[Arrhythmia and muscular exercise intolerance revealing lamin genetic defect in a young adult]. / Troubles du rythme et intolérance musculaire à l'effort chez un adulte jeune révélant une laminopathie.

INTRODUCTION: Arrhythmic disorders are infrequent in young adult and should evoke myopathy associated cardiomyopathy, even though muscular symptoms are moderate or absent. CASE REPORT: We report a 25-year-old woman who developed severe supraventricular rhythm disturbances with exercise intolerance and elevated serum creatine kinase level. Initially the echocardiography showed normal ventricular function. Mutation in the lamin gene (LMNA) was identified. During the disease course, arrhythmia and ventricular function worsened and required cardioverter defibrillator implantation. CONCLUSION: Laminopathies are genetic disorders among which dilated cardiomyopathy associated with skeletal muscular involvement is the most frequent phenotype, usually like Emery-Dreifuss muscular dystrophy. Other phenotypes are progeria, lipodystrophic syndromes and peripheral neuropathy. Cardiac involvement is responsible for syncope, thromboembolic events and sudden death and often requires early cardioverter defibrillator implantation.

Impact of transesophageal electrophysiologic study to elucidate the mechanism of arrhythmia on children with supraventricular tachycardia and no preexcitation.

An electrophysiologic study (EPS) of children and teenagers with paroxysmal supraventricular tachycardia (SVT) and normal electrocardiography (ECG) in sinus rhythm was evaluated. Generally, EPS is performed only before paroxysmal SVT ablation in these patients. In this study, 140 patients (mean age, 15 ± 3 years) with normal ECG in sinus rhythm were studied for SVT by a transesophageal route in baseline state and after isoproterenol. Idiopathic left or right ventricular tachycardia was diagnosed in four patients (3 %). Anterograde conduction over an atrioventricular (AV) left lateral (n = 10) or septal (n = 9) accessory pathway (AP) was noted in 19 patients (13.5 %) at atrial pacing. Orthodromic AV reentrant tachycardia (AVRT) was induced in these children. Five of the patients had a high rate conducted over AP (>240 bpm in baseline state or >290 bpm after isoproterenol). Two of the patients (a 10-year-old girl with well-tolerated SVT and a 17-year-old with syncope-related SVT) had the criteria for a malignant form with the induction of atrial fibrillation conducted over AP at a rate exceeding 290 bpm in baseline state. Of the 140 patients, 74 (53 %) had typical AV node reentrant tachycardia (AVNRT), nine had atypical AVNRT (6 %), 1 had atrial tachycardia (0.7 %), and 33 (23.5 %) had AVRT related to a concealed AP with only retrograde conduction. Electrophysiologic study is recommended for children with paroxysmal SVT and normal ECG in sinus rhythm. The data are helpful for guiding the treatment. Ventricular tachycardia or atrial tachycardia can be misdiagnosed. Masked preexcitation syndrome with anterograde conduction through AP was present in 13.5 % of the patients, and 1.4 % had a malignant preexcitation syndrome.

Sex-related differences in peri- and post-ablation clinical data for patients with atrial flutter.

UNLABELLED: Sex-related differences were not reported for the atrial flutter (AF). The purpose of the study was to look for the influence of gender on indications, clinical data and long-term results of AFl ablation. METHODS: 985 patients, [227 females (23%)] were referred for radiofrequency AFl ablation. Clinical history, echocardiography were collected. Patients were followed from 3 months to 10 years. RESULTS: Age of women and men was similar (65.5 ± 12 vs 64 ± 11.5 years). Underlying heart disease (HD) was as frequent in women as men (77.5 vs 77%), but women had more congenital HD (10 vs 2%;p<0.001), valvular HD (18 vs 10%;p<0.002), hypertensive HD (24 vs 18%;p<0.05), and less chronic lung disease (5 vs 10%;p<0.01), and ischemic HD (5 vs 20%;p<0.001). Atrial fibrillation (AF) history was more frequent in women (36 vs 27%;p<0.001). AFl-related tachycardiomyopathy (4.5 vs 8%;p<0.03) was more frequent, but 1/1 AFl (10 vs 6%;p=NS) as frequent. Failure of ablation (16 vs 10%;p<0.01), ablation-related major complications (3.5 vs 0.9%;p<0.005) were more frequent in women. After 3 ± 3 years, AFl recurrences were as frequent in women and men (10 vs 14%), AF occurrence more frequent in women (34 vs 19.5%; p<0.001). After excluding patients with previous AF, AF risk remained higher in women (19 vs 12%; p<0.004). CONCLUSIONS: In patients admitted for ablation, AFL was less common in women than in men, despite similar age and similarly prevalent HD. More than men, women had frequent AF history, a higher risk of failure of ablation and AFl ablation-related major complications and a higher risk of AF after ablation.

