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Biventricular resynchronisation is an additional therapeutic option in the management of refractory heart failure, with a functional and haemodynamic benefit as well as an improved morbidity and mortality. However, the rate of non-responsive patients has prompted a re-think about the presumed mechanisms of action for this procedure. This study aims to identify candidates more successfully. Based on five years experience in this centre, our work confirmed a medium and long term clinical benefit with multisite pacing. Nevertheless, there was evidence of a relative discordance between the functional benefit and the haemodynamic impact in terms of ejection fraction achieved with resynchronisation. While QRS narrowing appears to be a predictive factor for a successful procedure, the ECG alone is not sufficient to select 'unsynchronised' candidates. Statistical analysis reveals that before implantation the independent predictive factors to identify non-responsive patients include the presence of a complication of myocardial infarction and a low grade mitral leak. The limits of the ECG suggest a more mechanical than electrical approach to understanding the mechanisms of action for resynchronisation. Its effectiveness in cases of right bundle branch block confirm the hypothesis of left intra-ventricular conduction defects, not apparent on the surface ECG but accessible through new imaging techniques. Based on the hypothesis of delayed movement of the ventricular walls, the principle of resynchronisation aims to restore homogenous contraction. Echocardiography allows observation of electromechanical delay and opens new perspectives in the future for selecting patients for pacing. Ar

Endocavitary investigations showed that the ventricular extrasystoles originated in the common ventricular myocardium (pulmonary infundibulum) in only 9 cases whereas the majority arose from the Parkinje system either on the anterior wall of the right ventricle or in septal region of the left ventricle. The extrasystoles arising from the Parkinje system and pulmonary infundibulum differed in their duration and polymorphism (128 +/- 18 ms vs 145 +/- 13 ms, p = 0.05; 3.3 +/- 2.7 morphologies vs 1.1 +/- 0.4, p0.001, respectively). During the extrasystoles, the local Pukinje potential preceded the ventricular activation by variable intervals, some of which were very long, up to 150 ms. Seven applications of radiofrequency were delivered on average per patient on the most distal part of the Purkinje system leading to ablation of the specific activation. The clinical results were spectacular: 88% of patients had no further episodes of ventricular fibrillation as demonstrated by analysis of the defibrillator with an average follow-up period of more than 34 months.

Catheter ablation techniques for atrial fibrillation have undergone an extensive evolution, starting with linear lesions in the right, then the left atria before being superseded by ablation of triggers, mainly from the pulmonary veins. We investigate the feasibility and results of combined pulmonary vein and linear ablation utilizing a specific linear lesion connecting the lateral mitral annulus to the left inferior pulmonary vein (left isthmus).115 patients (101 M: 54 +/- 9 years) with paroxysmal atrial fibrillation (7 +/- 5 years) resistant to 4 +/- 1.6 anti-arrhythmic drugs were studied. After electrophysiologically guided disconnection of all four pulmonary veins, the left isthmus line was performed with an irrigated tip catheter. Complete linear block was demonstrated during coronary sinus pacing by local mapping looking for widely separated double potentials and confirmed by differential pacing. Mapping and ablation from within the coronary sinus was performed if an epicardial gap was detected after unsuccessful endocardial radiofrequency delivery.100% of pulmonary veins were successfully disconnected and the left isthmus line was complete with bi-directional block in 88% after a mean of 22 +/- 12 min of endocardial radiofrequency delivery in 44 patients. In 58 patients, additional radiofrequency delivery was required from within the coronary sinus for 5 +/- 5 min. After a follow-up of 6.5 +/- 2.6 months and a mean of 1.4 +/- 0.6 procedures/patient, 79% were in stable sinus rhythm without antiarrhythmic drugs.the left isthmus line is feasible and safe and when performed in addition to pulmonary veins isolation can contribute to an increased success rate.

Congenital isolated atrio-ventricular block (CAVB) is a rare pathology, and its management is still rather poorly described through international literature. Within the service of pediatric cardiology leaded by Pr Choussat and Dr Jimenez (Cardiologic Hospital Haut-Lévêque of Bordeaux), we collected from 1980 to 2003, 30 isolated congenital CAVB, constituting the purpose of this retrospective study. Average follow-up is 14 +/- 8.8 years. None death occurred. CAVB are discovered at an average age of 4.8 years old; 6 cases were diagnosed in utero, half of them were associated with maternal lupus. Twenty patients on 30 were fitted with stimulator at an average age of 8.7 +/- 6.9 years old, due to symptoms or bradycardy. Epicardic fitting in VVI mode represents 65% of first approaches, it is followed by endocavitary way for 81% of cases. Cardiac stimulation does not prevent from dilated cardiomyopathy. Among 30 patients 10 were not fitted with stimulator, half of them presents chronotrop insufficiency during effort. As a conclusion, our patients show a good long-term vital prognosis; although CAVB discovered in utero lead to worse prognosis for children.

