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Signal averaging of the ECG P wave is a recent technique used for obtaining predictive and prognostic information in atrial arrhythmias. There have been few publications of its evaluation in this setting. The authors report their results of temporal analysis of the P wave of patients who had undergone electrical cardioversion of atrial fibrillation (group 3, n = 22 patients) and compared them with those of a control group without atrial arrhythmias (group 1, n = 25 patients). After recording signals in three bipolar leads (Predictor 5.0 II Corazonix recorder-analyser), the total duration of the P wave, the root mean square of the P wave amplitude (RMSt) and of the last 20 milliseconds (RMS 20) and the integral under the curve of the P waves (IN) were determined. The comparison was continued with data obtained from a population of patients with paroxysmal atrial fibrillation (group 2, n = 22). All patients had normal left atria on echocardiography, had no valvular heart disease, had no myocardial infarction or signs of cardiac failure. Results showed that the most discriminating parameter was the P wave duration (Group 3: 159.45 +/- 15.1 ms; group 1: 123 +/- 8.5 ms; group 2: 144.6 +/- 12.03 ms; group 1 versus group 2, p < 0.001, group 2 versus group 3, p < 0.01; group 1 versus group 3, p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Patients with dilated cardiomyopathy often have unsustained VT (15 to 60% of cases) but sustained VT is much less common (0 to 10% of cases). The predictive value of sudden death of VT in Holter monitoring is not unanimously accepted. Therefore, it appears that, in patients with non-symptomatic VT, it is the degree of left ventricular dysfunction which is the best predictive factor of mortality because Holter monitoring, signal averaged ECG and programmed stimulation have a low positive predictive value although their cumulated negative predictive value seems to be very good. Programmed ventricular stimulation should be proposed to patients considered to be at high risk of sudden death, presenting with symptomatic unsustained VT or sustained VT. Approximately 3 out of 4 of these arrhythmias will be inducible and benefit from this method for orientating the choice of treatment. In these high risk subjects about 1 in 3 will be satisfactorily protected by antiarrhythmic drug therapy: non-inducible patients from the outset and those remaining inducible despite antiarrhythmic therapy remain at high risk of sudden death. This group of patients probably represents the best indication of implantable cardioverter defibrillators.

Many anti-arrhythmic drugs modify the pharmacokinetics of digoxin and increase serum levels. This possibility is considered for the majority of main anti-arrhythmics on the basis of a review of the literature. Quinidine, propafenone, flecainide, amiodarone and verapamil increase blood digoxin levels, sometimes to twice their baseline values. Suggested mechanisms involve above all a decrease in clearance of digoxin and changes in its volume of distribution. Reported accidents considered to be a direct consequence of these interactions are nevertheless rare in the literature, and the need for modifying dose and increased cardiological surveillance in the case of such a combination is essentially a question of precaution. Disopyramide, procainamide and mexiletine do not appear to have any reported effects on the pharmacokinetics of digoxin, their combined prescription never having had any effect on blood digoxin levels.

Atrial fibrillation is a daily cardiological problem which poses three types of questions, which, though old, are only partially mastered: anticoagulation, reduction and prevention of recurrence. It is a potent source of embolism. The risk is the greatest in patients with rheumatic valvular disease when the fibrillation is recent and when underlying cardiac disease is uncompensated. Long term anticoagulation is mandatory when the cause is rheumatic heart disease. In other pathologies, though anticoagulation has not been shown to reduce mortality, it significantly reduces the number of cerebrovascular accidents, including in the elderly and with low-dose vitamin K antagonist drugs. The efficacy of anticoagulation in preventing arterial embolism has not been established. Reduction of atrial fibrillation is not essential if the arrhythmia is well tolerated, chronic, especially in elderly patients and when several recurrences have occurred despite preventive therapy. In other cases, medical reduction is to be preferred to cardioversion if the fibrillation is recent and well tolerated. Of the oral and injectable preparations, amiodarone seems to be the drug with best benefit/risk ratio. Prevention of recurrence of fibrillation is unnecessary for many after a first episode, especially when idiopathic. In other cases, there are many available drugs but results are uncertain except in those observed in atrial fibrillation related to the autonomic nervous system. Strictly controlled and statistically exploitable studies show comparable efficacy of quinine and other Class I drugs. Beta-blockers are not very useful and the excellent long term results with amiodarone require confirmation.(ABSTRACT TRUNCATED AT 250 WORDS)