Does syncope require rhythmic and non-rhythmic evaluation in patients with previous MI?

BACKGROUND: Multiple factors, in addition to left ventricular ejection fraction (LVEF) influence the risk of mortality in coronary artery disease. The purpose of this study was to evaluate the main causes of syncope after myocardial infarction (MI) and to propose an algorithm of management. METHODS: 356 patients consecutively admitted for syncope and history of MI (>1 month), without ventricular tachycardia (VT), underwent echocardiography, Holter monitoring, head-up tilt test, exercise testing, signal-averaged ECG, electrophysiological study (EPS) and evaluation of coronary status. The mean follow-up was 4±2 years. RESULTS: Monomorphic VT, ventricular flutter or fibrillation (VF) and supraventricular tachyarrhythmia were respectively induced at EPS in 87, 63 and 39 patients; conduction disturbances were noted in 23 patients, and 57 patients had several abnormalities. Among the 144 patients with negative EPS, coronary ischaemia was identified in 37 patients, and hypervagotonia in 27 patients. All studies remain negative in 84 patients (23.6%), more frequently women (p<0.001). Four patients died suddenly during follow-up. A longer QRS duration, a lower LVEF and grade IVa,b of Lown on Holter ECG were associated with the induction of VT. LVEF<40% and VT/VF induction were predictors of cardiac mortality, VT was a predictor of sudden death, and low LVEF and advanced age were predictors of death by heart failure. CONCLUSION: Myocardial ischaemia, hypervagotonia, conduction abnormalities, ventricular or supraventricular tachyarrhythmias were identified in 76% of patients with syncope after MI. Several factors of syncope were found in 57 patients (16%). Non-invasive rhythmological and systematic coronary status assessment should be recommended in patients with syncope following MI.

[Comparison of patients with paroxysmal junctional tachycardia and syncope with those without syncope]. / Comparaison des sujets ayant des tachycardies jonctionnelles paroxystiques et des syncopes avec des sujets sans syncopes.

INTRODUCTION: The purpose of the study was to determine the possible mechanisms of presyncope in patients who have paroxysmal junctional tachycardias (PJT) and a normal surface ECG between tachycardias. METHODS: Among 419 patients consecutively recruited for PJT, aged from 10 to 88 years (47+/-19), 78 of them had presented at least one syncope; they had a normal ECG in sinus rhythm. Transesophageal programmed atrial stimulation was performed using one and two atrial extrastimuli delivered in control state and if necessary after infusion of 20-30 microg of isoproterenol; arterial blood pressure was monitored; vagal maneuvers and tilt test (n=25) were performed; echocardiogram was systematic. RESULTS: Age, sex, method of induction, tachycardia mechanism and the mean heart rate in tachycardia were similar in patients with and without syncope. Syncope was related to a vagal reaction induced by the PJT in 31 patients, to a fast rate during PJT in 15 patients, to a sinus node dysfunction in six patients, to a coronary ischemia in five patients, to a tetany induced by PJT in three patients, to an advanced age in three patients, to multiple causes in three patients and remained unexplained in eight patients. Radiofrequency ablation of reentrant circuit, performed in 28 patients, suppressed syncope in 26 of them. CONCLUSION: Presyncope or syncope occurred in 18% of patients who had a history of paroxysmal junctional tachycardia. Several mechanisms were implicated; the most frequent causes were coronary ischemia or sick sinus syndrome in old patients, vasovagal reaction or fast rate in tachycardia or tetany in patients of all ages.

[Significance of permanent atrial fibrillation in idiopathic dilated cardiomyopathy]. / Signification de la fibrillation auriculaire permanente dans la cardiomyopathie dilatée primitive.

