[Clinical evolution of patients following investigation of atrial vulnerability after a first cerebral ischaemic accident]. / Evolution clinique des patients ayant eu une recherche de vulnérabilité atriale après un premier accident ischémique cérébral.

Atrial vulnerability reflects the ability of the atrium to fibrillate. ISAV (Ischemic stroke and atrial vulnerability) is a French epidemiological registry whose main goal is to assess the evolution modalities of patients in whom an electrophysiological study of the atrium has been performed. A group of 269 patients with a history of non elucidated ischemic stroke and an electrophysiological study of the atrium performed in a mean delay of 3 months after the stroke has been included. Their mean age at the time of the stroke was 55 +/- 15.8 years. The electrophysiological study has measured the effective refractory period of the atrium, the locoregional right intra-atrial conduction time, the index of latent atrial vulnerability and assessed the inductibility. The mean delay between the date of the stroke and the date of the last news was 4.4 +/- 2.8 years. We observed 12 deaths and 11 patients presented during the follow up a spontaneous atrial arrhythmia and 17 a recurrence of stroke. If we consider the occurrence of the 28 combined events (atrial arrhythmia and/or stroke), it is not correlated with the presence of an atrial septal defect nor with the existence of an atrial vulnerability. On the contrary this occurrence is correlated with tobacco consumption and/or arterial hypertension; 82% of patients have these risk factors versus 54% of patients without events (p = 0.004). This association is not significant in patients younger than 55 years.

Long-term prognostic value of time domain analysis of signal-averaged electrocardiography in idiopathic dilated cardiomyopathy.

The aim of this study was to evaluate the long-term prognostic value of signal-averaged electrocardiography (SAECG) in idiopathic dilated cardiomyopathy (IDC). Time domain analysis of SAECG was assessed in 131 patients with angiographically confirmed IDC (age 52+/-12 years; 108 men; left ventricular ejection fraction 33+/-12%) using specific criteria in 44 patients with bundle branch block. Late potentials (LP) on SAECG were present in 27% of the patients. Patients with LP had a similar left ventricular ejection fraction and a similar left ventricular end-diastolic diameter than patients with a normal SAECG. With a follow-up of 54+/-41 months, 24 patients suffered cardiac death and 19 had major arrhythmic events (sudden death, resuscitated ventricular fibrillation, or sustained ventricular tachycardia). Patients with LP had an increased risk of all-cause cardiac death (RR 3.3, 95% confidence interval 1.5 to 7.5, p = 0.004) and of arrhythmic events (RR 7.2, 95% confidence interval 2.6 to 19.4, p = 0.0001). Using multivariate analysis, only LP on SAECG (p = 0.001), reduced SD of all normal-to-normal intervals (SDNN) (p = 0.002), increased pulmonary capillary wedge pressure (p = 0.005), and history of sustained ventricular tachyarrhythmia (p = 0.02) predicted cardiac death. A history of previous sustained ventricular tachyarrhythmia (p = 0.0001), reduced SDNN (p = 0.003), and LP on SAECG (p = 0.006) were the only independent predictors of major arrhythmic events. Results were not altered when considering separately patients with or without bundle branch block, or after exclusion of patients with a history of sustained ventricular tachyarrhythmia. This study is one of the first to suggest that LP on SAECG is an independent predictor of all-cause cardiac death and is of high interest for arrhythmia risk stratification in IDC.

[Comparison of the efficacy of moricizine and disopyramide in the treatment of ventricular extrasystoles]. / Comparaison de l'efficacité de la moracizine et du disopyramide dans le traitement des extrasystoles ventriculaires.

Moricizine chlorhydrate (Ethmozine), a relatively unknown antiarrhythmic agent in France, is a derivative of Phenothiazine, related to the Vaughan-Williams Class IB drugs. A randomised, double-blind, crossover trial with Disopyramide 600 mg/day after a placebo period in 10 patients with ventricular extrasystoles, half of whom had underlying cardiac disease, showed that moricizine 750 mg/day significantly reduced (p less than 0.05) the overall number of ventricular extrasystoles by 81 +/- 46% (disopyramide 72 +/- 69%; NS) and that this drug is effective in 2/3 of patients by suppressing 70 to 100% of ventricular extrasystoles, whereas disopyramide was effective in only 40% of the same patients and never gave better results than Moricizine. Cardiac and extracardiac tolerance of Moricizine was good in this study, confirming previously reported results and its superiority when compared with disopyramide (20% of unwanted effects in this series).