Atrial fibrillation, the most common arrhythmia, is frequently disabling and drug resistant and is associated with significant complications, especially thromboembolic events. Non-pharmacological approaches including surgery and catheter-based ablation have been developed for the most symptomatic patients. These new treatment strategies have dramatically increased our knowledge of the pathophysiology of this arrhythmia but most importantly have demonstrated that atrial fibrillation is curable. Since 1994, 2 different concepts have been used, aiming to modify the substrate responsible for AF maintenance using linear lesions, or to ablate the triggers located from within the pulmonary veins (PV) in about 90% of cases. The vast majority of the laboratories in the world are now using approaches centred on isolation of the PV. These approaches are far from being perfect but good enough to be offered in routine practice to selected patients in experienced centres. The importance of PVs in the initiation of AF has been clearly demonstrated and they also have a possible role in the maintenance of AF. However, the existence of non venous foci or a prominent substrate for AF maintenance limits the success rate to about 70%. As a consequence, a combination of PV isolation and linear lesions is commonly used. This more complex procedure carries a significantly higher success rate however with an increased risk of tamponade. As a consequence, we need to identify which patients will require linear lesions in addition to PV isolation. At the present time, AF ablation is restricted to symptomatic patients who have failed at least 1-2 antiarrhythmic drugs but future technical improvements based on presently applied concepts are likely to widen the indications for ablation therapy of AF.

We report the observation of a female 45 year old patient presenting with a post-surgery complex congenital cardiopathy, associated with serious ventricular rhythm disorders necessitating the placement of an implantable defibrillator. The palliative surgery performed (cavo-pulmonary Glenn anastomosis) does not allow the usual access to the right ventricle via the superior vena cava. The different possibilities for defibrillator implantation are discussed. These include associating a surgical approach to introduce the bipolar probe with subcutaneous tunnelling to connect the probe to the box.

Atrial fibrillation is the most frequently encountered arrhythmia in the human species. Its danger is widely appreciated but it remains for certain patients and their practitioners an awkward or even exasperating problem. Only surgery and radiofrequency ablation allow certain patients to be cured. The surgical approach is of course warranted in the case of an otherwise necessary cardiac intervention. In the absence of a surgical indication, endovenous ablation, which is less aggressive, is preferred. The procedure consists of disconnecting the pulmonary veins which "house" 80 to 95% of the foci, together with the ablation of further non-venous foci, which are always difficult to treat. Side effects in experimental centres are rare and 70% of patients are cured, which allows cessation of antiarrhythmic and anticoagulant treatments. The procedure is currently offered to symptomatic patients having had at least one episode every ten days in spite of antiarrhythmics.

The sleep apnoea syndrome is the best known apnoeic syndrome. It is observed in 4% of men and 2% of women. Nasal ventilation with continuous positive pressure is the best treatment for most patients. To date, electrical stimulation has a limited role in its treatment as it is used only when the apnoea requires ventilation by tracheotomy. This electrogenic ventilation requires so-called diaphragmatic stimulators. Although severe bradycardia may occur during sleep apnoea, there is usually no indication for cardiac pacing. However, recent publications have reported an anti-apnoeic effect of permanent atrial pacing. The modes of action remain unclear but these results support other recently reported data concerning the value of pacing in cardiac failure, the high incidence of sleep apnoea in cardiac failure patients and the possibility of diagnosing and monitoring apnoea by minute ventilation sensors. Therefore, there appears to be a field of research for cardiac pacing in apnoea syndromes. The authors review the principal reported data on the indications and possibilities of extra-cardiac and cardiac stimulation in apnoeic syndromes.

Atrioventricular nodal reentrant tachycardias which, for a long time, could only be treated medically, may now benefit from catheter ablation. The rapid retrograde pathway was an effective initial target but carried a risk of complete atrioventricular block of about 10%. Nowadays, most operators deliver the radiofrequency energy (endocavitary cautery) to the slow nodal pathway. Different techniques of guidance (anatomical, electrophysiological, rapid potential, slow potential) are associated with high success rates: 90 to 100%. However, experimental studies suggest that the slow potentials arise from transitional cells within the tachycardia circuit (the anatomical substrate of the slow pathway). There is still a risk of complete atrioventricular block (1 to 5%) which should be clearly explained to patients referred for ablation of this constantly benign arrhythmia.

