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Biomedical subjects

A Leenhardt

Publications and source records attributed to A Leenhardt.

At least 55 records · Page 3Linked to original sources
PubMed1997

[Pharmacological treatment of atrial fibrillation].

Atrial fibrillation is not a single entity. Many factors play a role in its genesis, its maintenance and termination. The presence of underlying cardiac disease and left ventricular dysfunction is a major factor due to the electrophysiological and haemodynamic consequences, the effect on autonomic nervous system and on the effect of antiarrhythmic drugs themselves. It is therefore essential to take this into account before deciding on a therapeutic approach. This also emphasises the difficulty of interpreting clinical trials comparing pharmacological treatments when the study population is poorly defined. In general, one molecule is not more or less effective than another, it is more or less adapted to the patient under treatment.

Adrenergic beta-Antagonists↗
PubMed1996

Drug therapy for prevention of atrial fibrillation.

Atrial fibrillation is not a homogeneous entity, and many factors are responsible for a number of different behaviors, clinical consequences, and reactions to therapy. Therefore, the conventional evaluation of preventive treatments is not really adapted to provide the correct answers to difficult problems of therapeutic indications, as the 2 components of the benefit-risk ratio are not really known. Like ventricular fibrillation, atrial fibrillation may be primary or secondary to organized tachyarrhythmias, and reentrant flutter or automatic atrial tachycardia may well form the actual target for treatment. The automatic nervous system is never absent as a determinant of the onset of arrhythmia, and the vagal as well as the sympathetic action may predominate and explain why a treatment may or may not be effective in situations that are identical only in appearance. The electrophysiologic milieu formed by the atrial tissue probably accounts for the perpetuation of the process of atrial fibrillation or its self-termination, and drugs themselves may contribute to modify the milieu in a way that in the end may be favorable or not. Finally, the presence or the absence of heart disease and heart failure largely contributes to the state of the vagosympathetic balance, to the hemodynamic consequences of atrial fibrillation, and ultimately to the proper toxic effects of drugs. The overall consequence of these complex situations is that any precise therapeutic decision algorithm for atrial fibrillation is always simplistic and that any global evaluation of drug efficacy or toxicity is not really meaningful as long as the category of patients treated is not precisely determined: no drug appears better or worse than others, but simply more or less adapted to various situations.

Anti-Arrhythmia Agents↗
PubMed1995

Catecholaminergic polymorphic ventricular tachycardia in children. A 7-year follow-up of 21 patients.

BACKGROUND: Primary ventricular tachyarrhythmias are rarely seen in children. Among them, catecholaminergic polymorphic ventricular tachycardia has a poor spontaneous outcome. Its diagnosis is often delayed after the first symptoms, which is unacceptable because treatment with the appropriate beta-blocker prevents sudden death. METHODS AND RESULTS: We observed 21 children (mean +/- SD age, 9.9 +/- 4 years) at the time of the diagnosis who had no structural heart disease and a normal QT interval on routine ECG. They were referred for stress- or emotion-induced syncope related to ventricular polymorphic tachyarrhythmias. The arrhythmia, consisting of isolated polymorphic ventricular extrasystoles followed by salvoes of bidirectional and polymorphic tachycardia susceptible to degeneration into ventricular fibrillation, was reproducibly induced by any form of increasing adrenergic stimulation. There was a familial history of syncope or sudden death in 30% of our patients. On receiving therapy with the appropriate beta-blocker, the patients' symptoms and polymorphic tachyarrhythmias disappeared. During a mean follow-up period of 7 years, three syncopal events and two sudden deaths occurred, probably due to treatment interruption. CONCLUSIONS: The entity of adrenergic-dependent, potentially lethal tachyarrhythmia with no structural heart disease deserves to be individualized. It may form a variant of the congenital long QT syndrome in which the ECG marker is lacking; this primary ventricular arrhythmia must be looked for in a pediatric patient with stress- or emotion-induced syncope because only beta-blocking therapy can prevent sudden death and therefore must be given for the patient's lifetime.

Adrenergic beta-Antagonists↗
PubMed1995

Holter functions of the implantable cardioverter defibrillator: what is still missing?

