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Primary hypertrophic cardiomyopathy is a genetic disease causing sarcomere dysfunction. The structural and functional myocardial changes combine to produce cardiac arrhythmias related to reentry phenomena and to triggered automatic activity. The commonest arrhythmias are atrial fibrillation and ventricular arrhythmias; junctional tachycardias via the bundle of Kent are rare. Atrial fibrillation and the Wolff-Parkinson-White syndrome are more commonly associated with certain genetic mutations. Their treatment is mainly based on medication with amiodarone or on radiofrequency ablation in cases of junctional tachycardia. Ventricular arrhythmias are mainly isolated ventricular extrasystoles and non-sustained ventricular tachycardia. The prognostic significance of the latter has been subject of debate for many years but recent studies report a poor prognosis with non-sustained ventricular tachycardia especially in the young patients. Sustained ventricular tachycardia and ventricular fibrillation, though life-threatening complications of hypertrophic cardiomyopathy, are rarely documented and justify implantation of an automatic defibrillator as the risk of recurrence is high. The main objective of the cardiologist in cases of primary hypertrophic cardiomyopathy is to identify the patient at high risk of sudden death. This requires analysis of several parameters: clinical, anatomical, haemodynamic, rhythmic, functional and genetic. The presence of at least two risk factors for sudden death justifies preventive measures. The implantation of an automatic defibrillator is the most reliable form of treatment.

Some of the classical concepts of mitral valve prolapse (MVP) should be reviewed in the light of recent publications. It is a condition, according to strict echocardiographic criteria excluding near physiological abnormalities, which affects 2 to 3% of the adult population in the industrialised world. Only repetitive atrial arrhythmias and complex ventricular arrhythmias are more common in this condition than in control groups, the differences being more pronounced in cases of mitral regurgitation. The risk of syncope or sudden death is 0.1% per year, hardly any different to that of the rest of the general adult population (0.2%). However, this risk may attain 0.9 to 2% in cases with mitral regurgitation. The causes of sudden death are unclear (haemodynamic, neurohumoral, arrhythmic, etc...), although there is evidence in favour of malignant ventricular arrhythmias. Detailed clinical, electrophysiological, isotopic and anatomopathological studies have raised doubts as to the direct responsibility of the vascular malformation (or its eventual consequences on the atrial and ventricular chambers) in this mode of fatal outcome. On the other hand, localised or diffuse myocardial disease is often observed, usually a- or pauci-symptomatic, associated with MVP, the responsibility of which is more plausible. Therefore, the physician should adopt a flexible attitude towards these patients, reassuring those with benign symptoms at low risk and following up or actively treating the rarer malignant forms (especially familial, syncopal with mitral regurgitation and/or severe arrhythmias).

The incidence and the nature of medium-term complications of automatic implantable cardiac defibrillators (AICD) were studied. Seventy-nine AICD were implanted in 50 consecutive patients (42 men, aged 54.5 +/- 13.7 years). Forty-six patients had spontaneous ventricular arrhythmia. These arrhythmias were resistant to treatment (N = 9), reproducible with treatment (N = 28). In 4 patients, the indication was prophylactic, in 2 a Brugada syndrome, in 2 syncope with reinducible ventricular tachycardia and in 1 patient, torsades with a short coupling interval. Forty-six patients had underlying cardiac disease (ischaemic, N = 28, primary dilated cardiomyopathy, N = 10, others, N = 8). The ejection fraction was > 40% in 32 patients. The average follow-up was 41.3 +/- 34.9 months. Eight patients died, 2 from cardiac failure. Twenty-one patients (42%) had 1 or more complications related to their AICD. These occurred: in the operative period (N = 3): 1 post-shock atrioventricular block, 1 ruptured electrode and 1 increased threshold with amiodarone; in the postoperative period (N = 6): infection in 3 cases, cerebrovascular accident in 1 case, deep venous thrombosis of the left arm in 1 case, pneumothorax in 1 case. In the medium-term, the complications were mainly inappropriate electrical shocks observed in 14 patients related to atrial arrhythmias in 7 cases, sinus tachycardia in 1 case, over-detection of myopotentials in 2 cases and electrode dysfunction in 4 cases. In addition, the authors observed complications related to the material: AICD failure in 1 case, electrode displacement in 1 case, and electrode rupture in 3 cases. The authors conclude that AICD are effective for the treatment of malignant ventricular arrhythmias which justify strict specialist follow-up given the incidence and diversity of their complications.

Cardiovascular mortality, the principal cause of early death in diabetics, is multifactorial. A prospective study was undertaken to analyse the different factors of excess cardiac complications in 40 patients with type 2 diabetes, whatever the symptomatology, by making an inventory of the cardiac abnormalities (systolic and diastolic left ventricular function, left ventricular hypertrophy, abnormalities of myocardial perfusion, heart rate variability and arrhythmias). Patients underwent 24 hour Holter monitoring, high amplification signal averaged electrocardiography, echocardiography, Thallium scintigraphy with a dipyridamole test followed by coronary angiography when positive. Patients were aged 60 +/- 8 years, diabetics for 11.8 +/- 6.8 years, and had associated cardiovascular risk factors: 85% were obese, 75% were hypertensive, 62.5% had hypercholesterolaemia and 60% were smokers. The HbA1C was 9.2 +/- 19%. An increased left ventricular mass was observed in 34.2% of patients. The left ventricular ejection fraction was normal (59.1 +/- 6.8%); 69.7% of patients had left ventricular diastolic dysfunction. Reduced heart rate variability was observed in 51.8% of cases. Late ventricular potentials were recorded on high amplification signal averaging in 39.5% of patients; 25.6% had significant ventricular extrasystoles and 52.2% had atrial extrasystoles. Twelve patients (45%) underwent Thallium myocardial scintigraphy with a positive dipyridamole test, 8 of whom had coronary lesions on angiography. The excess cardiac complications of diabetes is mainly due to ischaemic heart disease aggravated by autonomic neuropathy, left ventricular diastolic dysfunction, arrhythmias and left ventricular hypertrophy. In future, larger series are required to demonstrate that this detection can guide therapeutic intervention and reduce cardiac morbidity and mortality of diabetics.