Endocavitary catheter ablation by radiofrequency energy applied on the slow pathway is an effective method of treatment of nodal reentrant tachycardias. The aim of this report was to determine the criteria predictive of success during radiofrequency ablation of the slow pathway guided by the presence of slow potentials. Thirty-five patients (21 women, 14 men, mean age 44 +/- 14 years) with frequent attacks of junctional tachycardia were studied. After confirmation of the diagnosis by electrophysiological investigation, radiofrequency energy was delivered at a site characterised by the presence of slow potentials between the atrial (A) and ventricular (V) potentials. The criteria investigated at each site were: before application: A/V ratio; amplitude of A and V: maximum A/minimum A ratio; amplitude and duration of the A potential; during ablation: radiological stability of the catheter position and occurrence of a junctional rhythm. All 35 patients had successful procedures with no inducible tachycardia at the end of the procedure. The slow pathway was destroyed in 20 cases (57%) with no complication of atrioventricular block. The duration of the A potential was longer in the successful cases (56 +/- 16 vs 48 +/- 14 ms; p = 0.04). The appearance of junctional rhythm and catheter stability during the procedure were predictive of success (79% vs 48%; p = 0.02; 74% vs 43%; p = 0.01). The authors concluded that an ablation site with a long duration A potential and a slow potential is a good target. In addition, ablation should be started when the catheter is radiologically stable and should not be interrupted in the absence of a junctional rhythm.

Survival after His bundle ablation for supraventricular arrhythmias was analysed over 10 years (May 1982 to December 1992) in 312 consecutive patients (5 were lost to follow-up): 54 died (17.3%), 13 of sudden death (24%). The survival rates were 94.5% at 1 year (n = 256), 80.1% at 5 years (n = 88), 72.8% at 8 years (n = 20) and 51% at 10 years (n = 4); patients without apparent heart disease had a better prognosis. This series serves as a reference for other techniques of His bundle ablation.

The object of this study was to assess the efficacy and risks of radiofrequency ablation of common atrial flutter and to determine the optimal site of ablation in a large population of patients. Three different methods were used to determine the site of ablation: the first was anatomical and electrophysiological whilst the two others were based essentially on anatomical landmarks for localising the critical zone of the reentry circuit. Recent studies report that radiofrequency ablation is effective in interrupting and preventing recurrences of common atrial flutter both by using anatomical and electrophysiological methods. Nevertheless, a larger series of patients was necessary to establish the efficacy and to determine the optimal site of ablation. A series of 110 consecutive patients with common atrial flutter resistant to antiarrhythmic drugs was studied. The site of ablation of the first 50 patients was determined using both anatomical landmarks and electrophysiological parameters. The anatomical zones were: zone 1, between the septal leaflet of the tricuspid valve and the orifice of the inferior vena cava; zone 2, between the septal leaflet of the tricuspid valve and the ostium of the coronary sinus, and zone 3: between the orifice of the inferior vena cava and the ostium of the coronary sinus. The electrophysiological criterion was an endocavitary auriculogramme occurring during the plateau phase preceding the F wave of the flutter.(ABSTRACT TRUNCATED AT 250 WORDS)

A retrospective study of 192 patients centered on the outcome of supraventricular arrhythmias after catheter ablation of the atrioventricular junction provided some useful information concerning the choice of pacing mode in these patients. With the exception of atrioventricular bloc after ablation of the rapid nodal pathway where simple DDD pacing is adequate, rate adaptive pacing would seem to be essential. The VVIR mode should be the mode of choice in atrial flutter, permanent atrial fibrillation, poorly controlled atrial fibrillation and paroxysmal atrial fibrillation of elderly subjects (over 70 years) and/or of male sex, and/or complicating advanced cardiac disease (valvular, ischaemic or primary). The DDDR mode (with an algorithm to prevent endless loop tachycardia) is the mode of choice in sinus node dysfunction and/or in young patients (under 60), and/or females and/or in idiopathic arrhythmias and/or when retrograde VA conduction persists. When the pacemaker is replaced, the indication should be reviewed with respect to the outcome of the arrhythmia, which underlines the value of accurate implanted Holter systems.