The technology of the implantable cardioverter defibrillator (ICD) offers the opportunity to overcome the present limits of the invasive and noninvasive approaches of clinical electrophysiology. The invasive approach enables us to reproduce severe arrhythmias if they are inducible, but does not give information concerning the way they spontaneously arise. The noninvasive approach (Holter) gives this information, but it usually concerns only trivial arrhythmias with different therapeutic targets. One hopes in the future, by means of an important extension to ICD technology, which is not technically possible for the time being, to have access to pertinent information and to a better understanding of the circumstances leading to severe spontaneous arrhythmias, potentially lethal. For the moment, we only have the diagnostic certainty leading to the therapeutic intervention. It is based on an ECG and on the sequence of cardiac cycles preceding the rhythmic controlled accident. These data allow verification of but not explanation of the events. To have a chance to be understood and explained, these "events" must be replaced in the context of the "nonevents." Ideally, one should have all the gross information concerning the last 24 hours and subsequently analyze them. It is already a big step, thanks to the defibrillators the right to therapeutic error has been gained, a unique and fatal accident has been transformed into a repeatable event, and therefore, access is gained to the evolution of the responsible disease.

Defibrillators, Implantable↗
PubMed1995

[Value of the exercise test in the study of arrhythmia].

Exercise testing may be used to assess symptoms occurring on effort, to search for and evaluate arrhythmias or conduction defects, antiarrhythmic drugs, pacemakers or implantable cardioverter defibrillators. Interpretation of exercise testing is difficult because of the complexity of the factors in play. Exercise itself induces changes in myocardial metabolism and the autonomic nervous system, the nature and importance of which are influenced by the underlying cardiac disease and the presence of cardiac failure or myocardial ischaemia. This is particularly true when studying the behaviour of arrhythmias on effort, which depends on many parameters, in that they may appear or disappear during exercise, irrespective of their relationship to autonomic nervous system activation. The main problem lies in the interpretation of changes in the heart rate before the onset of an arrhythmia. The sinus rhythm is both a passive indicator of the vago-sympathetic equilibrium and one of the determining factor of the arrhythmia (relationship to the rate), but it is, itself, dependent on the presence of myocardial dysfunction, a source of arrhythmias, and its changes then become difficult to interpret. These reasons explain why exercise testing is certainly a valuable tool in assessing arrhythmias but the poor reproducibility, especially in the evaluation of ventricular arrhythmias, advises prudence in the interpretation of results.

Arrhythmias, Cardiac↗
PubMed1995

[Dynamics of ventricular repolarisation].

The clinical value of assessing the QT interval is obvious as it is a marker of ventricular depolarisation and repolarisation and it allows identification of clinical situations carrying a high risk of ventricular fibrillation and sudden death. Until the last few years, analysis of ventricular repolarisation was based on analysis of conventional surface electrocardiography. Technical difficulties explain the limits of our knowledge of the dynamics of ventricular repolarisation. This situation is beginning to change rapidly by computerised analysis of Holter monitoring, opening up a particularly complex and important field of research. The duration of the QT interval depends on different factors, especially changes in electrolyte balance, effects of certain drugs, and changes in heart rate and autonomic nervous system tone. The difficulty resides in selecting the pertinent data in order to study separately the effects of heart rate and those of the autonomic nervous system. The initial results show that this analysis provides important information for diagnosis and probably prognosis, on the status of the myocardium and the action of the autonomous nervous system. They require confirmation and validation on larger series of patients with different pathological conditions.

Action Potentials↗
PubMed1994

Antiarrhythmic drugs: how to evaluate them?