[Proarrhythmic effects of antiarrhythmic drugs]. / Les effets proarythmiques des antiarythmiques.

The proarrhythmic effects of antiarrhythmic drugs are complications which have been described over several decades but the mechanisms (reentry, increased automaticity, ectopic faci, induced repetitive activity, vagal or adrenergic triggers) and the predisposing factors (underlying cardiac disease, previous severe arrhythmia, metabolic disorders, ischaemia, etc...) have only recently been identified. The appreciation of their true frequency poses problems of methodology (mode of recruitment, therapeutic converse proof), of definitions and depends to a great extent on the methods of detection used. Their severity cannot be denied and has been demonstrated both in experience of isolated cases and in recent prospective studies, the conclusions of which must be interpreted critically. Proarrhythmic effects may be observed at atrial (vagal or sympathetic arrhythmias, 1/1 flutter, acceleration of atrial fibrillation in preexcitation syndromes), junctional (artificial unidirectional block created by the antiarrhythmic drug which may be very effective at higher dosages: biphasic effect) or ventricular (aggravation of ventricular extrasystoles, torsades de pointe, ventricular tachycardia/fibrillation) levels. It is curious that no antiarrhythmic drug seems to be statistically less exposed to this type of complication which may result from phenomena of toxicity or idiosyncrasy. Given the potential gravity measures must be taken to prevent this complication, by observing simple rules (respect of contraindication, use of progressive dosage regimens, avoidance of loading doses, elimination of predisposing factors and abstention from dangerous therapeutic associations) and by carefully following up high risk patients.

[Sinoatrial and atrioventricular conduction disorders in Lyme disease. Apropos of 2 case reports]. / Troubles conductifs sino-auriculaires et auriculo-ventriculaires de la maladie de Lyme. A propos de deux observations.

Lyme's disease due to Borrelia Burgdorferii is a rare cause of acute atrioventricular block (AVB) which is the commonest cardiac complication. Cutaneous, neurological and articular involvement complete the clinical picture of this condition. These two cases, confirmed by serology, support previously reported data describing the favourable prognosis of these conduction defects (suprahisian and/or hisian in our 2 cases) which regress completely, irrespective of their degree of severity. The authors also describe AVB occurring without extracardiac manifestations of this condition and a documented case of sinoatrial block, indicating a new zone of infestation.

[Injectable and oral propafenone in nodal reentry and pathways of ventricular preexcitation]. / Etude de la propafénone injectable et orale dans les rentrées nodales et les voies de préexcitation ventriculaire.

Propafenone, an antiarrhythmic drug of IC type, was applied to 10 patients with supraventricular tachycardia (SVT) produced by intranodal reentry (group I) and in 14 patients with reentry by an accessory atrioventricular (AV) pathway (group II), 10 of them suffering from orthodromic SVT. Propafenone given intravenously depresses or blocks the antegrade or retrograde conduction in the AV node and in the accessory AV pathway. The same effect is observed with orally given propafenone: 66% of antegrade blocking and 54% of retrograde blocking of the accessory conduction pathway. Intravenously given propafenone reduces within 2 to 3 min by antegrade or retrograde blocking 70% of SVT produced by intranodal reentry and by 85% of SVT produced by reentry by the accessory pathway. After injection it becomes impossible to induce intranodal SVT in 60% of cases and SVT by the accessory pathway reentry in 28% of cases. With oral treatment (600 mg/day) reinduction of intranodal SVT becomes impossible in 66% of cases and of SVT produced by reentry by the accessory pathway in 42% of cases. Long-term oral administration (17 +/- 3.7 months) of the same dose prevents 88% of SVT produced by internodal reentry and 80% of spontaneous SVT produced by reentry by the accessory pathway. Cardiologic tolerance is satisfactory: one case of atrioventricular and intraventricular dysrhythmia is observed. The same holds true for general tolerance: in 2 cases drug administration is discontinued and 11 patients present neurologic and digestive troubles improving after lowering the dosage or increasing the fractionation.(ABSTRACT TRUNCATED AT 250 WORDS)