The incidence of sudden death in the Wolff-Parkinson-White (WPW) syndrome is not well documented and probably underestimated. This retrospective study concerned 28 consecutive patients presenting with ventricular fibrillation either spontaneously (20) or during electrophysiological investigation (8) but whose characteristics allowed them to be assimilated into a single group. Their clinical and electrophysiological characteristics were compared with those of 60 consecutive patients with the WPW syndrome who had documented atrial fibrillation (and even reciprocating tachycardia) but never ventricular fibrillation. There were no significant differences between the two groups with respect to the following clinical parameters: sex, duration of symptoms, the type of tachycardia previously recorded, history of syncope and presence of underlying cardiac disease. With respect to the electrophysiological data, there were no differences in the point of anterograde block, the effective anterograde refractory period of the accessory pathway, the effective and functional refractory periods of the right atrium and atrial vulnerability. On the other hand, a significant difference was observed in the age of patients with ventricular fibrillation (29 +/- 13 years vs 36 +/- 12 years; p0.02), the prevalence of multiple accessory pathways (25% vs 7%; p0.04) with a dominant localisation in the postero-septal region (75% vs 47%, p0.026), preexcitation during exercise stress testing and under antiarrhythmic therapy (95% vs 68%, p0.037). The most discriminating parameter was the shorter RR interval during atrial fibrillation (172 +/- 23 ms vs 230 +/- 50 ms, p0.008). Multivariate analysis only showed one independent predictive factor: the minimum preexcited RR interval.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim is the analysis of the P wave on the signal averaged ECG in 31 pts: 12 control pts (6 M, 6 W, 40 +/- 10 y) 12 HTA (9 M, 3 W, 60 +/- 7 y), 7 pts (5 M, 2W, 48 +/- 7 y) with sustained paroxystic atrial fibrillation (AF) without organic heart disease, without antiarrhythmic drugs. We measured the filtered P wave duration (Ad), the integral of Ad, the root mean square voltage of Ad for the last 10, 20, 30, 40, 60 msec and the duration of P wave on the ECG in lead II (P II) and the echocardiographic dimensions of the atria (LAd). HTA Ad (132 +/- 12 msec)* etcontrol Ad (116 +/- 10 msec) HTA LAd (38 +/- 3 mm) etcontrol LAd (31 +/- 0.7 mm) HTA PII (120 +/- 1.5 mm)* etcontrol PII (88 +/- 10 mm). The difference between HTA Ad (132 +/- 12 msec) and AF Ad (129 +/- 7 msec) is not significant. The linear regression tests don't show correlation between P II and Ad and between LAd and Ad in HTA group. There is a correlation between Ad and LAF in AF group (r = 0.83, p 0.02). HTA RMS 2o (2.2 + 0.6 microV), control RMS 2o (3.9 + 1.8 V) but HTA RMS 2o and AF RMS 2o (2.4 +/- 0.6 microV) are not significantly different and are not correlated with LAd and PII. A long duration of P filtered P wave and a low RMS 2o observed in HTA group and AF group would be a criteria of atrial vulnerability. p0.05.

Epidemiological data has established a relationship between left ventricular hypertrophy (LVH) and sudden cardiac death. This relationship is independent. The search for ventricular and atrial arrhythmias in hypertensives confirms a greater prevalence of these arrhythmias in patients with LVH. The mechanism of these arrhythmias is multifactorial: ischemia, subendocardial fibrosis, increased sympathetic tone, electrolyte disturbances, age, and hemodynamic changes may be arrhythmogenic substrates both at the ventricular and auricular levels. The relationship between LVH (marker or cause) and the detected arrhythmias remain obscure. The most sensitive markers of severity seem to be the ECG parameters (LVH with overload), echocardiographic mass (greater than + 20%) and septal thickness (greater than 12 mm). The evolution of arrhythmias with regression of LVH is unknown. Respect of electrolyte equilibrium would seem to be the only unquestioned therapeutic intervention.

Left ventricular hypertrophy which is the adaptive mechanism of the heart to hypertension may become a cardiovascular risk factor independent of the hypertension which induced it: the regression of left ventricular hypertrophy therefore constitutes one of the medium-term objectives of antihypertensive therapy. Some antihypertensive drugs make the left ventricular hypertrophy regress early and permanently: methyldopa, betablockers, converting enzyme inhibitors, calcium antagonists. The reduction of myocardial mass is slight or debatable with diuretics and absent or inconstant with vasodilator therapy. The regression of left ventricular hypertrophy in hypertension raises several problems: the reliability of methods of measurement; inter-individual and inter-drug variations; the beneficial nature of this regression; the preventive effect of regression of left ventricular hypertrophy on cardiovascular complications. In the light of recent trials, early treatment of hypertension may prevent the development of left ventricular hypertrophy.

The electrophysiological properties of of 0,6 mg/Kg SOTALOL administered intravenously were studied in 15 subjects aged between 32 and 81 years. The following parameters were recorded: sinus rate (SR), corrected sinus node recovery time (SNRT), sinoatrial conduction time (SACT), PA interval, right atrial effective refractory period (ERP), right atrial functional refractory period (FRP), AH interval at rest, at 100 bpm, Luciani-Wenckebach point (LWP), AV node ERP and FRP, HV interval, His-Purkinje ERP, right ventricular ERP, corrected QT interval. At this dosage, intravenous SOTALOL displays two types of behaviour: --That common to the betablocker drugs: slowing SR by 16%, increasing the AV nodal conduction, increasing the AH interval at rest (5%), at 100 bpm (23%), increasing AV nodal ERP (26%) and FRP (20%), decreasing the LWP (18%). --Other properties: increasing intraatrial PA interval (3%), increasing right atrial ERP (II%), FRP (I7%), increasing right ventricular ERP (8%), increasing His-Purkinje ERP (when measurable) (about 6%), no change in corrected QT interval. At this dosage, SOTALOL exhibits electrophysiological behaviour similar to drugs in Class III (Touboul): those with a "wide electrophysiological spectrum".

