Determinants of spontaneous occurrence of sustained monomorphic ventricular tachycardia in right ventricular dysplasia.

OBJECTIVES: We sought to demonstrate the determinants of spontaneous onset of ventricular tachycardia in right ventricular dysplasia. BACKGROUND: Sudden death during athletic activities has been described in patients with right ventricular dysplasia, but few data are available on the clinical circumstances of well tolerated ventricular tachycardias. METHODS: The spontaneous occurrence of 43 episodes of sustained monomorphic ventricular tachycardia was recorded during ambulatory electrocardiographic (Holter) monitoring in 12 patients. RESULTS: The ventricular tachycardia usually occurred without a significant immediate precipitating arrhythmic event: Atrial arrhythmia was never present, and long-short cycle sequences by postextrasystolic pauses or runs of polymorphic extrasystoles were also unusual (four episodes of ventricular tachycardia each). Finally, no arrhythmia was present immediately before the tachycardia in 36 (84%) of the 43 episodes and in 8 of 12 patients. Examination of the sinus rate before the initial episode of tachycardia in each patient showed a continuous increase from 30 min to the few cycles before the tachycardia (mean RR decrease from 876 +/- 778 to 830.5 +/- 189 ms, with a mean slope of approximately 8.4 ms/min; both p = 0.01 by Wilcoxon test). A within-patient comparison showed that the first cycle of the ventricular tachycardia was shorter than that of runs or couplets (389 +/- 88 vs. 453 +/- 121 and 520 +/- 133 ms, p = 0.03 and p < 0.01, respectively, by paired t test) and that the second cycle was shorter than that of runs (383 +/- 96 vs. 435 +/- 120 ms, p = 0.03). Sinus rate measured 15 beats before the event was higher for ventricular tachycardia than for isolated beats (mean RR interval 835 +/- 184 vs. 908 +/- 153 ms, p < 0.01). CONCLUSIONS: Increased heart rate and shortening of the coupling intervals of the first cycles before the tachycardia are due to a change in the vagosympathetic balance with an increased sympathetic tone. This increase appears to be the main determinant of the ventricular tachycardia in this disease in contrast to the multifactorial origin of ventricular tachycardia due to coronary heart disease. It should be considered in patients participating in strenuous athletic activities.

Determinants of the spontaneous ectopic activity in repetitive monomorphic idiopathic ventricular tachycardia.

Twenty-four hour ambulatory electrocardiographic tape recordings of 30 patients (16 men and 14 women, mean age 42 +/- 17 years) with repetitive monomorphic idiopathic ventricular tachycardia were analyzed using a new computerized system designed to study 15 RR cycles and mean heart rate of the 3 minutes preceding any defined event. The mean (+/- SD) number of events analyzed per patient in 24 hours was 610 +/- 483 for single premature ventricular complexes, 622 +/- 490 for couplets, 260 +/- 411 for runs of 3 complexes, 186 +/- 476 for runs of 4, 108 +/- 173 for runs of 5, 82 +/- 129 for runs of 6 to 10 and 83 +/- 116 for runs of more than 10 complexes. The heart rate was faster before runs of ventricular tachycardia than before isolated extrasystoles (p less than 0.01) and a positive linear correlation was observed between the mean preceding heart rate and the type of extrasystolic activity, the length of the runs increasing with increasing preceding heart rate (r = 0.98, p less than 0.001). A long RR interval just before the occurrence of runs was present in 77% of the cases (23 of 30) with or without an oscillatory pattern of RR intervals due to bigeminy or trigeminy, and the length of the runs correlated positively with the duration of this long preceding diastole (r = 0.90, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Predictive value of electrophysiologic studies during treatment of ventricular tachycardia with the beta-blocking agent nadolol. The Working Group on Arrhythmias of the French Society of Cardiology.