[Estimation of the long-term efficacy of anti-arrhythmia treatment with flecainide in ventricular tachycardia]. / Prévision de l'efficacité à long terme du traitement antiarythmique par flécaïnide dans les tachycardies ventriculaires.

Flecainide, a Class IC antiarrhythmic agent, was used in 12 patients with an average age of 57 years to treat spontaneous monomorphic sustained ventricular tachycardia (S-VT, n = 9), with a ventricular rhythm of 203 +/- 41 bpm (5 right bundle branch and 4 left bundle branch block pattern) and non-sustained ventricular tachycardia (NS-VT, n = 3). The patients had ischaemic heart disease (n = 5, including 2 cases of aneurysm), idiopathic dilated cardiomyopathy (n = 1), ventricular dysplasia (right, n = 1; left n = 2; biventricular, n = 1). The remaining 2 patients had no overt cardiac disease on coronary angiography. None of the patients had signs of cardiac failure; the left ventricular ejection fraction was 0.49 +/- 0.7. Before treatment, programmed ventricular stimulation (PVS) induced 12 S-VT (214 +/- 41 bpm) which reproduced the clinical VT in 8 out of 10 cases. A second series of electrophysiological studies was performed after an average of 5 weeks treatment with Flecainide 300 mg/day (200-400 mg). It was not possible to induce VT in 2 patients (17% total prevention); NS-VT replaced S-VT in 4 patients (33%); S-VT was less rapid in 5 patients (at least 50 bpm slower) (41%); one patient had S-VT as rapid as before treatment (9%). The 12 patients were prescribed long-term Flecainide therapy. During follow-up there were 4 early (7, 10 and 15 days) and one late recurrence (16 months) (42% failure rate) whilst the other 7 patients had no further attacks of VT (follow-up of 19.1 +/- 5 months) (58% success rate).(ABSTRACT TRUNCATED AT 250 WORDS)

[Treatment of supraventricular and paroxysmal ventricular tachycardia with bepridil]. / Traitement des tachycardies supraventriculaires et ventriculaires paroxystiques par le bépridil.

Bepridil is a molecule which, apart from its anti-anginal properties, also has antiarrhythmic effects due to its calcium antagonist action which depresses antero and retrograde AV conduction in the physiological pathways. Conduction in accessory AV pathways is also depressed to a lesser and more variable extent. It also has an anti-ventricular arrhythmic action probably due to an associated membrane-stabilising effect. This drug was used intravenously to treat attacks of reciprocating supra-ventricular tachycardia (SVT) (60 p. 100 conversion to sinus rhythm: 6 out of 10 cases of intra-nodal reentry, 6 out of 10 cases of reentry via an accessory pathway) and also in ventricular tachycardia (VT) (7 conversions in 15 patients within 2 to 9 minutes). It was impossible to induce attacks of SVT after administering the drug in about a third of patients; better results were obtained in intra-nodal SVT (5 cases of effective prevention out of 10) than in SVT involving an accessory pathway (1 case out of 10). It was not possible to reinitiate VT after treatment in 3 out of 6 cases (very aggressive pacing methods, a long QT interval and accelerated idio-ventricular rhythm were responsible for the failures). Oral therapy (400 to 800 mg, usually 600 mg daily in 3 doses) prevented any recurrence of SVT in over half the patients (prevention of intranodal SVT: 80 p. 100; prevention of SVT involving an accessory pathway: 13 p. 100) and in 4 out of 6 patients with VT. Provocative pacing studies after intravenous or oral bepridil provide a good indication of long-term efficacy. The drug is generally well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

[Comparative study of the efficacy of propafenone and amiodarone in the treatment of chronic ventricular extrasystole]. / Etude comparative de l'efficacité de la propafénone et de l'amiodarone dans le traitement des extrasystoles ventriculaires chroniques.

