a sinus rhythm on a normal electrocardiogram. Fifty-two patients (group I) had presyncope and/or syncope associated with tachycardia. The remaining patients (group II) had no loss of consciousness. Transesophageal programmed atrial stimulation used 1 and 2 atrial extrastimuli, delivered in a control state, and if necessary, after infusion of 20 to 30 microg of isoproterenol. Arterial blood pressure was monitored. Vagal maneuvers and echocardiogram were performed in all patients. Paroxysmal tachycardia was induced in 51 group I patients and 227 group II patients. Comparisons of groups I and II revealed that age (50 +/- 21 vs 49 +/- 17 years), presence of heart disease (10% vs 10%), mechanism of tachycardia with a predominance of atrioventricular nodal reentrant tachycardia (70.5% vs 76%), and rate of tachycardia (196 +/- 42 vs 189 +/- 37 beats/min) did not differ between the groups. However, there were differences in both groups with regard to significantly higher incidences of positive vasovagal maneuvers (35% vs 4%, p <0.01), isoproterenol infusion required to induce tachycardia (55% vs 17%, p <0.001), and vasovagal reaction at the end of tachycardia (41% vs 4%, p <0.05). Thirty-seven group I patients underwent radiofrequency ablation of the reentrant circuit, which suppressed presyncope and/or syncope in 36 of the 37 patients. Thus, presyncope and/or syncope frequently complicated the history of patients with paroxysmal junctional tachycardia (18.5%). Several mechanisms are implicated, but vasovagal reaction was the most frequent cause. Treatment of the tachycardia typically suppressed presyncope and/or syncope.
The purpose of this study was to evaluate the influence of age on the mechanism of paroxysmal supraventricular tachycardia (PSVT). Previous studies have shown age and sex differences between certain arrhythmias and especially changes in electrophysiological characteristics of Wolff-Parkinson-White syndrome. Four hundred and eighty five patients aged 9-86 years, with PSVT and without Wolff-Parkinson-White syndrome in sinus rhythm, were studied. The esophageal or intracardiac electrophysiological study used a standardized atrial pacing protocol. Paroxysmal junctional tachycardia was induced in 475 patients. The mechanism of tachycardia was not influenced by age and atrioventricular nodal reentrant tachycardia (AVNRT) was found as the main cause of PSVT in all ranges of age. Atrioventricular reentrant tachycardia (AVRT) using a concealed accessory pathway (AP) had a similar incidence from youth to elderly. The ratio male/female (M/F) and the inducibility of other arrhythmias (atrial flutter/fibrillation) (AF/AFl) were also found to be similar in all ranges of age. The age of the patients did not influence the mechanism of the tachycardia. Most of PVST were related to a AV nodal reentrant tachycardia. Concealed accessory pathway was identified with a similar incidence in young and old patients.
OBJECTIVES: The purpose of the study was to look for the predictor factors of atrial proarrhythmic effects of class I antiarrhythmic drugs. BACKGROUND: Class I antiarrhythmic drugs may induce or exacerbate cardiac arrhythmias. The predictors of ventricular proarrhythmia are known. The predictors of atrial flutter with 1:1 conduction are unknown. METHODS: Clinical history, EGG, signal-averaged EGG (SAECG) and electrophysiologic study were analysed in 24 cases of 1:1 atrial flutter with class I AA drugs and in 100 control patients without history of 1:1 atrial flutter with class I AA drugs. RESULTS: The ages of patients varied from 46 to 78 years. Underlying heart disease was present in nine patients. The surface EGG revealed the presence of a short PR interval (PR<0.13 ms), visible in leads V5, V6 in eight (35%) patients with normal P wave duration; in other patients with prolonged P wave duration, PR seemed normaL On SAECG recording, there was a pseudofusion between P wave and QRS complex. The electrophysiologic study revealed some signs indicating a rapid AV nodal conduction (short AH interval or rate of 2nd degree AV block at atrial pacing >200 beats/mm) in 19 of the 23 studied patients. All patients, except one, had at least one sign indicating a rapid AV nodal conduction (short PR and/or P wave-QRS complex continuity on SAECG). In the control group, seven patients (7%) had a short PR interval (P<0.01) and 11 (11%) had a pseudofusion between P wave and QRS complex on SAECG (P<0.001). The P wave-QRS complex pseudofusion on SAECG had a sensitivity of 100% and a specificity of 89% for the prediction of an atrial proarrhythmic effect with class I antiarrhythmic drug. CONCLUSION: We recommend avoiding class I AA drugs in patients with a short PR interval on surface EGG and to record SAECG in those with apparently normal PR interval to detect a continuity between P wave and QRS complex, which could indicate a rapid AV nodal conduction, predisposing to 1:1 atrial flutter with the drug.
