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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
PubMed1989

Reduced sensitivity of human platelets to PAF-acether following ticlopidine intake.

We investigated in 9 patients the effect of a 7-day treatment by Ticlopidine (250 mg b.i.d.) on washed platelets activation by PAF-acether in comparison with adenosine 5'-diphosphate (ADP) and arachidonic acid (AA). Aggregations induced by ADP were totally suppressed upon drug administration. AA-induced aggregations were partly but significantly inhibited (p less than 0.05). Responses of platelets to PAF-acether before treatment differed from patient to patient. A paired Student's test and a two-way analysis of variance showed a significant inhibitory effect of Ticlopidine treatment on PAF-acether-induced aggregation. The inhibitory effect of Ticlopidine or its metabolite(s) was evidenced after platelet washing procedure, suggesting a persistent effect of this drug on platelet after administration of the drug has been stopped.

Adenosine Diphosphate↗
PubMed1988

Effect of diltiazem on myocardial infarct size estimated by enzyme release, serial thallium-201 single-photon emission computed tomography and radionuclide angiography.

Diltiazem is a calcium antagonist with demonstrated experimental cardioprotective effects. Its effects on myocardial infarct size were studied in 34 patients admitted within 6 hours after the first symptoms of acute myocardial infarction. These patients were randomized, double-blind to placebo or diltiazem (10-mg intravenous bolus followed by 15 mg/hr intravenous infusion during 72 hours, followed by 4 X 60 mg during 21 days). Myocardial infarct size was assessed by plasma creatine kinase and creatine kinase-MB indexes, perfusion defect scores using single-photon emission computed tomography with thallium-201 and left ventricular ejection fraction measured by radionuclide angiography. Tomographic and angiographic scanning was performed serially before randomization, after 48 hours and 21 days later. Groups were comparable in terms of age, sex, inclusion time and baseline infarct location and size. Results showed no difference in creatine kinase and creatine kinase-MB data between controls and treated patients, a significant decrease in the perfusion defect scores in the diltiazem group (+0.1 +/- 3.0 placebo vs -2.2 +/- 1.9 diltiazem, p less than 0.02) and a better ejection fraction recovery in the diltiazem group (-4.2 +/- 7.4 placebo vs +7.7 +/- 11.2 diltiazem, p less than 0.05). Myocardial infarct size estimates from perfusion defect scores and enzyme data were closely correlated. These preliminary results suggest that diltiazem may reduce ischemic injury in acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Enzyme Tests↗
PubMed1988

Mode of action of antiarrhythmic drugs and the implicated arrhythmogenic risk.

The mode of antiarrhythmic action of drugs usually cannot be extrapolated from their electrophysiologic properties despite extensive in vitro and in vivo assessment: in most cases, the mechanism of arrhythmias remains uncertain and cannot be established by clinical evaluation including electrophysiologic study; in specific cases where the arrhythmia substrate is fully described, the exact origin of antiarrhythmic action is unknown, especially when chronic preventive treatment is considered where triggering events are probably important. Nevertheless, the profound electrophysiologic changes resulting from antiarrhythmic drugs alter several delicate balances, at the cellular level (repolarizing and depolarizing currents) and at the tissue level (refractory period/conduction time ratio). Some afterdepolarizations can be elicited, especially when repolarization is delayed by long cycle lengths and K+ current inhibition; reentry is enhanced when conduction impairment occurs without similar change in refractoriness. Proarrhythmic effects of drugs seem to relate to these alterations and caution should be exerted when ECG shows drug-induced QT or QRS prolongations.

Animals↗
PubMed1987

Phase mapping of radionuclide gated biventriculograms in patients with sustained ventricular tachycardia or Wolff-Parkinson-White syndrome.

Accuracy of Fourier phase mapping of radionuclide gated biventriculograms in detecting the origin of abnormal ventricular activation was studied during ventricular tachycardia or preexcitation. Group I included six patients suffering from clinical recurrent VT; 3 gated blood pool studies were acquired for each patient: during sinus rhythm, right ventricular pacing, and induced sustained VT-Group II included seven patients with Wolff-Parkinson-White syndrome and recurrent paroxysmal tachycardia; 3 gated blood pool studies were acquired for each patient: during sinus rhythm, right atrial pacing and orthodromic reciprocating tachycardia. Each acquisition lasted 5 min, in 30 degrees-40 degrees left anterior oblique projection. In Group I, the Fourier phase mapping was consistent with QRS morphology and axis during VT (5/6), except in one patient with LV aneurysm and LBBB electrical pattern during VT. Origin of VT on phase mapping was located in the right ventricle (n = 2) or in left ventricle (n = 4), at the border of wall motion abnormalities each time they existed (5/6). In Group II, the phase advance correlated with the location of the accessory pathway determined by ECG and endocardial mapping (n = 6) and per-operative epicardial mapping (n = 1). Discrimination between anterior and posterior localisation of paraseptal pathways and location of intermittent preexcitation was not possible. We conclude that Fourier phase mapping is an accurate method for locating the origin of VT and determining its etiology. It can help locate the site of ventricular preexcitation in patients with only one accessory pathway; its accuracy in locating multiple accessory pathways remains unknown.

Adult↗
PubMed1986

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↗
PubMed1986

[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↗
PubMed1984

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↗
PubMed1983

[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↗
PubMed1982

[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↗
PubMed1981

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↗