[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.

Comparative study of atrial vulnerability in patients with unexplained ischemic stroke or lone atrial paroxysmal fibrillation.

Strokes have a high prevalence, with a high rate of recurrence, and about 30-40% remain of unknown cause. Some patients might have asymptomatic paroxysmal atrial fibrillation (AF) which remains the main cause of embolic events. A latent atrial arrhythmogenic substrate may induce recurrent arrhythmias, including functional abnormalities such as nonuniform refractoriness and/or anatomic abnormalities such as atrial septum aneurysm (ASA) and patent foramen ovale (PFO). In 175 patients divided into three groups (Group I: 103 patients with unexplained ischemic stroke, Group II: 48 patients with paroxysmal AF and Group III or control group: 24 patients explored for another cause), such an atrial arrhythmogenic substrate was assessed by electrophysiological study. Groups I and II had a similar high rate of inducible atrial arrhythmias compared to control group III where no arrhythmia was induced. An induced atrial arrhythmia was observed in more than 50% of patients of Group I and in more than 70% of patients of Group II without any significant difference according to age. However, in 26 young patients of Group I who had a transesophageal echocardiography, both a high rate (46%) of ASA and/or PFO and a frequent latent atrial vulnerability (LAV) were observed, compared to older patients where an atrial septum abnormality was observed in only 21% of cases. Thus, among patients with stroke of unknown cause, a high percentage of them might have asymptomatic atrial paroxysmal arrhythmia. The predictive value of the electrophysiological study for spontaneous arrhythmias and recurrence of stroke remains to be demonstrated.

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.

[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).

[Comparative study of cibenzoline and flecainide by oral route for preventing recurrence of paroxysmal atrial tachyarrhythmias]. / Etude comparative de la cibenzoline et du flécaïnide administrés par voie orale dans la prévention de récidive des tachyarythmies auriculaires paroxystiques.

Although paroxysmal atrial arrhythmias are the commonest form of arrhythmia, their therapeutic management still remains controversial. Seventy one patients were included in a multicentre, randomized double-blind, double-placebo study, in parallel groups (37 in group C and 34 in group F) to compare the efficacy of cibenzoline (C) and flecainide (F), administered orally, in the prevention of recurrent atrial arrhythmia. The arrhythmia usually consisted of atrial fibrillation (n = 65), while 6 patients presented with paroxysmal atrial flutter. The mean daily dosages were 221 +/- 60 mg (C) and 165 +/- 49 mg (F). The mean age was 63 +/- 12 years in group C and 63 +/- 16 years in group F. In this trial, atrial arrhythmia was idiopathic in almost two-thirds of cases. The duration of follow-up of this study was 6 months, during which recurrences of arrhythmia were evaluated in terms of the symptoms experienced and in terms of ECG and Holter examinations repeated at the 3rd and 6th months. Supplementary ECG and Holter examinations were also performed in the presence of a clinical suspicion of recurrent symptoms. Comparison of the percentages of patients not developing a documented recurrence and who tolerated treatment, by Kaplan-Meler curves, showed a significant difference between cibenzoline (58%) and flecainide (56%). In the not-responders, the mean time to recurrence was 75 +/- 48 days in group C and 75 +/- 62 days in group F(NS). Six patients dropped out of the trial because of adverse events, including 3 cardiac adverse events (2 case of ventricular proarrhythmic activity). Four extracardiac adverse events led to discontinuation of treatment in group C. In conclusion, the efficacy of cibenzoline and flecainlde in the secondary prevention of atrial arrhythmia was found to be comparable, with 58% and 58% of patients in sinus rhythm, respectively, with a follow-up of 6 months.

[Cibenzoline versus propafenone by the oral route for preventing recurrence of atrial arrhythmia: multicenter, randomized, double-blind study]. / Cibenzoline versus propafénone par voie orale dans la prévention de la récidive des arythmies auriculaires: étude multicentrique randomisée réalisée en double aveugle.

