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Biomedical subjects

P Coumel

Publications and source records attributed to P Coumel.

At least 19 recordsLinked to original sources
PubMed1992

[Effect of atropine therapy on sudden infant death. A multicenter survey of 7851 children at risk].

The results of a multicentre inquiry started in 1988 in reference centres of sudden infant death are presented. This study concerns the sudden and unexplained mortality of infants under 1 year of age who were treated with atropinics for an alleged risk of sudden death. The 7,851 infants involved were divided into 2,605 siblings, 1,067 premature babies and 4,179 infants who experienced malaises. Only one of the 2,034 infants treated with atropinics (385 siblings, 435 prematures, 1,214 with malaise) died, as opposed to 27 deaths among the 5,817 infants who where not treated (10 deaths among 2,220 siblings, 6 among 632 premature and 11 among 2,965 infants with malaise); P = 0.005. These results are encouraging, but they suffer from the limitations and biases inherent in all large inquiries. They certainly do not allow us to conclude without reservation that vagal hyperreflectivity is the mechanism responsible for sudden infant death and that atropinics must be systematically given to all infants at risk. Wide and randomized prospective studies are highly desirable in this particular field.

Drug Evaluation↗
PubMed1992

[Pro-arrhythmia effect of pyridostigmine. Apropos of a case].

A coronary patient with myasthenia gravis with a previous myocardial infarction presented with severe ventricular arrhythmias after the replacement of neostigmine by pyridostigmine for the treatment of the myasthenia. These arrhythmias were resistant to antiarrhythmic therapy associating betablockers and amiodarone throughout treatment with pyridostigmine but regressed when this drug was withdrawn. A test of reintroduction of pyridostigmine under medical surveillance led to the reappearance of the ventricular hyperexcitability, so confirming the responsibility of this drug. This would seem to be the first reported case of severe ventricular arrhythmias due to a proarrhythmic effect of pyridostigmine. The possible mechanisms of this effect are discussed.

Coronary Disease↗
PubMed1992

[Clinical aspects of polymorphic ventricular tachycardia].

Polymorphic ventricular tachycardia is defined as constant change of the QRS morphology. The diagnosis has important etiological, therapeutic and prognostic implications. This term covers several different entities which may be artificially distinguished by the electrocardiographic appearances during tachycardia, by changes of the resting electrocardiogramme, the mode of onset, the presence or absence of underlying cardiac disease and of intercurrent drug therapy. However, as the resting ECG may not be available in an emergency situation, or difficult to interpret, the clinical context is the key to diagnosis and treatment. Polymorphic ventricular tachycardia is classified according to the absence or presence of underlying cardiac disease respectively as torsades de pointe with long QT, torsades de pointe with a short coupling interval and catecholamine-induced ventricular tachycardia of childhood on the one hand, and, iatrogenic torsades de pointe, ventricular tachycardia in acute or chronic infarction and other cardiac diseases, on the other hand. Finally, the authors discuss the problem of polymorphic ventricular tachycardia induced by programmed ventricular stimulation.

Anti-Arrhythmia Agents↗
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↗
PubMed1979

Multilevel block in the atrioventricular node during atrial tachycardia and flutter alternating with Wenckebach phenomenon.

The electrocardiograms of 100 patients with rapid and regular PP intervals during atrial arrhythmias (because of atrial tachycardia or flutter, or pacing) were examined for periods of irregular atrioventricular conduction. This irregular conduction corresponds to an alternating Wenckebach phenomenon, of a type that can be determined from simple rules. The different types of conduction encountered in different patients and the changes seen in the same patient suggest that the atrioventricular node functions physiologically with 3 levels of sequential block. The different prevalence of the 2 types of alternating Wenckebach block may reflect functional differences at the level of the atrioventricular node.

Atrial Flutter↗
PubMed1979

[Intracorporeal cardiac pacemakers for refractory tachycardia (excluding atrial disease). Apropos of 18 cases].