Sixty patients with recurrent inducible sustained ventricular tachycardia were prospectively treated with nadolol (40 or 80 mg/day). Old myocardial infarction was present in 43 patients and dilated cardiomyopathy in 12. In group I (n = 36), nadolol was given alone, whereas in group II (n = 24), previously ineffective treatment with amiodarone was continued in combination with nadolol. Left ventricular ejection fraction was higher in patients in group I (0.40 +/- 0.12) than in group II (0.30 +/- 0.10, p less than 0.01) patients. Electrophysiologic study was repeated after short-term treatment with nadolol, which was continued regardless of the results of this test, according to the scheme of the parallel approach. Recurrence of spontaneous tachycardia or sudden death occurred in 21 patients after 10 +/- 9.2 months; sustained tachycardia was inducible in 19 on nadolol therapy. The remaining 39 patients (of whom 21 had inducible tachycardia while taking the drug) have had no recurrence of tachycardia after 27.8 +/- 9.3 months of follow-up study. Sensitivity, specificity and predictive value of a positive and negative test were 90.5%, 46%, 47.5% and 90%, respectively. The results differ between group I and group II patients, the latter having a high percent of false positive responses. This difference is even more obvious with respect to left ventricular ejection fraction: the predictive value of a positive test was 86% when ejection fraction was greater than 0.40 and 39% when it was less than 0.40.(ABSTRACT TRUNCATED AT 250 WORDS)

[The coexistence of a para hisian accessory pathway and a complete atrioventricular block in a 32 years old patient]. / Un faisceau accessoire chez un patient de 32ans pas si accessoire !

The present case report describes a 32-year-old patient with complete atrioventricular block coexisting with a permanent ventricular preexcitation. The patient ended up with pacemaker implantation without requiring ablation of accessory pathway.

Comparison of four beta-blockers as assessed by 24-hour ECG recording.

beta-Blockers are used as if they were equivalent. With ECG recordings in 42 patients we investigated the effect on sinus heart rate of four beta-blockers given at three successive daily doses. Heart rate was dose-dependently decreased by all drugs except acebutolol, the effect of which decreased at a higher dosage. The maximal effects of metoprolol, nadolol, and propranolol were similar but the drugs differed in potency (dosage producing 50% of maximal effect, calculated from the dose-effect relationships; nadolol, 0.3 mg/day; metoprolol, 120 mg/day; propranolol, 47 mg/day). Similar relationships were found with drug plasma concentrations (concentration producing 50% of maximal effect: nadolol, 3.5 ng/ml; metoprolol, 21 ng/ml; propranolol, 36 ng/ml) and with supine or upright heart rates and blood pressures. However, the drugs were not equivalent: In addition to its greater potency, nadolol differed from propranolol and metoprolol in the slope of its dose-response curve. We conclude that beta-blockers can be compared by ECG recordings and that nadolol is different from the other beta-blockers without intrinsic sympathomimetic activity.

European experience with the antiarrhythmic efficacy of propafenone for supraventricular and ventricular arrhythmias.

Seventy-one patients (mean age 53 years) were treated with oral propafenone, 900 mg/day, for a mean of 6.6 months. A large spectrum of arrhythmias was encountered, and particular attention was paid to their relation with the autonomic nervous system. Drug efficacy was graded from 1 (no effect) to 5 (complete control) according to the clinical result and Holter recording. This method permitted comparisons to be made between propafenone and 3 other antiarrhythmic agents: quinidine, beta-blockers and amiodarone. Among the 32 patients with supraventricular arrhythmias, 9 cases of vagally dependent atrial flutter and fibrillation were less sensitive to propafenone (mean effect 1.4) than to quinidine (mean effect 2.0) or amiodarone (mean effect 2.3). However, 8 cases of adrenergically dependent atrial tachycardia and fibrillation were more sensitive to propafenone (mean effect 4.1) than to beta blockers (3.0) or amiodarone (mean effect 3.5). In 12 cases of miscellaneous atrial arrhythmias the response to propafenone was intermediate. However, 3 patients with resistant junctional tachycardia were improved with propafenone. Among 42 ventricular arrhythmias, 5 patients with extrasystole who were responsive to quinidine (mean effect 3.8) were also improved with propafenone (mean effect 4.6). Propafenone (mean effect 4.1) was much more effective than quinidine (mean effect 2.4) in treating 8 cases of idiopathic benign ventricular tachycardia and even more successful in treating 13 cases of more severe arrhythmias in diseased hearts (propafenone's mean effect 4.1, quinidine's mean effect 1.9 and amiodarone's mean effect 1.9). Propafenone was less effective (mean effect 3.3) than amiodarone (mean effect 4.0) in 4 cases of severe, adrenergically dependent idiopathic ventricular tachycardia (VT).(ABSTRACT TRUNCATED AT 250 WORDS)