This multicentre, randomized, double-blind study, conducted in parallel groups, was designed to compare the efficacy and safety of cibenzoline (C) and oral propafenone (P) in the prevention of recurrent atrial arrhythmias (M) over a 6-month period. Patients of either sex with reduced atrial fibrillation or flutter and predominantly in sinus rhythm (> 50%), with a left ventricular shortening fraction greater than or equal to 20% and not receiving any antiarrhythmic treatment were included. Patients presenting severe conduction disorders, severe heart failure (NYHA class III or IV), marked hypotension or recent myocardial infarction were not included. Treatments were administered at the dosage of one tablet twice a day, i.e. 260 mg/day of cibenzoline or 600 mg/day of propafenone. This dosage was reduced by one half in elderly patients (> 70 years). Patients were seen on inclusion (Dzero), and at the third and sixth months or in the case of recurrence of symptoms. Recurrent arrhythmias were assessed by ECG and 24-hour Holter monitoring and according to the symptoms experienced by the patients. Sixty-five patients, 36 men and 29 women, between the ages of 34 to 86 years and presenting an atrial arrhythmia-atrial fibrillation (80%) or atrial flutter (20%)-were included in the trial: 34 patients received cibenzoline and 31 received propafenone. The arrhythmia had already been treated in 78% of cases. Its aetiology was related to hypertensive heart disease (32%), valvular heart disease (8%), other (17%) or idiopathic (43%). The arrhythmia was symptomatic in 91% of patients on inclusion. The ultrasonographic left ventricular shortening fraction was 32.8 +/- 8.1% in group C and 32.6 +/- 6.4% in group P. The two groups were comparable before treatment. The efficacy of the two treatments was comparable: no significant difference in the number of recurrences was demonstrated: 11 patients treated with C and 12 patients treated with P; cumulative percentages of patients without recurrence with good tolerance of treatment (Kaplan-Meier acturial curves) at 6 months were 55.9% with C and 48.4% with P(NS); probability of no recurrence at 6 months (0.63 +/- 0.09 in group C and 0.57 +/- 0.09 in group P); mean time to recurrence (53.4 +/- 44.3 days in group C and 61.6 +/- 35.3 days in group P). Adverse events leading to discontinuation of treatment occurred in 4 patients from each group, and one proarrhythmic effect at 6 months in a patient in group P. The treatments were well tolerated in the majority of cases: there was no significant difference in the number of patients presenting at least one adverse event: 9(26.5%) in group C, 11(35.5%) in group P. Most events were considered to be mild or moderate. The effects of the two treatments on the course of blood pressure, heart rate, PR interval and QT interval calculated at 3 and 6 months compared to DO were not statistically different. The QRS interval increased to a significantly greater extent in group C that in group P (p = 0.02 at 3 months; p = 0.0005 at 6 months). No significant difference was observed between the two groups for the course of laboratory parameters at 3 and 6 months compared to DO in the patients present at these three visits. Cibenzoline can therefore constitute a good alternative to propafenone in the prevention of symptomatic recurrences of atrial tachyarrhythmias. The preferential use of one or other treatment can be guided by individual factors, including tolerance.

[Comparative study of the efficacy and tolerability of 2 modalities of intravenous cibenzoline administration in the reduction of recent spontaneous atrial arrhythmia]. / Etude comparative de l'efficacité et de la tolérance de deux modalités d'administration de la cibenzoline intraveineuse dans la réduction des arythmies auriculaires spontanées et récentes.

This multicentre, single blind, parallel group study compared the efficacy and clinical and electrocardiographic tolerance of a 2 minute intravenous administration of cibenzoline at a dose of 1.2 mg.kg-1 with that of a 10 minute 1.75 mg.kg-1 infusion in patients presenting with spontaneous atrial fibrillation (AF) for less than 6 weeks. Sixty-two patients (40 men and 22 women) with an average age of 62 years and presenting with sustained AF for at least 30 minutes with a ventricular rate greater than or equal to 80 bpm were randomly assigned to groups and received via the intravenous route either one of the two treatments. Efficacy (return to sinus rhythm) was assessed by an ECG recording every 5 minutes and at 45 and 60 minutes thereafter. Sixty-one of the 62 randomised patients were assessed for efficacy. Cibenzoline, administered in the form of a bolus or infusion, proved effective within one hour in 4 patients in each group (13%) and arrhythmia persisted with ventricular rate of less than 80 bpm in 10 (33%) and 5 (16%) of the patients respectively. In patients in whom sinus rhythm was not restored, ventricular rate was significantly reduced by cibenzoline. The patients in whom normal rhythm was restored under one of these treatment regimens were significantly younger. Patients in whom rhythm returned to normal following the administration of the bolus had AF of significantly more recent onset than that of the patients in whom abnormal rhythm persisted, whilst the history of the AF did not differ significantly between these two types of response after the infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

[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)

[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.

[Study of the efficacy and tolerability of oral administration of cibenzoline in the prevention of recurrence of symptomatic atrial fibrillation]. / Etude de l'efficacité et de la tolérance de la cibenzoline administrée par voie orale dans la prévention des récidives de fibrillation auriculaire symptomatique.

The efficacy and safety of oral cibenzoline were evaluated in 42 patients aged 67 +/- 7 (55-80) and with recurrent symptomatic atrial fibrillation for at least a year and for which at least one previous anti-arrhythmic agent had been stopped for inefficacy or intolerance. Cibenzoline was administered for 6 months at the dose of 260 to 390 mg per day in patients aged under 70, with the possibility of reducing this dose in those aged over 70. Clinical, electrocardiographic and 24-hour Holter evaluation took place at inclusion and after 3 and 6 months' treatment or at the time of trial termination for documented recurrence (atrial arrhythmia persisting for 60 seconds or more). The mean duration of atrial fibrillation was 5.6 +/- 5 years (1-26). It was related to ischemic (22%), valvular (17%), hypertensive (17%), hypertrophic (7%) or dilated (7%) heart disease. No etiology was found in 45% of cases. All patients had taken at least one anti-arrhythmic agent in the past (mean of 2 drugs, range 1 to 6). All patients were symptomatic, the commonest symptoms being palpitations (82%), chest pain (28%), feelings of vertigo (11%) or episodes of acute dyspnea (9%). Thirteen patients (31%) had a documented recurrence (> 60 seconds) during the six months of the trial. Recurrence occurred during the first months of treatment in the majority of patients (11 out of 13). The number of symptomatic patients decreased considerably during treatment with cibenzoline, with the disappearance of palpitations in 83% of cases.(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.