Temporal and spectral analysis of heart rate variability over 24 hours (HRV) was undertaken in 89 patients with primary dilated cardiomyopathy (DCM) confirmed by left ventriculography with normal coronary angiography and compared with 60 control subjects. The left ventricular ejection fraction was 35 +/- 12% in the DCM patients (71 men and 18 women: age 51 +/- 11 years). Clinical signs of cardiac failure were observed in 66% of patients, requiring medication in 62% of patients (diuretics: 47%, digitalis: 45% and ACE inhibitors: 33%). The HRV was significantly lower in the DCM patients than in the control group, even in the absence of clinical signs of cardiac failure. The global HRV was correlated to left ventricular fractional shortening (r = 0.5, p < 0.001) and peak oxygen consumption on exercise (r = 0.56, p < 0.01), but was independent of the degree of left ventricular dilatation, pulmonary capillary pressure and cardiac index. It was not significantly different in cases of sustained or non-sustained ventricular tachycardia on Holter ECG or in cases with late ventricular potentials on signal averaging of the surface ECG. During follow-up of 51 +/- 35 months, patients with decreased HRV on the global indices and those reflecting sympathetic activity had a much higher risk of cardiovascular death and of cardiac transplantation (p < 0.01). The authors conclude that HRV is decreased in DCM. This is mainly related to the degree of left ventricular dysfunction and is independent of the ventricular arrhythmogenic substrate. The HRV may also identify subgroups of patients with DCM at high risk of cardiovascular death or of haemodynamic decompensation requiring cardiac transplantation.

ECG gated blood pool tomography has been performed in sixteen patients with right ventricular arrhythmias in whom the diagnosis of arrhythmogenic right ventricular cardiomyopathy was made based on the finding of abnormalities on contrast angiography. They were compared both to control subjects and to patients with primary dilated cardiomyopathy. Thick slices of ventricles were obtained throughout the cardiac cycle in three orthogonal planes: horizontal long axis and short axis thick slices for analysis of right and left ventricular regional wall motion abnormalities and analysis of the spread of the contraction by means of Fourier phase imaging, vertical long axis slices (one for each ventricle) for ejection fractions, because of easy and reproducible determination of valvular planes and analysis of all right ventricular segments, especially the pulmonary infundibulum. Five typical right ventricular abnormalities were seen: decreased ejection fraction (32 +/- 15% vs 55 +/- 3% in control; p < 0.001), increased diameter (ratio of right to left diameters = 1.2 +/- 0.3 vs 0.9 +/- 0.1; p < 0.01), global delayed contraction versus that of the left ventricle (22 +/- 20 degrees vs -2 +/- 6%; p < 0.01), increased dispersion of contraction (32 +/- 16 degrees vs 13 +/- 4 degrees; p < 0.01) and presence of segments with decreased and/or delayed contraction. Right ventricular disease was observed in all the patients: localized form (56%), diffused form (44%). This method provides accurate functional data for diagnosis and follow-up of patients. In future, this wall motion evaluation method may replace planar nuclear angiography as myocardial SPECT have replaced myocardial planar scintigraphy.

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

Left and right ventricular wall motion was studied in mitral valve prolapse with or without ventricular arrhythmias. Regional and global ventricular wall motion was evaluated by isotopic methods, based in ejection fraction and Fourier phase analysis representing the progression of wall contraction. The synchronisation of the ventricles was characterized by the difference of the mean phase of each ventricle. The heterogeneity of contraction of each ventricle was defined by the dispersion around the mean (standard deviations of the phases). Fifteen of the 36 patients had complex ventricular arrhythmias (Lown grade > or = III). 12 had LVP and 16 had mitral regurgitation. In mitral valve prolapse, the RV EF was decreased compared with normal controls (30 +/- 9% vs 40 +/- 10% ; p < 0.001), especially in patients with mitral regurgitation (26 +/- 7% vs 30 +/- 10%; p = NS) and complex ventricular arrhythmias (26 +/- 7% vs 32 +/- 10%; p < 0.01). The SDP of the LV was greater than those of controls (18 +/- 11 degrees vs 11 +/- 5 degrees ; p = NS) whereas the SDP of the RV was greater (27 +/- 17 degrees vs 12 +/- 5 degrees ; p < 0.05) especially in those with complex ventricular arrhythmias (36 +/- 21 degrees vs 21 +/- 10 degrees : p < 0.01). The SDP of LV and RV were greater in patients with mitral regurgitation: 20 +/- 11 degrees versus 17 +/- 10 degrees (NS) and 35 +/- 21 degrees versus 20 +/- 8 degrees (p < 0.01). Heterogenous ventricular contraction, more marked in the right ventricle in mitral valve prolapse suggests severe myocardial disruption in this valvular disease, reflected by the high incidence of LVP and complex ventricular arrhythmias.

Idiopathic monomorphic ventricular tachycardia (IVT) represents 10% of all cases of VT and is usually observed in young subjects. The origin of the VT may be right ventricular, especially in the infundibulum, giving rise to runs of VT with inter-critical ventricular extrasystoles of the same morphology, or to paroxysmal sustained exercise-induced VT; they usually show left bundle branch block with right axis deviation: the triggering mechanism is probably a parasystole incompletely protected from the sinus rhythm (for the runs of VT) whereas the mechanism of maintenance is probably that of triggered repetitive activity (for the runs and paroxysmal forms of VT). When the origin is in the left ventricle, the VT shows right bundle branch block and left axis deviation and is typically paroxysmal and sustained, triggered by coupled atrial stimulation and followed by a post-tachycardial syndrome; these forms are probably due to reentry into or near to the left posterior hemibranch. These forms of IVT are unique by: 1) their triggering by acceleration of the heart rate, especially during the day, on effort or during an emotion; 2) the usual absence of late ventricular potentials on surface recordings; 3) their capricious outcome, usually good with 92% survival at 10 years; 4) their response to drugs (verapamil, betablockers and/or adenosine) which are relatively ineffective against other forms of VT; 5) their tendency to recur often leading to radiofrequency ablation procedures (80% success rate). The exclusion of underlying inapparent cardiac disease (especially arrhythmogenic right ventricular dysplasia) is an essential part of diagnosis.