Flecainide in quinidine-resistant atrial fibrillation.

Flecainide (100 mg twice daily) was used for prevention of paroxysmal atrial fibrillation (PAF) in 52 patients with frequent symptomatic attacks that were resistant or intolerant to quinidine (600-900 mg/day). Underlying heart disease was present in only 8 cases and left ventricular ejection fraction was always greater than 30%. No patient had had a myocardial infarction. Vagally induced PAF was clinically documented in 35 patients. Amiodarone, previously used and ineffective, was combined with flecainide in 33 patients. After 1-5.8 years of follow-up, complete disappearance of PAF was observed in 38 patients (73%). The success rate was slightly higher in patients with vagally induced PAF (p = 0.07). Extracardiac side effects necessitated withdrawal in only 3 cases. Permanent pacemaker was needed in 7 patients on amiodarone and flecainide because of excessive sinus bradycardia. Two patients, with previously documented atrial flutter, experienced presyncopal episodes of atrial flutter with 1:1 atrioventricular (AV) conduction and wide QRS complex. No death occurred during the follow-up. In this series, quinidine proved to be unsuccessful in 46 patients and it was withdrawn in 6. We concluded that flecainide is efficient and well tolerated for long-term prevention of PAF in patients resistant to quinidine. The possibility of 1:1 AV conduction during atrial flutter may suggest the use of verapamil or beta blockers in combination with flecainide in patients with previously documented atrial flutter.

Direct-current cardioversion of atrial tachyarrhythmias under oral flecainide therapy.

Results of direct-current cardioversion of 48 patients with atrial arrhythmia taking oral flecainide were compared with those of 96 control-matched patients. After completion of 3 shocks, 98% of flecainide patients were converted versus 78% of control patients (p <0.01). Thus, despite an experimental increase in defibrillation threshold, flecainide given before cardioversion seems to have a beneficial effect.

Results of electrical fulguration in arrhythmogenic right ventricular disease.

Eleven patients with sustained ventricular tachycardia (VT) refractory to antiarrhythmic drugs due to right ventricular disease shown by angiography underwent fulguration. Seven patients always had VT with the same morphology, and 4 had clinical VT with 2 or 3 different QRS waveforms. Five patients underwent a single fulguration and the other 6 underwent from 2 to 5 procedures; 2 to 14 shocks (mean 6) of 150 to 250 J were used. No serious complications occurred. At 31.5 +/- 9 months of follow-up, the arrhythmia was controlled in 8 patients, with continuation of previously ineffective antiarrhythmic drug therapy in 6 of 8. The number of VT episodes the year before and after fulguration was 0.5 +/- 0.7 vs 3.5 +/- 1.7 (p less than 0.001). There was no statistically significant difference between the success rate and the degree of prematurity of the onset of the local electrogram during VT: -36 +/- 31 ms for successes and -38 +/- 13 ms for failures. In 7 patients with monomorphic VT, there were 6 successes and 1 failure, and in 4 patients with several morphologies of VT, there were 2 successes and 2 failures (1 due to the appearance of a "new" VT). Thus, electrical fulguration of VT in patients with right ventricular disease is safe and most often effective, particularly in patients with monomorphic VT, when combined with antiarrhythmic drugs. In these patients, the usually recommended endocardial mapping criteria for the determination of the optimal fulguration site were not predictive of outcome. Further studies are necessary to better define the optimal site for fulguration.

