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Biomedical subjects

G Lascault

Publications and source records attributed to G Lascault.

At least 37 records · Page 2Linked to original sources
PubMed1994

[Ablative methods, therapeutic alternative to medical treatment for junctional tachycardia].

The clinical syndrome corresponding to junctional tachycardia is generally known as Bouveret's disease, but actually corresponds to two quite separate entities: 1) tachycardia related to a secondary atrioventricular pathway or Kent bundle; 2) intranodal tachycardia arising in the atrio-ventricular node. Until recently, anti-arrhythmics were used to treat most of the cases of accessory pathways. If this was unsuccessful or if the anti-arrhythmics induced adverse effects and in life-threatening cases affecting Kent bundles, surgical section was sometimes proposed, carrying a non-negligible risk of morbidity and mortality. Intranodal arrhythmia is not a serious, but may call for prophylactic antiarrhythmic treatment if it becomes too frequent and disabling. Before the advent of ablative treatment, there was no satisfactory alternative to antiarrhythmic treatment. Ablation of the accessory pathways or selection ablation of the slow pathway of the atrio-ventricular node (sometimes of the rapid pathway) is not achieved by applying a high-frequency current (radiofrequency), which has virtually replaced fulguration (destruction using a modified electrical current). In both types of tachycardia, a cure is obtained in 90% of cases with a low incidence of complications and virtually no risk of mortality, which contrasts favorably with long-term antiarrhythmic treatment (or surgical section of Kent bundles), which justifies the large-scale development of radiofrequency ablation.

Catheter Ablation↗
PubMed1994

[Repolarization and intraventricular conduction disorders in arrhythmogenic right ventricular dysplasia].

Right ventricular dysplasia may lead to sudden cardiac death an adolescent or adult with little or no symptoms. Identification of this condition in the high-risk population appears to be an objective to be attained in the near future. Thorough ECG analysis seems to be a non-invasive and inexpensive technique which could be used as a first approach for screening of the disorder. In a series of 50 cases of arrhythmogenic right ventricular dysplasia compared with a control group, the diagnosis of ARVD could be determined by ECG with 84% sensitivity and 100% specificity if QRS duration in leads V1, V2 or V3 was longer than 110 ms, T wave was negative in V2 or if T wave was negative in V1, but in this latter case only provided incomplete right bundle branch block was present.

Adolescent↗
PubMed1993

[Holter and sudden death: value in a case of arrhythmogenic right ventricular dysplasia].

The authors report the first case of arrhythmogenic right ventricular dysplasia presenting with a sudden death due to primary ventricular fibrillation (ventricular fibrillation not preceded by ventricular tachycardia) recorded by the Holter method. The patient was a 56 year old man whose only complaint was near syncopal case is the fact that it is the first documented case of ventricular fibrillation revealing arrhythmogenic right ventricular dysplasia, the diagnosis of which was made at autopsy. In addition, the Holter recording showed the factors which triggered the arrhythmia: the "trigger" of 4 monomorphic ventricular extrasystoles during the minute preceding the ventricular fibrillation; the arrhythmogenic substrate giving rise to late ventricular potentials and, finally, the analysis of the R-R intervals suggesting a role of the sympathetic and parasympathetic nervous systems. Holter recordings could help identify subjects at high risk of severe ventricular arrhythmias.

Adipose Tissue↗
PubMed1993

[Sustained monomorphic ventricular tachycardia in non ischemic heart diseases].

Sustained ventricular tachycardia in the absence of coronary artery disease is mainly observed in diffuse left ventricular cardiomyopathy especially dilated but sometimes hypertrophic, and in right sided cardiomyopathies such as ventricular dysplasia, more difficult to diagnose. More rarely, other localised abnormalities, mitral valve prolapse, cardiac tumour and idiopathic aneurysm, may give rise to this arrhythmia. Irrespective of the case, sustained ventricular tachycardia carries a poor prognosis during the most advanced stages of a myocardial disease. The therapeutic strategy remains the same as that of other cases of sustained ventricular tachycardia, drug therapy generally orientated by the results of programmed ventricular stimulation with the exception of Class I antiarrhythmics when the ejection fraction is under 30%, and non-pharmacological methods when drug therapy fails.

Anti-Arrhythmia Agents↗
PubMed1993

[Arrhythmogenic right ventricular dysplasia. A new clinical entity].