A comparison of the haemodynamic and electrocardiographic data was carried out in 180 coronary patients. All underwent catheterisation and coronary angiography for angina. They were divided into three main groups: 53 patients with coronary atheroma without significant stenosis; 43 patients with at least one coronary stenosis greater than 50%; 84 patients had myocardial infarction with ECG changes of transmural necrosis and coronary thrombosis (or greater than 80% stenosis). Parameters of left ventricular function (LVF), especially ejection fraction (EF), systolic work (LVESW), end diastolic pressure (LVEDP), end diastolic volume (LVEDV), myocardial mass calculated from angiography (LMV) and volumic compliance were analysed in all cases. Each patient had at least 5 ECG recordings analysed by a HP 6 calculator which determined the values of the principal numeric ECG parameters and the means of the 5 recordings. Particular attention was given to the sum of the R waves in the 12 leads (sigma R mV) and Macruz's index (duration of P/PR - P in Lead II). A satisfactory correlation was found overall between sigma R and EF (r = 0,45, p less than 0,001). sigma R was the only ECG variable related to LVF in patients without infarction. In this group of 96 patients, sigma R correlated with LVEDV (r = 0,46, p less than 0,001) with LVM (r = 0,46, p less than 0,001), with LVESW (r = 0,52, p less than 0,001). There was a discordance between angiographically measured LVM and the mass of electrically active myocardium in patients with infarction. sigma R was independent of LVM, LVEDV, and LVESW.(ABSTRACT TRUNCATED AT 250 WORDS)

The clinical data and presenting signs of 17 cases of atrial myxoma (14 left atrial, 3 right atrial myxomas) were analysed. The aim of the study was to assess changes in the presenting features since the introduction of non-invasive methods of cardiovascular investigation. Two groups of patients were identified according to whether the tumour has been diagnosed before (Group A) or after (Group B) the advent of echocardiography. The diagnosis of cardiac tumour, especially myxoma, has become easier with echocardiography and radio-isotope techniques. The presentation of myxoma, recognised earlier, has changed; the features of advanced valvular disease with resistant heart failure are no longer seen. Variable, atypical clinical signs are now encountered (syncope, pyrexia of uknknown origin, transient ischaemic attacks). The average delay between the first sign and diagnosis was 30 +/- 32 months in Group A, compared to 4,6 +/- 6,5 months in Group B (p0, 005). Of the 7 patients in Group B, three had normal cardiac auscultation, and normal ECG, and four had normal ESRs. The diagnosis of myxoma should be considered at the least doubt and an echocardiographic examination, preferably with 2-dimensional echo should be requested. It not only allows positive diagnosis but also orientates the patient to surgery without further investigation.

Hypertensive heart disease has been studied by means of the maximal exercise test, mechanographic techniques and echocardiography. The patients have been divided into three groups according to their electrocardiogram and the size of their heart as measured radiologically: I: normal ECG, normal size; II: ECG shows left atrial hypertrophy, heart of normal size; III: ECG shows left ventricular hypertrophy, heart is dilated. The total work on exercise decreases from group I to group III. The parameters of the pumping action (PEP/TEVG, VCF, FE) were identical in all three groups and were normal. The relationship A/H on the apexogram and the left ventricular mass/volume relationship on the echocardiogram increased from group I to group III. One possible interpretation of these findings suggests an alteration in diastolic compliance of the left ventricle in the early stages of hypertensive heart disease. The response to beta-blockers as measured on the echocardiogram also argue in favour of this theory.

The diagnosis of atrial myxoma, the most common cardiac tumour, has been greatly facilitated by the introduction of echocardiography. The principal echocardiographic features and the diagnostic pitfalls encountered in a personal series of 7 atrial myxomas (5 left and 2 right) studied by M mode and 2-dimensional echocardiography are reported. In M mode, left atrial myxoma is a relatively easy diagnosis when the tumour prolapses into the mitral orifice. On standard mitro-aortic scanning, it is recorded behind the anterior mitral leaflet as a mass of abnormal echos appearing shortly after mitral valve opening. The diagnosis is much more difficult or even impossible in nonprolapsing tumours. Right atrial myxomas, prolapsing into the tricuspid orifice, do not usually pose any diagnotic problems. 2-dimensional echocardiography shows its superiority in the early diagnosis of small, localised, relatively immobile and non-prolapsing tumours. The parasternal (long axis and transverse views), the apical (4 and 2 chamber views) and subxiphoid positions were the most useful incidences and the tumour was visualised as a more or less circumscribed mass of echos. In all cases, 2-dimensional echo provided information on the size, mobility, insertion and the length of the pedicle of the tumour. Atrial myxoma is being recognised more easily and more often nowadays by echocardiography, the diagnostic method of choice, and 2-dimensional studies should be preferred.

Recent studies have shown the high incidence of concealed Bundles of Kent in the reentry circuits of paroxysmal supraventricular tachycardia. Arguments in favour of the nodal or junctional level of reentry were observed in supraventricular tachycardia with complete atrioventricular dissociation. Two such cases under went electrophysiological investigation. In the first case, tachycardia was terminated by a complete infrahisian block. However, during atrioventricular dissociation, tachycardia could be initiated by a single atrial stimulus after an increased nodal conduction time and terminated by a single atrial stimulus or cardiac message. In the second case the supraventricular tachycardia presented with complete atrioventricular dissociation due to a retrograde ventriculo-atrial block. Atrial stimulation at progressively higher rates and premature atrial extra stimuli initiated the tachycardia but could not terminate it, so confirming the non-participation of the atrium in the reentry circuit. These two cases suggest that the ventricle (case I) and the atrium (case II) are not indispensable links in junctional or nodal reentry circuits. Case II was suggestive of a common initial pathway developing retrograde unidirectional block during tachycardia.