The danger in utilizing electrocautery during a surgical procedure on a pacemaker patient depends, to a great extent, on the position of the electrodes. We have studied this influence in an experimental model consisting of a plexiglass tank filled with a saline solution. Seven pacemakers were successively attached to an immersed and fixed frame and connected to a lead whose tip remains in the same location throughout the experiments. An ERBOTOM T 400 C generator (450 kHz) was used in an unmodulated unipolar mode at a maximum output (400 W). The high frequency current was delivered between a patch located successively at six preset positions in the tank and another electrode applied to 176 surface locations. For each position, we measured the currents in the lead with a separate measurement circuit connected in parallel on the same lead. Results were displayed on a map. Regardless of the patch position, currents were: (1) at a maximum when high frequency was delivered close to the pacemakers and around the tip of the lead; (2) negligible when applied to the path followed by the lead; and (3) a function of the distance between electrodes. These results may help to formulate recommendations to prevent accidents when using electrocautery in pacemaker patients.

One of the hazards of high frequency electrical interference (electrocautery) with cardiac pacing is thought to be related to an increase in the threshold values leading to loss of pacing. This hypothesis was examined in an experimental study performed on 5 dogs. A pacing catheter was introduced via the right jugular vein and positioned at the apex of the right ventricle and connected successively to several stimulators implanted in a latero-cervical subcutaneous pocket. A Bovie 400 CT generator was used to deliver a high frequency 1.75 MHz current between a probe applied near to the pacemaker pocket and an electrode placed under the right leg. One or two 5 second bursts were applied for each make of pacemaker, making a total of 3 to 6 applications per animal. A detecting circuit enabled the measurement of the currents in the catheter during the application. The thresholds of pacing were measured before and after each manipulation for several pacing impulse durations. At the maximal output of the generator, the highest recorded current was 117 mA (modulated) and 141 mA (unmodulated). The thresholds of stimulation did not change significantly and the pacing catheter impedance was also stable. This study suggests that high frequency current does not modify the threshold of stimulation in cardiac pacemaker patients. The loss of pacing sometimes observed after the use of electrocautery is probably related to pacemaker dysfunction.

The aim in treating chronic atrial fibrillation, is not limited to simply achieving immediate regularization. What matters, is sustaining the sinus rhythm. The various methods of regularization, using either medical procedures or cardioversion, involve constraints and risks. Investigation of the relapse predicting factor is of great value in evaluating the benefit/risk ratio. For regularization, the absence ultrasound signs of heart disease, an undilated left atrium, recent atrial fibrillation and all forms of heart disease which are curable, albeit surgically, are indicative of success. With regard to prophylaxis, relapses occur more frequently in cases involving mitral valve disease, long-standing atrial fibrillation or a dilated left atrium.

Systemic embolism secondary to chronic atrial fibrillation usually affect the cerebral circulation. The risk of a cerebrovascular accident in patients with chronic atrial fibrillation, irrespective of the aetiology, is 1.8 to 7.5 times that of the general population. The embolic risk is 18 times greater in patients with atrial fibrillation related to the rheumatic heart disease. The risk of patients under 60 years of age with idiopathic atrial fibrillation does not seem to be different to that of the general population. The risk of early recurrence of embolism in the first 30 days ranges from 8 to 15%. The risk of late recurrence varies but seems to be higher than that of the general population. The prognosis of embolic cerebrovascular accidents is poor with a 20% mortality rate. The benefits of preventive therapy of embolism with oral anticoagulants have been clearly established in rheumatic atrial fibrillation and in other indications. In non-valvular atrial fibrillation the benefits have to be compared with the risks of treatment. The incidence of hemorrhage due to anticoagulant therapy is between 3 and 5% per year per patient (about 1% of severe haemorrhage). Three randomised studies of primary prevention have shown a significant reduction of the embolic risk in non-valvular atrial fibrillation treated by warfarin compared to patients on placebo. Only one study has shown a significant reduction of the embolic risk in patients under 75 years of age with non-valvular atrial fibrillation treated with 325 mg/day of aspirin. However, anticoagulant therapy does not seem necessary in carefully selected patients under 60 years of age with idiopathic atrial fibrillation (less than 5% of all patients).

