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Forty patients with normal resting ECGs and a history of paroxysmal junctional tachycardia underwent endocavitory electrocardiography. Accessory atrioventricular pathways were demonstrated in 34 patients (82.5%), 14 of whom (35%) had Kent bundles. The ventriculo-atrial conduction time during ventricular stimulation was constantin 85% of the 40 patients but increased after injection of striadyne (ATP). This may suggest a reentry circuit partially bypassing the atrioventricular node.

Between 1974 and 1984, 207 patients with Wolff-Parkinson-White syndrome (WPW) were admitted to our hospital department; 195 of them were followed up for periods ranging from 1 to 12 years (6 years in children, 3 years and 9 months in adults on average); 160 had undergone electrophysiological exploration. Fifty-seven patients were less than 16 years old: 7 died, including 6 with associated congenital heart disease; an asymptomatic 12-year old girl died suddenly while taking part in a sporting event. The signs of WPW disappeared in 5 out of 10 children under 1 year of age. One hundred and thirty-eight patients were older than 15: 15 of them died, but only 3 deaths were related to WPW: one was consecutive to surgery for WPW and one to fulguration; the third patient died of WPW tachyarrhythmia; the refractory period of his Kent's bundle was short, but his compliance with treatment was irregular. We found no correlation between changes in functional symptoms and Kent's bundle refractory period values; paradoxically, the frequency of attacks and resistance to treatment was higher in cases with long refractory period. On the whole, this series confirms that WPW usually is a benign disease. However, the risk of sudden death, of which it offers an example, indicates that all patients with WPW should be evaluated with at least an exercise test and, depending on its results or on the socio-professional context, an electrophysiological exploration.

A group of 6 patients operated for Fallot's tetralogy (4 cases) or a similar congenital cardiac malformation (2 cases) were studied to assess the prevalence, severity and predictive factors of late post-operative ventricular tachycardia. These 6 patients were compared with a control group of 44 patients undergoing complete correction of Fallot's tetralogy. The age at operation (6 +/- 2 years), the length of follow-up (8 +/- 2.5 years) and surgical technique were comparable in both groups. The clinical parameters and results of non-invasive investigations (resting ECG, Holter monitoring) were compared. The first attack of tachycardia occurred on average 3 years after surgery. A triggering factor was found in 3 cases (a blow on the chest--2 cases--, general anaesthesia--1 case). These postoperative tachycardias are characterised by poor clinical tolerance, a tendency to recur, resistance to therapy and reserved prognosis. They are significantly commoner in patients operated late and in those with a poor haemodynamic result: right ventricular systolic pressure greater than 60 mmHg and recurrence of the ventricular septal defect. The combination of ventricular tachycardia and a poor haemodynamic result is associated with a mortality rate of 33 p. 100. The functional status of the patient, conduction defects and the surgical technique used were not predictive of ventricular tachycardia. The detection of a ventricular arrhythmia on the resting ECG, and, particularly, on Holter monitoring, and the induction of ventricular tachycardia by ventricular stimulation should lead to treatment against malignant ventricular arrhythmias and sudden death. The choice of anti-arrhythmic agent may be guided by endocavitary stimulation techniques to assess its efficacy.

In order to study the importance of atrial systole, the authors used different stimulus modalities at the same rate; they stimulated the right ventricle, the right atrium, and the two. The haemodynamic parameters were monitored by microcatheterisation of both right and left sides. A comparative study using controls and patients with left ventricular failure showed the improvement in the haemodynamic picture which was obtained in the latter group when the atrio-ventricular sequence was correct.

The purpose of this study was to evaluate the usefulness of two-dimensional echocardiography of the left coronary artery (LCA). This vessel could be visualized in about 80% of the patients, and its pathological features (stenosis, density, irregularities) are described. The first prospective studies seem to have demonstrated the high predictive value of this method for LCA lesions (75%). Two-dimensional echocardiography deserves to be more widely used for non-invasive exploration of patients with coronary disease.