30 patients (mean age 56 +/- 18 years) suffering from multiple ventricular extrasystoles (VES) of various origin, like ischemic, hypertensive, valvular and congenital cardiopathy, and arrhythmogenic ventricular dysplasia, were treated during 12 days by a daily dose of 900 mg of propafenone (15 cases) or 600 mg of amiodarone (15 cases). The study was randomized and a portable ECG was used for 24 h. At the time of entering into the study (H0) the patients were without any therapy. The mean total number of VES was 16,878 +/- 9,212 in the propafenone group (2,062 +/- 2,342 of them being repetitive) and 19,497 +/- 7,930 in the amiodarone group (2,907 +/- 3,615 of them being repetitive). The difference between the two groups was not statistically significant, even with the use of Holter (H1) ECG monitoring one week later. After 12 days of treatment (H2) a significant decrease in the number of total VES was noted: by 78% with propafenone (76% isolated and 89% repetitive VES) and by 77% with amiodarone (74% isolated and 91% repetitive VES). The difference between the effect of the two drugs was not significative. After 12 days of wash-out (H3) the number of VES returned to initial values with propafenone but not with amiodarone where the values were still decreased after 82 days of wash-out (H4). Both drugs produced significant bradycardia which was more apparent and more spread out during the nyctohemeral with amiodarone. Propafenone affected rather the maximal and diurnal frequencies. No correlation was found between the bradycardic and antiarrhythmic effect. Amiodarone was well tolerated and propafenone produced minor digestive and neurosensory troubles in about half the cases, only in one patient a more pronounced arrhythmogenic effect was observed. In conclusion, the efficacy and the good hemodynamic tolerance of the two drugs was found to be similar in the short-term treatment of chronic, isolated or repetitive VES, irrespective of their etiology.

[Study of the arrhythmogenicity of cardiomyopathies. Hypertrophic cardiomyopathies]. / Etude du potentiel arythmogène des myocardiopathies. Les myocardiopathies hypertrophiques.

Forty-four cases of hypertrophic cardiomyopathy (23 men, 21 women; 55 +/- 15 years) referred for evaluation of chest pain (28 cases), dyspnoea (26 cases), palpitations (25 cases), dizziness (11 cases) and syncope (4 cases), were investigated prospectively between February 1983 and February 1989. The cardiomyopathy was concentric (N = 16), obstructive (N = 24) or apical (N = 4) and the diagnosis confirmed by angiography. Twenty-four hour Holter monitoring showed no ventricular extrasystoles in 43% of patients: the others had Grade I (25%), Grade III (2%), Grade 4A (14%) or 4B (16%) ventricular arrhythmias with diurnal predominance in half the cases. Patients with greater than or equal to Grade III ventricular extrasystoles had greater left axis deviation but did not differ from the others from the hemodynamic point of view. Exercise stress testing induced an isolated ventricular arrhythmia in 23% of patients and repetitive extrasystoles in 23%. The prevalence of surface late ventricular potentials was no greater in these patients than in normal subjects (4% vs 1%; NS). Programmed ventricular stimulation (N = 37) induced a repetitive response in only 25% of patients, with only two cases of sustained monomorphic ventricular tachycardia. There were no correlations between the results of programmed ventricular stimulation and those of Holter monitoring, exercise stress testing or late ventricular potential recording, but patients with inducible ventricular tachycardia or fibrillation had proportionally more syncopal episodes and greater than or equal to Grade III ventricular extrasystoles on Holter monitoring, but the difference was not statistically significant in this series.(ABSTRACT TRUNCATED AT 250 WORDS)

[Arrhythmogenic potential of cardiomyopathies. Dilated cardiomyopathies]. / Etude du potentiel arythmogène des myocardiopathies. Les myocardiopathies dilatées.