The clinical and electrophysiological data in 52 consecutive patients with bundle branch block and followed-up for an average period of 20.8 +/- 10.4 months was reviewed. The patients were divided into two groups: Group A with normal AH intervals (36 patients) and Group B with prolonged AH intervals (16 patients). These two groups differed in age, the average being higher in Group B (p0.05), in history of syncope (more common in Group A: p0.01) and in the duration of PR interval (p0.05). On electrophysiological investigation the Wenckebach point was lower in Group B (118 +/- 29 ms) than in Group A (160 +/- 33) (p0.001). The effective right atrial refractory period was significantly longer in Group B (321 +/- 111 ms) than in Group A (246 +/- 59 ms) (p0.05). The effective refractory period of the atrioventricular node was also significantly longer in Group B (492 +/- 190 ms) than in Group A (333 +/- 125 ms (p0.05). On the other hand, there was no significant difference in the HV interval or in the number of patients managed by permanent pacing.

Evaluating the cost of coronary artery disease is difficult because it must take into account not only the cost of the disease process itself, but also that of prevention and research. 1. The cost of the disease process itself may be assessed by: a) an analytical study of the real cost of diagnostic and therapeutic procedures; b) a synthetic study of the procedures according to the clinical forms of the disease. Although this task is simple for a given patient, extrapolation of the results to a whole group of patients is more aleatory; c) an epidemiological study of the different forms of coronary artery disease: although global data is available the absence of a coronary artery disease register makes this a difficult problem; d) an evaluation of the socio-professional repercussions of coronary artery disease with integration of the cost and loss in gross national product. 2 The cost of prevention can be assessed by taking the following factors into consideration: a) cost of individual primary prevention which poses the problems of check-up examinations; b) cost of community primary prevention; c) cost of research including fundamental research on the atheromatous process and myocardial ischemia plus clinical research such as secondary prevention enquiries. In conclusion, it appears that: --it is difficult to determine the cost of coronary artery disease without a specialist register; --the cost of coronary artery disease should be considered from positive (source of economic activity) and negative points of view (socio-professional repercussions); --a reduction in the cost of coronary artery disease requires a deeper understanding of the disease, better prophylaxis and socio-professional rehabilitation, and improved organisation of exciting health structures.

Fourteen patients with permanent electrocardiographical features of the Wolff-Parkison-White syndrome in sinus rhythm referred for electrophysiological investigation also underwent maximal exercise tolerance tests. The working hypothesis was that in patients with the Wolff-Parkinson-White syndrome with accessory pathways of longer effective refractory periods than the normal pathway (group I) the delta wave should disappear on exercise, whilst in patients with accessory pathways with shorter refractory periods than the normal pathway (group II) the delta wave should persist. Of the 9 patients in group I,the delta wave regressed in 8 and persisted in 1 patient; of the 5 patients in group II, the delta wave persisted in 4 of them. Three patients had attacks of tachycardia during or just after the exercise tolerance test. These results suggest that the exercise tolerance test may help in the identification of patients with accessory pathways with long refractory periods, less susceptible to rapid ventricular rhythms should atrial fibrillation occur, and therefore with better prognoses.

Twenty-two hypertensive patients with normal coronary arteriograms underwent a complete study of left ventricular performance. The patients were classified into three groups according to the findings on X-ray and ECG investigation: group I--ECG normal, X-ray normal (6 cases); group II--ECG showed left atrial hypertrophy, X-ray normal (7 cases); group III-ECG showed left ventricular hypertrophy, X-ray showed cardiac dilatation (9 cases). The results of this study were as follows:--cardiac ouptut was lowered in groups II and III;--end-diastolic volume was lowered in group II and raised in group III;--LVEDP was raised in groups II and III;--V max and VEC max were lower in groups II and III than in group I;--left ventricular compliance was diminished in groups I and II. Myocardial rigidity of the left ventricle was similar in the three groups. Hypertensive heart disease is therefore characterised by early changes in compliance of the left ventricle. These are associated with geometrical changes in the ventricle: disturbance of the volume/mass ratio of the left ventricle. These findings have therapeutic implications for the importance of beta-blockers.

Measurement of the blood volume in cases of essential hypertension has shown a negative correlation with increase in blood pressure. We have been able to distinguish a group of moderate hypertensives who are hypervolemic, and whose systemic effect is more marked than in the moderate hypovolemic type. Such cases respond poorly to single drug therapy with beta blockers, but well to diuretics. The authors propose a general treatment scheme for essential hypertension: single therapy (beta blockers or diuretics) in mild cases of hypertension; single therapy by diuretics in the moderate types with the increased volume; single therapy by beta blockers in the moderate types with low volume, multiple treatment with the drugs together in cases of severe hypertension.