Complete data concerning long-term results of transcatheter electrical ablation of the atrioventricular junction is not available. At the request of the French Cardiac Arrhythmia Working group we undertook an inquiry in October 1983. All centers potentially able to perform such procedures were asked to report their experience. Eight centers have performed one case or more, over a period of 3 years, for a total of 91 patients. The mean follow-up completed in all patients in April 1986 was 12 +/- 10 months. The procedure was indicated for a supraventricular arrhythmia resistant to a mean of 3.9 +/- 1.3 classes of antiarrhythmic agents. Atrial flutter or fibrillation in 54 (59%) and atrioventricular nodal reentry in 17 (18%) were the most common arrhythmias. A mean of 2.6 +/- 2.3 electrical shocks (range 1-14 shocks) with a stored energy of 130-400 joules was delivered during 1-5 sessions. Complete heart block was obtained in 83 patients and persisted at the time of discharge from the hospital in 46 patients (50.5%). The immediate complication (within 24 hours after the procedure) included ventricular fibrillation successfully converted (one patient) and nonsustained ventricular tachycardia (three patients). Late complications included one death 3 days after the procedure, in a patient in whom sustained ventricular tachycardia was documented, nonsustained ventricular tachycardia in two patients, sepsis in three patients and pericardial effusion in one patient. At the time of the follow-up, there were three additional deaths related to sepsis due to pacemaker pocket infection in one patient and to preexisting congestive heart failure in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors advocate a semiquantitative evaluation of mitral regurgitation (MR), based on the extent of the left intra-atrial systolic jet. Their study was performed in a series of 63 consecutive patients explored by: (1) catheterization with left ventriculography on two planes for either ischaemic heart disease (24 cases) or cardiac valve disease (39 cases including 2 with mitral valve prosthesis), and (2) pulsed Doppler ultrasound combined with two-dimensional echocardiography for evaluation of MR carried out 24 or 48 hours prior to catheterization. Five grades of MR (0 to IV) were determined by ventriculography according to the time and degree of left atrial opacification. Similarly, five grades of MR (0 to IV) were determined by Doppler ultrasound, considering only the maximum distance from the mitral annulus plane. This distance was evaluated on at least 3 projections: apical for the 4 and 2 cavities, parasternal for the greater axis. The Doppler method correlated fairly well with the angiography, whether or not grade 0 was included (r = 0.87 and r = 0.72 respectively). However, some major MR may be underestimated; thus, out of 13 RM of angiographic grade III or IV, three (23 p. 100) were graded II by the Doppler technique. Conversely, some minute or moderate MR may be overestimated: out of 33 MR of angiographic grade I or II, four (12 p. 100) were graded III or IV by the Doppler technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Bidirectional ventricular tachycardia, defined as the rapid alternation of the QRS complexes with successive opposing axial deviation, is a rare arrhythmia. In the rare cases which have undergone endocavitary investigations, an infrahisian origin has generally been proved. However, the mechanism of these tachycardias remains poorly understood and is discussed with respect to a new case. Bidirectional tachycardia occurred in a 79 year old woman with previous diaphragmatic and anterior wall infarction. It was a wide QRS tachycardia at 180/min with a succession of ventriculogrammes of opposing axis in the frontal plane and permanent right bundle branch block over the right precordium. The two types of tachycardia were observed, monomorphic type A or Type B or a combination of the two realising an A-B bidirectional tachycardia. The origin of these episodes, which occurred on a background of atrial tachycardia at about 100/min, was ventricular as shown by the absence of a His potential before the ventricular complexes in tachycardia. The presence of ventricular extrasystoles with relatively fixed coupling intervals, and the results of endocavitary investigation were suggestive of a reentry phenomenon ventricular extrastimuli were capable of transforming the bidirectional into monomorphic tachycardia and vice versa; this suggests that A was at times the origin of a reentry B, but protected by A, tachycardia B could be sustained. In the light of previously reported cases with documented endocavitary investigation and this new case, it seems possible to talk in terms of true "bidirectional ventricular tachycardia", a tachycardia whose mechanism is obscure but certainly not univocal.

The electrophysiological properties of carocainide a new Class I antiarrhythmic agent (Delalande Research Centre) were studied after intravenous injection of 3.5 mg/kg in 5 minutes in 16 patients aged 24 to 66 years. Five minutes after the injection there was a significant increase (p less than 0.01) in the HV (+/- 12.8 +/- 10.5 msec), AH (+ 21.8 +/- 14 msec) and PR intervals (+ 43.8 +/- 24.2 msec) and in the duration of QRS (+ 20.6 +/- 9.9 msec). The anterograde and retrograde Wenckebach points were decreased (-42 +/- 43 bpm and - 52 +/- 36 bpm respectively, p less than 0.05). All these effects reverted progressively 20 minutes after injection and disappeared by the 40th minute, which corresponds to the pharmaco-kinetic profile of the patient. There were no changes in blood pressure, sinus node function or refractory periods except for the retrograde refractory periods which were prolonged (+ 87 +/- 41 msec). Atrial fibrillation was induced in 2 patients and atrial flutter in 2 others by the extrastimulus technique. These arrhythmias could not be reproduced in these 4 patients during the 40 minutes after injection of carocainide. Five other patients with reciprocating nodal tachycardia induced by atrial extrastimuli had their arrhythmia interrupted by the carocainide injection. We conclude that carocainide acts mainly on atrio-ventricular and intra-ventricular conduction. The results obtained in patients with tachycardias suggest that the product is effective in atrial arrhythmias and paroxysmal junctional tachycardia.

