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Biomedical subjects

J F Leclercq

Publications and source records attributed to J F Leclercq.

At least 109 records · Page 6Linked to original sources
PubMed1981

Computer quantitated evaluation of cardiac arrhythmias.

The identification of a cardiac arrhythmia depends on the interpretation of both the QRS complexes and the P waves. P wave detection is unreliable and hence automated diagnostic systems are often imperfect. An alternative is a system which detects QRS only and which classifies the QRS events; the physician then has a detailed quantitated QRS analysis to aid in diagnosis. The ATREC system has an analog QRS detector, which suppresses the P wave and the T wave frequencies and feeds a minicomputer (Mitra 15/35) with signals for the RR interval, the QRS duration, and polarity. The computer classifies these signals as either narrow or wide complexes. The narrow complexes are analyzed for irregular rhythm, bradycardia, pauses, transient or continuous tachycardia, and fibrillation. The wide complexes are classed by their coupling interval, bi- or trigeminy, doublets, or salvos, and the number per hour. The system gives a trend of the 16 beat mean, and the minimum and maximum heart rate. The data is presented on several displays.

Analysis of Variance↗
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↗
PubMed1981

Effects of intrinsic sympathetic activity of beta-blockers on SA and AV nodes in man.

The authors compare the effects of beta-blockers without intrinsic sympathetic activity (ISA) (propranolol, 160 mg/day), moderate ISA (acebutolol, 800 mg/day) and high ISA (pindolol, 20 mg/day). The sinus rate decreases more with propranolol than with acebutolol, during the day (P less than 0.01) and during the night (P less than 0.001), whereas pindolol does not change the daylight rate and increases the nighttime rate (P less than 0.001). The ventricular rate during atrial fibrillation (AV nodal transmission) is modified as is sinus rate. There is no significant difference between propranolol and acebutolol, and a highly significant difference between pindolol and propranolol (P less than 0.001) or acebutolol (P less than 0.01). Moreover, the eurythmic effect of beta-blockers, making RR intervals more regular, is maximal with propranolol and minimal with pindolol, as judged on RR interval histograms. The ISA of the beta-blockers is of major importance for the clinical use of these drugs, and in the case of SA or AV node dysfunction ISA can be useful, but it can obscure the beneficial effects of beta-blocking therapy.

Acebutolol↗
PubMed1981

[Limits of quantitative evaluation methods].

Technical considerations limit the arrhythmias quantifiable by Holter monitoring to atrial and ventricular extrasystoles. However, benign atrial extrasystoles are often neglected and are not considered a target of importance for the study of antiarrhythmic drugs. As regards quantification of ventricular extrasystoles, possible causes of bias should be recognised: the exclusion of patients with dominant irregular and/or wide QRS rhythms, the failure to take global heart rate into account, the qualitative approach to assessment of important parameters such as QRS morphology, coupling interval, grouping which are only considered statistically in terms of prevalence. As a result of these limitations major arrhythmias both at atrial level (salvos of extrasystoles, atrial tachycardia, flutter, fibrillation) and junctional (paroxysmal reciprocating tachycardia) and ventricular levels (ventricular tachycardias of differing origins and types) are systematically disregarded by quantitative standardised protocols, although modern antiarrhythmic agents have been introduced precisely for their treatment. To consider minor arrhythmias more reliable models for study than serious ones because they are easier to quantity, is an error which has been well demonstrated, as in many respects we still do not know how to quantify relatively important parameters. A good example of this situation is the confusion and contradictions in the literature about the long-term prognosis of myocardial infarction evaluated by methods of counting ventricular extrasystoles: the most formal conclusions are drawn from reports containing the least and most qualitative data and which include bias unrelated to the techniques, chosen consciously or not by the authors.

Anti-Arrhythmia Agents↗
PubMed1981

[Comparison of the efficacy of aprindine and quinidine in chronic ventricular rhythm disorders].

The object of this study was to compare the efficacity and the side effects of Aprindine and Quinidine in patients with stable ventricular arrhythmias. A series of 33 patients with chronic stable ventricular arrhythmias were given successively Aprindine and Quinidine on the principle of extrasystoles (VES) determined by computer analysis of Holter recordings. The VES were counted every hour and the statistical study used analysis of variance followed by linear contrast and also the sign test. The stability of the arrhythmia was verified by several control Holter recordings without therapy (average : 3,3 per patient). Low dose regimes were used in 17 patients (an average of 50 to 60mg/day Aprindine, and 481 mg Quinidine base), and Quinidine was shown to be the more active (p less than 0.05 to 0.003 according to the test used), reducing the number of VES by 39% compared to an average of 21% for Aprindine. In the other 16 patients with a higher dosage regime, 109 mg Aprindine and 707 mg Quinidine base, there was no significant difference between Quinidine and Aprindine (p less than 0.08 to 0.12), Quinidine reducing the number of VES by an average of 54%, and Aprindine by 36%. Quinidine caused diarrhoea in I patient on the low dose and 4 patients in the high dose regime. Aprindine caused neurological side effects in 2 patients on the low dose, and 7 patients on the high dose regime. Aprindine at 100 mg/day may therefore be used in the same manner as Quinidine at usual dosages as regards the incidence of side effects of the two drugs. However, the ratio of effective dose/toxic dose is lower with Aprindine than with Quinidine.