All aortic aneurysms require a positive diagnosis, a differential diagnosis and an assessment of extension. Several exploratory methods can be contemplated. In patients with warning symptoms, conventional radiology may point to the diagnosis. The reference method remains retrograde aortography which may be either conventional and seriographic or, better, radiocinematic with orthogonal projections and, if possible, digital. The site and morphology of the aneurysm, and in particular its inner channel are thus demonstrated. Computerized tomography is less invasive and usually of great value, notably for the horizontal, thoracic and abdominal aorta, not only to confirm the diagnosis but also to determine the size of the inner channel, parietal thrombi and aortic walls, as well as relations with nearby structures. Other, totally non-invasive methods are widely utilized to explore aortic aneurysms. These are ultrasonography and its variants (notably Doppler-echocardiography and the transoesophageal route), and magnetic resonance imaging which provides three-dimensional and anatomical views of the vessel. These last two examinations alone usually confirm and outline the aortic aneurysms. They must therefore be utilized as first-line examination, arteriography it is various forms being reserved for emergencies or special cases.

A 63 year old man with ischemic heart disease underwent two sessions of catheter ablation in the inferior right atrium for poorly tolerated resistant and recurrent atrial flutter. After endocavitary mapping and comparison with surface recordings of the f waves, a shock of 50 joules was delivered to the zone situated anteriorly to the inferior vena cava, under the orifice of the coronary sinus and behind the tricuspid valve. Early recurrence of the arrhythmia led to a second attempt and another 50 joules shock was administered to the same area. Another short term recurrence led to definitive nodohisian interruption with a 270 joules shock. Thirty months later, the patient died suddenly during an episode of cardiac failure. Macroscopic examination of the right atrium showed a zone of parietal congestion measuring 4 x 3 cm with a very thin, translucid, central zone measuring 3 x 1.5 cm, just anterior to the inferior vena cava in the right atrial free wall. Histological examination of this zone showed an intense, mutilating fibrosis dissociating the muscular fibres, of the pectinate muscle and even replacing the myocardium in certain regions. In the Eustachian valve, there were muscular fibres, probably representing the posterior internodal pathway, which were also fibrosed. These observations suggest that: 1) in view of the extreme thinness of the atrial wall at the site of ablation there is a high risk of perforation even when right endoatrial catheter ablation is performed with low energy shocks; 2) the posterior internodal pathway does not seem to be an essential component for atrial flutter.

Complete atrioventricular block (AVB) following radiotherapy has been reported rarely, usually after high dose mediastinal irradiation for Hodgkin's disease or lung or breast carcinoma. We report six new cases of episodic complete infranodal AVB, requiring permanent pacemaker implantation. The mean age was 48-years old (ranging from 25-60) at the first Adams Stokes attack, mean delay was 12 years after irradiation (10-18), and mean radiation dose was 5,200 rads (4,000-6,500). All patients had abnormal interval electrocardiograms (right bundle branch block in two, left bundle branch block in three, alternating left and right bundle branch block in one). Electrocardiograms during the episode of AVB or Holter recordings were consistent with infranodal block in all patients; electrophysiological study performed in five patients confirmed infranodal AVB in four, and one was normal. Pericardial disease was constant, which included pericardial constriction in four patients. Two patients died after failure of pericardiectomy to improve congestive heart failure, due to epicardial, myocardial, and endocardial involvement. Noncardiac mediastinal lesions were present in four cases. Since this delayed complication may occur in patients of such age that the relation between the AVB and the chest irradiation is questionable, we propose the following etiologic criteria; high radiation dose (over 4,000 rads); delay of 10 years or more; abnormal interval tracings; pericardial involvement; and associated cardiac or mediastinal radiation-induced lesions.

Almost 50 percent of patients with chronic heart failure die of sudden death often due to arrhythmia. In these patients the prognosis is related to the severity of myocardial lesions and also, probably, to the presence of ventricular arrhythmias. The potential severity of which can be assessed by various methods, including ECG, Holter monitoring, late potentials study and programmed ventricular stimulation tests. The first therapeutic measure to improve the prognosis of heart failure is to improve the myocardial function by prescribing converting enzyme inhibitors. The second measure consists of acting on potentially dangerous ventricular arrhythmias with few or no symptoms. Among antiarrhythmic agents, only beta-blockers and amiodarone seem to be valuable.