Sixty-nine cases of non-ischemic dilated cardiomyopathy were studied prospectively from February 1983 to February 1989 (52 men: 53 +/- 13.5 years of age). There were 6 cases of sustained ventricular tachycardia. Thirty-seven patients were in Class III or IV of the NYHA Classification. In addition to echocardiography, radionuclide studies, cardiac catheterisation and coronary angiography, they all underwent 24 hour Holter monitoring, signal-averaged electrocardiography and, in 46 cases, endocavitary electrophysiological investigations. Holter monitoring showed ventricular extrasystoles greater than or equal to Grade 3 of Lown's classification in 72% of patients (26% had nonsustained ventricular tachycardia) and these patients had a significantly lower cardiac index. Twenty five per cent of patients had late ventricular potentials (versus 2% in 50 normal subjects; p less than 0.02); this proportion rose to 32% in those patients with greater than or equal to Grade 3 ventricular extrasystoles and to 66% in the patients with spontaneous ventricular tachycardia; the cardiac index was lower in patients with late ventricular potentials (2.3 vs 2.8 l/min/m2; p less than 0.01) and they had a higher incidence of greater than or equal to Grade 3 ventricular extrasystoles (94% vs 65% in patients without late ventricular potentials, p less than 0.05). Programmed ventricular stimulation induced sustained or nonsustained monomorphic ventricular tachycardia and ventricular fibrillation in 15% of cases. The 6 cases of induced sustained ventricular tachycardia were only observed in the 6 patients with spontaneous sustained ventricular tachycardia and they had the same electrocardiographic appearances.(ABSTRACT TRUNCATED AT 250 WORDS)

[Mitral valve prolapse, arrhythmias and sudden death]. / Prolapsus valvulaire mitral, troubles du rythme et mort subite.

Some of the classical concepts of mitral valve prolapse (MVP) should be reviewed in the light of recent publications. It is a condition, according to strict echocardiographic criteria excluding near physiological abnormalities, which affects 2 to 3% of the adult population in the industrialised world. Only repetitive atrial arrhythmias and complex ventricular arrhythmias are more common in this condition than in control groups, the differences being more pronounced in cases of mitral regurgitation. The risk of syncope or sudden death is 0.1% per year, hardly any different to that of the rest of the general adult population (0.2%). However, this risk may attain 0.9 to 2% in cases with mitral regurgitation. The causes of sudden death are unclear (haemodynamic, neurohumoral, arrhythmic, etc...), although there is evidence in favour of malignant ventricular arrhythmias. Detailed clinical, electrophysiological, isotopic and anatomopathological studies have raised doubts as to the direct responsibility of the vascular malformation (or its eventual consequences on the atrial and ventricular chambers) in this mode of fatal outcome. On the other hand, localised or diffuse myocardial disease is often observed, usually a- or pauci-symptomatic, associated with MVP, the responsibility of which is more plausible. Therefore, the physician should adopt a flexible attitude towards these patients, reassuring those with benign symptoms at low risk and following up or actively treating the rarer malignant forms (especially familial, syncopal with mitral regurgitation and/or severe arrhythmias).

[Surgical treatment of atrial fibrillation]. / Traitement chirurgical de la fibrillation auriculaire.

The persistence of atrial fibrillation with a controlled ventricular response with medical treatment or ablation of the His bundle, suppresses troublesome palpitations but leaves potential haemodynamic problems and the risk of thromboembolism. Surgical treatment of this arrhythmia, by leaving an anatomic bridge between the sinus and atrioventricular nodes, aims to allow acceleration of the ventricular rhythm on exercise whilst preventing by partial, total or selective exclusion of atrial tissues, the multiple intra-atrial reentries responsible for atrial flutter or fibrillation. The first method proposed was isolation of the left atrium (Cox, 1980) which allows acceleration of the ventricular rhythm during exercise, leaving little or no haemodynamic disturbance, but, in theory, the same risk of embolism. The second method, the "corridor" operation (Guiraudon, 1985) consists in isolating both atria, but significantly alters the haemodynamic efficacy without reducing the embolic risk, and hardly offers any advantage over ablation of the nodo-hisian pathway completed by implantation of a ventricular, rate responsive, pacemaker. The recently described "maze" procedure (Cox and Boineau, 1991) would seem to be more promising with judiciously chosen incisions (at the base of the atria, around the pulmonary veins, between the vena cavae, along the interatrial septum, etc.) and points of cryoablation in the region of the coronary sinus, allowing modulation of the ventricular response with activation of sufficient atrial tissue to prevent reentry and recurrence of atrial fibrillation without affecting haemodynamic efficacy. The results of this technique are encouraging in the hands of its inventors but require confirmation in larger series of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