Precapillary pulmonary hypertension was diagnosed in a 29 year old woman who became progressively more breathless (NYHA Class III) after her pregnancy, two years previously: systolic pulmonary artery pressure was 120 mmHg with an arterio-capillary pressure gradient of 30 mmHg. She had anti-nuclear autoantibodies detectable at 1/1000 and anti-DNA autoantibodies at 1/800 without any other manifestation of lupus. Treatment with prednisone (2 mg/kg/day) resulted in regression of her dyspnoea with a decrease of systolic pulmonary artery pressure to 65 mmHg, and of the arterio-capillary gradient to 15 mmHg; the lupus serology became negative with a clinical follow-up of 37 months. This observation shows that systemic lupus erythematosus may present with precapillary pulmonary hypertension, the conventional treatment of which may be successfully completed by steroid therapy.

The authors report a case illustrating the causality between the appearance of contact eczema and the implantation of a cardiac pacemaker. To the authors' knowledge, only 11 cases of eczema secondary to the implantation of a pacemaker have been previously reported, all in dermatological journals. In 60% of caes, the lesions were observed over the pacemaker implantation and the appearance of the rash varied from 2 days to 24 months. The causal allergens were mainly the metallic and plastic components. The physiopathological mechanisms, though not completely understood, are related to cellular immunity and therefore, to delayed hypersensitivity reactions. From the therapeutic point of view, locak steroid applications to limited excema lesions have been suggested but recurrence is common. The only effective treatment is removal of the allergen.

In cardiac failure, continuous ambulatory electrocardiographic recording for 24 hours (Holter system) enables detection of 60 to 80% of complex ventricular arrhythmias, 15 to 40% of atrial arrhythmias and sudden death accounts for about 40% of fatalities but its causes are multiple and sometimes unrelated to arrhythmias. Abnormalities of cardiac structure, metabolic and neuro-hormonal changes and some drug therapies are implicated in the genesis of these arrhythmias, the management of which is discussed in two different situations with respect to the functional incapacity: in paucisymptomatic ventricular arrhythmias in patients with cardiac failure, class I antiarrhythmics and d-sotalol should be avoided and betablockers prescribed with caution; the indications of amiodarone have not yet been determined. When the arrhythmia is symptomatic (sustained ventricular tachycardia or ventricular fibrillation), class I antiarrhythmics are not effective enough in the prevention of sudden death; betablockers and amiodarone may give good results but should be compared with implantable defibrillators in the future. The multiplicity and complexity of the mechanisms of arrhythmias in cardiac failure, and the inadequate results obtained with classical antiarrhythmics necessitate the development of new antiarrhythmics based on blockade of non-selective channels probably activated in cardiac failure by the stretching of myocardial fibres.

The persistence of atrial fibrillation with a controlled ventricular response with medical treatment or ablation of the His bundle, suppresses troublesome palpitations but leaves potential haemodynamic problems and the risk of thromboembolism. Surgical treatment of this arrhythmia, by leaving an anatomic bridge between the sinus and atrioventricular nodes, aims to allow acceleration of the ventricular rhythm on exercise whilst preventing by partial, total or selective exclusion of atrial tissues, the multiple intra-atrial reentries responsible for atrial flutter or fibrillation. The first method proposed was isolation of the left atrium (Cox, 1980) which allows acceleration of the ventricular rhythm during exercise, leaving little or no haemodynamic disturbance, but, in theory, the same risk of embolism. The second method, the "corridor" operation (Guiraudon, 1985) consists in isolating both atria, but significantly alters the haemodynamic efficacy without reducing the embolic risk, and hardly offers any advantage over ablation of the nodo-hisian pathway completed by implantation of a ventricular, rate responsive, pacemaker. The recently described "maze" procedure (Cox and Boineau, 1991) would seem to be more promising with judiciously chosen incisions (at the base of the atria, around the pulmonary veins, between the vena cavae, along the interatrial septum, etc.) and points of cryoablation in the region of the coronary sinus, allowing modulation of the ventricular response with activation of sufficient atrial tissue to prevent reentry and recurrence of atrial fibrillation without affecting haemodynamic efficacy. The results of this technique are encouraging in the hands of its inventors but require confirmation in larger series of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Cibenzoline, a Vaughan-Williams Class I antiarrhythmic agent, was studied in 26 patients with orthodromic supraventricular tachycardia (SVT) by nodal reentry (n = 10) or an accessory pathway (AP) (n = 16). IV cibenzoline accelerated sinus rhythm, prolonged PR, AH, HV and QT, widened QRS and depressed or blocked anterograde and retrograde conduction in the accessory pathway, significantly, without significantly modifying conduction capacity in the AV node, nor atrial, nodal or ventricular refractory periods. It converted 6/10 of nodal reentries and 9/16 of reentries due to an AP, by a mean dose of 1 mg/kg, in 2 to 3 minutes, in 12 cases out of 16 by blocking retrograde conduction in the reentry circuit. It prevented reinduction of 12 of the 26 cases of SVT, significantly slowing the cycle of induced SVT in other patients. Oral cibenzoline (260 to 390 mg/day) prevented induced SVT in 11 cases out of 25 and spontaneous SVT in 14 cases out of 26, with a follow-up of 11 +/- 4 months (6 to 16), and this regardless of the reentry mechanisms. Intravenous cibenzoline was not associated with any clinical or hemodynamic intolerance but there was facilitation of episodes of SVT in one patient. Oral administration caused only one case of digestive intolerance, leading to lowering of the dose. Plasma levels showed no significant differences between successes and failures, for both the injection and oral formulations of cibenzoline, whether in terms of the conversion or prevention of episodes. Electrophysiological investigations had a 60% positive and 50% negative predictive value, a sensitivity of 64% and a specificity of 50%. Cibenzoline thus appears to be useful for the conversion and prevention of episodes, SVT, regardless of the reentry circuit, and seems justified, in view of its good safety/acceptability, as first line treatment in this diagnostic indication, measurement of plasma levels and electrophysiological investigations being of little apparent value in terms of guiding treatment and predicting its results.