A case of atrioventricular block (AVB) complicating hypertrophic obstructive cardiomyopathy is reported and analysed with respect to the results of cardiac catheterisation. The installation of 2nd degree AVB was associated with an increase of the intraventricular pressure gradient from 36 to 128 mmHg. This aggravation was related to the lenghtening of diastole which lowered the aortic diastolic pressure and allowed a more forceful ventricular contraction with a reduction in the calibre of the intraventricular stenosis. The sudden lenghtening of diastole also led to an increased contractility of the following systole. In complete AVB the increased gradient was related to a reduction in ventricular volume secondary to the loss of atrial systole. The 33 mmHg pressure gradient disappeared when spontaneous atrial systole or an atrial systole provoked by sequential atrioventricular pacing preceded ventricular contraction. Sequential atrioventricular pacing would seem to be the most appropriate pacing technique in hypertrophic obstructive cardiomyopathy complicated by complete AVB.

Ninety patients admitted to a neurology unit for cerebral ischaemic accident without evidence of embolism from the heart were examined by ambulatory electrocardiographic monitoring (AEM) and by echocardiography assessable in 76 cases. On the basis of a standard cardiac evaluation (SCE) including physical examination, chest radiography and electrocardiography, the patients were divided into 3 groups: 42 with normal SCE (group I), 19 with isolated arterial hypertension (group II) and 36 with patent cardiac disease (group III). Significant abnormalities were detected by AEM in 10.5% of group I patients, 18.5% of group II patients and 33% of group III patients. A structural cardiopathy was discovered at echocardiography in 33%, 62% and 91% respectively of patients in these 3 groups. The greatest number of mitral valve prolapses (7/9 cases) was found in group I. The main echocardiographic abnormality detected in group II was dilatation of the left cardiac cavities: atrium more than 38 mm in 8 cases, ventricle more than 50 mm in 3 cases. Comparisons between the two explorations showed that arrhythmias were often associated with dilatation of the left cardiac cavities (39%) and much less frequently with mitral valve prolapse (11%) and myocardial hypertrophy (16%). Our results suggest that when examinations cannot be routinely performed in hospital patients with a cerebral ischaemic accident echocardiography should be reserved to patients with heart disease or hypertension, and AEM to those with heart disease or hypertension and with dilatation of the left cardiac cavities.

A population of 236 patients with dilated cardiomyopathy (DCM) was studied and followed up for an average of 38.8 +/- 27 months. The most common atrial arrhythmia was atrial fibrillation (AF) which was observed in 27 p. 100 of cases. Patients with AF (n = 43) and without it (n = 193) at the time of diagnosis were compared: the subjects with AF were older (p = 0.036), had a higher left ventricular ejection fraction and lower end diastolic pressures (p = 0.022). AF was associated with mitral valve prolapse (p = 0.007) and with signs of adiastole (p = 0.0015); the most significantly correlated variable was echocardiographic dilatation of the left atrium (p = 0.0012). AF was the presenting symptom of DCM in 13 cases (5.5 p. 100); in 10 cases (4 p. 100) it was the main clinical and therapeutic problem, realizing an arrhythmic form of DCM. Electrical conversion was successful in 7 out of 11 patients with a 2 year follow-up: 3 patients remained in sinus rhythm for over 6 years and have no clinical symptoms, posing the problem of the dominant if not exclusive underlying role of AF in these cases of DCM. An example illustrated by several echocardiographic examinations is presented. Embolic complications were observed in a quarter of the cases with AF and this arrhythmia was present in half the patients with embolic phenomena. However, the prognosis in the groups with and without AF was not significantly different.

62 of 100 cases of acute pericarditis observed over 15 years were so-called acute benign pericarditis. 20 of these patients (30%) had multiple relapses. Relapse could not be predicted. The interval between the initial affection and first relapse was usually more than one month (18/20). Each relapse was accompanied by pain, fever, ST-T changes, slight cardiomegaly and acceleration of the ESR. Corticotherapy appeared to be responsible for relapse in 13 cases. In 6 cases the eradication of a deep septic focus prevented further relapses. In two cases the duration of anti-inflammatory therapy was thought to have been insufficient. Antibiotic therapy did not seem to be a provocative factor. Relapses may be numerous (10 to 12) and prolonged (24-36 months) especially in the corticodependant forms in which steroids should be tailed off gradually according to a strict protocol.