UNLABELLED: The significance of atrial fibrillation (AF) in idiopathic dilated cardiomyopathy (IDCM) remains discussed. The purpose of the study was to evaluate the clinical significance of permanent atrial fibrillation in patients with IDCM. METHODS: Systematic noninvasive and invasive studies including Holter monitoring, measurement of left ventricular ejection fraction (LVEF), electrophysiological study and coronary angiography were performed in 323 patients with IDCM; all patients had a left ventricular ejection fraction (LVEF)<40%. The studies were indicated for spontaneous ventricular tachycardia (VT) in 69 patients, syncope in 103 patients and nonsustained VT on Holter monitoring in 151 asymptomatic patients. Sixty-five patients were in permanent AF (group I). Remaining patients were in sinus rhythm at the time of evaluation (group II). Programmed ventricular stimulation using up to 3 extrastimuli in control state and if necessary after isoproterenol was systematic. Patients were followed 3+/-2 years. RESULTS: Mean age was significantly older in group I (61+/-8 years) than in group II (52+/-12) (P<0.01). Syncope (31 vs 36%), spontaneous sustained VT (18 vs 23%); mean LVEF (28+/-9% vs 29+/-9%), VT induction (25 vs 35%) were similar in both groups. During the follow-up, there were no statistical differences between groups I and II concerning each event: sudden death occurred in 13 patients, 1.5% of group I patients and 5% of group II patients (NS); a death related to heart failure occurred 22 patients, 5% of group I patients and 7% of group II patients (NS); heart transplantation was performed in 13 patients, 8% of group I patients and 3% of group II patients (NS). CONCLUSIONS: An older age is the only significant clinical factor associated with the presence of a permanent atrial fibrillation in idiopathic dilated cardiomyopathy. The presence of permanent AF does not increase the induction of a sustained ventricular tachycardia and does not affect the general prognosis of IDCM.

Supraventricular tachyarrhythmia as a cause of sudden cardiac arrest.

INTRODUCTION: Supraventricular tachyarrhythmias (SVTA) are an accepted cause of cardiac arrest in patients with Wolff-Parkinson-White syndrome (WPW) and hypertrophic cardiomyopathy but their participation in other conditions is less well understood. The purpose of the study was to examine the role of SVTA in sudden cardiac arrest (SCA) by comprehensive evaluation of patients successfully resuscitated from SCA. METHODS: A total of 169 survivors of SCA in the absence of acute myocardial infarction underwent systematic evaluation that included echocardiography, Holter monitoring, coronary angiography and electrophysiological study (EPS) with additional testing in selected cases using provocative drug testing with isoproterenol, ajmaline or ergonovine. RESULTS: SVTA was found as the only possible cause or as the cause facilitating SCA in 29 patients: (1) 3 had a WPW syndrome related to accessory pathway with short refractory period; (2) for 12 patients, SVTA was the cause of cardiovascular collapse; heart disease (HD) was present in 11 cases, but disappeared in two of four with dilated cardiomyopathy after the restoration of sinus rhythm; (3) in 14 patients, SVTA degenerated either in a VF or ventricular tachycardia (VT); HD was present in 12 cases, but disappeared in one; two had no HD and recurrent similar arrhythmia was documented by cardiac defibrillator in one of them. SVTA induced coronary ischemia was the main cause of SCA. CONCLUSION: Rapid SVTA was a cause of SCA, either by cardiovascular collapse or by the degeneration in VT or VF. The complication generally occurred in patients with advanced HD or with rapid SVTA-induced cardiomyopathy and rarely in patients without HD. The incidence of SVTA as the only cause or the facilitating cause of SCAs is probably underestimated, because it is difficult to prove.

[Significance of isuprel infusion in unexplained syncope after myocardial infarction]. / Intérêt de la perfusion d'Isuprel dans le bilan des syncopes inexpliquées après infarctus du myocarde.

UNLABELLED: The prognosis for patients with complications and syncope following myocardial infarction depends on the left ventricular ejection fraction (LVEF) and the mechanism of the syncope. The aim of this study was to evaluate the results of an electrophysiological study (EPS) following isoproterenol infusion in patients with a negative EPS under basal conditions. The population included 60 patients, aged 60 +/- 12 years, 5 of whom had syncope on effort or with stress. The EPS included measurement of AV conduction, with programmed atrial and ventricular stimulation. It was repeated following infusion of 2 to 4 microg/kg of isoproterenol. RESULTS: An arrhythmia was identified as preceding the syncope in 27 patients (45%): ventricular tachycardia (VT) n = 16, supraventricular tachycardia (n = 5), 2nd or 3rd degree AV block (n = 3), vaso-vagal reaction (n = 3): 3 subjects developed coronary ischaemia. The subjects with VT on Isuprel differed from those without VT, with a lower LVEF (34 +/- 8 vs 45 +/- 14%) (p < 0.05), a higher incidence of effort related syncope (4 vs 1) and a higher risk of cardiac death (6/16 vs 2/44) (p < 0.01). In conclusion, we recommend repeating the electrophysiogical test under Isuprel in patients with complications after MI and a negative EPS in the basal state whether or not they have exercise related syncope, which will reveal an arrhythmia in 45% of cases. Subjects with inducible VT are at high risk of cardiac death.