Ventricular arrhythmias are frequent, sometimes complex and severe, in primary hypertrophic cardiomyopathy. They carry a poor prognosis. Some workers have reported that these arrhythmias are more common in patients with abnormal myocardial perfusion. Other groups have underlined the important role of the sympathetic nervous system in the development of ventricular hypertrophy and the genesis of ventricular arrhythmias. Therefore, a population of 28 patients with primary hypertrophic cardiomyopathy (PHCM) were studied by thallium 201 myocardial scintigraphy and sympathetic innervation was assessed using a structural analogue of noradrenaline, meta-iodobenzyl-guanidine (MIBG). Then, perfusion and innervation were correlated with ventricular arrhythmias observed on 24 hours holter monitoring electrocardiogram. Perfusion abnormalities were observed in 60% of patients: stable in mild left ventricular hypertrophy, labile in severe left ventricular hypertrophy. They were not related to the presence of muscular bridges and systolic compression of septal arteries demonstrated by coronary angiography. These perfusion abnormalities were closely correlated to ventricular extrasystoles observed on Holter monitoring. In this series, and compared to controls, the fixation of MIBG as determined by the Heart/Mediastinum (H/M) ratio was significantly decreased (2.27 +/- 0.31 versus 2.57 +/- 0.33 in controls). Uniform myocardial uptake of MIBG with no defect or significant global hypofixation was observed in 32% of PHCM. Regional and occasionally global hypofixation was observed in 68% of patients. In moderate hypertrophy, reduced uptake was not uniform, the lateral wall and apex being the most abnormal. Uptake of MIBG was significantly correlated to septal wall thickness and to left ventricular mass index. These defects were related to abnormal neuronal uptake of MIBG.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to determine the predictive value for ventricular arrhythmias of ventricular late potentials (LP) in mitral valve prolapse (MVP) the authors performed high amplification signal-averaging ECG (SA) and 24 hours ambulatory ECG (Holter) monitoring in 68 consecutive patients (34 men, 34 women, average age 48 +/- 17.7 years) with echocardiographically diagnosed MVP. Patients with bundle branch block or associated cardiac disease were excluded. Echocardiography showed 26 patients to have floppy mitral valves (38.2%), 50 patients to have posterior deplacement > or = 5 mm of the mitral valves in systole (73.5%) and 35 patients to have mitral regurgitation (51.4%). Holter monitoring showed 17 patients without ventricular extrasystoles (VES), 15 had Lown Grade I, 6 had Lown Grade II, 3 had Lown Grade III, 15 had Lown Grade IV A and 12 had Lown Grade IV B ventricular arrhythmias. Therefore, 30 patients had complex ventricular arrhythmias (> or = Lown Grade III) and 13 patients had spontaneous non-sustained ventricular tachycardia (NSVT) (one patient had NSVT on resting ECG but not on Holter monitoring). Eighteen patients had LP (26.5%). The incidence of complex ventricular arrhythmias was higher in patients with mitral regurgitation (62.8% versus 27.7%; p < 0.005) whereas the incidence of NSVT was not significantly different (25.7% versus 17.1%; p = 0.15). On the other hand, the frequency of complex ventricular arrhythmias was not significantly different in the presence or absence of LP (61.1% versus 40%: NS) whereas the incidence of NSVT was higher in patients with LP (44.4% versus 10%; p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Mitral valve prolapse (MVP) a common condition easily recognised by echocardiography with, however, strict criteria to avoid diagnosis by excess, may be complicated by arrhythmias. Two very different situations oppose severe decompensated mitral regurgitation due to myxoid dystrophy and quasi-asymptomatic MVP with a good prognosis and a low risk of complications. The important question is therefore to detect risk criteria of sudden death in patients with few symptoms. Unfortunately, no isolated factor or association of factors resolves this problem in a given patient. However, it is usually young women without severe mitral regurgitation but with thickened valves and, sometimes, a long QT interval, who are involved. Programmed ventricular stimulation and the detection of later ventricular potentials do not seem to be useful in the present state of our knowledge.

With the improvement in the results of cardiac transplantation, more and more cardiologists are called on to follow up cardiac transplant patients. Cardiological follow-up requires a knowledge of the electrocardiographic and electrophysiological features of the transplanted heart after surgery and the suppression of autonomic innervation. The transplanted heart ECG is characterised by the presence of 2 P waves of different morphology and frequency (from the native and transplanted atria), an acceleration of the sinus rhythm, clockwise rotation of the longitudinal axis, right bundle branch block and ST-T segment changes. The increase in heart rate during exercise is catecholamine-dependent, more progressive and less important than in normal subjects, as is the deceleration of the cardiac rhythm when exercise is stopped. The observation of early sinus node dysfunction is not rare (6.6%) and though usually asymptomatic and transient, implantation of a pacemaker is commonly proposed with different modes of stimulation (VVI, VVIR, AAIR, AAT). The authors have observed changes in the electrophysiological properties of experimental transplanted hearts during acute rejection. The most important of these were in the conduction of the activation within the atrium and in the atrioventricular node, and a reduction in the amplitude of the ventricular potential. The recording of these changes in humans by a non-invasive method could help early diagnosis of acute rejection and limit the number of endomyocardial biopsies. Of the non-invasive techniques under assessment, signal-averaged electrocardiography (temporal and/or frequency analysis) seems to be the most promising.

In patients with supraventricular rhythm disorders ambulatory electro-cardiographic recording (Holter system) is an indispensable examination as it detects attacks that pass unrecorded by conventional ECG, being asymptomatic, too brief or too rare. It confirms the diagnosis, defines the factors triggering the attacks, detects the association of rhythm and conduction disorders, guides the treatment and monitors its effectiveness. Sequential ambulatory recording lends itself particularly well to this last objective. Biochemical examinations explain the cause of certain relapses (potassium depletion, high alcohol blood level) or detect the origin, clinically more or less obvious, of these disorders of rhythm (essays of thyroid hormones). Measuring blood levels of therapeutic drugs makes the handling of these various drugs safer. Finally, echocardiography detects an underlying heart disease, evaluates the size of the left atrium (a factor of relapse when it is dilated and of embolism when it harbours thrombi) and assesses the left ventricular function before administration of antiarrhythmics which, to varying extents, are all negative inotropic drugs.

