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D Babuty

Publications and source records attributed to D Babuty.

At least 73 records · Page 4Linked to original sources
PubMed1996

Detection of acute cardiac allograft rejection with high resolution electrocardiography: experimental study in rats.

BACKGROUND AND METHODS: To diagnose early acute cardiac rejection, we evaluated high-resolution electrocardiography in rats. Heterotopic heart transplantations were performed in allogeneic animals, either treated with cyclosporine or untreated, and in syngeneic animals. High-amplification electrocardiograms were recorded daily, under anesthesia, with two intra-abdominal leads. After amplification (x 5000 to 20,000), the electrocardiographic signal was acquired and analyzed with P-Clamp software. We measured the amplitude (millivolts) and duration (milliseconds) of the auriculogram (P wave) and the ventriculogram (QRS wave), the duration of auriculoventricular conduction (milliseconds; PQ interval) and the heart rate. Twenty-five grafted hearts were fully studied in recipients not treated with cyclosporine (allogeneic n = 16, syngeneic n = 9). RESULTS: In the allogeneic group, acute cardiac rejection was always accompanied by an early and progressive increase in P wave duration and PQ interval, whereas an increase in QRS duration was subsequently recorded. No significant change in P wave, PQ interval, or QRS wave duration was recorded in the syngeneic group, which showed no histologic rejection lesions. A decrease in P wave and QRS wave amplitude was recorded in both groups of animals. In the allogeneic group treated with cyclosporine (n = 21), grafted hearts were removed early (4.5 +/- 0.5 days): 10 cardiac grafts were rejected and 11 were not. An increase in P wave duration > or = 20% was associated with mild rejection in most cases. The sensitivity and specificity of this electrocardiographic sign were excellent (100%). The auricular (right and left atria) and the ventricular (right and left ventricles) tissues were evaluated histologically. In the allogeneic groups (n = 26), the histologic lesions during acute rejection were greater in the auricular myocardium than in the ventricular myocardium. Rejection in the atrial and ventricular myocardium was most often differentiated by one degree according to the Billingham classification. CONCLUSIONS: We concluded that acute cardiac rejection in rats is associated with early conduction disturbances in the atrial myocardium which can be shown by high-resolution electrocardiography.

Abdomen↗
PubMed1995

Cibenzoline versus flecainide in the prevention of paroxysmal atrial arrhythmias: a double-blind randomized study.

In a randomized, double-blind, parallel clinical trial, the authors tested and compared flecainide and cibenzoline, a new antiarrhythmic drug, on atrial arrhythmias. Sixty-eight patients (36 men, 32 women, mean age 62.5 +/- 1.6 years) with documented symptomatic paroxysmal atrial arrhythmias (fibrillation in 56, flutter in 12) were recruited and received either cibenzoline 260 mg/day (n = 33) or flecainide 200 mg/day (n = 35). Patients were assessed with physical examination, resting ECG, 24-hour ambulatory ECG recording, two-dimensional echocardiography, and standard biologic titrations before the inclusion day, and 3 months and 6 months after the randomization day. Sixteen patients were withdrawn (7 were lost to follow-up, 7 had side effects, 2 had another medical event). Seventeen patients had documented recurrence of atrial arrhythmia (9 in the cibenzoline group, 8 in the flecainide group) during the study. The efficacy of cibenzoline and flecainide for preventing recurrence of atrial arrhythmias was not significantly different (62.5% versus 71.4%). Eleven patients complained of one or more side effects (cibenzoline, n = 6; flecainide, n = 5), justifying leaving the trial in 6 cases (cibenzoline, n = 3; flecainide, n = 3). Two ventricular proarrhythmic effects were observed. No atrial proarrhythmic effects were reported. The efficacy of cibenzoline and flecainide for preventing atrial arrhythmia is good and similar during a follow-up period of 6 months. In view of these results, cibenzoline may be administered first to prevent atrial arrhythmia.

Aged↗
PubMed1995

[Anti-arrhythmic therapy and cardiac failure].

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.

Adrenergic beta-Antagonists↗
PubMed1994

Ventricular arrhythmia factors in mitral valve prolapse.