[Prevalence of supraventricular tachycardia and tachyarrhythmias in resuscitated cardiac arrest]. / Incidence des tachycardies et tachyarythmies supraventriculaires dans les morts subites récupérées.

Supraventricular arrhythmias are considered to be benign when the ventricular rate is slowed and treated by anticoagulants. The aim of this study was to determine the possible influence of these arrhythmias in resuscitated cardiac arrest. Between 1980 and 2002, 151 patients were admitted after a cardiac arrest. Supraventricular arrhythrmias were identified as a possible cause of the cardiac arrest in 21 patients. They underwent echocardiography, exercise stress test, Holter ECG monitoring , coronary angiography and electrophysiological investigation. After these investigations, three patients had a malignant form of the Wolff-Parkinson-White syndrome, two were asymptomatic and, in the third patient, ventricular fibrillation was induced by treatment with diltiazem. In 8 patients, a rapid supraventricular arrhythmia was considered to be the cause of cardiac arrest by cardiogenic shock; 2 patients had hypertrophic cardiomyopathy, 5 had severe dilated cardiomyopathy which regressed in one patient. In ten patients, cardiac arrest due to ventricular tachycardia or fibrillation was provoked by a rapid (> 220 beats/min) supraventricular arrhythmia; two patients had no apparent underlying cardiac pathology. In the others, myocardial ischaemia or acute cardiac failure were considered to be the cause of the cardiac arrest. The authors conclude that rapid supraventricular arrhythmias may cause cardiac arrest either by cardiogenic shock or degenerescence to ventricular tachycardia or fibrillation. Usually, this event occurs in patients with severe cardiac disease but it may occur in subjects without cardiac disease or by an arrhythmia-induced cardiomyopathy.

[Does syncope change the results of programmed ventricular stimulation in patients with previous myocardial infarction?]. / La syncope change-t-elle les résultats de la stimulation ventriculaire programmée chez les patients ayant un antécédent d'infarctus du myocarde?

UNLABELLED: The induction of a ventricular tachycardia (VT) after myocardial infarction (MI) is associated with a high risk of VT and sudden death (SD) in asymptomatic patients; the purpose of the study was to know if syncope modifies the results of programmed ventricular stimulation (PVS) and the clinical consequences. METHODS: PVS using two and three extra stimuli delivered in two sites of right ventricle was performed in 1057 patients without spontaneous VT or resuscitated SD at least 1 month after an acute MI; 836 patients (group I) were asymptomatic and were studied for a low ejection fraction or nonsustained VT on Holter monitoring or late potentials; 228 patients (group II) were studied for unexplained syncope. The patients were followed up to 5 years of heart transplantation. RESULTS: Sustained monomorphic VT (< 280 b/min) was induced in 238 group I patients (28%) and 62 group II patients (29%); ventricular flutter (VT > 270 b/min) or ventricular fibrillation (VF) was induced in 245 group I patients (29%) and 42 group II patients (18%) (P < 0.05); PVS was negative in 353 group I patients (42%) and 124 (55%) group II patients (NS). The patients differ by their prognosis; cardiac mortality was 13% in group I patients and 34% in group II patients with inducible VT < 280 b/min (P < 0.01), 4% in group I patients and 13% in group II patients with inducible VF (P < 0.05), 5% in group I patients and 7% in group II patients with negative study (NS). In conclusion, syncope did not change the results of programmed ventricular stimulation after myocardial infarction. However, syncope increased significantly cardiac mortality of patients with inducible ventricular tachycardia, flutter or fibrillation.

[Causes and prognosis of syncope in patients with primary dilated cardiomyopathy]. / Causes et pronostic des syncopes chez les patients avec une cardiomyopathie dilatée primitive.