Certain drugs can induce ventricular tachycardia (VT) by creating reentry, ventricular after potentials or exaggerating the slope of phase 4. These may or may not be symptomatic, sustained or non-sustained and have variable ECG appearances: monomorphic or polymorphic, bidirectional, torsades de pointes. They risk degenerating into ventricular flutter of fibrillation and have been held responsible for the increased mortality observed unexpectedly in some long-term treatments. The drugs responsible are mainly those used in cardiology, probably due to predisposing circumstances (cardiomegaly, cardiac failure, previous severe ventricular arrhythmias, therapeutic associations, metabolic abnormalities). These include primarily the antiarrhythmic drugs (IA, IC, sotalol and bepridil), digitalis, sympathomimetics and phosphodiesterase inhibitors. These complications may be toxic or idiosyncratic, in patients with or without cardiac disease, and may also occur with other drugs: vasodilators and anti-anginal drugs (lidoflazine, vincamine, fenoxedil), psychotropic agents (phenothiazine and imipramine), antimitotics, antimalarials (chloroquine) or antibiotics (erythromycin, pentamidine). The prognosis is severe and the treatment is often difficult which makes prevention, helped by repeated surface ECG (or Holter monitoring), very important with careful assessment of patients at risk.

Without treatment, about 60% of atrial arrhythmia patients suffer a relapse within 3 months and 70% within one year. Antiarrhythmic treatment intended to reduce this percentage is therefore justified, on condition that it is well tolerated. Several preliminary questions have to be settled before this medical prophylaxis: 1) Justification of antiarrhythmic treatment (sometimes pointless to deal with very occasional episodes); 2) Treatment of the underlying heart disease (valve disease, cardiothyrotoxicosis, etc.) or promoting factors (potassium depletion etc.); 3) Accurate assessment of any associated conduction abnormalities, which may constitute a contraindication to antiarrhythmic treatment (WPW syndrome in the case of verapamil and the digitalis-like drugs) or require additional treatment (pacemaker); 4) Definition of the mechanism (vagal or sympathotonic) inducing arrhythmia; 5) Evaluation of the hemodynamic parameters of the underlying heart disease (size of the atria, ventricular function, coronary or valvular lesions) which may limit the efficacy of the treatment. Once these parameters have been identified, the primary treatment should be type la or lb antiarrhythmics, which have been shown to be effective, despite the fact that they are not without arrhythmic risks (the Ib antiarrhythmics are less effective and have a poor safety profile). The beta-blockers have preferential indications (hypersympatheticotonia, hyperthyroidism, hypertrophic myocardiopathy, mitral prolapse, angina etc.) and can be replaced by verapamil or bepridil if there are non-cardiac contraindications (ulcers, asthma, diabetes). Amiodarone is extremely effective, but its poor extracardiac safety restricts its long-term use. Complementary treatments (digitalis-like, anticoagulants or anti-PAF and cardiostimulant drugs) should be added if necessary. Recurrences (to be confirmed by ECG or Holter) should lead to rigorous confirmation of therapeutic compliance and observance of simple hygienic and dietary measures (no excessive exertion, elimination of stimulants etc.). With strict clinical and ECG monitoring, it would then be possible either to increase the dose levels (accompanied by plasma determinations if possible) or to switch to a treatment with more effective, but more aggressive drugs (amiodarone, flecainide) or to use drug associations (la and lb, la and II etc.). Repeated failure of such attempts should lead to a non-medical approach to treatment.

Unlabelled: We studied atrial arrhythmias during a continue prospective work in 48 hypertensive patients referred to the OMS criteria. Hypertension was confirmed by a blood pressure ambulatory monitoring and stress testing blood pressure trend. All cardiovascular drugs were stopped at admission. Patients with associated valvular or coronary artery disease were excluded from analysis. In all patients, we realized a twelve lead-ECG, stress testing, 24 hour Holter monitoring, a blood pressure ambulatory monitoring, two-dimensional echocardiography with Doppler study and cardiac radio-nuclide angiography with diastolic function study. Atrial arrhythmias were considered significant if more than 100 premature atrial beats (PAB) and/or more than three successive PAB were present during Holter monitoring. Significant atrial arrhythmias were found in 39.5% of patients (group II, n = 19), not significant in 60.5% of patients (group I, n = 29). The duration of hypertension was longer in group II (140 vs 66 months, p < 0.05). There was no difference between the two populations considering left atrial size or blood pressure level. Furthermore, we were surprised to find a normal E/A ratio on mitral Doppler recording in patients with atrial arrhythmias (1.23 vs 0.9; p < 0.05). Others diastolic parameters didn't significantly differ. Left ventricular mass index was similar in the two groups but patients with atrial arrhythmias had more asymmetric hypertrophy (1.23 vs 1.13 septum/posterior wall ratio: p < 0.05)., Conclusion: atrial arrhythmias in our study seem to be more dependent from duration of HTA and left ventricular asymmetric structure than from left atrial size.(ABSTRACT TRUNCATED AT 250 WORDS)

The proarrhythmic effects of antiarrhythmic drugs are complications which have been described over several decades but the mechanisms (reentry, increased automaticity, ectopic faci, induced repetitive activity, vagal or adrenergic triggers) and the predisposing factors (underlying cardiac disease, previous severe arrhythmia, metabolic disorders, ischaemia, etc...) have only recently been identified. The appreciation of their true frequency poses problems of methodology (mode of recruitment, therapeutic converse proof), of definitions and depends to a great extent on the methods of detection used. Their severity cannot be denied and has been demonstrated both in experience of isolated cases and in recent prospective studies, the conclusions of which must be interpreted critically. Proarrhythmic effects may be observed at atrial (vagal or sympathetic arrhythmias, 1/1 flutter, acceleration of atrial fibrillation in preexcitation syndromes), junctional (artificial unidirectional block created by the antiarrhythmic drug which may be very effective at higher dosages: biphasic effect) or ventricular (aggravation of ventricular extrasystoles, torsades de pointe, ventricular tachycardia/fibrillation) levels. It is curious that no antiarrhythmic drug seems to be statistically less exposed to this type of complication which may result from phenomena of toxicity or idiosyncrasy. Given the potential gravity measures must be taken to prevent this complication, by observing simple rules (respect of contraindication, use of progressive dosage regimens, avoidance of loading doses, elimination of predisposing factors and abstention from dangerous therapeutic associations) and by carefully following up high risk patients.