The purpose of this study was to evaluate the value of esophageal programmed stimulation in children and teenagers with normal sinus rhythm ECG and normal noninvasive studies, having palpitations and syncope, and no documented tachycardias. Paroxysmal tachycardias are frequent in children and are often related to accessory connection. These tachycardias are sometimes difficult to prove. Transesophageal atrial pacing was performed at rest and during infusion of isoproterenol in 31 children or adolescents aged 9-19 years (16 +/- 3 years) with normal sinus rhythm ECG and suspected or documented episodes of paroxysmal tachycardia. Sustained tachycardia was induced in 27 patients, at rest in 13 patients, and after isoproterenol in 14 remaining patients. Atrioventricular nodal reentrant tachycardia was found as the main cause of paroxysmal tachycardia (22 cases). Six patients were followed by a vagal reaction and dizziness. These patients had spontaneous tachycardia with syncope. In three other patients, atrial fibrillation was also induced. Concealed accessory pathway reentrant tachycardia was identified in three patients. In two patients, a regular wide tachycardia with right bundle branch block morphology was induced; the diagnosis of verapamil-sensitive ventricular tachycardia was made in a second study by intracardiac study. In conclusion, atrioventricular nodal reentrant tachycardia was found as the main cause of symptoms in children with normal sinus rhythm ECG. Syncope is frequently associated and provoked by a vagal reaction. This diagnosis could be underestimated in adolescents frequently considered as hysterical because noninvasive studies are negative.
Sudden death might be the first event in patients with asymptomatic WPW. The purpose of the study was to know if the age of the patient modifies the electrophysiological characteristics of asymptomatic WPW. Transesophageal stimulation was performed on 92 asymptomatic WPW patients from the following age groups: 10-69 years (n = 14), 20-29 years (n = 33), 30-39 years (n = 15), 40-49 years (n = 17), and 50-69 years (n = 13). The procedure consisted of atrial pacing up to the second AV block, programmed atrial stimulation using one and two extrastimuli delivered on two driven rhythms in the control state, and after infusion of isoproterenol. In thefive age groups, paroxysmal junctional tachycardia occurred, respectively, in 1 (7%), 1 (3%), 2 (13%), 2 (12%) patients, and not at all in the oldest group. AF > 1 minute occurred, respectively, in 3 (21%), 9 (27%), 5 (33%), 3 (18%), and 4 (31%) patients. The dangerous form of WPW (rapid conduction in the Kent bundle > 240/min in the control state or > 300/min after isoproterenol + AF induction) occurred, respectively, in 3 (21%), 9 (27%), 4 (27%), 1 (6%), and 3 (23%) patients. In conclusion, electrophysiological data of asymptomatic WPW are not modified by age of the patient. Elderly patients remain at risk of a dangerous form of WPW; systematic evaluation of WPWis recommended in patients with an active life independent of age.
UNLABELLED: The prognosis of patients with bundle branch block (BBB) and myocardial infarction (MI) is poor, particularly for patients suffering from syncope. The purpose of this study was to investigate the diagnostic value of some techniques for the evaluation of the mechanism of syncope in patients with MI and BBB and their prognosis. METHODS: We prospectively obtained the results of clinical history, 24 h Holter monitoring, left ventricular ejection fraction (LVEF), signal-averaged ECG (SAECG) and programmed ventricular stimulation in 130 patients with syncope, MI and BBB. 81 of them had right (R)BBB and 49-left (L)BBB. RESULTS: Ventricular tachycardia (VT) was identified as the main cause of syncope in patients with MI and BBB: 68% of them had inducible VT. The sensitivity (se) and specificity (sp) of non sustained VT on Holter monitoring for the detection of VT were respectively 42.5 and 47% in patients with RBBB, 62 and 36% in those with LBBB; se and sp of LVEF <40% were 67.5% and 65% in patients with RBBB, 85 and 9% in those with LBBB; se and sp of the combination of 2 of the 3 SAECG criteria, QRS duration > 155 ms, LAS duration >30 ms and RMS 40 < 17 microV were respectively 50 and 57% in patients with RBBB; se and sp of the combination of 2 of the 3 criteria QRS duration >165 ms, LAS duration >40 ms and RMS 40 <17 microV were 73 and 55.5%) in patients with LBBB. During the follow-up (4.7 years +/- 2.5), 12 patients died suddenly and 12 patients died from heart failure. Univariate and multivariate analysis revealed than only the induction of VT was a significant predictor of sudden death. A long QRS duration (> 165 ms) and induction of VT were independent predictors of total cardiac mortality. CONCLUSION: Among noninvasive studies, only the determination of filtered QRS duration was a significant predictor of cardiac mortality in the case of a prolongation (> 165 ms). Sudden death was only predicted by the induction of sustained VT. Because of the high incidence of inducible sustained VT, the low value of Holter monitoring and decreased LVEF for the prediction of ventricular arrhythmias and the poor prognosis of patients with inducible VT and low LVEF, systematic programmed ventricular stimulation is indicated in patients with MI, syncope and BBB, whatever the non-invasive studies results.