The causes of adverse prognosis of patients with primary dilated cardiomyopathy remain controversial. Classically, it is thought that syncope is associated with an increased risk of mortality. The aim of this study was to try and identify the causes and prognostic significance of syncope in patients with primary dilated cardiomyopathy. Sixty-five patients aged 31 to 80 with primary dilated cardiomyopathy were admitted for investigation of syncope. The average ejection fraction was 27 +/- 10%. Invasive and non-invasive investigations including complete electrophysiological investigations, were performed. Sustained monomorphic ventricular tachycardia was induced in 14 patients (21.5%), ventricular flutter or fibrillation was induced in 9 patients (14%), a supraventricular arrhythmia in 17 patients (26%), and a conduction defect alone or associated with another arrhythmia in 7 patients (11%). A pathological result of tilt testing was observed in 5 patients (8%). No cause of syncope could be demonstrated in 15 patients (23%). During follow-up (4 +/- 2 years) there was a mortality of 15% which was only correlated with the reduction in left ventricular ejection fraction. The authors conclude that there are many causes of syncope in primary dilated cardiomyopathy: ventricular arrhythmias represent only 35% of cases and do not impact on the prognosis; above all, left ventricular ejection fraction is the most important prognostic factor.

[Risk factors for cardiac mortality in cases of syncope with previous history of myocardial infarction]. / Facteurs de risque de mortalité cardiaque en cas de syncope et d'antécédents d'infarctus du myocarde.

Syncope is considered to be a clinical sign predictive of sudden death in patients with a previous history of myocardial infarction. The aim of this study was to determine the prognostic factors in this population. The study population included 228 patients with myocardial infarction over one month old and who had no documented ventricular tachycardia. The patients were referred for investigation of syncope. The left ventricular ejection fraction (LVEF) was measured by echocardiography or radionucleide technique. Complete electrophysiological study including programmed atrial and ventricular stimulation was performed in all cases. The patients were followed up for 6 months to 5 years or until cardiac transplantation (average 3+/-1 years). One hundred and nineteen patients had a LVEF <40% (Group I) and 109 patients had a LVEF >40% (Group II). Sustained monomorphic ventricular tachycardia (VT) with a rate inferior to 280/min was induced in 44 patients in Group I (37%) and in 18 patients in Group II (16.5%), p<0.05. Ventricular flutter or fibrillation was induced in 24 patients in Group I (19%) and in 19 patients in Group II (17%) (NS). Different causes of syncope (conduction disturbances, supraventricular tachycardia, increased vagal tone, severe coronary ischaemia) were found in 23 patients in Group I (19%) and 32 patients in Group II (29%) (NS). Syncope was unexplained in 43 patients in Group I (36%) and 40 patients in Group II (37%) (NS). The prognosis was very different. In Group I, the cardiac mortality was 49% in patients with inducible monomorphic VT <280/min, 35% in those with inducible ventricular flutter or fibrillation but only 9% in patients without inducible ventricular arrhythmias. In Group II, the prognosis was independent of the results of programmed stimulation and much better: cardiac mortality was 5.5% in patients with inducible VT, 5% in those with inducible ventricular flutter or fibrillation and 4% in patients without inducible ventricular arrhyhtmias. The authors conclude that LVEF is the most powerful predictor of cardiac mortality and sudden death in cases of syncope with a past history of myocardial infarction. The prognosis also depends on the results of programmed ventricular stimulation when the LVEF is inferior to 40%. Sustained monomorphic VT is the most frequently induced arrhythmia in this case and the prognosis of these patients is particularly poor. On the other hand, syncope does not appear to be a poor prognostic factor in the group with normal LVEF, even when it is possible to induce VT.

Predictors of atrial flutter with 1:1 conduction in patients treated with class I antiarrhythmic drugs for atrial tachyarrhythmias.

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.

[Action of sotalol on high-amplification electrocardiogram]. / Action du sotalol sur l'électrocardiogramme haute amplification.

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.

Long-term reproducibility of ventricular tachycardia induction with electrophysiological testing in patients with coronary heart disease and depressed left ventricular ejection fraction.

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.

[Predictive value of induction of atrial flutter or fibrillation in paroxysmal junctional tachycardia]. / Valeur prédictive de l'induction d'un flutter ou d'une fibrillation auriculaire chez un sujet exploré pour tachycardie jonctionnelle paroxystique.

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.