For two decades, the evaluation of antiarrhythmic drugs has essentially been based on the count of premature beats during Holter monitoring and the inducibility of tachyarrhythmias during electrophysiologic studies. These approaches are convenient to provide firmly established short-term evaluations of the effects of type I agents in relatively benign arrhythmias occurring in patients with good cardiac function. However, the situation is much more uncertain for long-term outcome in serious tachyarrhythmias occurring in severely diseased patients with an altered myocardium. In addition, indications for type I agents are not really adapted to beta-blockers and type III drugs, the effects of which are much more difficult to assess and depend at least in part on the target arrhythmia. There is an interest in evaluating drug efficacy in terms of responders and nonresponders and in understanding the reasons for a response rather than reliance on pure quantitative data, the meaning of which may be less relevant in the final analysis. We must also recognize the need to reconcile the multiple obstacles encountered when severely diseased patients must be managed efficaciously and safely in the long term with new drugs, the effects of which need objective assessment.

Adrenergic beta-Antagonists↗
PubMed1994

Short-coupled variant of torsade de pointes. A new electrocardiographic entity in the spectrum of idiopathic ventricular tachyarrhythmias.

BACKGROUND: Torsade de pointes is characterized not only by its particular ECG pattern but by its context of congenital or acquired long QT syndrome and the long coupling interval of the initial premature beat. METHODS AND RESULTS: We observed 14 patients aged 34.6 +/- 10 years (mean +/- SD) with no structural heart disease who presented with syncope related to a typical ECG aspect of torsade de pointes. However, there was no evidence of long QT syndrome, and the torsade had the unusual particularity of an extremely short coupling interval of the first beat or of the isolated premature beats (245 +/- 28 milliseconds). In 10 cases they deteriorated into ventricular fibrillation. Four patients had a familial history of sudden death. Only 2 patients had a tachyarrhythmia inducible by programmed stimulation. At Holter recordings the heart rate variability was globally and significantly depressed, the vagal limb of the autonomic nervous system being predominantly affected. During a mean follow-up of 7 years there were 5 deaths (4 sudden). Nine patients are alive, 3 with implanted defibrillators and 6 treated with verapamil alone. Unlike the other types of antiarrhythmic agents including beta-blockers and amiodarone, verapamil is in our experience the only drug apparently active on the arrhythmias; however, it does not prevent sudden death. CONCLUSIONS: The short-coupled variant of torsade de pointes should be identified because of their ECG pattern and the risk of sudden death in young adults with no structural heart disease.

Adult↗
PubMed1994

[Pericardial constriction caused by epicardial patches of automatic implantable defibrillators. Apropos of 3 cases].

The authors report three cases of pericardial constriction secondary to implantation of an automatic defibrillator. In one case, the pericardial constriction occurred 1 year after implantation and was associated with ascending infection of the patch electrodes from the stimulator; the patient died when the patch electrodes were removed, the infection having eroded the left ventricular wall. In the other two cases, signs of constriction appeared 2 years after implantation. In one of these patients, surgery showed a fibrous pericardial reaction deforming the patch electrodes with a favourable outcome when the electrodes were removed. The other patient refused surgery. In the three cases, the diagnosis was confirmed by right heart catheterisation and ventriculography which showed signs of adiastole and severe deformation of the ventricular contours. Pericardial constriction due to patch electrodes is a potentially serious complication of implantable automatic defibrillators, the prevalence of which may be underestimated. The use of endocavitary or extra-pericardial electrodes should avoid this complication.

Defibrillators, Implantable↗
PubMed1994

[Catheter ablation of atrioventricular nodal reentrant tachycardia].

Electrophysiological data of atrioventricular nodal reentrant tachycardia recensed over the last 40 years in the animal and in man has not resolved the question as to the exact site of the reentry circuit: an exclusively intranodal pathway or a pathway involving part of the atrium? The remarkable efficacy of modern radical therapy of this arrhythmia with preservation of atrioventricular conduction reinforces the concept of reentry involving not only the atrioventricular node but also the juxta nodal atrium and the superior and inferior atrionodal connections. Radical treatment was initially surgical and then by catheter ablation. The technique of specific ablation of the rapid anterior pathway was the first to be described. Its limitation is the relatively high risk (about 10%) of complete atrioventricular block. Very quickly, radiofrequency ablation of the slow posterior pathway became the method of reference. Most patients do not have retrograde conduction in the slow pathway. The pathway is located in sinus rhythm by recording its specific potentials: either the rapid potential described by Jackman et al or the fragmented potential described by Haïssaguerre and Warin. The former is recorded from the posterior septal position anterior to the orifice of the coronary sinus; the second is recorded at the same level but slightly above in the mid septal position. Ablation of the slow pathway can be performed on these purely anatomical criteria. Using these approaches, an immediate success rate of over 90% may be obtained. The recurrence rate is 0 to 5%; that of complete atrioventricular block ranges from 0 to 4%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[Automatic implantable defibrillators: long-term results].