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Cardiac causes explain 5 to 30% of the syncopes and their incidence increases with age. Prognosis is poor in case of misdiagnosis. Mechanical causes are related principally to obstruction of left ventricular outflow, and responsible for exertional syncope. Diagnosis is easy through clinical examination and echocardiography. Arrhythmic causes are due either to brady-cardia (diagnosed by surface electrocardiogram, 24-hour holter monitoring and electrophysiologic study in patients with bundle branch block) or to supraventricular or ventricular tachycardia. Arrhythmic syncope is easily prevented by antiarrhythmic drugs or non medical treatments such as radiofrequency ablation of tachycardia, pace-maker or defibrillator implantation.
The Multicenter Automatic Defibrillator Implantation Trial (MADIT) has recently confirmed the role of programmed ventricular stimulation (PVS) to identify the high risk patients of sudden death after myocardial infarction and to prevent this risk. The purpose of this study was to evaluate the long-term reproducibility of PVS in these patients. Thirty patients with coronary heart disease without spontaneous documented sustained ventricular tachycardia (VT) underwent two programmed stimulations in the absence of antiarrhythmic drug treatment between 2 and 6 years (mean 4 years). No patient had a myocardial infarction or intervening cardiac surgery during this period. The protocol of study was similar using up to three extrastimuli in two sites of the right ventricle, delivered in sinus rhythm and driven rhythm (600 ms, 400 ms, respectively). On the first PVS, 17 patients had inducible sustained VT (group I). Thirteen patients did not have inducible VT (group II). On the second PVS all group I patients but one had inducible VT, but the cycle length was significantly modified in 11. In group II, five patients had inducible VT and in the other patients the PVS remained negative. In conclusion, in patients with coronary heart disease, but without documented VT, the long-term reproducibility of PVS was excellent in those with inducible VT (94%); the patients remain at risk of VT and a prophylactic implantable cardioverter defibrillator could be considered. In patients with initially negative study, reproducibility of PVS was lower (61.5%), probably because of the progressive remodeling after myocardial infarction. Therefore, the occurrence of new symptoms in patients with previously negative study requires a second programmed ventricular stimulation.
The induction of atrial tachyarrhythmias (ATAs) is used to guide the medical or ablative treatment of these tachycardias. To date no information is available regarding the reproducibility of programmed atrial stimulation (PAS) induced ATA. The purpose of the study was to look for the reproducibility of PAS. Two baseline electrophysiological tests were performed in the drug-free state and within 6 months to 3 years of one another (mean 18 months) in 62 patients. Twenty-six patients had spontaneous documented ATAs (group I); 36 patients did not have spontaneous ATAs (group II). PAS used one and two extrastimuli delivered during three cycle lengths (sinus rhythm, 600 ms, 400 ms). The results were as follows. In group I, sustained (> 1 minute) ATA was induced in 23 patients on the first PAS and remained inducible in 22 patients in the second study. In three patients with noninducible ATA, PAS remained negative in only one; the reproducibility of PAS was 88%. In 17 (47%) group II patients, a sustained ATA was induced in the first study, and the ATA remained inducible in 10 patients in the second study. Nineteen other patients did not have inducible ATA on the first study, but 10 of them had an inducible ATA on the second PAS; the reproducibility of PAS was 53%. In conclusion, long-term reproducibility of PAS induced ATA in patients with spontaneous and documented ATA was good. In patients without spontaneous ATA, the reproducibility of PAS induced ATA was low and the induction of ATA in these patients should be interpreted cautiously in light of this observed variability in induced atrial arrhythmias.