An evaluation of the ventricular arrhythmia potential was conducted 3 months after a myocardial infarction (anterior n = 32, inferior n = 58) in 90 patients with a group mean age of 58 +/- 9.3 years, using 24-hour ambulatory ECG monitoring, an exercise test, recording of late ventricular potentials and programmed right ventricular stimulation. Eighteen patients (20%) had a ventricular extrasystole > or = Lown grade III on the Holter, which was more frequent in patients with ventricular dyskinesia (41% vs 15%; p < 0.05); 10 patients (11.1%) had ventricular extrasystoles > or = Lown grade III during the exercise test; 19 patients had late ventricular potentials. Programmed ventricular stimulation induced monomorphic ventricular tachycardia in 10 patients (11.1%) (sustained, n = 5, unsustained n = 5) and the prevalence of late ventricular potentials was higher in this group (60% vs 16.2%; p < 0.01). In the medium term (32 months), 2 patients had died: one suddenly and the other of a recurrence of myocardial infarction. Five patients had an episode of spontaneous ventricular tachycardia. The risk of sudden death or ventricular tachycardia was higher in patients with late ventricular potentials (positive predictive value = 21%) and in patients with electro-induced ventricular tachycardia (positive predictive value = 66%). In the absence of late ventricular potentials, the risk of a serious arrhythmic event is slight (2.8%). After myocardial infarction, the presence of late ventricular potentials can be used to isolate a group of patients with a high risk of serious ventricular arrhythmia; this risk is higher if programmed ventricular stimulation triggers monomorphic ventricular tachycardia.

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

Moricizine chlorhydrate (Ethmozine), a relatively unknown antiarrhythmic agent in France, is a derivative of Phenothiazine, related to the Vaughan-Williams Class IB drugs. A randomised, double-blind, crossover trial with Disopyramide 600 mg/day after a placebo period in 10 patients with ventricular extrasystoles, half of whom had underlying cardiac disease, showed that moricizine 750 mg/day significantly reduced (p less than 0.05) the overall number of ventricular extrasystoles by 81 +/- 46% (disopyramide 72 +/- 69%; NS) and that this drug is effective in 2/3 of patients by suppressing 70 to 100% of ventricular extrasystoles, whereas disopyramide was effective in only 40% of the same patients and never gave better results than Moricizine. Cardiac and extracardiac tolerance of Moricizine was good in this study, confirming previously reported results and its superiority when compared with disopyramide (20% of unwanted effects in this series).

Forty-four cases of hypertrophic cardiomyopathy (23 men, 21 women; 55 +/- 15 years) referred for evaluation of chest pain (28 cases), dyspnoea (26 cases), palpitations (25 cases), dizziness (11 cases) and syncope (4 cases), were investigated prospectively between February 1983 and February 1989. The cardiomyopathy was concentric (N = 16), obstructive (N = 24) or apical (N = 4) and the diagnosis confirmed by angiography. Twenty-four hour Holter monitoring showed no ventricular extrasystoles in 43% of patients: the others had Grade I (25%), Grade III (2%), Grade 4A (14%) or 4B (16%) ventricular arrhythmias with diurnal predominance in half the cases. Patients with greater than or equal to Grade III ventricular extrasystoles had greater left axis deviation but did not differ from the others from the hemodynamic point of view. Exercise stress testing induced an isolated ventricular arrhythmia in 23% of patients and repetitive extrasystoles in 23%. The prevalence of surface late ventricular potentials was no greater in these patients than in normal subjects (4% vs 1%; NS). Programmed ventricular stimulation (N = 37) induced a repetitive response in only 25% of patients, with only two cases of sustained monomorphic ventricular tachycardia. There were no correlations between the results of programmed ventricular stimulation and those of Holter monitoring, exercise stress testing or late ventricular potential recording, but patients with inducible ventricular tachycardia or fibrillation had proportionally more syncopal episodes and greater than or equal to Grade III ventricular extrasystoles on Holter monitoring, but the difference was not statistically significant in this series.(ABSTRACT TRUNCATED AT 250 WORDS)

Sixty-nine cases of non-ischemic dilated cardiomyopathy were studied prospectively from February 1983 to February 1989 (52 men: 53 +/- 13.5 years of age). There were 6 cases of sustained ventricular tachycardia. Thirty-seven patients were in Class III or IV of the NYHA Classification. In addition to echocardiography, radionuclide studies, cardiac catheterisation and coronary angiography, they all underwent 24 hour Holter monitoring, signal-averaged electrocardiography and, in 46 cases, endocavitary electrophysiological investigations. Holter monitoring showed ventricular extrasystoles greater than or equal to Grade 3 of Lown's classification in 72% of patients (26% had nonsustained ventricular tachycardia) and these patients had a significantly lower cardiac index. Twenty five per cent of patients had late ventricular potentials (versus 2% in 50 normal subjects; p less than 0.02); this proportion rose to 32% in those patients with greater than or equal to Grade 3 ventricular extrasystoles and to 66% in the patients with spontaneous ventricular tachycardia; the cardiac index was lower in patients with late ventricular potentials (2.3 vs 2.8 l/min/m2; p less than 0.01) and they had a higher incidence of greater than or equal to Grade 3 ventricular extrasystoles (94% vs 65% in patients without late ventricular potentials, p less than 0.05). Programmed ventricular stimulation induced sustained or nonsustained monomorphic ventricular tachycardia and ventricular fibrillation in 15% of cases. The 6 cases of induced sustained ventricular tachycardia were only observed in the 6 patients with spontaneous sustained ventricular tachycardia and they had the same electrocardiographic appearances.(ABSTRACT TRUNCATED AT 250 WORDS)