[Drug-induced ventricular tachycardia]. / Les tachycardies ventriculaires d'origine médicamenteuse.

Certain drugs can induce ventricular tachycardia (VT) by creating reentry, ventricular after potentials or exaggerating the slope of phase 4. These may or may not be symptomatic, sustained or non-sustained and have variable ECG appearances: monomorphic or polymorphic, bidirectional, torsades de pointes. They risk degenerating into ventricular flutter of fibrillation and have been held responsible for the increased mortality observed unexpectedly in some long-term treatments. The drugs responsible are mainly those used in cardiology, probably due to predisposing circumstances (cardiomegaly, cardiac failure, previous severe ventricular arrhythmias, therapeutic associations, metabolic abnormalities). These include primarily the antiarrhythmic drugs (IA, IC, sotalol and bepridil), digitalis, sympathomimetics and phosphodiesterase inhibitors. These complications may be toxic or idiosyncratic, in patients with or without cardiac disease, and may also occur with other drugs: vasodilators and anti-anginal drugs (lidoflazine, vincamine, fenoxedil), psychotropic agents (phenothiazine and imipramine), antimitotics, antimalarials (chloroquine) or antibiotics (erythromycin, pentamidine). The prognosis is severe and the treatment is often difficult which makes prevention, helped by repeated surface ECG (or Holter monitoring), very important with careful assessment of patients at risk.

[Treatment of ventricular tachycardia with propafenone. Parallel study of ventricular provocation tests]. / Traitement des tachycardies ventriculaires par la propafénone. Etude "en parallèle " des tests de provocation ventriculaire.

Propafenone (P), a class IC antiarrhythmic drug, was tested intravenously and orally in the curative and preventive treatment of sustained (VTS) and non-sustained (VTNS) ventricular tachycardia. The 16 patients involved included 11 men and 5 women of mean age 49 years. They all had heart disease: ischaemia in 3, right ventricular arrhythmogenic dysplasia in 6, dilated myocardiopathy in 5 and left ventricular aneurysm in 2. Intravenous P in doses of 1.5 mg/kg controlled VT within 2 or 3 minutes on average in 9 out of 12 patients. Following the injection VT could not be reinduced in 2 out of 10 patients; other inductions were harder to obtain or resulted in VTNS instead of VTS (n = 3), or remained unchanged (n = 5). When P was administered orally (mean dose 900 mg) to 14 patients reinduction of VT was no longer possible in 2 cases, more difficult in 1 case, remained unchanged in 7 cases and was easier in 4 cases. Long-term oral therapy at the same dosage level prevented recurrences of VT in 7 out of 14 patients; the drug was discontinued in 2 patients owing to its arrhythmogenic effect on induced VT. The patients were followed up for 5 to 36 months (mean: 16.4 +/- 11.7 months). In this trial the results of long-term treatment could not be predicted from Holter recordings or measurements of plasma levels.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of oral and injectable flecainide in patients with an accessory atrioventricular pathway]. / Effets de la flécaïnide injectable et orale chez les patients ayant une voie accessoire auriculo-ventriculaire.