The treatment of paroxysmal tachycardia by the use of permanent pacing to prevent or terminate attacks is discussed. The series comprises 18 patients with follow-up periods ranging from 1 to 12 years. In 6 cases the indication for pacing was atrial tachy-arrythmias favourised by bradycardia (5 of whom had vagally- induced atrial arrythmias). The atrial pacemaker successfully prevented attacks in 4 out of 6 cases. Three cases of chronic reciprocating tachycardia were successfully treated by simultaneous atrial and ventricular pacing or using sequential pacing with a very short P-R interval. Eight cases of paroxysmal orthodromic reciprocating tachycardia in the WPW syndrome were paced: in 5 cases pacing was employed to terminate attacks by atrial (3 cases) or ventricular (2 cases) stimulation, in the other 3 cases pacing was used to prevent the bradycardia which favourised the initiation of tachycardia. Good results were obtained in all 8 cases. Ventricular stimulation was used to terminate attacks in one patient with refractory ventricular tachycardia but the patient had a sudden death probably caused by the pacemaker. The place of these different pacing techniques with respect to medical treatment and specialised arrhythmia surgery is discussed.

Heart↗
PubMed1979

[Quantitative evaluation of the efficacy of anti-arrhythmia agents in chronic ventricular arrhythmia].

The authors describe a computer system for the analysis of ventricular arrhythmias and its use in the evaluation of anti-arrhythmic drugs. Provided the arrhythmia is stable, this method allows an estimation of the onset and duration of action of the drug and gives guidelines for the choice of an appropriate drug regimen. Using this system, a comparison can be made between different drugs based on quantification of their efficacy.

Amiodarone↗
PubMed1979

[Technical characteristics of a new computerized system for quantitative evaluation of cardiac arrhythmias (author's transl)].

The ATREC system is designed to carry out at sixty times real time the quantitative evaluation of arrhythmias in 24 hour magnetic tape recordings. A preprocessing unit eliminates the low frequency waves (P and T) and artefacts, and furnishes the computer (Mitra 15/35, 16 K words of core) with information on R-R interval, QRS duration, regular or irregular rhythm, bradycardia or pauses, transient to sustained tachycardia, and ventricular fibrillation. Extrasystoles are analyzed in terms of enlargement, number, coupling interval, bi or trigeminy, doublets or salvos. Trends of mean and extreme cardiac rate, and R-R interval histograms, are also available. The system is also available for ECG real time monitoring of patients in coronary care units. The computer can analyze 8 ECG tracings simultaneously. The ATREC system provides an important aid in the quantification of arrhythmias and improves the evaluation of antiarrhythmic drugs efficacy.

Anti-Arrhythmia Agents↗
PubMed1978

[2 or 3 level blocks in the Tawara node during atrial tachycardia].

In atrial flutter (or paroxysmal atrial tachycardia), the ventricular response is dependant on the passage through 3 superposed zones of conduction in the Tawara node, the zone of decremential conduction being the central zone N. When the ventricular response is between half and a quarter of the atrial rate there are two possible explanations: type B alternate Wenckebach period (mobitz I block in the central zone N, 2/1 block at the nodo-ventricular junction) or type A alternate Wenckebach period (Mobitz I block in the central zone N and 2/1 block at the atrio-nodal junction). These two responses may alternate in the same patient depending on the drug therapy or vagal activity due to a phenomenon similar to the "GAP" phenomenon. Inexactitudes in the working out of the arithmetic formulae may easily be explained by a certain degree of concealed conduction of blocked activation in one zone or more rarely by hisian extrasystoles. Type A alternate Wenckebach periods are always easier to construct than type B. Perfect 3/1 atrial flutter can only be explained by a type B alternate Wenckebach period with a 3/2 period with a 3/2 period in the N zone and a 2/1 block in the NH zone. When the ventricular rhythm is permanently very slow or when the RR intervals are greater than four times the atrial cycle, 3 zones of block are usually at issue (the third being located in the inferior part of the node or superior part of the bundle of His). Examples of 5/1, 6/1 flutter are thereby analysed. Rapid atrial pacing after termination of the atrial arrhythmia allows a better analysis of its mechanism and the successive reproduction of conduction defects in each zone of block.

Atrioventricular Node↗
PubMed1978

[The atrial arrhythmia syndrome of vagal origin].