Two new cases of ventricular tachycardia (VT) in the infant are reported, and reviewed in the light of the 23 case histories found in the literature. The diagnosis rests upon eliminating a pre-excitation syndrome, which is so common in this age group. The VTs found in infants are rapid, irregular, and take many different forms. They often necessitate urgent treatment with electric shocks. Preventive treatment consists of a combination of procainamide and beta-blockers in relatively large doses. The search for an aetiological agent should include a haemodynamic and angiocardiographic study of all the chambers of the heart to exclude cardiomyopathy, tumours, papyraceous right ventricle and congenital heart defects. Where no cause can be demonstrated, preventive treatment should be given, with regular electrical testing and other follow-up investigations. An attempt to reduce the drug dosage should be made every 6 months, in hospital. In cases which prove resistant despite adequate treatment, it seems justifiable to carry out a pericardial exploration with the aim of diathermising the ectopic focus; this approach is suggested because of the poor natural history of this type of case.

The antiarrhythmic efficiency of quinidine arabogalactan-sulphate (QAGS) and disopyramide were determined in 38 patients showing chronic, stable frequency premature ventricular beats (PVB). The study which was carried out in 4 medical Centers, used a longitudinal cross-over design. After a baseline evaluation which consisted of two 24 hours electrocardiograms, the patients were randomised to one of the two drugs during a period of 6 or 7 days. The drug sequence were followed by a placebo sequence. A 24 hours electrocardiogram was performed at the end of each sequence. The daily doses were equivalent to 660 mg of quinidine base for QAGS and 600 mg for disopyramide. Among the 38 patients who entered in the study, 32 went through each sequence of the test. The average number of PVB was significantly reduced by QAGS and disopyramide (p less than 0.0001). With QAGS 18 patients had more than 65 p. 100 reduction of PVB and 12 of them more than 80 p. 100. With disopyramide, 14 patients had more than 65 p. 100 reduction of PVB and 12 of them more than 80 p. 100. There was no statistical difference in the overall efficiency of the two drugs. Three patients died, one from myocardial reinfarction, one from ventricular fibrillation; in one other case, the cause of the death remained undetermined. QAGS was better tolerated than disopyramide; adverse effects occurred in 6 patients with QAGS and in 10 with disopyramide. The responsibility of disopyramide in the occurrence of two severe ventricular arrhythmia may be questioned.

Ventricular tachycardia occurred with chest pain in a 64 year old man with coronary artery disease after an intravenous injection of atropine. The particular feature of this case as compared to the other 8 reported cases is the restoration of sinus rhythm after a passage of accelerated idioventricular rhythm by the administration of oxygen and nitroglycerin. The increased oxygen consumption and myocardial ischaemia due to the tachycardia seem to be the factors responsible for these ventricular arrhythmias. Such cases, though rare, incite caution in the administration of atropine to patients with coronary artery disease.

Nine patients aged 47 to 74 years underwent endocavitary destruction of the bundle of His because of paroxysmal arrhythmias resistant to medical therapy. Four patients had paroxysmal atrial fibrillation, 2 had paroxysmal atrial flutter, 1 had reentrant atrial tachycardia, 1 had paroxysmal atrial tachycardia and 1 had an intranodal reentrant tachycardia. One patient had already undergone "surgical ablation" of the His bundle without success. A tripolar or bipolar catheter was introduced via the femoral vein and the His potential localised by bipolar and then unipolar recordings. The lead with the greatest His potential was connected to an external defibrillator and the other pole connected to a metal plaque positioned under the patient's left shoulder. An electrical shock of 200 to 400 joules was administered, in some cases repeatedly. Eight of the 9 patients developed complete atrioventricular block after the shock. This was only temporary in 3 cases, necessitating another shock in 2 cases; the procedure was not repeated in the 3rd case. After 30 minutes of persistent AV block a pacemaker was implanted; 7 of these 8 patients had VVI and I patient (intranodal reentry) DDD pacing. The follow-up period ranges from 1 to 18 months. None of the patients have had symptoms of paroxysmal arrhythmia; in the long-term, there was one initial failure. Of the other 8 cases, 4 remain in complete AV block, 2 have 2nd degree and 21st degree AV block. Three patients have associated antiarrhythmic therapy with quinidine or verapamil. No side effects were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

The clinical significance and mechanism for changes in the axis of the QRS complex during attacks of angina pectoris (excluding cases of Prinzmetal's angina) are unknown. Previous work has suggested that left anterior hemiblock under these circumstances is a sign of unstable angina indicating a lesion in the anterior descending artery. Two cases with left anterior hemiblock associated with frequent attacks of angina have been the subject of careful study. In case one, atrial stimulation tests showed that the left axis deviation was not related to tachycardia. It only occurred when atrial stimulation was carried out for long enough to induce myocardial ischaemia as witnessed by precordial pain and disorders of repolarisation. In case two, the left anterior hemiblock came on at first at the same time as the attacks of angina, and then became permanent. Bypass graft of the anterior descending artery restored the QRS axis to normal, and corrected the repolarisation disorders which were of ischaemic origin. These findings argue in favour of an ischaemic origin of this conduction defect. Unlike ischaemia of the left anterosuperior subbranch, anterior left hemiblock is indicative of extensive ischaemia of the anterior wall of the left ventricle relative to an obstruction in the anterior descending artery or in the main trunk of the left coronary artery.