Flecainide, a new Vaughan-Williams Class Ic anti-arrhythmic agent, was used in 21 patients with an accessory AV conduction pathway which was apparent in 16 cases (WPW syndrome), latent in 1 case and concealed in 4 cases (block in the anterograde direction). Seventeen patients had spontaneous and inducible arrhythmias; 13 supraventricular tachycardias (SVT) due to orthodromic reentry including the accessory AV pathway and 4 atrial arrhythmias. Intravenous flecainide (2 mg/kg over 5 minute period) terminated the 13 cases of SVT in an average of 3 minutes by depressing then blocking retrograde conduction in the accessory pathway and 3 out of 4 cases of atrial arrhythmias. Conduction in the accessory pathway was blocked in the anterograde direction in 75% of cases and depressed in the rest; it was blocked in the retrograde direction in about half the cases and depressed in the rest. Intravenous flecainide completely prevented the induction or arrhythmias in 13 out of 17 patients (76%). Oral flecainide blocked the accessory pathway in the anterograde direction in 68.7%, and in the retrograde direction in 62% of patients, and prevented arrhythmias during provocative testing in 82% of patients (14 out of 17). With an average follow-up of 20.7 +/- 2.6 months with oral doses adapted to body weight and to the response to IV flecainide only one recurrence of atrial fibrillation was observed, a 100% prevention of spontaneous SVT and 94% prevention of all arrhythmias (16 out of 17 cases). The predictive value for the response to oral therapy of the tests of regularisation of SVT by IV flecainide and of the tests of non-provocation of SVT with oral or IV flecainide was excellent (100%). The cardiac tolerance was very good in these 21 patients (17 of whom had no valvular or myocardial lesion). There were 6 minor cases of general intolerance to oral therapy which were not dose related, only 1 of which required interruption of therapy. Flecainide appears one of the best choices for the treatment of preexcitation syndromes and their related arrhythmias at the present time.

[Interruption of the infra-renal inferior vena cava with azygos continuation. Case report]. / Interruption infra-rénale de la veine cave inférieure avec continuation azygos. A propos d'un cas.

The authors report a case of congenital interruption of the inferior vena cava with azygos continuation with a deep venous thrombosis of the left lower extremity. It is a rare congenital abnormality which is most of the time asymptomatic. However such an abnormality may be a problem in case of cardiac catheterization or thoracic surgery.

[Value of esophageal stimulation for decreasing auricular flutter]. / Intérêt de la stimulation cesophagienne pour la réduction du flutter auriculaire.

The purpose of this study was to evaluate the effectiveness of trans-esophageal atrial stimulation in decreasing atrial flutters. 31 patients, aged between 26 and 86 years, underwent 38 esophageal stimulations between August 1986 and April 1987. Esophageal stimulation was carried out with a device delivering major stimuli (10 to 20 ms) as well as high voltages (10 to 20 volts). A bipolar probe of permanent intracardiac stimulation was placed behind the left atrium, via a trans-esophageal approach under ECG guidance. Stimulations were carried out at a slightly faster rhythm than that of the atrial flutter, for 1 to 30 seconds with a progressive increase of the stimulation frequency (280 to 960 impulses/min) until either a sinus rhythm or an atrial fibrillation was obtained. A sinus rhythm was obtained immediately (21 times out of 38; 55.3%) and at the 24th hour after temporary atrial fibrillation in 8 additional patients (21%). The reduction percentage at 24 hours was therefore 76.3 p. cent. In 6 patients (15.8%), esophageal stimulation failed and in 3 additional patients, after atrial fibrillation, there was either relapse into flutter, or persistence of atrial fibrillation at the 24th hour. Esophageal stimulation was well tolerated in all cases. There were no local or rhythm complications. In conclusion, trans-esophageal atrial stimulation appears to be effective, easy to implement, economical and well tolerated. Its primary use to decrease atrial flutter seems justified, permitting to avoid in 75 p. cent of the time, recourse to intracardiac atrial stimulation or external shock.

[Injectable and oral cibenzoline in the treatment of supraventricular tachycardia related to intranodal reentry or accessory atrioventricular conduction pathway]. / Etude de la cibenzoline injectable et orale dans le traitement des tachycardies supraventriculaires liées à une rentrée intranodale ou à une voie de conduction auriculo-ventriculaire accessoire.