Internal cardioversion is a new method of treating atrial fibrillation. It consists in delivering an electric shock between an electrode positioned in the right atrium and a dorsal electrode. A quadripolar electrophysiological catheter is used as the proximal electrode, the two distal poles of which are used to locate the His bundle deflection. Care is taken that the electrode used for cardioversion is not in contact with the atrial wall by using biplane fluoroscopy and unipolar endocavitary recordings. Twenty-eight patients (18 men and 10 women) average age 55 years, underwent this treatment for chronic atrial fibrillation resistant to one or two attempts at external cardioversion. Each patient was given one or two shocks (average 1.68) in the same session. There were 22 immediate reversions to sinus rhythm, giving a primary success rate of 78.57%. Four patients relapsed in the 3 days following the procedure, giving a short term success rate of 64.28%. The minimum effective energy would seem to be 200 joules. The only rhythm complications were sinus bradycardia and/or atrioventricular block lasting a few seconds, both countered by prophylactic ventricular pacing : no traumatic complications due to electric shock were observed. The long term results show sinus rhythm maintained in 66.66% of patients at 6 months and more. In conclusion, internal cardioversion is an effective method of treating cardiac arrhythmias resistant to external cardioversion. The procedure would seem to be reliable and relatively atraumatic. The long term results are promising, particularly the stability of sinus rhythm which seems to be longer than after external cardioversion, by they need further confirmation.

The authors report their experience involving 21 right endoatrial electroversions aimed at converting chronic atrial fibrillation resistant to external electroversion. All prior precautions were taken to ensure that the shocks were not in contact with an atrial wall nor over the node-His bundle (two dimensional radiological identification, endocavitary recordings). A total of 37 internal electric shocks were administered. Results were: 16 immediate successes out of 21 (72.2 per cent) and 12 short term successes out of 21 (57 per cent). The mean effective energy value was 200 Joules. There were no traumatic complications. The authors conclude that this technique is effective and reliable in the management of atrial fibrillation resistant to external electroversion.

We report a case of severe subacute autonomic and sensory neuropathy in a 52 year-old man. Cerebrospinal fluid protein was 275 mg/dl. Electrophysiological data were consistent with an axonal sensory neuropathy. Nerve biopsy showed a severe decrease in myelinated fibers, and a less severe loss of unmyelinated fibers. No cause was found and recovery was almost complete over 4 years, with minimal persistent dysautonomia. This case and 4 similar reported cases are compared with pure dysautonomia and with sensorimotor dysautonomic neuropathy. The site of damage is discussed and it is suggested that these cases are axonal forms of inflammatory polyneuropathy.

The authors studied the possible consequences of the use of high frequency electrical currents of cardiac pacemaker function. Twenty-five unipolar pacemakers (22 single and 3 double chamber) were tested. They were connected to a pacing catheter, emerged in a saline bath and submitted to a modulated and then unmodulated current of 348 KHz in as many pacing modes as possible for each unit. Three dangerous deprogrammations were observed which could nevertheless be easily corrected. Five pacemakers immediately adopted the reversion mode specified by their manufacturer. The other changes observed only lasted as long as the electric current was applied. The commonest abnormality was a drop in the output voltage proportional to the energy delivered which sometimes led to true inhibition of the pacemaker. Two abnormal rate increases were observed reaching frequencies higher than 250/mn. No particular pacing mode seemed to protect the pacemakers from the effects of high frequency currents.

We report a new case of non-familial dysautonomia. The patient was a boy with no known Jewish ancestry in whom psychomotor retardation in early infancy failed to lead to specialized evaluation. Regressive episodes of ataxia developed at the age of three and infrequent generalized seizures occurred between four and seven. Diagnosis was first considered at the age of seven after neuroparalytic keratitis developed and rapidly became bilateral. This case has remained highly unusual throughout the course since none of the commonly reported complications (swallowing disorders, aspiration pneumonia, and dysautonomic "attacks") has occurred. No life-threatening manifestations have developed. Peripheral nerve biopsy specimens showed that myelinated fibers, especially of large diameters, were abnormally scarce, and that the histogram failed to exhibit the normal bimodal aspect. Ultrastructural studies also disclosed a marked reduction in the caliber of unmyelinated fibers, whose axons were flattened or occasionally missing. No evidence of regeneration was found. The atypical clinical features in our patient are discussed.

