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The case of a patient presenting syncopal catecholergic ventricular tachycardias associated with abnormalities of the interval QTu is reported. EKG at rest shows a normal or sometimes lengthened repolarization. The least effort or emotion produces a His rhythm accompanied with lengthening of QTu. Three stress tests disclose the caricatural picture of a catecholergic ventricular tachycardia. Treatment with quinidin derivatives causes a constant lengthening of QTu without modifying the profile of the stress test. The patient died suddenly. This case seems to represent an intermediate form between catecholergic ventricular tachycardia and the syndrome of long congenital QT.

The authors report the case of a 70 year old woman who had 3 episodes of acute ischaemia of the lower limbs in the space of 2 months. She was admitted to the Cardiology Unit after the second embolism: successive ECG recordings showed signs of the sick sinus syndrome justifying permanent pacing and anti-arrhythmic and anticoagulant therapy. The standard 2D echocardiographic views showed no signs of intracardiac disease, but a modified high short axis view demonstrated an oblong thrombus in the left auricle. Unfortunately, therapeutic non-compliance led to a third episode of embolism 2 weeks later; a repeat 2D echocardiogram showed the left auricle to be completely free of thrombosis. The authors review the medical literature of this condition. Echocardiography only began to play a useful diagnostic role from 1984 when technical improvements and the use of new and more appropriate views of the left auricle were introduced.

The potential short-term arrhythmogenic role of catheter-mediated electrical ablation was studied in 61 patients of mean age 44 years (range 15-80 years) who underwent this procedure for Wolff-Parkinson-White syndrome (36 patients) or ventricular tachycardia (VT, 25 patients). Continuous ECG monitoring was pursued during the 24 hours that preceded and followed ablation. Only bursts of 3 consecutive beats or more were considered significant. Recordings were performed with either a Hewlet Packard 78720 A arrhythmia recorder or a Holter readout system (Oxford Medilog 2, Marquette). In 36 patients with an accessory conduction pathway the 160 J were delivered at the annulus fibrosus cordis. Post-ablation recordings showed: VT bursts in 16 patients (17%); the bursts disappeared in every case before 3 days; in 3 patients the electrogram at the site of ablation was predominantly ventricular (p less than 0.05); frequent or subintrant attacks of reciprocal orthodromic rhythm (RR); in 3 cases RR began on simple variations of heart rate; it reflected a loss of the anterograde conduction hidden in the accessory pathway and required a second ablation; in 1 case RR initiated by VT bursts revealed the presence of a second accessory pathway; atrial tachycardia bursts, spontaneously resolved, in 4 patients (11%). No atrial fibrillation of flutter was recorded. In patients with VT ablation was delivered in the right ventricle (160 J, 9 patients) or in the left ventricle (240 J, 16 patients). The effects of ablation could only be interpreted in 21 patients who underwent 25 ablations.(ABSTRACT TRUNCATED AT 250 WORDS)

The electrocardiographic expression of preexcitation results from the electrophysiological behaviour of the 2 conduction pathways: the normal pathway and the accessory pathway (AP). Its interpretation can only be deductive since the electrical activities of these 2 pathways are not recorded simultaneously. The validation of a K potential likely to represent Kent's bundle activation is based on criteria of exclusion of other origins (atrium, His bundle, ventricle). The K potential could be obtained in 16 of 32 consecutive studies. In 2 cases the unusual behaviour of the AP could be reliably studied owing to recording of the K potential. In case n. 1 a 35 ms increment in conduction was reproducibly observed by atrial extrastimulation at the atrium-Kent's bundle interface. In case n. 2 preexcitation was expressed on ECG only when the atrial rate was 70 to 100/mn. With lower atrial rates conduction in the AP was impaired by a 1st degree block with an atrium-Kent's bundle delay of 100 ms. Atrial acceleration reduced this delay to 40 ms, showing that this improvement in conduction reflected an initial block on the AP in phase IV. With higher atrial rates a block was observed on the AP in phase III either as an abrupt rupture of the atrium-Kent's bundle conduction, or as a block following progressive increment of the Luciani-Wenckebach type. Injection of ATP 20 mg produced and anterograde block on the AP at the atrium-Kent's bundle interface. Retrograde conduction seemed to be lacking in the AP since atrial activity was completely dissociated from induced ventriculograms.(ABSTRACT TRUNCATED AT 250 WORDS)