A prospective study of arrhythmias was performed in 33 patients with hypertrophic cardiomyopathy with obstruction by Holter monitoring. The aim of the study was to assess the incidence of "occult" arrhythmias in this condition and to establish a "profile" of high risk patients from clinical, echocardiographic and haemodynamic data. The Holter monitoring demonstrated asymptomatic arrhythmias in 31 of the 33 patients (94%). A supraventricular arrhythmia was detected in 15 cases (45%), including 7 episodes of supraventricular tachycardia (21%). Ventricular arrhythmias were observed in 28 patients (85%), including 5 episodes of ventricular tachycardia (15%). Some patients presented several types of arrhythmia. A number of patients with arrhythmia including short bursts of ventricular tachycardia were asymptomatic during Holter monitoring; conversely, other patients complained of dizziness or syncope but had no arrhythmias. A retrospective study of clinical, echocardiographic and haemodynamic data showed no difference between patients with and patients without arrhythmias. Medium-dose betablocker therapy (propranolol, 110 mg/day) did not seem to protect patients with hypertrophic cardiomyopathy with obstruction from arrhythmias. We conclude that Holter monitoring should form part of the routine evaluation of patients with cardiomyopathy with obstruction, and that potentially dangerous arrhythmias should be treated by anti-arrhythmic agents other than betablockers. This attitude could reduce the incidence of syncope and eventually decrease the risk of sudden death in this condition.

This study compared the phase images of 12 normal subjects and 14 patients with right ventricular and 5 patients with left ventricular preexcitation. The phase images obtained from equilibrium radionuclide ventriculographies in the left anterior oblique portion with an ECG trigger: Fourier analysis was used to measure the phase and amplitude of the variations. In normal subjects the mean difference in phase was nearly zero: in 12 of the 14 patients with right ventricular preexcitation, right ventricular preceded left ventricular contraction (LV phase - RV phase = + 23 degrees); injection of Ajmaline normalised the ECG and suppressed the premature right ventricular contraction during right ventricular preexcitation (LV phase - RV phase = nearly zero), demonstrating a direct relationship between the abnormal depolarisation and abnormal contraction. In left sided Kent bundles, phase imaging did not seem to show significant premature ventricular contraction under basal conditions. Atrial pacing, which accentuated both left and right electrical preexcitation, increased the difference in ventricular phase. Finally, a satisfactory correlation was observed between the presumed locations of the accessory pathways and the zones of premature right and left ventricular contraction.

Programmed ventricular stimulation (PVS) has been advocated as being capable of identifying patients with idiopathic non obstructive dilated cardiomyopathy (NOCM) and at high risk of sudden death. We have studied the results of that method in 56 patients aged from 29 to 69 years (mean 53 years) presenting with idiopathic NOCM. The patients were divided into two groups according to the presence or absence of ventricular tachycardia (VT). Group I (controls) comprised 23 patients without documented VT. Group II consisted of 33 patients with documented VT which was sustained in 5 cases. Finally, 7 patients from both groups experienced losses of consciousness. Ventricular stimulation was performed on 2 sites of the right ventricle, using 1 to 3 extrastimuli on 2 imposed cycles. It was repeated under isoprenaline on 25 occasions. PVS induced non sustained ventricular tachycardia (NSVT) in only 2 patients of group I; it reproduced the sustained ventricular tachycardia (SVT) observed in the 5 patients with spontaneous SVT. PVS was negative in 14 of the 28 patients with NSVT; it induced NSVT in 8/28 and SVT in 6/28 (including 4 with more than 280 beats/min). The isoprenaline test failed to induce SVT. 7 patients died suddenly: 3 presented with SVT and 4 had syncopes and NSVT; ventricular stimulation induced SVT in 3 of these 4 patients. It is concluded that induction of sustained VT is uncommon in NOCM, but a history of syncope should prompt a search for SVT. Patients with spontaneous symptomatic NSVT and inducible SVT must be considered at high risk of sudden death.

The effects of isoprenaline on the induction of supraventricular tachycardia by programmed stimulation were studied in 67 patients to see whether they correlated with spontaneous catecholamine mediated symptoms during exercise testing and Holter monitoring. Thirty seven control patients (group 1) did not have spontaneous arrhythmias either during exercise testing or Holter monitoring. Thirty patients (group 2) had documented exercise or stress related supraventricular tachycardias--that is paroxysmal junctional tachycardia (24) or atrial arrhythmia (6). Programmed electrical stimulation was performed before and during the infusion of isoprenaline. No group 1 patient developed sustained supraventricular tachycardia during isoprenaline infusion. In 21 patients with paroxysmal junctional tachycardia and all the patients with atrial arrhythmias electrical stimulation during isoprenaline infusion produced the same tachycardia that had been seen during exercise testing and Holter monitoring. Changes in electrophysiological variables and the concentrations of serum potassium were not associated with the induction of supraventricular tachycardia by isoprenaline. Infusion of isoprenaline safely facilitated the induction of supraventricular tachycardia by programmed stimulation in patients who had spontaneously occurring catecholamine mediated symptoms.