The exploration of 113 cases of myocardiopathy (69 cases of dilated myocardiopathy (DMC) and 44 of hypertrophic myocardiopathy (HMC) by a 24-hour Holter recording, exercise tests, recording of surface-delayed ventricular potentials (DVPs) and forced right ventricular stimulation (PVS), revealed an arrhythmogenic potential in both forms of this disorder. In cases of DMC, ventricular arrhythmias were common (81% of cases), frequently recurrent and may constitute one sign of the disease, although they are fairly independent of hemodynamic changes. The presence of DVPs in cases of DMC (25% of cases) was significantly correlated with ventricular extra-systole greater than or equal to grade 3 on the lown scale revealed by the Holter with induction of tachycardia or ventricular fibrillation in response to PVS. Ventricular arrhythmia is less common in HMC (57%). DVPs were rare, and spontaneous or induced ventricular arrhythmia appeared to be more closely correlated with syncope than with any other hemodynamic factor. This study of the arrhythmogenic potential therefore appears to be necessary in myocardiopathy in order to obtain a better definition of the prognostic risk.

Flecainide, a Class IC antiarrhythmic agent, was used in 12 patients with an average age of 57 years to treat spontaneous monomorphic sustained ventricular tachycardia (S-VT, n = 9), with a ventricular rhythm of 203 +/- 41 bpm (5 right bundle branch and 4 left bundle branch block pattern) and non-sustained ventricular tachycardia (NS-VT, n = 3). The patients had ischaemic heart disease (n = 5, including 2 cases of aneurysm), idiopathic dilated cardiomyopathy (n = 1), ventricular dysplasia (right, n = 1; left n = 2; biventricular, n = 1). The remaining 2 patients had no overt cardiac disease on coronary angiography. None of the patients had signs of cardiac failure; the left ventricular ejection fraction was 0.49 +/- 0.7. Before treatment, programmed ventricular stimulation (PVS) induced 12 S-VT (214 +/- 41 bpm) which reproduced the clinical VT in 8 out of 10 cases. A second series of electrophysiological studies was performed after an average of 5 weeks treatment with Flecainide 300 mg/day (200-400 mg). It was not possible to induce VT in 2 patients (17% total prevention); NS-VT replaced S-VT in 4 patients (33%); S-VT was less rapid in 5 patients (at least 50 bpm slower) (41%); one patient had S-VT as rapid as before treatment (9%). The 12 patients were prescribed long-term Flecainide therapy. During follow-up there were 4 early (7, 10 and 15 days) and one late recurrence (16 months) (42% failure rate) whilst the other 7 patients had no further attacks of VT (follow-up of 19.1 +/- 5 months) (58% success rate).(ABSTRACT TRUNCATED AT 250 WORDS)

Two randomized series of 60 cases of myocardial infarction or menace syndrome have been treated at the acute stage, one by Heparin alone, the other by the combination Urokinase-Heparin. The average dosage was 300 mg Heparin in the first series, of 2,700,000 CTA units of Urokinase combined with 240 mg of Heparin in the second series. After the first 24 hours, equal heparinization was performed in both series up to the third week. Significantly different results were obtained in the two series. They favour Urokinase and concern: -- the disappearance time of pain, -- the course of the arrhythmias and of cardiac failure, -- the regression or limitation of the necrosis q waves and the lesion areas on the electrocardiogram. Finally the 30th-day overall mortality was 13% in the Heparin series and 3% in the myocardial infarction on the way of constitution, or which have done so for less than 24 hours.

The aim of this study of 20 young subjects (28 +/- 10.6 years) with no apparent cardiac disease on clinical examination and chest X-ray was to determine the origin of complex ventricular arrhythmias: monomorphic or polymorphic ventricular extrasystoles, isolated or in valves (average 18 158 +/- 12 388 per 24 hours) and/or ventricular tachycardia (5 cases, sustained in 3). These arrhythmias were aggravated (N = 6), disappeared (N = 8) or remained unchanged (N = 5) during exercise. The inter-critical ECG showed ST changes in 5 cases. The extrasystoles had a left bundle branch block configuration in 14 cases and a right bundle branch block configuration in 9 cases. Nine patients were Grade 2 (45%) and 11 patients Grade 4B of Lown's classification. Complementary investigations (echocardiography), radionuclide investigations, right and left heart catheterisation, selective right and left ventriculography and coronary angiography) showed a high incidence of arrhythmogenic right ventricular dysplasia (N - 14) associated with left ventricular abnormalities in 13 cases: hypofixation of Thallium (N = 14) associated with left ventricular abnormalities in 13 cases: hypofixation of Thallium (N = 11), abnormal global left ventricular function (N = 13) with decreased ejection fractions in half the cases, left ventricular dilatation in a third of cases (average and diastolic volume: 109.8 ml/m2), mean velocity of circumferential fibre shortening decreased in 86% of cases (average 0.88 cir/sec), angiographic abnormalities of segmental left ventricular wall motion in 36% of cases; 2 clinically silent cases of mitral valve prolapse were associated with these left ventricular changes; these cases represent forms of arrhythmogenic cardiac disease localised to the right ventricle or involving both ventricles which should be searched for routinely in young patients with apparently normal hearts but with idiopathic and severe ventricular arrhythmias. The diagnosis can only be established by angiography. In other cases, isolated left ventricular abnormalities are detected: two cases of hypertrophic non obstructive cardiomyopathy including one apical form, a condition which may be suspected from analysis of the surface ECG and careful 2D echocardiographic study; phonomechanography may be normal; one idiopathic left ventricular aneurysm which was only diagnosed at ventriculography; one dilated cardiomyopathy affecting the left ventricle. In our series, none of the patients had coronary artery disease and two patients even had no abnormality of any of these investigations.(ABSTRACT TRUNCATED AT 400 WORDS)

Two cases of anterior transmural myocardial infarction occurring after closed chest injuries in young adults (26 and 29 years) are reported. In one case, the infarct was detected after 42 days when the patient gradually developed left ventricular failure after thoracic injury (fracture of the left 9th rib). In the other case, the diagnosis was made during the initial evaluation of a patient with multiple injuries by routine electrocardiography. Radio-isotopic investigations showed an antero-septo-apical and lateral defect with akinetic wall motion in the first case, and apical hypofixation with limited akinesis in the second one. Coronary angiography with left ventriculography was performed after 2 and 3 months respectively, and showed a prolonged non-atheromatous stenosis of the proximal left anterior descending artery with anterior wall hypokinesia, apical akinesia and mitral incompetence (Case n 1) and slight changes of the distal part of the left anterior descending artery with apical hypokinesia (Case n 2). These two cases bring the number of documented reported cases to 37 and illustrate the two possible mechanisms of myocardial infarction after closed chest trauma: direct trauma to the coronary arteries with vascular lesions and secondary myocardial infarction associated with a poor prognosis, and myocardial contusion resulting in random myocardial lesions which usually carry a better prognosis.