Cardiac involvement in Friedreich's disease is classically a hypertrophic myocardiopathy, concentric or assymmetrical with or without dilatation. It has nothing specific in comparison to other myocardiopathies. Nevertheless, forms with a dilated myocardiopathy are also possible, but much more unfrequent. A propos of three cases, we have studied the different aspects of myocardiopathies in Friedreich's ataxia. The problem raised by the case of an hypertrophic myocardiopathy evolving toward a dilated form, unusual element of this pathology, is presented. The therapeutic potential of hypertrophic myocardiopathies is classically represented either by beta-blockers or by the more recent slow calcium inhibitors.

Many in vitro and animal experimental studies seem to support the hypothesis of reentry as the physiopathological mechanism of atrial flutter. Clinically, these studies are much more difficult because of problems in determining the different sequences of atrial depolarisation. In this study, the authors attempted to improve the technique of endocavitary atrial mapping. Three or four multi-recording electrodes were positioned in the atria using biplane 30 degrees RAO and 60 degrees LAO incidences. Right atrial angiocardiography showed up the atrial borders and enabled the recording catheters to be more accurately positioned. Thirty to 47 recordings points were thereby determined within the atrial cavities, the left atrium being studied via the coronary sinus, right pulmonary artery, patent foramen ovale or by the endooesophageal approach. This method of spatial orientation of the catheters associated with recording of the endocavitary potentials allowed the construction of an isochronic map of atrial depolarisation, which was then analysed for each case of flutter. The study confirmed two hypotheses: the asynchronism of right and left atrial depolarisation, and the circus motion of depolarisation. Three types of flutter were observed: --The first two types were similar with cirus motion within the right atrium. The wave front ascended in part or all of the septum and descended in the external free wall of the right atrium. There was a transitional zone, possibly reentrant, in the groove located anterior to the inferior vena cava. --The third type of flutter was atypical and was associated with cirus motion in the left atrium. Two transitional zones, similar to those encountered in the right atrium, were detected in one patient between the orifices of the pulmonary veins, and, in another patient, on the anterior part of the roof of the left atrium. These transitional zones seem to be at the basis of the physiopathological mechanism of flutter. Unfortunately, their small size makes their analysis by endocavitary mapping difficult.

The superficial peroneal nerve was taken from 12 arteriosclerotic non-diabetic patients just after amputation of a leg. Preparations of teased fibers were performed in 8 cases. Specimens were studied by light and electron microscopy in all cases. Histograms of myelinated fibers in transverse semi-thin sections showed that depletion of myelinated fibers varied from case to case, with no selective vulnerability in either the large or the small diameter group. There was a dramatic loss of myelinated fibers in only one case. No real nerve infarct was observed. In most cases, regions of Wallerian-like degeneration were prevalent; however, myelino-axonal changes were severe only in a few cases. Axons with organelle aggregates were seen in some cases. Figures of segmental demyelination were not numerous in this series. Unmyelinated fibers were also damaged, and the degree of involvement differed from case to case. Pathological changes observed in this study confirm the relative resistance of peripheral nerve to ischemia.

Correlation between the endocardial electrocardiographic recording and the histological findings of the conduction pathways in one case of apparent atrial standstill makes it possible to state the following facts: 1. The presence of a supranodal block through an intraatrial conduction disturbance. 2. The presence of James' fibres by-passing the upper part of Tawara node. 3. The functional character of these James' fivres which constitute, in view of the presence of lesions of the upper part of the Tawara node, the only possible pathway from the atria to the ventricles in this case. 4. The possibility to record the action potentials of James' fibres in that exceptional case. The histological examination made it possible also to recognize the anatomical lesions responsible for the idiopathic dilatation of the right atrium and of the apparent atrial standstill which represented the end-stage of an atrial rhythm disease.

A 25 year old patient presented with several types of paroxysmal tachycardia. Analysis of the recordings and the results of endocavitary electrophysiological investigation suggest the presence of nodoventricular and atrio-ventricular fibres. These two accessory pathways were latent in sinus rhythm but formed part of reentry loops. The reciprocating rhythms used the Kent bundle in the retrograde direction, and either the normal nodo-hisian or the Mahaim fibres in the anterograde direction. Simple echos ascending by the nodo-hisian pathway and descending by the nodo-ventricular pathway were also observed. The patient died of an unassociated cause and a pathological examination of the heart was performed. This confirmed the presence of a left posterior paraseptal Kent bundle and the presence of fibres relaying the inferior part of the atrioventricular node to the septal ventricular myocardium, this being made possible by a dehiscence of the central fibrous body.