Aprindine↗
PubMed1981

[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↗
PubMed1980

Prevention of intra-atrial reentry by chronic atrial pacing.

The authors describe a case of so-called "intra-atrial reentry," associated with sinus node dysfunction. The spontaneous initiation of the tachycardia was always preceded by a sinus pause, and external atrial pacing prevented the appearance of tachycardia. Thus an atrial pacemaker was implanted, and after several months, the atrial dysrhythmias disappeared completely, despite interruption of the antiarrhythmic drugs. When a pacemaker dysfunction occurred, the sinus node dysfunction and the tachycardia reappeared. This is analogous with the "incessant" tachycardias seen in the WPW syndrome, and must be differentiated from the usual forms of the sick sinus syndrome which require both a pacemaker and antiarrhythmic drugs.

Adult↗
PubMed1980

[Ventricular tachycardia in bursts. Electrophysiological and therapeutical study].

22 patients with salvoes of ventricular tachycardia were investigated electrophysiologically and pharmacologically to determine the mechanism of the arrhythmia. The appearance of the ventricular complexes was suggestive of a septal origin. The arrhythmia appeared to occur and regress within precise limits of sinus rhythm. 24 hour ECG recording and endocavitary stimulation techniques showed its essentially variable character, but occasionally a fixed coupling interval with the first extrasystole was observed, suggesting the presence of an unprotected parasystolic focus. The repetition of the extrasystolic activity, which could be triggered and terminated at will, is explained by phenomena of delayed after potentials. The results of the systematic investigation of the effects of quinidine-like drugs, beta-blockers and verapamil do not invalidate these hypotheses and show a difference of degree but not of nature between the two populations A and B of patients classified according to the quantitative character of the extrasystolic activity over 24 hours (more or less than 1000/hour). The observation of intermediate forms with simple extrasystoles and other forms with sustained tachycardia extends the significance of these results to many forms of ventricular arrhythmia.

Adolescent↗
PubMed1980

[Ventricular arrhythmias and mitral valve prolapse. A study of 35 cases].

35 patients with mitral valve prolapse (MVP) underwent investigation by Holter monitoring with computerised analysis. Ventricular arrhythmias were observed in 70% patients with MVP. There does not seem to be a close correlation between the severity of the arrhythmia and the degree of prolapse. The mechanisms of the ventricular arrhythmia are variable: two patients had the necessary criteria for ventricular reentry, at least six had parasystolic foci, protected or not from the sinus rhythm. The most severe ventricular arrhythmias are characterised by their variable morphology (but usually showing right bundle branch block), a clear diurnal rhythm, the inducing role of exercise or emotion and a greater diurnal variation of the sinus rhythm suggesting increased sympathetic tone. The results of beta blockade are better in the patients with the most marked diurnal rhythms.

Arrhythmias, Cardiac↗
PubMed1979

Sustained intra-atrial reentrant tachycardia. Electrophysiologic study of 20 cases.

Twenty cases of sustained tachycardia due to intra-atrial reentry were investigated in patients aged 17 to 80 years (mean 47). The average frequency of the tachycardia was 128.6/min (extremes 95 and 180). Three modes of onset of the tachycardia were observed: atrial extra-stimulus (19 times), progressively accelerated atrial pacing (9 times) and atrial escape beat (10 times). The tachycardia was stopped in all cases by a premature stimulation. When spontaneous, the termination was either sudden (10 times) or preceded by a progressive slowing (9 times) or an alternating phenomenon of long-short cycle (13 times). Precise atrial mapping allowed to localize the first atrial depolarization less frequently in the sinus node area (1 case) than in the mean right atrium (21 cases), the low right atrium (2 cases), the interatrial septum (2 cases), and the left atrium (4 cases). The macroscopic size of the reentry circuit was demonstrated in only 3 cases. A junctional reentry was accurately ruled out in all cases thanks to the existence of a second or third-degree AV or VA black, or by studying the sequence of retrograde atrial activation. A true junctional reciprocating tachycardia was associated with the intra-atrial reentry in 2 cases.

Adolescent↗