Suppression of arrhythmias within hours after a single oral dose of amiodarone and relation to plasma and myocardial concentrations.

In 65 patients a single oral dose of amiodarone (30 mg/kg) produced an antiarrhythmic effect on supraventricular or ventricular arrhythmias within 3 to 8 hours and lasted for 17 to 19 hours. On the second day a 15-mg/kg dose reproduced this effect within 3 to 9 hours. Plasma concentration of amiodarone increased to a maximum (2.2 +/- 1.7 mg/liter) mean +/- standard deviation) at 6 +/- 3.5 hours and plasma levels of N-desethylamiodarone (NDA) rose to 0.2 +/- 0.08 mg/liter at 12 +/- 6.4 hours. Sixty-one other patients were given a single 30-mg/kg dose 7 hours to 4 days before open heart surgery. Biopsies of the right atrial and left ventricular walls were taken during surgery. Myocardial concentration of amiodarone was maximal in the atrium after 7 hours (13 +/- 8 mg/kg) and in the ventricle after 24 hours (17 +/- 11 mg/kg). NDA myocardial concentration increased progressively until 24 hours and then remained stable over 4 days (1.5 mg/kg). The amiodarone myocardial to plasma concentration ratio was similar in the atrium and in the ventricle and averaged 22 and 10 for amiodarone and NDA, respectively. A significant relation existed between amiodarone concentration and the effect on ventricular premature complexes (r = 0.74, p less than 0.001) and between amiodarone plasma concentration and the effect on the atrioventricular conduction (r = 0.58, p less than 0.001). The plasma concentration of amiodarone corresponding to a 60% decrease in arrhythmias averaged 1.5 to 2 mg/liter.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of drug-induced QT interval modifications in dynamic electrocardiography: the case of bepridil.

Drug-induced modifications of QT interval are usually assessed through formulae defining the corrected QT interval "QTc". They are all based on the assumption that the correction is adequate, and that drug-induced heart rate variations and rate-dependent QT changes are proportional. Holter ECG allows to study the repolarization in selected RR cycles while controlling environmental rate-related and circadian influences. Repolarization duration was evaluated in 15 normal individuals and 13 patients with stable coronary artery disease and no heart failure who did not differ in terms of 24-hour heart rate, age and sex. The effects of a 3-month treatment with bepridil were assessed in the latter. Using the conventional evaluation through the corrected QT (Bazett formula), no difference was found between the two groups at baseline, and bepridil induced a non-significant 5% prolongation of QTc. At Holter recordings, the QTa (Q-T apex) duration was linearly correlated with the heart rate over 24 hours. To specifically study day-to-night variations and to exclude the rate-dependent and short-term autonomic influences. QTa was studied in populations of averaged QRS-T selected according to i) the last RR cycle length and ii) an identical mean RR interval during the preceding minute. Both RR values were fixed at 800 ms to obtain the "QTa-800" measured directly or extrapolated from linearly correlated, other RR values.(ABSTRACT TRUNCATED AT 250 WORDS)

Surgery for the Wolff-Parkinson-White syndrome in 73 consecutive patients: what have we learnt from intraoperative mapping?

Intraoperative epicardial mapping data obtained in 73 consecutive patients operated upon for the Wolff-Parkinson-White syndrome were reviewed. Fifty-six patients had single and 17 patients had multiple accessory pathways. Except for right free wall pathways, all bypass tracts were divided using an endocardial approach. There were 2 operative deaths, 1 of which occurred after a concomitant mitral valve replacement. A total of 78 of the 87 pathways present in the 71 survivors were successfully ablated (90%). All failures occurred in patients with left posterior septal pathways. Epicardial mapping performed prior to bypass was found helpful in identifying multiple distinct accessory pathways which had been missed preoperatively. This occurred in 6 patients and led to appropriate combinations of classic operative approaches which resulted in all of these pathways being successfully divided. Further, by demonstrating that Kent bundles often presented as multiple closely-spaced or arborized accessory pathways, intraoperative mapping led to widening of the margins of surgical dissection, and in particular to an additional left atriotomy in all cases of left posterior septal accessory pathways which resulted in a substantial improvement in our rate of success.