Arrhythmogenic right ventricular dysplasia has been identified in 1977. It affects the right ventricle and its etiology is unknown. It has been recently included in the group of cardiomyopathies since it affects mainly the right ventricular muscle. It is found in young adults, frequently sportsmen who have a nearly normal cardiac physical examination. Ventricular arrhythmias could lead to palpitations, syncopes or even sudden death. This accident could be the first presenting sign of the disease. Two physiopathogenic mechanisms have been considered: heredo-familial origin or the result of a burned out myocarditis which could be the result of an abnormal immunological response. Its treatment mainly involves antiarrhythmic drugs. In the resistant cases ablative techniques, implantable defibrillator or surgery and even cardiac transplantation could be considered. Correctly treated, ARVD has a good prognosis. More extensive studies are necessary both on the clinical as well as the basic science standpoints.

Adolescent↗
PubMed1992

Comparison of DDD and 'VVI-R like' pacing during moderate exercise: echo-Doppler study.

The non-invasive haemodynamic comparisons of DDD and 'VVI-R like' pacing at rest and during moderate exercise by echo Doppler are reported. Twelve patients (six males, six females, mean age 48.2 years) with a dual chamber pacemaker were submitted to a series of two exercise tests in a semi-supine position, the first test in DDD mode and the second test in a 'VVI-R like' mode: VVT mode, during which pacing rate was externally increased by chest wall stimulation. During the second test, the workload profile was matched to that of the first test (66 watts and same exercise stages) and ventricular pacing rate was incremented via chest wall stimulation and reproduced exactly the heart rate profile of the first test in DDD mode. The heart rate averaged 81 beats.min-1 at rest and reached 116 beats.min-1 during exercise. At rest and throughout exercise tests, aortic blood flow velocity spectra were continuously recorded on video tape and analysed with the calculation program of the echocardiograph. At rest, ejection time, flow velocity integral, flow acceleration and stroke volume differed between DDD and 'VVI-R like' mode while other parameters did not. During exercise all but two parameters differed. DDD mode especially was associated with a larger stroke volume (81.9 vs 70.9 ml; P less than 0.001) and cardiac output (9.24 vs 8.011.min-1; P less than 0.001) than VVI-R mode.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Right ventricular dysplasia].

Arrhythmogenic right ventricular dysplasia is responsible for ventricular tachycardia affecting an apparently healthy heart. It can sometimes lead to sudden death, which may be the presenting symptomatology of the disease. It results from fibro-adipose infiltration of the free wall of the right ventricle, and sometimes of the septum, possibly secondary to myocarditis. The prognosis depends upon the quality of the left ventricle. If it is healthy, the only risk is that of arrhythmia. Treatment using anti-arrhythmic drugs is most often effective and, with proper management, the prognosis is good and the risk of sudden death eliminated. If the left ventricle is abnormal, there is the risk that dysplasia associated with arrhythmia will progress to right then congestive cardiac failure in the context of a dilated idiopathic cardiomyopathy with ventricular tachycardias originating on the right side. Arrhythmogenic right ventricular dysplasia is a notable cause of sudden death in athletes. Routine screening of such individuals is justified, as is that of those with high risk occupations (locomotive and vehicle drivers, etc.).

Adolescent↗
PubMed1992

[VVI mode cardiac pacing: cause or risk factor of cerebral embolism?].

Epidemiological studies suggest that VVI pacing is associated with a higher risk of embolic complications than atrial or dual chamber pacing. However, no studies have been performed on pacemaker patients admitted to a neurological department with a cerebral embolism. The authors report the cases of 8 patients (6 men and 2 women) with an average age of 74 years and having the following characteristics: 1) a cerebral embolism, 2) a permanent cardiac pacemaker (7 VVI and 1 DDD mode). The average delay between implantation of the pacemaker and the neurological complication was 31 months. Cardiological investigations at the time of admission showed: a clinically evident cause of cardiac embolism in 3 cases (2 with VVI and 1 with DDD pacing); paroxysmal or permanent atrial fibrillation in 4 cases with VVI pacing at the time of the embolic event (in only one case at the time of implantation); various echocardiographic abnormalities in 6 of the 7 patients who underwent this examination, mainly left atrial dilatation (6/7), septal wall motion abnormalities in all related to ventricular pacing and unexplained left ventricular dilatation in 2 patients with VVI pacemakers. These results suggest that although the etiology of cerebral embolism was probably multifactorial in some patients, VVI packing probably a predisposing role, though not the only cause, and could be considered to be an embolic risk factor as suggested by previous epidemiological studies. These preliminary retrospective data should be interpreted cautiously taking into account the small population size. Prospective studies on pacemaker patients with cerebral embolism are required.

Aged↗
PubMed1992

[Ventricular tachycardia in a patient with rate-responsive cardiac pacemaker].

The authors report a case of syncopal ventricular tachycardia in a patient with a respiratory-dependent rate responsive pacemaker, followed-up for valvular heart disease with severe left ventricular dysfunction and sustained atrial and ventricular arrhythmias. The introduction of low dose betablocker therapy with reinforcement of the treatment of cardiac failure controlled the ventricular arrhythmia, after suppression of the data responsive function had been shown to be ineffective. The authors discuss the role of the rate responsive function in the triggering of the ventricular tachycardias.

