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Biomedical subjects

C Sebag

Publications and source records attributed to C Sebag.

At least 37 records · Page 2Linked to original sources

Triple antegrade nodal pathway in a patient with supraventricular paroxysmal tachycardia.

A 69-year-old patient is described in whom programmed atrial extrastimulus testing revealed dual discontinuity of atrioventricular nodal conduction suggesting a triple antegrade nodal pathway. In this patient, programmed right ventricular pacing initiated two types of tachycardia due to intranodal reciprocating rhythms. In both cases, antegrade conduction occurred via the slow nodal pathway, and retrograde conduction by the fast and intermediate pathways, respectively. During ventricular extrastimulus testing, a single echo beat was elicited via a third circuit: the intermediate nodal pathway in a retrograde direction, and the fast pathway in an antegrade direction.

Aged

[Infranodal chronic auriculo-ventricular block in subjects under 50 years of age].

The aetiology and evolution of chronic infranodal atrioventricular block (AVB) of young patients are not well known: are they the first sign of subclinical myocardial disease which can only be diagnosed by long term follow-up or do they represent isolated degenerative disease of the conduction tissue (Lenegre's disease)? Eighteen patients (15 men, 3 women) aged 25 to 49 years (average 41.5 years) were followed up for periods of 2 to 20 years (average 7.33 years) after pacemaker implantation for syncopal AVB. Follow-up was focused on the evolution of the conduction defects and the cardiovascular status. The patients were divided into two groups at the initial assessment: Group I: 15 patients with documented AVB; Group II: 3 patients in whom all basal recordings showed sinus rhythm (SR). Apart from one patient with an early non-ischaemic dilated cardiomyopathy, there was no previous cardiovascular disease. There was no history of ischaemic heart disease, drug effects, infection or inflammation in favour of an acute AVB. Three patients had permanent AVB, either 2nd degree with bundle branch block (N = 2) or 3rd degree block (N = 1). The other 15 patients were in sinus rhythm with bundle branch block: left bundle branch block (LBBB) in 5 cases, right bundle branch block (RBBB) in 3 cases; RBBB with left anterior hemiblock in 5 cases, RBBB and left posterior hemiblock in 2 cases. Paroxysmal AVB was recorded in 12 of these 15 patients on at least one occasion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adams-Stokes Syndrome

Physiopathology of ventricular tachyarrhythmias.

Ventricular arrhythmias may be the result of three mechanisms: abnormal automaticity, triggered activity complicating early or late after-depolarizations, and reentry by circular pathway or by reflection. These three fundamental mechanisms have been observed in the intact heart in experimental models of myocardial ischemia and digitalis intoxication. In man, the arguments in favor of a given mechanism are indirect and may be determined by their response to stimulation. It may be possible to state the following conclusions: (1) reentry is at the origin of ventricular fibrillation, certain ventricular tachycardias of bundle branch reentry and probably most chronic sustained ventricular tachycardias that are easily inducible; (2) the mechanism of certain other ventricular arrhythmias sustained remains unknown; (3) even when arrhythmias are associated with reentry, the triggering extrasystole can arise from a focal origin.

Action Potentials

[Reciprocating tachycardia and anterograde conduction by a nodoventricular pathway].

Two patients were investigated for paroxysmal regular tachycardia with left bundle branch block centrifugation. A right-sided nodo-ventricular accessory pathway was demonstrated in both cases at electrophysiological investigation with His bundle recording and atrial and ventricular programd pacing techniques. However, the function of this pathway was different in the two cases. In the first case, there were no signs of an accessory pathway on the surface ECG in sinus rhythm but it could be unmasked by simple right atrial pacing at the same rhythm (widening of the QRS and shortening of HV from 40 to 25 ms). The tachycardias could be only initiated by ventricular extrastimulus. They showed major pre-excitation with left sided delay and a 1/1 atrio-ventricular response. There was no His potential before the ventriculogramme which retained the same configuration throughout the attack. The investigations also suggested the presence of a dual nodal pathway with the accessory pathway connected to the slow pathway. In the second case, the presence of an accessory pathway could be suspected from the appearance of the QRS complex in sinus rhythms. Tachycardia was initiated by an atrial extrastimulus with initially a first complex showing slightly more marked pre-excitation and a distinct His potential before the QRS but with a shorter HV interval than in sinus rhythm. Then the reciprocating tachycardia had appearances of major pre-excitation, left-sided delay and a 1/1 atrio-ventricular response. However, in contrast to the first case, all ventricular complexes were preceded by a His potential and the degree of pre-excitation was variable with a HV interval ranging from 0 to 15 ms. These two cases merit attention because of: --their points in common: nodal duality and an accessory pathway which was not atrio-ventricular (decremental conduction) but nodo-right ventricular, conducting well in the anterograde direction but more or less masked in sinus rhythm; the presence of the accessory pathway was clearly visible during reciprocating tachycardia; --the differences: in the first case the nodo-ventricular pathway formed part of the circuit of the reciprocating tachycardia which was antidromic: descending limb, the slow nodal pathway and then the accessory nodo-ventricular pathway; ascending limb, the His bundle and then the rapid nodal pathway. In the second case, the reciprocating tachycardia was entirely intranodal, the accessory pathway not being involved in the circuit but connected to it in parallel with the normal Hisian pathway.

Adult

[Late recurrence of atrioventricular block in acute anterior and/or septal myocardial infarcts. Discussion of the implantation of a permanent pacemaker. Apropos of 2 cases].