Sustained intra-atrial reentrant tachycardia. Electrophysiologic study of 20 cases.

Twenty cases of sustained tachycardia due to intra-atrial reentry were investigated in patients aged 17 to 80 years (mean 47). The average frequency of the tachycardia was 128.6/min (extremes 95 and 180). Three modes of onset of the tachycardia were observed: atrial extra-stimulus (19 times), progressively accelerated atrial pacing (9 times) and atrial escape beat (10 times). The tachycardia was stopped in all cases by a premature stimulation. When spontaneous, the termination was either sudden (10 times) or preceded by a progressive slowing (9 times) or an alternating phenomenon of long-short cycle (13 times). Precise atrial mapping allowed to localize the first atrial depolarization less frequently in the sinus node area (1 case) than in the mean right atrium (21 cases), the low right atrium (2 cases), the interatrial septum (2 cases), and the left atrium (4 cases). The macroscopic size of the reentry circuit was demonstrated in only 3 cases. A junctional reentry was accurately ruled out in all cases thanks to the existence of a second or third-degree AV or VA black, or by studying the sequence of retrograde atrial activation. A true junctional reciprocating tachycardia was associated with the intra-atrial reentry in 2 cases.

[Quantitative evaluation of the efficacy of anti-arrhythmia agents in chronic ventricular arrhythmia]. / Evaluation quantitative de l'efficacité des anti-arythmiques dans les troubles du rythme ventriculaire chroniques.

The authors describe a computer system for the analysis of ventricular arrhythmias and its use in the evaluation of anti-arrhythmic drugs. Provided the arrhythmia is stable, this method allows an estimation of the onset and duration of action of the drug and gives guidelines for the choice of an appropriate drug regimen. Using this system, a comparison can be made between different drugs based on quantification of their efficacy.

[Prognostic factors for success in catheter ablation of the right Kent bundle: report of 27 patients]. / Factores pronóstico de éxito en la fulguración de los haces de Kent derechos: a propósito de una serie de 27 pacientes.

In 27 patients with atrial fibrillation and/or reciprocating tachycardia, ablation of right-sided Kent bundles (23 in the right posterior paraseptal region and four of the right free wall) was performed. The anterograde refractory period of the accessory pathways was 253 +/- 70 msec and the shortest R-R interval during atrial fibrillation 211 +/- 47 msec. Cumulative energies of 589 +/- 396 J per patient were used, with 3 +/- 2 shocks and 195 +/- 312 J per shock. Accessory pathway ablation was effective in 16/27 patients (59%) during an 11 +/- 8 months of follow-up (in 15/16 pre-excitation disappeared; in nine of them the anterograde and retrograde conductions were abolished and in the other six the anterograde and retrograde conductions were severely altered; ablation was partially ineffective in 1/16 patients who remained asymptomatic on medical treatment and without inducible reciprocal rhythm). Ablation was ineffective in 11/27 patients. Three hours after ablation a patient died from electromechanical dissociation; during ablation a 200 J shock cancelled preexcitation, not being possible to produce reciprocal rhythm. The emergency echocardiography only showed a minimum posterior pericardial effusion. Ablation was effective in 15/23 patients (65%) right posterior paraseptal. Overall success in 1989 (10/27 patients) was 70% (7/10 patients). The success in 1989 was 70% (6/8 patients) right posterior paraseptal. The shortest RP' interval (was 82 +/- 19 msec) during the reciprocal rhythm, where the ablation was performed, was 82 +/- 19 msec (74 +/- 17 msec with success and 99 +/- 19 msec with failure).(ABSTRACT TRUNCATED AT 250 WORDS)

[The surgical section of the bundle of Kent as an operative treatment of the Wolff-Parkinson-White syndrome: apropos a series of 82 operated cases]. / Sección quirúrgica del fascículo de Kent como tratamiento cruento del síndrome de Wolff-Parkinson-White: a propósito de una serie de 82 casos operados.