To assess the prevalence of ventricular arrhythmias and late potentials (LPs) in mitral valve prolapse (MVP) and to identify clinical, ECG, and echocardiographic markers of spontaneous ventricular arrhythmias, we studied 58 consecutive patients (mean age 46.6 +/- 17.8 years; 29 males, 29 females) with MVP diagnosed by echocardiography. Patients underwent ambulatory ECG recording (n = 58), exercise stress test (n = 56), signal-averaged ECG (n = 58), and programmed ventricular stimulation (n = 52). Ten patients (17.2%) had spontaneous nonsustained ventricular tachycardia (NSVT), 26 patients (44.8%) had premature ventricular contractions (PVCs), Lown grade > or = 3 during 24-hour ECG, and 19 had Lown grade > or = 3 PVCs during exercise stress test; 13 patients had LPs (22.4%). We provoked sustained VT in one case and NSVT in ten cases. Patients with complex ventricular arrhythmias during 24-hour ECG and exercise stress test were older and more often had mitral regurgitation. There was a statistical correlation between the presence of LPs and spontaneous VT (46.1% vs 8.9%; P < 0.005) and induced ventricular arrhythmias (50% vs 12.8%; P < 0.005). No correlation was found between spontaneous ventricular arrhythmias and thickness or posterior displacement of the mitral valve. In conclusion, complex ventricular arrhythmia (especially VT) and LPs are frequent in MVP. Patient age and mitral regurgitation seem to be determinant factors of complex ventricular arrhythmias in MVP. On signal-averaged ECG, absence of LPs seems to be a good additional marker to identify MVP patients without spontaneous VT. On the other hand, programmed ventricular stimulation does not appear valuable in determining a MVP subgroup with a high risk of ventricular arrhythmias.

Adult↗
PubMed1994

Electrocardiographic and electrophysiologic properties of cardiac allografts.

The increasing number of heart transplant patients requires that physicians be able to recognize the electrocardiographic (ECG) and electrophysiologic properties of cardiac allografts. Cardiac allografts are characterized by modifications of resting ECGs and frequent arrhythmias in the postoperative period, and the loss of autonomic nervous control illustrated by permanent tachycardia and loss of heart rate variability during 24-hour ambulatory ECG recording. Some clinical and experimental observations suggest a mid-term reinnervation of the cardiac allograft, but this requires histologic confirmation. The electrophysiologic characteristics of the denervated myocardium are similar to those of the innervated myocardium at rest. However, supersensitivity to circulating catecholamines has been observed in cardiac allografts as in experimentally denervated hearts, which is responsible for a progressive increase in heart rate during exercise and a slow decrease during recovery. Supersensitivity of the denervated heart to acetylcholine may explain the high prevalence of donor sinus dysfunction due to impairment of its automaticity. More often, the sinus node dysfunction is transient and can be treated with an adenosine antagonist, such as theophylline, before permanent implantation of a pacemaker. In the case of pacemaker implantation, synchronization of the donor atria with the recipient atria is desirable, and an endocardial lead implantation is preferred. Several electrophysiologic changes have been observed during acute cardiac allograft rejection. From experimental studies, the most important of these are the disturbance of conduction in the atria and the atrioventricular node and a decrease in the amplitude of the ventricular potential. Initial studies on isolated myocytes show profound changes in membrane conductance during experimental cardiac rejection. The development of new noninvasive detection methods of cardiac allograft rejection, such as intramyocardial voltage electrogram monitoring and high-resolution ECG, could help early diagnosis.

Animals↗
PubMed1994

[Surgical treatment of atrial fibrillation].

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)

Age Factors↗
PubMed1994

[Late ventricular potentials and mitral valve prolapse].

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)

Action Potentials↗
PubMed1993

[Non-invasive exploration methods of supraventricular arrhythmia in current practice].

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.

Arrhythmias, Cardiac↗
PubMed1993

[Drug-induced ventricular tachycardia].

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.

Anti-Arrhythmia Agents↗
PubMed1993

[Electrophysiological properties of the transplanted heart. Clinical applications].

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.

Animals↗
PubMed1992

[Preventive drug therapy of recurrence of atrial fibrillation].

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.

Anti-Arrhythmia Agents↗
PubMed1992

[Proarrhythmic effects of antiarrhythmic drugs].

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.

Anti-Arrhythmia Agents↗
PubMed1992

[Evaluation of the arrhythmogenic potential 3 months after myocardial infarction].

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.

Action Potentials↗
PubMed1992

[Prevalence of atrial arrhythmia in 48 hypertensive patients: research of predictive criteria].

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)

Adult↗
PubMed1992

[Comparison of the efficacy/tolerability ratio of cibenzoline and propafenone in the treatment of ventricular arrhythmia].

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.

Anti-Arrhythmia Agents↗
PubMed1991

[Comparison of the efficacy of moricizine and disopyramide in the treatment of ventricular extrasystoles].

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).

Adolescent↗
PubMed1991

[Arrhythmogenic potential of cardiomyopathies. Dilated cardiomyopathies].

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)

Adult↗