Cardiac arrhythmias are common causes of syncope and malaise in elderly patients, but they are sometimes difficult to demonstrate without invasive procedures. The aim of this report was to demonstrate the value of transoesophageal electrophysiological investigation in cases of negative classical non-invasive studies. The authors report 18 cases of patients, aged 70 to 88, mainly in poor general condition, who were admitted for the investigation of malaise or syncope. The ECG was normal or subnormal and Holter monitoring non-contributive to the diagnosis. Transoesophageal electrophysiological study enabled initiation of an arrhythmia, bradycardia or tachycardia, which reproduced the symptoms of spontaneous malaise. In 10 cases, paroxysmal junctional tachycardia was demonstrated, by nodal reentry in 8 cases, and in a latent Kent bundle in 2 cases. The malaise was caused by tachyarrhythmia in 3 patients and by a vagal reaction or sinus arrest after the tachycardia in the other patients. In 6 other patients, atrial fibrillation reproduced the malaise either due to the rapid rhythm, or to bradycardia after the arrhythmia in 3 cases. In another 2 patients, conduction defects were demonstrated by atrial stimulation (alternating bundle branch block in one patient, complete atrioventricular block at the end of atrial stimulation in another patient). The authors conclude that transoesophageal electrophysiological study is a simple technique which allows diagnosis of unexplained malaise in elderly patients when non-invasive methods are unable to demonstrate the causal arrhythmia. Supraventricular arrhythmias seem to be a common and probably underestimated cause of malaise or syncope in elderly patients.
D,l sotalol is an antiarrhythmic widely used for treating ventricular excitability, especially ventricular tachycardia (VT). The means of assessing its efficacy is 24 hour Holter monitoring and programmed ventricular stimulation. High amplification ECG has also been proposed for predicting the effects of the drug on the induction of VT. The aim of this study was to assess the results of high amplification ECG before and after taking sotalol and to compare them with those of programmed ventricular stimulation. This study was performed in 24 patients with spontaneous and inductible ventricular tachycardia due to ischaemic heart disease. The two investigations were performed under basal conditions and after treatment with 160 to 320 mg/day of d,l-sotalol for 8 days. Nine patients had VT which could not be induced after treatment. In the other 15 cases, the VT remained inducible and was not significantly slowed. Analysis of different parameters of high amplification ECG, the QRS duration, RMS 40 and LAS did not show any difference after treatment in cases with inducible VT or VT suppressed by treatment. In conclusion, d,l sotalol, even at antiarrhythmic doses, does not seem to change the parameters of high amplification ECG, and it is therefore not necessary to stop treatment to carry out this investigation. Moreover, it was impossible to predict the effect of d,l sotalol on VT by high amplification ECG.
Curative radiofrequency ablation of the reentry circuit of paroxysmal junctional tachycardia is a relatively common method of treating this condition. The aim of this study was to determine whether the age of the patients should be taken into account for assessing the indication. The study population was 178 patients aged 18 to 86 years (average 56 +/- 19 years), who had paroxysmal junctional tachycardia and normal interatrial ECGs. One hundred and thirty-five patients were under 70 years of age (Group I) and 43 were over 70 (Group II). No significant differences in the mechanism of reentry, which was intranodal in 67% of cases, in the risk of immediate complications (11%) or in recurrence of tachycardia were observed between the two groups. Functional improvement was more spectacular in Group II with regression of the symptoms of associated cardiac disease and, above all, in reduction in the number of hospital admissions. The common association of cardiac disease and other pathologies in Group II should however lead to more careful management and follow-up of the more elderly patients. The authors conclude that radiofrequency ablation of paroxysmal junctional tachycardia in the over 70s is feasible and often provides better clinical results than observed in younger patients.
The object of this study was to assess the incidence and significance of atrioventricular block (AVB) induced by radiofrequency ablation of intranodal reentrant tachycardias. The study population was 18 patients aged 44 to 83, selected from a total population of 144 patients treated for recurrent, refractory tachycardias. These patients developed complete AVB (9 cases), 2nd degree ABV (3 cases) and 1st degree AVB (6 cases) either immediately or in the chronic phase after radiofrequency ablation. The outcomes were as follows: 1. In the 9 patients with complete AVB, the block regressed in a period ranging from 7 seconds to 5 minutes. It recurred as complete AVB 1 to 4 days later in 2 patients, and regressed again after a maximum of 10 days. One 47 year old woman had definitive complete AVB; 2. In the 3 patients with 2nd degree AVB, the block regressed within 7 days; 3. In the 6 cases of 1st degree AVB, 2 patients developed transient complete AVB the following day. The possible causes of AVB were: increased vagal tone in 1 case, ablation of the rapid pathway located in a postero-septal site in 8 cases and, in the remainder, pre-existing conduction defects. The authors conclude that transient complete AVB is common and usually has a good prognosis. Definitive complete AVB is a rare but possible (0.7%) complication of radiofrequency ablation of reentrant intranodal tachycardias; other forms of AVB generally regress quickly and, although they may recur within days, they carry a good prognosis in the following months. However, long-term follow-up remains necessary.