Eighty two patients diagnosed of the Wolff-Parkinson-White syndrome (WPW) underwent operation for the surgical section of the Kent-His bundle. In these cases, posteroseptal localization (PS) occurred in 32, left lateral (LL) in 25, right lateral (RL) in six, anteroseptal (AS) in one, posteroseptal and left lateral in 14, right and left posteroseptal in two, anteroseptal and left lateral in one, and left lateral and right and left posteroseptal in one. All of the patients presented an invalidating clinical of palpitations and/or loss of consciousness, and episodes of atrial fibrillation and/or reciprocal rhythm were registered in all cases. The mean anterograde refractory period in the accessory pathways was 244 +/- 60 msec, and the shortest RR in atrial fibrillation was 190 +/- 36 msec. A mitral commissurotomy was carried out in 3 patients during surgery, mitral prostheses were implanted in two, a double aorto-coronary bypass was made in three and an interventricular communication was closed in one. After a follow-up of 36 +/- 18 months, the surgical section of the Kent bundle was found to be effective in 77 out 82 patients (94%). (In 70 out of 77 cases, both anterograde and retrograde conduction were totally abolished and in seven out of 77 obtunded. All patients were asymptomatic during the follow-up period). In 5 out of 82 patients, surgical treatment was ineffective all five showed a PS Kent-His and two presented a second Kent-His fascicle (LL).(ABSTRACT TRUNCATED AT 250 WORDS)

[Ventricular tachycardia of ischemic cardiomyopathies]. / Les tachycardies ventriculaires des cardiopathies ischémiques.

Ventricular tachycardia in patients with ischemic heart disease are almost always observed after myocardial infarction without preservation of the border zone (thrombolysis or early angioplasty). Monomorphic tachycardias are related to permanent electrophysiological substrate with a zone of slow conduction. This may be affected by initiating factors such as extrasystoles, especially with alternating long and short cycles, and the sympathetic nervous system before the appearance of clinical tachycardia. Cardiac mortality is mainly due to sudden death after an initial episode of sustained monomorphic ventricular tachycardia. The prognostic value of left ventricular function as assessed by the ejection fraction is essential: the 5-year mortality is 30% if LVEF is > 0.3 compared with 51% if LVEF is < 0.3 (p < 0.01). On the other hand, the frequency of spontaneous VT and VT induced by programmed stimulation does not affect the prognosis. The mortality after an initial episode of syncopal tachycardia is greater than after a well tolerated tachycardia. This is why the clinical history of the patient is essential to guide management. The persistence of inducible VT despite antiarrhythmic therapy increases the mortality; it is therefore important to find a drug which prevents induction VT. The patient is then classified as "responder". The number of "responders" patients, however, is low when the ejection fraction is < or = 0.30. The choice of treatment seems important when the ejection fraction is < or = 0.30: in this case, patients receiving Class I antiarrhythmics have a higher mortality and those taking betablockers have a reduced mortality. After polymorphic VT, if VT or VF is inducible, the risk of mortality is very high.(ABSTRACT TRUNCATED AT 250 WORDS)

[Value of electrophysiological studies in the evaluation of atrial fibrillation]. / Intérêt de l'exploration électrophysiologique dans l'évaluation de la fibrillation auriculaire.

Electrophysiological studies of the atrium provide a means of evaluating the parameter involved in the process of fibrillation. The study of atrial vulnerability, initially limited to the test of provocation of the arrhythmia, has widened to include analysis of the substrate. Shortened refractory periods and regional conduction defects play a role in the creation of reentry pathways. Variations in the heart rate influence these parameters and explain the fundamental role of the autonomic nervous system on the uniformity of the activation front. The risk of atrial fibrillation is related essentially to thrombo-embolism: atrial vulnerability was investigated in 70 patients with unexplained cerebrovascular accidents. Globally, one out of two patients had pathological substrates. This study of atrial vulnerability showed that it was possible to identify a group of patients at risk of atrial fibrillation, even before the arrhythmia was recorded. This prognostic approach could also be applied to the investigation of preexcitation and syncope, and to the evaluation of the effects of pharmacological intervention.