[Prolongation of the averaged QRS complex. A simple prognostic factor in patients with post-infarction bundle branch block and a history of syncope]. / Prolongation de la durée du QRS moyenné. Elément simple de pronostic des patients avec bloc de branche, séquelle d'infarctus et histoire de malaises.

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.

[Paroxysmal junctional tachycardia and normal ECG in sinus rhythm. Is their mechanism influenced by the age of the patient at the time of the study?]. / Tachycardies jonctionnelles paroxystiques et ECG intercritique normal. Leur mécanisme est-il influencé par l'âge d'exploration du patient?

At the time of the curative treatment of paroxysmal junctional tachycardias, to determine the mechanism of the tachycardia is important. Five-hundred forty intracardiac or esophageal electrophysiological studies were performed in patients aged from 9 to 86 years and then revieved. There was no preexcitation syndrome on surface ECG. Programmed atrial stimulation was performed in basal state and if necessary repeated after infusion of isoproterenol. Atrioventricular nodal reentrant tachycardia was the most frequent cause of junctional tachycardia (72%) since childhood and in all stages of life. Concealed accessory pathway reentrant tachycardias were identified in 22% of tachycardias with a stable incidence during the course of life. Various mechanisms of tachycardia were identified in the remaining patients. In conclusion, the mechanism of paroxysmal junctional tachycardia is not correlated with the age of the patient.

[Influence of time (4 years) on the results of programmed ventricular stimulation]. / Influence du temps (4 ans) sur les résultats de la stimulation ventriculaire programmée.

The reproducibility of programmed ventricular stimulation has been previously demonstrated for periods of a few hours to several months. It has not been studied over longer intervals. The aim of this study was to assess the reproducibility of the method at long-term (> 2 years). Forty-six patients with underlying cardiac disease underwent two programmed ventricular stimulations in the absence of antiarrhythmic treatment at intervals of 2 to 6 years (mean 4 years). None of the patients had myocardial infarction or cardiac surgery during this period. The protocol was identical: up to 3 extra-stimuli were delivered in the two right ventricular sites over 3 cycles. Twenty-eight patients had inducible sustained monomorphic ventricular tachycardia during the first investigation (Group I): the investigation was negative in the remaining 18 patients (Group II). During the second investigation, 26 of the 28 patients in Group I had inducible ventricular tachycardia, the rate of which decreased from 206 +/- 50 bpm to 196 +/- 54 bpm. The induced ventricular tachycardia was slower in 15 patients and faster in 5 patients. The mode of induction was different in 12 cases. In Group II, 4 patients (22%) had inducible sustained ventricular tachycardia at the second investigation. The authors conclude that the reproducibility of programmed ventricular stimulation remains good in the long-term in subjects within inducible tachycardia, demonstrating the stability of the arrhythmogenic substrate; the frequency of this tachycardia is generally slower. In subjects with an abnormal initial investigation who became symptomatic, it may be useful to repeat programmed ventricular stimulation.

Increased atrial vulnerability in arrhythmogenic right ventricular disease.

Supraventricular tachyarrhythmias (SVTA) may occur in patients with the arrhythmogenic right ventricular dysplasia (ARVD). The purpose of the study was to evaluate the incidence of SVTA in 47 patients with ARVD proved by right ventricular angiography. Thirty-three men and 14 women, aged 21 to 72 years (mean 44 +/- 18) were admitted for nonsustained or sustained ventricular tachycardia. Eight patients had a history of spontaneous SVTA several years before ventricular tachycardia occurrence. Protocol of the study consisted of programmed atrial stimulation with one and two extrastimuli delivered during sinus rhythm and two driven rhythms (600 and 400 msec), programmed ventricular stimulation with up to three extrastimuli and was performed in the control state and after infusion of isoproterenol. The results of programmed atrial stimulation were compared with those obtained in 36 asymptomatic subjects without heart disease and with a mean age of 50 +/- 18 years (control group). Sustained SVTA (> 1 minute) was induced in seven of eight patients with spontaneous SVTA, in 27 (69%) of those with ARVD, who did not have spontaneous SVTA, and in two control subjects (5.5%) (p < 0.001). SVTA was inducible in the control state, but ventricular tachycardia induction required isoproterenol in 11 of 27 patients. Two patients without SVTA history but with inducible SVTA developed later spontaneous SVTA. ARVD was associated with a significantly higher incidence of inducible SVTA than in a control population. Supraventricular tachycardias may precede ventricular tachycardias. This association argues for a diffuse myocardial disorder in ARVD.