Does the high incidence of post hospital sudden death in patients surviving acute anterior and or septal infarction complicated by transient intraventricular or atrioventricular block have any relation to a late recurrence of the conduction defect and is prophylactic permanent pacing justified from the outset? These questions remain controversial and, to illustrate the problem, two cases of infarction, one an extensive anterior infarct and the other a deep septal infarct are reported. Both developed late recurrences of atrioventricular block without recurrent myocardial infarction requiring permanent pacing. In practice, the usual poor prognosis of these infarcts make comparative survival studies very difficult. The authors suggest permanent pacing for a very restricted group of patients surviving acute anterior and or septal infarction complicated by transient complete atrioventricular block.

Electrocardiography

Double Wenckebach phenomenon in atrioventricular node and His bundle. Electrophysiological demonstration in a case of atrial flutter.

In a case of atrial flutter with a 9:2 atrioventricular response, the only possible way to explain the conduction pattern was 3:1 block in the atrioventicular node (which is 3:2 Wenckebach sequence in the N zone and a 2:1 block at the junction of the node with the bundle of His) plus 3:2 Wenckebach sequence distal to the H deflection. The recording of the His bundle deflection confirmed this analysis.

Aged

[Fragmenting of the His potential after atrial stimulation].

Splitting of the His potential (H) in sinus rhythm is generally considered to be pathological but its significance during programmed atrial stimulation is not clear. This phenomenon was observed in 10 out of 53 patients aged between 19 and 45 years (average 31.8 years) not suspected of having paroxysmal intranodal block (asymptomatic, sinus rhythm without bundle branch block). Under basal conditions the H and the HV interval (35 to 50 ms; average 41 ms) were normal. Split H was observed with pacing periods of 680 to 885 ms (average 754 ms) and H1 H2 intervals of 325 to 450 ms (average 395 ms). The maximal interval between the split potentials ranged from 80 to 130 ms (average 100 ms). Splitting disappeared at the shortest periods when variable pacing cycles were used. The response to regular atrial pacing up to 150 bpm (10 cases) and to Ajmaline (1 mg/Kg) (4 cases) was normal. All patients but one were followed up to 10 to 41 months (average 21.4 months); the clinical and ECG parameters remained stable during this period. The presence of fragmented potentials between the atrial and ventricular complexes during programmed atrial stimulation may pose a difficult diagnosis problem, especially with respect to delayed atrial potentials. Splitting of the H is generally attributed to dispersion of the depolarisation wave front in the His bundle due to the persistence of the functional refractory state. Other mechanisms, especially longitudinal dissociation of the His bundle, may be discussed. From a prognostic point of view, this finding does not seem to carry more serious implications than simple lengthening of the HV interval or intranodal conduction delay, phenomena usually considered to be non-pathological.

Adolescent

[Double Wenckebach phenomenon at nodal and His levels. Electrophysiological demonstration in slow and irregular flutter].

The authors describe the analysis of a case of atrial flutter with a slow ventricular response, the block being 9:2 with a first RR interval measuring between 3 and 4 PP intervals and a second RR interval between 5 and 6 PP intervals, the second of the 2 RR intervals being exactly 9 PP intervals. The only possible explanation of this sequence is firstly a 3:1 intranodal block (Wenckebach 3:2 in the central zone N of the node and 2:1 block at the nodo-hisian junction) followed by a 3:2 infra- or intra-hisian Wenckebach phenomenon. The His bundle recordings during flutter confirmed this hypothesis with the recording of a 3:2 block after the H potential. When sinus rhythm was restored at atrial level, the intrahisian conduction defect persisted (2:1 or 3:2 Wenckebach block).

Aged

[Atrioventricular block disclosing an isolated congenital aneurysm of the sinus of Valsalva, extending into the septum and not ruptured].

A case of a congenital aneurysm of the right anterior sinus of Valsalva (ASV) extending into the septum is reported. The patient, a 20 year old male Central-African, presented with syncopal complete atrioventricular block (AVB) or recent onset. There were no clinical or radiological signs of associated cardiac disease. After implantation of a pacemaker, the diagnosis of an ASV extending into the septum was suggested on routine M mode echocardiography. It was confirmed by two-dimensional echocardiography and aortography. These investigations provided data on its size, its relationship to the cardiac chambers and also showed absence of rupture. The neck of the aneurysm was closed by an endo-aortic approach. There was moderate postoperative aortic regurgitation. This case underlines the value of systematic echocardiography in young patients with AVB of recent onset and obscure origin.

Adult

[Bitachycardia].

One or several episodes of bitachycardia (a simultaneous ventricular tachycardia and atrial tachycardia or fibrillation) were observed in 13 patients. An oesophageal or right atrial endocavitary recording is usually necessary to show the atrioventricular dissociation: even then the diagnosis may be difficult in cases of isorhythmic dissociation or when the ventricular tachycardia is irregular. In 5 cases the double tachycardia appeared to be coincidental. In 7 patients the ventricular tachycardia seemed to be dependant on the atrial tachycardia and could be initiated by a simple spontaneous atrial extrasystole in 3 cases. In one patient the ventricular tachycardia, after a phase of retrograde conduction to the atria, initiated the atrial arrhythmia. The therapeutic indications depend in part on the eventual relationship between the two arrhythmias.

Aged

[Acute myocarditis simulating myocardial infarct with regressive heart failure].

Two patients were hospitalised with severe heart failure and hypotension thought initially to be due to acute anterior myocardial infarction because of very suggestive electrocardiographic appearances. Heart failure rapidly regressed in both cases. The young age of these two patients, the pyrexia, rapid and total regression of the ECG appearances, the absence of atheromatous lesions at coronary angiography and clinical cure with a follow-up of 10 years in one of the cases, were factors in favour of the diagnosis of acute myocarditis.

Adult