This study provides detailed information on the echocardiographic data obtained before and during an intravenous infusion of isoprenaline in a group of 16 patients under 50 years of age presenting with early repolarization syndrome and in a control group of 16 patients of the same age-group. The stereotyped echocardiographic features of early repolarization syndrome are described. They include: in the basal state, ventricular hyperkinesia, anterior motion of the mitral valve and reduction of the left ventricular outflow tract; these data were significant when compared with the control group; under isoprenaline, dynamic obstruction of the left ventricle. The authors discuss the electrical significance of the early repolarization syndrome, the relationship between that syndrome and the borderline forms of obstructive hypertrophic cardiomyopathy and the role of catecholamines in the pathogenesis of obstructive hypertrophic cardiomyopathy.

We applied a new technique of catheter ablation to treat atrioventricular nodal reentrant tachycardia and preserve anterograde conduction, performing this procedure in 21 patients with repetitive episodes of tachycardia refractory to antiarrhythmic drugs. Using atrial activation in the His-bundle lead as a reference, we selected the optimal site of ablation by positioning an electrode catheter so that atrial activation occurred simultaneously with or earlier than the reference activation during tachycardia. At this site, the His-bundle deflection was completely absent or was present only at a low amplitude (less than 0.1 mV). In the majority of patients, these criteria could be met by withdrawing the catheter 5 to 10 mm from the site of the His-bundle recording (adjacent to the reference catheter). Shocks of 160 or 240 J were delivered at this site (cumulative energy [mean +/- SD], 689 +/- 442 J). Treatment resulted in preferential abolition or impairment of retrograde nodal conduction. Anterograde conduction, although modified, was preserved in 19 patients; complete heart block persisted in 2 patients. Sixteen patients remained free of arrhythmia, without medication or implantation of a pacemaker, for a mean follow-up period of 14 +/- 8 months (range, 7 to 42). Tachycardia was not inducible in 14 patients in a follow-up electrophysiologic study performed 3.6 +/- 6 months after the procedure. We conclude that catheter ablation is an effective alternative for the treatment of atrioventricular nodal tachycardia in patients with drug-resistant tachycardia.

Intracardiac electrode catheter ablation of arrhythmogenic foci, using cumulative high energy, was attempted in 29 patients (mean age 57 +/- 15 years) presenting with ventricular tachycardia (VT) refractory to antiarrhythmic drugs. A heart disease, present in 25 patients, was responsible for severe heart failure in 10 of them; 13 patients had myocardial infarction, 7 had arrhythmogenic dysplasia of the right ventricle, 5 had cardiomyopathy (dilated in 4, hypertrophic in 1). The myocardium was apparently normal in 4 patients, 2 of whom had mitral valve prolapse. Morphologically, VT was single in 20 cases, double in 4 cases and more than triple in 5 cases; arrhythmia was continual or occurred several times a day in 17 cases. In one (20 patients) or several (9 patients) catheter ablation sessions, 1 to 16 cathodic shocks of 160 to 240 Joules (1.180 +/- 1.062 J) were delivered after mapping and focal stimulation without irreversible adverse reaction. The cumulative energy delivered was 840 +/- 558 J in the right ventricle (11 patients) and 1.390 +/- 1.244 J in the left ventricle (18 patients). During a 23.4 +/- 12 months follow-up period, 4 patients died (2 of heart failure, 1 of a hitherto undocumented VT, 1 suddenly of bradycardia-asystole). VT was regarded as being controlled in 23/27 patients, 15 of whom were not taking antiarrhythmic agents. The presystolic potential during VT was -5 + 5 ms in the 4 failure cases versus -41 + 29 ms in the successful cases (p less than 0.05). It is concluded that electrode catheter ablation is an effective curative treatment of VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Fulguration is a new technique of palliative treatment (ablation or alteration of the atrioventricular junction) of refractory supraventricular tachycardias. It can be too a curative treatment of arrhythmias unresponsive to medial therapy and not suitable for surgery or implantable defibrillator (ventricular tachycardias - refractory arrhythmias of the Wolff-Parkinson-White Syndrome and permanent or incessant form of reciprocating tachycardia). An original indication of this method is the ablation of the retrograde pathway alone in refractory intranodal reciprocating tachycardias. The results of these indications are herein analysed.