Patients with a history of myocardial infarction and complete bundle branch block with syncopal episodes have a high risk of sudden death: the identification of the cause of the syncope is therefore essential. The aim of the study was to assess the diagnostic value of non-invasive techniques used in the investigations of syncope: 24 hour Holter recording, high amplification ECG and measurement of left ventricular ejection fraction. The results of these investigations were compared with those of complete electrophysiological investigation evaluating atrioventricular conduction and the inducibility of tachycardia. The patient population was 134 patients, 83 with right bundle branch block and 51 with left bundle branch block. Ninety one patients had inducible sustained ventricular tachycardia and 24 had atrioventricular conduction defects: of these, 14 also had ventricular tachycardia. During follow-up, there were 12 sudden deaths and 13 deaths from cardiac failure. Uni- and multivariate analysis showed induction of ventricular tachycardia to be a significant risk factor for global mortality and sudden death but prolongation of the averaged QRS complex (> 165 msec) was also an independent risk factor of global cardiac mortality. The authors conclude that simple prolongation of the averaged QRS duration > 160 ms in patients with right bundle branch block and > 170 ms in patients with left bundle branch block after myocardial infarction and syncope is a significant poor prognostic factor. However, this sign is not predictive of sudden death.
Sudden death may be the presenting symptom of a Wolff-Parkinson-White syndrome. Electrophysiological investigation is the best method of identifying high risk cases. The aim of this study was to determine whether this investigation should be proposed to all patients, irrespective of age. Transoesophageal stimulation was performed in 85 asymptomatic patients with the Wolff-Parkinson-White syndrome. Of the 85 subjects, 13 were under 20 years of age, 30 under 30 years, 15 under 40 years, 16 under 50 years and 11 between 50 and 69 years of age. A protocol of incremental stimulation until 2nd degree AVB was attained and programmed atrial stimulation with one or two extrastimuli delivered on 2 paced cycles (600 and 400 ms) was used under basal conditions and with Isoprenaline. A malignant form of the condition was defined as the demonstration of two abnormalities: rapid conduction in the bundle of Kent (over 240/min) under basal conditions or over 300/min after Isoprenaline, and if it induced sustained atrial fibrillation (> 1 min). The results were: [table: see text] In conclusion, the number of malignant forms of the Wolff-Parkinson-White syndrome is exactly the same, irrespective of age. Elderly patients remain at risk of malignant WPW syndrome because of the increased incidence of atrial fibrillation. Therefore, the authors recommend systematic evaluation of this syndrome if the patient has an active life-style especially with regard to sporting activities.
The association of different types of tachycardia in a given patient is a well-known phenomenon and the development of ablative methods rises hopes that treatment of one of them may suppress the others. The aim of this study was to determine the significance of induction of atrial flutter or fibrillation (AF) during electrophysiological investigation of patients investigated for paroxysmal junctional tachycardia. The initial population of 500 patients was limited to 485 patients, aged 12 to 86, with a normal intercritical ECG and without a Wolff-Parkinson-White syndrome, who underwent electrophysiological investigation for junctional tachycardias since 1978 and in whom the tachycardia could be reproduced. The study was performed by the endocavitary approach in 262 cases and by the transoesophageal approach in 213 cases with a similar protocol, programmed atrial stimulation with 1 and 2 extrastimuli under basal conditions, eventually completed by the repetition of the protocol with low doses of isoproterenol. The electrophysiological study showed that the tachycardia involved a latent bundle of Kent in 103 cases, a double nodal pathway in 343 cases or another circuit in 39 cases. During this study, sustained AF was induced in 66 cases (13.5%) with a similar incidence in Kent bundles (14.5%), intranodal reentry (11%) and other forms of reentry (11%). During follow-up, ranging from 6 months to 10 years, 7 patients with induced AF and 9 without inducible tachycardia, developed permanent AF. The occurrence of the arrhythmia was significantly correlated with the mechanism of reentry (latent Kent 8/103 cases, intranodal reentry 8/343 cases, p < 0.05), and with the induction of the same arrhythmia by oesophageal investigation alone (p < 0.001). The initiation of the arrhythmia by endocavitary stimulation did not seem to have any positive predictive value. In conclusion, the induction of atrial flutter or fibrillation during investigation of a subject with paroxysmal junctional tachycardia without a patent Wolff-Parkinson-White syndrome, does not seem to be predictive of future development of atrial flutter or fibrillation, unless the investigation was undertaken by the oesophageal approach.