Aged↗
PubMed1992

[Ventricular anti-arrhythmic treatments during postinfarction].

Antiarrhythmic agents may be prescribed in the post-infarction period either as systematic therapy to prevent sudden death or as prophylactic treatment against recurrences of documented life-threatening arrhythmias. Systematic therapy or even the treatment of symptomatic ventricular extrasystoles by Class IC anti-arrhythmics is associated with an increased risk, especially in patients with a low risk of sudden death at the outset. Betablockers are effective on symptoms: they are not always effective on the arrhythmia but at least they do not aggravate the mortality of these patients. However, for high risk patients with post-infarction left ventricular dysfunction, betablockers are the only drugs which have a proven efficacy: they should therefore be prescribed, especially those whose efficacy has been demonstrated, at the same dosages as those used in clinical trials. Preventive treatment of sustained ventricular tachycardia should be chosen with respect to the patient's hemodynamic status. When the ejection fraction is under 40%, amiodarone and betablockers are the drugs of first intention, with controls of their efficacy by the inability to induce or the slowing of the tachycardia rhythm during endocavitary electrophysiological studies.

Adrenergic beta-Antagonists↗
PubMed1992

[Environment and permanent cardiac pacing].

The increasing technological sophistication of cardiac pacemakers make them potentially more vulnerable to electrical interference. The clinical consequence are of variable importance depending on the type of pacemaker and the nature of the interference. Electrical interference is present in the domestic, industrial and, above all, the medical environment. Apart from controlling the sources of emission, prevention requires standards of protection for the casing and electronic circuitry. Patient education remains primordial.

Electric Countershock↗
PubMed1991

[Search for emboligenic heart disease in case of ischemic cerebral accidents].

The demonstration of a cardiac source of systemic embolism in patients who have suffered a cerebral ischemic event may have important therapeutic implications. This explains the large demand for echocardiography and Holter monitoring in these patients. The frequency of cerebral embolism of cardiac origin, the simplification of the diagnostic approach by non-invasive investigations and the precision of ultrasound techniques explains the tendency towards the indiscriminate generalisation of this attitude. However, the large number of potential patients for investigation, the limited facilities of investigation and the incertitude over the responsibility of certain cardiac abnormalities with respect to the context and age, are arguments in favour of a more selective investigative approach. The keystone of diagnosis is careful history taking and clinical examination with interpretation of the ECG and chest X-ray. Three clinical situations may then be identified: 1) A cardiac abnormality known to be highly embolic is diagnosed from the outset (e.g. mitral stenosis, valve prosthesis, endocarditis, myocardial infarction). The diagnostic work-up is no longer etiological: echocardiography may show intracardiac thrombi or a valvular vegetation, reinforcing the causal relationship, but the complementary investigations are mainly useful for evaluation the cardiac disease and for deciding on curative or preventive therapy. 2) A cardiac abnormality is diagnosed but its responsibility is doubtful due to its high prevalence and low embolic potential. This is the case of patients with mitral valve prolapse, mitral annular calcification, calcific aortic stenosis and VVI pacing. Complementary investigations are not discriminative for the etiological diagnosis of the cerebral embolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1991

[Doppler echocardiography of the effect of atrioventricular delay on transmitral flow in dual chamber pacing. Role of associated cardiopathy].

Doppler echocardiography was used to analyse transmitral blood flow in 23 patients undergoing DDD pacing under basal conditions at a pacing rate of 70/min. Changes in the atrioventricular delay led to changes in Doppler parameters corresponding to the different phases of ventricular filing. When the atrioventricular interval was increased, the maximum velocity, the velocity time integral and the duration of the E wave decreased and the maximum velocity, the velocity time integral and duration of the A wave increased. The atrial contribution to left ventricular filing increased by 15 to 46% (p less than 0.001). The changes of the Doppler parameters with respect to the duration of the atrioventricular interval varied according to the patient group studied. Patients without ventricular dilatation with or without hypertrophy had greater maximum velocities and velocity time integrals of the A wave than patients with left ventricular dilatation. However, for the same changes in atrioventricular delay, the A wave and atrial contribution to left ventricular filing were more variable in patients without left ventricular dilatation than those with left ventricular dilatation confirming the greater sensitivity of patients without left ventricular dilatation to the setting of the atrioventricular interval. These results confirm the great variability of transmitral flow with changes in atrioventricular delay. They illustrate the need for appropriate programming of the atrioventricular delay especially in patients in whom the mitral flow is most sensitive to this adjustment.

Aged↗