The automatic implantable defibrillator is an essential component of the preventive management of sudden death of patients with malignant ventricular arrhythmias. Though its efficacy in this indication is not contested, the data concerning its influence on global cardiac mortality is more controversial. The elements of this controversy are reviewed. Several prognostic factors are implicated, the principal of which being the patient's haemodynamic status as assessed by objective evaluation of left ventricular function. Prospective randomised studies comparing medical therapy with the automatic implantable defibrillator are under way and should provide a better understanding of its indications in the future.

Arrhythmias, Cardiac↗
PubMed1994

[Right accessory pathways with slow and decremential anterograde conduction. Electrophysiological changes during ablation of the proximal atrial poles].

Right sided accessory pathways with slow and decremential anterograde conduction differ from the anatomical substrates of the nodo-ventricular connections described by Mahaim. The connection may also be atrio-ventricular or atrio-fascicular. The authors report a series of 6 patients (2 men, average age 31 +/- 9 years) with antidromic reciprocating tachycardia implicating accessory pathways with decremential conduction (wide QRS complexes with left bundle branch block) the radiofrequency ablation of which was centered on the proximal atrial pole. The increment of pre-excitation was 75 +/- 18 ms. No nodo-ventricular or nodo-fascicular connections were observed. One patient had an atrio-ventricular connection, the mapping and ablation (5 applications) of which were performed on the annulus, as if it were a bundle of Kent. Five patients had a nodo-fascicular connection which was masked during sinus rhythm. The localisation of the proximal atrial insertion on the tricuspid annulus was initially estimated by studying the superior junction of the circuit and by endocavitary stimulation, and then by recording the M potential (activation of the accessory pathway). This was recorded in 4 patients, either at a specific point on the annulus (lateral or postero-lateral) which was the target of ablation (3 patients, 5 +/- 3 applications) or over a wider region (2 cm) at which ablation failed (1 patient: 13 applications). The site of the increment was determined in 2 patients and was proximal to the M potential. The M potential could not be recorded on the annulus in one patient. In 2 patients, the M potential was also recorded along the side of the pathway on the antero-lateral wall of the right ventricle of the tricuspid valve at its distal pole. In 2 patients, ablation was centered on the distal pole in second intention, near to the terminal part of the right bundle where it was localised in one of the two (18 applications). Finally, ablation was obtained in 5 out of 6 patients. They remain asymptomatic after 12 +/- 7 months follow-up. These cases show that accessory pathways with slow decremential conduction usually behave like a complete conduction pathway with an accessory laterally situated atrioventricular node on the tricuspid, an accessory bundle and a distal insertion which are all accessible to ablation.

Adolescent↗
PubMed1994

[Value of searching ventricular late potentials in patients recovering from ventricular fibrillation].

The prognostic value of ventricular late potentials (VLP) was studied in 38 survivors of ventricular fibrillation (VF) resuscitated after cardiac arrest. Thirty-seven patients had coronary artery disease, 24 within one month of myocardial infarction, and one patient had valvular heart disease. There were 7 deaths within 2 years, including 5 sudden deaths, the average follow-up in the remaining patients being 46 +/- 30 months. Bad prognostic factors included low left ventricular ejection fraction, anterior myocardial infarction, VF occurring after the first 24 hours of myocardial infarction and the presence of VLP. The 2 year mortality rate was 35% in patients with VLP compared with only 5% when they were absent (p < 0.05). The subgroup with the highest risk of death was that of anterior myocardial infarcts with VLP (45% 2 year mortality). The clinical circumstances surrounding VF were important; patients with clinical and electrical signs of ischaemia at the time of VF tended to have a better prognosis than the others, especially in the absence of VLP: in this subgroup of 12 "ischaemic" VFs without VLP the mortality at 2 years was nil, whereas the other 26 patients had a 27% death rate (0.05 < p < 0.10). Programmed ventricular stimulation was only carried out in 14 cases: it showed that the long-term mortality was very high (60%) in patients with VLP and inducible ventricular tachycardia (VT). Therefore, the implantation of an automatic defibrillator device would seem to be justified in patients resuscitated from VF who have both VLP and inducible VT, but of no value in cases of "ischaemic" VF without VLP.