The electrophysiological effects of flecainide acetate were studied in 30 patients (10 men, 20 women, mean age 48.3 +/- 18 years) suffering from sustained re-entrant intranodal tachycardia. A 2 mg/kg dose of flecainide administered over 10 minutes was given after the onset of sustained tachycardia within 3.8 +/- 2.3 min in 25 of the 30 patients; this was effected by a block in the retrograde leg of the circuit in 22 patients and by a block in the anterograde leg in 3 patients. In the remaining 5 patients the tachycardia was slowed down (367 +/- 27 ms vs 431 +/- 48 ms) chiefly by prolongation of the atrioventricular anterograde conduction. No significant side-effect was observed while the drug was being injected. Following treatment with flecainide, tachycardia was no longer inducible in 24 out of 30 patients (A) and it remained inducible in 6 patients (B, non-responders). The initial electrophysiological exploration revealed differences between these two groups in retrograde conduction: prolongation of the ventriculoatrial time during incremental ventricular stimulation (A: 41 +/- 32 ms vs B: 81 +/- 142 ms, p less than 0.05) and prolongation of the atrioventricular time above 100 ms (A: 2/24 patients, B: 3/6 patients, p less than 0.01). The following electrophysiological parameters were significantly (p less than 0.01) ,modified after intravenous flecainide: AH and HV conduction intervals, atrial refractory periods, anterograde and retrograde atrioventricular conduction. Complete retrograde block was observed in 12 patients of group A. Thus, in this study flecainide arrested a reciprocal intranodal rhythm in 25 out of 30 patients and prevented the reinduction of tachycardia in 24 of these.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors present 8 cases of aneurysms of the interauricular septum (AIAS). The diagnosis was established in all cases by two-dimensional echocardiography (E2D) which was requested, three times following a cerebral vascular accident (CVA). The AIAS manifest themselves as localised "hernias" of the inter-auricular septum, mobile during the cardiac cycle. Their topography was strictly right inter-auricular in 6 cases, whereas in the other 2 patients the AIAS passed into the left atrium at protosystole and returned to the right atrium at telesystole. Catheterization with angiography was carried out 5 times: the inter-auricular septum was crossed 4 times without gasometric reasons for an associated shunt; the AIAS was opacified in all cases. An anti-coagulant treatment was prescribed for 3 patients who had suffered a CVA, and for a fourth presenting numerous supraventricular extrasystoles which were sometimes grouped. A review of the literature of the last fifty years enabled a compilation of 93 cases of AIAS to be made, 49 of which had been examined by E2D, 35 had had a hemodynamic and angiographic exploration and 47 an anatomical and/or surgical confirmation. The main results obtained are described and commented on. The diagnostic, etiopathological and prognostic problems raised by the "updating" of this pathology are discussed.

The authors have compared the anti-arrhythmic activity and tolerance of disopyramide and amiodarone in the treatment of ventricular extrasystoles (VES) by using two quantitative methods of assessment. The stability of the rhythmic disorder was confirmed by two control Holter recordings in 20 patients without treatment, 16 of whom were bearers of an organic cardiopathy. The ventricular extrasystole was greater than 90 VES/hour in 18 patients. After the first control, Holter recording, each patient was treated successively with 400 mg of disopyramide/day in 4 doses for average period of 31 days, then a second Holter control recording without treatment, then 600 mg/day of amiodarone for 8 days followed by a maintenance dose varying from 200 to 400 mg/day: this second period of treatment lasted for an average of 38 days. The reduction of the number of VES was greater than 65 percent (SAMI criterion) in 2 of the 20 patients treated with disopyramide and in 13 of the 20 patients treated with amiodarone. Using the method of variance analysis, disopyramide was found to be efficacious in 5 cases out of 20 and amiodarone in 15 cases out of 20. Both methods indicate that the greater efficacy of amiodarone is statistically significant (p less than 0.01). All of those who did not respond to amiodarone were also non-responders to disopyramide.

The efficacy of orally administered propafenone in the prevention of paroxysmal supraventricular dysrhythmias (atrial fibrillation, atrial tachysystole, reciprocal tachycardia) resistant to Vaughan-Williams class Ia drugs was investigated in 10 patients. Propafenone controlled dysrhythmia very well in 4 out of the ten patients, and satisfactorily in another one at a dosage ranging from 450 to 900 mg/day in 3 or 4 divided doses; this result was documented using continuous 24 hr. Holter ECG monitoring. Among the 5 clinical failures, 1 patient had atrial fibrillation primarily at night, and another poorly tolerated this agent which led to interrupt therapy.