[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.

[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.

[Comparison of the efficacy/tolerability ratio of cibenzoline and propafenone in the treatment of ventricular arrhythmia]. / Comparaison du rapport efficacité/tolérance de la cibenzoline et de la propafénone dans le traitement des arythmies ventriculaires.

Cibenzoline (C) was compared with propafenone (P) in 18 adult patients (7 women and 11 men) aged 50 +/- 7 in double-blind, placebo-controlled crossover trial. After a therapeutic wash-out period corresponding to 5 times the half-life of previous anti-arrhythmic drugs, patients with more than 100 premature ventricular contractions (PVC) per hour in two 24 hour Holter records obtained at an interval of 7 days were treated in succession and after randomised by C (390 mg/day in 3 divided doses) and P (900 mg/day in 3 divided doses) for a period of two weeks, each active sequence being followed by a two week wash-out period. Efficacy (based upon the decrease in PVC/hour in a 24 hour Holter) and tolerability were evaluated at the end of each sequence, with samples drawn at the same times for assay of the study drugs. Three patients dropped out of the trial, 1 with each active drug (for epigastric pain) and 1 with dummy. No significant difference was seen between the two drugs regarding the decrease in the total number of PVC/hour in the 15 patients completing the cross-over protocol. A reduction in PVC/hour of more than 70 per cent was seen in 7 patients with C and in 9 patients with P. C was better tolerated than P on the basis of both clinical and electrocardiographic parameters. One patient developed troublesome adverse reactions with C as compared with 4 patients in the case of P. A more than 20 per cent increase in QRS was seen in 7 patients with C and in 10 patients with P, the figures for PR being 2 and 6 patients respectively. One patient showed a proarrhythmic effect with P. Plasma levels of C were significantly higher in responders (328 +/- 149 ng/ml) than in non-responders (137 +/- 41 ng/ml, p less than 0.05). No significant difference was found concerning plasma levels of P (578 +/- 477 ng/ml compared with 646 +/- 457 ng/ml, p greater than 0.05). In conclusion, the efficacy/tolerability ratio in this population with a low risk of serious rhythm events appeared to be better with C than with P.

[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.

[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).

[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)

[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)

Late ventricular potentials and spontaneous and induced ventricular arrhythmias in dilated or hypertrophic cardiomyopathies. A prospective study about 83 patients.

In a series of 83 patients with dilated (DCM) (n = 56) or hypertrophic cardiomyopathies (HCM) (n = 27), were performed 24-hour-Holter monitorings, exercise stress testings, noninvasive recordings of late ventricular potentials (LVP), and programmed ventricular stimulations (PVS) (sinus rhythm and three cycles of stimulation, two extrastimuli, two right ventricle sites) (n = 53), in order to appreciate the frequency of ventricular premature depolarisations (VPDs), to correlate these results with myocardial vulnerability to TV induction, and to compare electrophysiologic and hemodynamic results. Holter monitoring showed that 80% of group A patients had VPDs (75% Lown's grade 3 or over) and 63% in group B (37% greater than or equal to grade 3). LVP were found in 15/56 DCM, and 2/27 HCM; in comparison with a control group of 32 normal subjects, the prevalence of LVP was only significant for DCM group. LVP were more frequent in cases of VPD's greater than or equal to Lown's grade 3 at Holter monitoring in DCM group, (33% versus 7% if VPDs less than or equal to Lown's grade 3) and HCM group (20% versus 0) but the correlation was not significant. Exercise stress testing, conducted only in group B, revealed about 20% of VPDs. PVS provoked ventricular arrhythmia (greater than 5 QRS) in 13 out of 33 cases in group A and in 2 out of 20 cases in group B. There was no significant correlation between the results of these methods of study and those of hemodynamic or echocardiographic explorations except for cardiac index in group A (lower when LVP were present, and VPDs greater than or equal to grade 3 during Holter) and end diastolic diameter (larger when PVS provoked fewer ventricular arrhythmias). In group B, PVS induced monomorphic VT in 2/3 patients with syncopes. Thus: (1) ventricular arrhythmias are frequent in cardiomyopathies but LVP had a significant prevalence only in dilated forms; (2) in DCM monomorphic induced VT reproduce spontaneous crisis, whereas in HCM it is possible to provoke VT in patients with syncopes but without this clinical arrhythmia; (3) in DCM as in HCM, ventricular arrhythmia can be independent from hemodynamic disorders.