Episodic mitral regurgitation due to ischaemia of one or both papillary muscles was studied in a review of 39 cases with complementary investigations and compared with previously reported data. The condition occurred after myocardial infarction in 69 p. 100 of cases (usually after inferior infarction: 54 p. 100) associated with ischaemia of the controlateral territory; there was no history of myocardial infarction in 31 p. 100 of cases. The patients were usually elderly (73 years), often hypertensive (77 p. 100) and diabetic (62 p. 100). The clinical syndrome was that of severe anginal pain, mitral regurgitation and left ventricular failure which was critical in some cases. The ECG showed typical ST depression (4.1 +/- 1.6 mm) especially in the antero-lateral leads; left bundle branch block (28 p. 100) with left axis deviation (18 p. 100), sometimes associated with changes of chronic infarction (64 p. 100) was also recorded. Mitral regurgitation and left ventricular failure regressed almost completely in typical cases between attacks, whilst the ECG showed slight residual sub-endocardial ischaemia (ST depression of 1.5 +/- 0.4 mm) in 30 cases and/or subepicardial ischaemia observed in the anterolateral leads in 13 cases. Phonomechanographic recordings (n = 32) showed moderate mitral regurgitation (1-2/6), usually parasystolic (47 p. 100) or early and mid systolic (36 p. 100) in 87.5 p. 100 of cases between attacks, aggravated by handgrip exercise and improved by trinitrin administration. Echocardiography (n = 27) only showed mitral valve changes in 2 patients (increased density of the papillary muscle in 1 case and prolapse of the anterior leaflet in 1 case); however, segmental wall hypokinetic (51 p. 100) or dyskinetic (15 p. 100) motion, was common with increased left ventricular end diastolic dimensions (mean 56.3 +/- 8.0 mm) and decreased fractional shortening (mean 0.30 +/- 0.07) (67 p. 100). Left atrial dimensions were increased (mean 39.7 +/- 6.4 mm) in 52 p. 100 of patients. Thallium 201 myocardial scintigraphy (n = 32) showed hypofixation in 57 (36 p. 100) and a lacuna in 23 (14 p. 100) of the 160 segments analysed. Left ventricular angioscintigraphy (n = 27; 135 segments) showed hypokinesia in 72 segments (53 p. 100); 2.7 segments per patient), akinesia in 19 segments (15 p. 100; 0.7 segment per patient) and dyskinesia in 2 segments (1.5 p. 100); 0.1 segment per patient). The global ejection fraction was 46 +/- 13 p. 100. Coronary angiography (n = 8) showed significant diffuse atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)

44 cases of paroxysmal sinoatrial tachycardia (PAT) due to reentry within the sinus node or between the sinus node and the atrium are reported; these tachycardias are usually quite well tolerated clinically as the rhythm is rarely faster than 140/min and they are often degraded by functional AV block. They can be triggered and terminated by one (or two) atrial stimuli, and reduced by carotid sinus massage but relapse in the short term. They often alternate with a disturbance of atrial excitability in patients who also have binodal disease. Their diagnosis implies endocavitary investigation showing sinusal anterograde atrial activation and atrial and ventricular stimulation to differentiate them from other types of paroxysmal tachycardia, especially those due to reentry involving concealed right sided Kent bundles. Studies of sinus node function by atrial extrastimulus techniques in 38 patients usually showed an isolated and prolonged Zone I followed, without a transitional plateau, by a Zone IV of sinus echos during which the tachycardia could be triggered. This type of tachycardia, without doubt as common as junctional tachycardia, may respond to treatment with Quinidine, Amiodarone, Verapamil, or beta-blockers, associated with permanent pacing in cases of binodal block.

In normal patients, Mac Carthy has demonstrated that there was a very close correlation between the ventricular contractile activity, evaluated by Fourier's isotopic phase analysis, and electrical depolarization, evaluated by endocardial mapping. It has therefore been possible to study asynchronisms or asymmetries of the ventricular contraction-depolarization and particularly the syndromes of ventricular pre-excitation and ventricular tachycardias. In Wolff-Parkinson-White syndromes (WPW), the mapping obtained by heart cavity tomography in addition to dual-plane gamma-angiography, provides most useful informations, due to additional section planes permitting tridimensional location of the earliest site of ventricular activation. It is quite useful to locate the bundle of Kent always difficult on surface electrocardiogram, or when the endocardial exploration does not permit to precisely locate the site of the excentric atrial activation in case of multiple bundles of Kent or without retrograde conduction. When the left bundle of Kent is barely identified, the isotopic image may be improved by oesophageal stimulation. Additional parameters (use of several harmonics, factorial analysis) will permit to improve the localization of accessory pathways, to be destroyed by fulguration or surgery. In case of ventricular tachycardias with limited functional tolerance, only gamma-angiography, lasting only 3 to 5 minutes, may be used. Combined with endocardial tomography or even gamma-angiography performed in sinus rhythm, not only the site of origin of the ventricular ectopy may be localized, but it also can be correlated with ventricular kinetics abnormalities and the cardiopathy in question may be identified. Most authors consider that there is a close relationship between isotopic site, electrocardiographic appearance and the site found by endocardial mapping or "pace-mapping". In patients with ventricular tachycardias of different morphologies, isotopic mapping permits to differentiate those originating from a same lesion (which may be treated by surgery of fulguration) from those originating in remote areas. Therefore, this technique is a non aggressive and rapid method providing accurate informations on severe rhythm disorders currently treated by eradication of their anatomical substratum.