Action Potentials↗
PubMed1994

[Long term course of catecholaminergic polymorphic ventricular tachycardia in children. Apropos of 20 cases with an 8 year-follow-up].

BACKGROUND: Primary ventricular arrhythmias are rarely seen in children. Some of them have a poor prognosis; they should be diagnosed because adequate treatment can prevent sudden death. POPULATION AND METHODS: Twenty children (11 male, nine female), aged 3 to 16 years (mean: 7.7 +/- 4), with apparently normal hearts and normal QTc intervals were referred for stress or emotion-induced syncope. Primary ventricular arrhythmia, consisting of isolated polymorphic ventricular extrasystoles followed by salvos eventually degenerating into ventricular fibrillation, was reproducibly induced by physical exertion. The syncopal events and "torsades de pointe" disappeared with beta-blocking therapy. A total of four syncopal events and two sudden deaths occurred during a mean follow-up of 8 years, probably due to discontinuation of treatment. DISCUSSION: Fifty-four-cases of stress-induced severe polymorphous ventricular arrhythmia have been reported in the literature. There were four sudden deaths in 37 patients on beta-blocking therapy, and ten sudden deaths in 21 untreated patients. CONCLUSION: Clinically close to the congenital long QT syndrome, this primary ventricular arrhythmia must be looked for in cases of stress or emotion-induced syncope. The diagnosis relies on Holter monitoring and a stress test. Life-long beta blocker therapy is required.

Adolescent↗
PubMed1994

[Indications for implantable automatic defibrillators].

The automatic implantable defibrillator is an effective therapeutic tool for palliative treatment of severe ventricular arrhythmias. There is a significant reduction in sudden death in implanted patients. However, reliable data on the long term global mortality is not yet available. The indications are difficult to define apart from special cases. A large number of factors has to be taken into consideration: the clinical presentation of the arrhythmia, and the different medical and non-medical therapeutic options. At present, it is not possible to arrive at a consensus on the indications of automatic implantable defibrillators. Therefore, it is illusory to construct decisional algorithms. The authors suggest therapeutic orientations rather than strict clinical indications, based on recommendations published by the working groups on cardiac arrhythmias and pacing of the European Society of Cardiology and on their own personal experience.

Death, Sudden, Cardiac↗
PubMed1993

[Ventricular arrhythmia and halofantrine intake. Probable deleterious effect. Apropos of 3 cases].

Incidence and malignant forms of imported Plasmodium falciparum malaria are increasing, and chemoprevention is more and more replaced by stand-by treatment and radical cure in preventing access on return from malaria areas. Halofantrine is recommended for this radical cure: it's an habitually well-tolerated amino-alcohol with very few side-effects. We report three cases of long QT-interval due to halofantine: three different young women coming back from Africa took halofantrine (500 mg (2 tablets) six hourly for three doses on the first and the seventh day) and all presented with syncopal episodes. Serum electrolyte concentrations and echocardiograms were normal. In one case only, a diagnosis of Plasmodium falciparum malaria was made, without severe manifestations, and in the two other cases, treatment was a radical cure. In two cases, several bursts of torsades de pointes ventricular tachycardia due to halofantrine were proven and electrophysiological cardiac tests concluded that they had a congenital long QT-interval/Romano-Ward syndrome). So far halofantrine cardiac toxicity was unknown with single dose of 24 mg/kg/d. This phenomenon can be very severe in case of preexisting cardiopathy. In spite of the rarity on the congenital Romano-Ward syndrome, systematic electrocardiogram is necessary before giving halofantrine.

Adult↗