Cibenzoline, a Vaughan-Williams Class I antiarrhythmic agent, was studied in 26 patients with orthodromic supraventricular tachycardia (SVT) by nodal reentry (n = 10) or an accessory pathway (AP) (n = 16). IV cibenzoline accelerated sinus rhythm, prolonged PR, AH, HV and QT, widened QRS and depressed or blocked anterograde and retrograde conduction in the accessory pathway, significantly, without significantly modifying conduction capacity in the AV node, nor atrial, nodal or ventricular refractory periods. It converted 6/10 of nodal reentries and 9/16 of reentries due to an AP, by a mean dose of 1 mg/kg, in 2 to 3 minutes, in 12 cases out of 16 by blocking retrograde conduction in the reentry circuit. It prevented reinduction of 12 of the 26 cases of SVT, significantly slowing the cycle of induced SVT in other patients. Oral cibenzoline (260 to 390 mg/day) prevented induced SVT in 11 cases out of 25 and spontaneous SVT in 14 cases out of 26, with a follow-up of 11 +/- 4 months (6 to 16), and this regardless of the reentry mechanisms. Intravenous cibenzoline was not associated with any clinical or hemodynamic intolerance but there was facilitation of episodes of SVT in one patient. Oral administration caused only one case of digestive intolerance, leading to lowering of the dose. Plasma levels showed no significant differences between successes and failures, for both the injection and oral formulations of cibenzoline, whether in terms of the conversion or prevention of episodes. Electrophysiological investigations had a 60% positive and 50% negative predictive value, a sensitivity of 64% and a specificity of 50%. Cibenzoline thus appears to be useful for the conversion and prevention of episodes, SVT, regardless of the reentry circuit, and seems justified, in view of its good safety/acceptability, as first line treatment in this diagnostic indication, measurement of plasma levels and electrophysiological investigations being of little apparent value in terms of guiding treatment and predicting its results.

[Preventive drug therapy of recurrence of atrial fibrillation]. / Prévention médicamenteuse des récidives de fibrillation auriculaire.

Without treatment, about 60% of atrial arrhythmia patients suffer a relapse within 3 months and 70% within one year. Antiarrhythmic treatment intended to reduce this percentage is therefore justified, on condition that it is well tolerated. Several preliminary questions have to be settled before this medical prophylaxis: 1) Justification of antiarrhythmic treatment (sometimes pointless to deal with very occasional episodes); 2) Treatment of the underlying heart disease (valve disease, cardiothyrotoxicosis, etc.) or promoting factors (potassium depletion etc.); 3) Accurate assessment of any associated conduction abnormalities, which may constitute a contraindication to antiarrhythmic treatment (WPW syndrome in the case of verapamil and the digitalis-like drugs) or require additional treatment (pacemaker); 4) Definition of the mechanism (vagal or sympathotonic) inducing arrhythmia; 5) Evaluation of the hemodynamic parameters of the underlying heart disease (size of the atria, ventricular function, coronary or valvular lesions) which may limit the efficacy of the treatment. Once these parameters have been identified, the primary treatment should be type la or lb antiarrhythmics, which have been shown to be effective, despite the fact that they are not without arrhythmic risks (the Ib antiarrhythmics are less effective and have a poor safety profile). The beta-blockers have preferential indications (hypersympatheticotonia, hyperthyroidism, hypertrophic myocardiopathy, mitral prolapse, angina etc.) and can be replaced by verapamil or bepridil if there are non-cardiac contraindications (ulcers, asthma, diabetes). Amiodarone is extremely effective, but its poor extracardiac safety restricts its long-term use. Complementary treatments (digitalis-like, anticoagulants or anti-PAF and cardiostimulant drugs) should be added if necessary. Recurrences (to be confirmed by ECG or Holter) should lead to rigorous confirmation of therapeutic compliance and observance of simple hygienic and dietary measures (no excessive exertion, elimination of stimulants etc.). With strict clinical and ECG monitoring, it would then be possible either to increase the dose levels (accompanied by plasma determinations if possible) or to switch to a treatment with more effective, but more aggressive drugs (amiodarone, flecainide) or to use drug associations (la and lb, la and II etc.). Repeated failure of such attempts should lead to a non-medical approach to treatment.