A study has been conducted into the morphological arrangement of the atrioventricular junctional area of human heart. The area was investigated in infantile, child, young adult, middle-aged, and old nodes. Although marked individual and ageing variations were observed, a general pattern of nodal architecture could be distinguished. The junctional area was therefore divided into four areas: (1) a transitional zone, (2) the compact node, (3) the penetrating bundle, and (4) the branching bundle. The transitional zone was intermediate between atrial myocardium and compact nodal specialized myocardium, but itself exhibited specialized characteristics. An important connection of the zone was to the myocardium of the left side of the interatrial septum. The compact node was itself composed of two segments which approached each other anteriorly from the mitral and tricuspid extremities of the septal anulus fibrosus. The junction of compact node and penetrating bundle could not be distinguished using cytological criteria. It was arbitrarily defined as the last point to make contact with transitional cells. Tissue distal to this was considered as penetrating bundle. A bypass tract was defined as any fiber contacting the bundle distal to this point, but such tracts were not observed in normal hearts. The branching bundle originated at the point of bifurcation of the penetrating bundle.

The introduction of data processing techniques into the interpretation of electrocardiograms and the rapid progress towards automatization require a multiplication of the criteria of decision and an exact evaluation of their performance. The ECG diagnosis of left ventricular hypertrophy depends on a large number of parameters. Only the aVR lead has not been fully exploited to date. This study proposes a corrected measurement of S in aVR, with an amplitude of S aVRc greater than or equal to 11 mm being the parameter with the best performance and the best predictability.

A 58 year old man who died of metastatic carcinoma had undergone electrophysiological investigation 4 years previously for a Wolff-Parkinson-White syndrome (Rosenbaum Type A, Frank and Boineau Type IV) associated with supraventricular tachycardia (SVT) at 180/mn, atrial fibrillation and flutter and slow junctional (or low atrial) rhythm at 70-80/mn. Atrial extrasystoles or appropriate atrial stimulation not only induced and terminated the SVT but also the junctional rhythm and allowed passage from one arrhythmia to another. These studies showed the presence of a left lateral Kent bundle responsible for orthodromic SVT with retrograde conduction through the accessory pathway, and suggested that the junctional rhythm might be due to longitudinal dissociation of the AV node. Autopsy findings confirmed the presence of the left posterolateral Kent bundle in an almost horizontal position, parallel to the mitral annulus (it might therefore have escaped eventual surgical section) and the longitudinal dissociation of the AV node.

Residual arterial hypertension after excision of a pheochromocytoma of the Zuckerkandl organ, has brought the problem of its etiology. The short term approach consisted in performing, after specific biochemical dosages, a scintigram with IMBG, a scan and a magnetic resonance imaging, to look for a second pheochromocytoma. A negative workup enabled to conclude to an essential arterial hypertension. Nevertheless, this does not exclude the possibility of a long term malignancy, requiring clinical monitoring and IMBG scintigraphy.

Acute inflammatory muscular syndromes secondary to clofibrate therapy are rare. They usually present with muscular pain in all four limbs with biochemical signs of rhabdomyolysis. The outcome is favourable as a rule with rapid regression of the clinical and biochemical changes after stopping the responsible drug. The authors report an atypical case of this syndrome with chest pains suggestive of angina.