[Flecainide: a new antiarrhythmic agent]. / La flécaïnide: un nouvel antiarythmique.

The authors report their clinical experience with flecainide, a new Class I antiarrhythmic drug, in 44 patients classified into three groups. The first group (7 cases) comprised patients with a wide range of arrhythmias sensitive to the usual antiarrhythmic agents. The second (17 cases) were atrial arrhythmias resistant to the usual antiarrhythmic agents and were mainly vagal atrial arrhythmias. The last group (20 cases) comprised patients with resistant VT, 14 of whom had underlying cardiac disease (8 chronic infarcts). The results obtained were analysed by a score test because of the wide range of arrhythmias and the wide variations in their spontaneous recurrent rate. The antiarrhythmic effect was checked by repeated Holter monitoring correlated with the results of interrogation. Provocative pacing studies were performed in 5 cases of inducible VT under therapy. The results with flecainide were compared with those obtained with reference Class I antiarrhythmics: quinidine, 700 to 1100 mg/day or disopyramide, 600 mg/day. Amiodarone was often associated with each Class I antiarrhythmic because of the resistant nature of these arrhythmias. In group I the results with flecainide were equivalent to those of quinidine. In the other two groups the results were significantly better than those of the reference antiarrhythmic: mean scores: group II 3,20 +/- 0,5 compared to 1,9 +/- 0,4 (p less than 0,01); group III 3,70 +/- 0,37 compared to 1,85 +/- 0,22 (p less than 0,001). Tolerance was good apart from neurosensory side effects (loss of accomodation, vertigo) which were dose dependent and which led to the withdrawal of therapy in only 4 cases. Four types of cardiac side effects were observed: aggravation of existing sinoatrial block (1 case); aggravation of existing intraventricular block (2 cases); aggravation of contractile function which was very poor before therapy (2 cases); and sudden death during therapy in patients with ischemic heart disease in cardiac failure and with incessant resistant VT (2 cases). In these instances the role of the drug cannot be confirmed. These complications were observed with doses of more than 5 mg/kg/day and in patients with cardiac failure. Two of these patients had serum flecainide levels which were very high. It may therefore be possible to reduce the incidence of these complications by adapting dosage to the patient's clinical state and to the serum drug levels.(ABSTRACT TRUNCATED AT 400 WORDS)

[Late potentials and mitral valve prolapse]. / Potentiels tardifs et prolapsus valvulaire mitral.

Signal averaged electrocardiogrammes were recorded in 100 consecutive patients with echocardiographic mitral valve prolapse (MVP) and compared with 50 normal control subjects. Criteria of normality were defined in the reference population: QRS duration after averaging < 113 ms, Simson's vector of the last 40 ms (RMS40) > or = 17 microV, and duration of the terminal potential within the 40 microV range < 38 ms, using a high-pass bidirectional 40 Hz filter. Of the 100 patients with MVP, late ventricular potentials (LP) were recorded in 38 cases with at least 2 criteria of positivity, compared to only 3 out of 50 (6%) in the control group (p < 0.01). The prevalence of LP was very dependent on the appearances of the valve; when the valve was of normal thickness and only showed slight systolic bulging there were only 5/46 cases of LP (10.9%) which did not differ significantly from the control group. On the other hand, when the valve showed myxoid changes, the prevalence of LP was very high: 33/54 = 61% (p < 0.001 versus controls). Six patients had severe ventricular arrhythmias (sustained ventricular tachycardia or ventricular fibrillation): all had LP. In cases of MVP with frequent ventricular extrasystoles (VEs) the prevalence of LP was the same with normal valves (2/23 = 9% and 2/22 = 9%, NS) whereas LPs were more common in cases of VEs with myxoid valve (23/33 = 70% versus 5/16 = 31%; p = 0.01). The high prevalence of LP in MVP with myxoid valves is a convincing argument in favour of myocardial abnormality in this disease.(ABSTRACT TRUNCATED AT 250 WORDS)