To study the effects of an atrial premature beat on atrial refractory periods, we investigated 11 patients (group A) who were the control group, 12 patients suffering from paroxysmal atrial fibrillation (group B), and 10 patients (group C) without arrhythmias but with cardiopathy or cardiomyopathy. At every eighth complex of a constant atrial electrostimulated rhythm a fixed premature extrastimulus was introduced, and effective and functional refractory periods (ERP and FRP) were measured in three different sites of the right atrium, before and after introduction of this extrastimulus. Average ERP and FRP shortened respectively in group A, from 220.28 +/- 25.68 msec and 281.17 +/- 28.15 msec before extrastimulation, to 190.58 +/- 22.74 msec and 245.88 +/- 19.86 msec after; in group B, from 219.44 +/- 27.38 msec and 284 +/- 30.06 msec to 191.66 +/- 28.72 msec and 253.23 +/- 34.01 msec; and in group C from 229.03 +/- 29.65 msec and 289.67 +/- 51.62 msec to 194.19 +/- 24.6 msec and 237.74 +/- 39.59 msec. The average dispersions of ERP and FRP in group A were, respectively: 41.81 +/- 21.36 msec and 36.36 +/- 18.04 msec before extrastimulation, 28.18 +/- 18.14 msec and 35.45 +/- 15.72 msec after. In group B: 26.66 +/- 19.46 msec and 41.66 +/- 16.96 msec versus 45.83 +/- 23.91 msec and 45 +/- 34.77 msec and in group C: 27 +/- 11.59 msec and 45 +/- 29.15 msec versus 29 +/- 18.52 and 27 +/- 18.88.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors report the case of a pheochromocytoma of the organ of Zuckerkandl in a 46 year old man. The clinical presentation was severe paroxysmal hypertension; the tumour was located by arteriography, CT scanning, and by scintigraphy with iodine labelled benzylguanidine. The blood pressure returned to normal after surgery. The embryological, anatomical and physiological features of the organ of Zuckerkandl are reviewed: the authors discuss briefly the modern methods of diagnosis and localisation of the tumour.

The diagnostic value of magnetic resonance imaging (MRI) was assessed in 30 patients with congenital heart disease, including 7 patients with postoperative sequellae. The images obtained by synchronizing the MRI spectrometer with the electrocardiogramme were recorded in 2 or 3 different planes (sagittal, frontal and transverse) and compared to clinical, angiographic and/or echocardiographic data. The MRI provided high resolution tomographic images enabling spatial reconstitution of the heart by the use of different planes. These images were particularly useful for showing the position and dimensions of the ventricles (both chamber size and wall thickness) and their relationship to the atria and great vessels. These results confirm the value of this new non-invasive imaging technique in the diagnosis of congenital heart disease, not counting the additional information on blood flow and tissue characterisation that will soon become available.

If endovenous thromboses on permanent cardiac stimulation catheter are rather frequent, it is usual to note the absence of complications, especially embolic complications. On the contrary, intracardiac thromboses, occurring always on a permanent stimulation catheter, are rare but may generate embolisms: the authors report a new case discovered on bidimensional sonocardiography recorded following pulmonary embolisms.

The authors described seven cases of supraventricular tachycardia with atrio-ventricular dissociation, associated with the activity of an automatic focus in the bundle of His. These tachycardias, which appear at birth or are discovered at a very young age, appear to be congenital and sometimes familial, and are always isolated, having no associated cardiac abnormality. They give rise to cardiac failure, which is more marked when the rate is high (180-260/mn) and particularly resistant to treatment. The most effective form of treatment is amiodarone, almost always used in combination with digitalis. The anatomical abnormality, which was studied in the first case, is a contricting fibrosis around the main trunk of the bundle of His, and the appearances are reminiscent of those found in conditions of congenital atrio-ventricular block.

The electrophysiological properties of bepridil suggest a possible ventricular antiarrhythmic effect. This prospective multicentre trial was undertaken to study the antiarrhythmic efficacy of oral bepridil on ventricular arrhythmias in patients with stable coronary insufficiency and more than 1 000 ventricular extrasystoles per 24 hours or ventricular tachycardia. The patients were divided into 3 groups according to the arrhythmias observed and the dosage used. In group I, the dosage was 300 mg/day and 12 out of 44 patients (27%) responded favourably to two criteria of efficacy (decrease of 84% of the number of ventricular extrasystoles; suppression of complex ventricular extrasystoles). In group II, the dosage was 300 mg/day, and then increased to 500 mg in non responders. Using the same criteria of efficacy, 13 out of 19 positive results were observed (68.4%). Group III comprised all cases of ventricular tachycardia; bepridil was effective in 3 out of 6 cases, associated with amiodarone in 1 case. The results demonstrate an antiarrhythmic effect of bepridil which is modest at 300 mg/day but which becomes more marked at the dosage of 500 mg/day.

Tocolysis was carried out in a case of paroxysmal junctional tachycardia (Bouveret) and there was an attack of paroxysmal tachycardia which resolved spontaneously. In a case of Wolff-Parkinson-White syndrome and in two cases of ventricular double extra-systoles, tocolysis was very well tolerated. A short discussion based on these four case histories is presented. The indication for the use of tocolytic drugs was discussed with the cardiologist. The cardiac state of these pregnant women under treatment was very closely monitored.