Having observed 18 cases, the authors describe a syndrome of recurrent paroxysmal atrial arrhythmia which was very homogeneous from the clinical and ECG point of view. It was usually found in middle aged males, with no demonstrable underlying heart disease, whose disorder of intra-atrial conduction occurred during sinus rhythm. The condition developed slowly over the course of years towards a maximum incidence of several short daily attacks of an arrhythmia which alternated between an atrial fibrillation and atrial flutter. Vagal overactivity is the precipitating cause of these attacks which are usually not completely nocturnal. The condition never progressed to sino-atrial block nor to permanent fibrillation. The beginning of each attack, often heralded by atrial coupling with a long enough interval to cause re-entry, is accompanied by slowing of the sinus rate down to the threshold level. The vagal effect of shortening the action potential and refractory period is recognised to be non-homogeneous in the atrial wall, and suggests a re-entry mechanism rather than hyper-excitability. This would explain the usual resistance of atrial arrhythmias of vagal origin to digitalis, beta blockers and quinidine. Amiodarone alone is usually effective because of the prolongation of the action potential which it causes. In 5 particularly resistant cases a good clinical result was obtained by the insertion of an atrial pacemaker with a fairly rapid rate.

Adrenergic beta-Antagonists↗
PubMed1977

Mechanisms of atrioventricular junctional tachycardia. Role of reentry and concealed accessory bypass tracts.

Electrophysiologic investigations with programmed stimulation of the human heart have clearly established the participation of the atrioventricular (A-V) junction in three different types of junctional reciprocating tachycardia: (1) paroxysmal supraventricular tachycardia in the Wolff-Parkinson-White syndrome: (2) the vast proportion of "paroxysmal atrial tachycardia" without evidence of preexcitation during sinus rhythm with antegrade conduction; and (3) the permanent or almost permanent (chronic relapsing) form of supraventricular tachycardia with its characteristic rate-dependent initiating mechanism. The obvious presence of the Wolff-Parkinson-White syndrome during sinus rhythm does not necessarily imply that the accessory pathway will be utilized during supraventricular tachycardia. Conversely, in the absence of preexcitation, the mechanism of A-V junctional reciprocating tachycardia has been traditionally attributed to pure intranodal dissociation, often without definite direct proof. Concealed accessory pathways (with unidirectional block) may be more frequent than realized and should be carefully searched for. Proof that supraventricular tachycardia utilizes an accessory pathway for retrograde conduction to the atrium often requires meticulous electrophysiologic studies- Conslucions based on the absence of various findings may be misleading. Emphasis must be placed on positive viagnostic features. One or more of the following observations may prove or disprove participation of a Kent bundle during supraventricular tachycardia: (1) induction of A-V block during tachycardia: (2) influence of electrically induced ventricular premature beats upon tachycardia; (3) patterns of retrograde atrial activation during tachycardia; or (4) influence of functional bundle branch block on the rate of the tachycardia. Analysis of events at the onset of rather than during the tachycardia is probably less important but may also provide suggestive clues about the mechanism of reentry. Observation of the following variables may be helpful: (1) behavior of antegrade conduction at the onset of tachycardia; (2) relation of atrial and ventricular activation at the onset of tachycardia; (3) presence of retrograde ventriculoatrial (V-A) conduction; (4) prolongation of the H-V interval at the onset of tachycardia; and (5) atrial stimulation at various sites. Precise understanding of the pathophysiology of supraventricular tachycardia is important because specific therapy (pharmacologic, pacemaker or surgical) may ultimately depend on accurate knowledge of the underlying mechanisms.

Anti-Arrhythmia Agents↗
PubMed1977

XXII. Intractable paroxysmal tachycardias which proved fatal in type A Wolff-Parkinson-White syndrome.

Paroxysmal tachycardias proved fatal in a middle-aged man with type A Wolff-Parkinson-White syndrome. Efforts to control his arrhythmias included a surgical incision into the left atrium, based on discovery of early left ventricular activation during epicardial mapping. The incision did not alter any electrocardiographic or clinical feature; at later necropsy examination it was found that the incision had not cut a nearby left atrioventricular (A-V) connection. Serial section study of the entire A-V rings and septal junction of this heart also demonstrated a second unusual A-V connection, between the atrial septum and the region of the His bundle. This latter connection was anatomically eccentric to the normal organization of this region and may have caused an alteration in the local electrophysiological behavior. The left lateral A-V connection may have been of no electrophysiological significance since it was composed of ordinary working myocardial cells. These and other possible correlations are discussed in the context of the clinical features, numerous electrophysiological observations, and the meticulously determined anatomical findings.

Atrioventricular Node↗
PubMed1977

[Arrhythmias and chronobiology].

The cyclical changes in biological events have seldom been studied by cardiologists. No complete systematic method of study has ever been applied to them. It is, however, certain that the circadian rhythms play a very important role in cardiac patients. This can be seen to be so in the arrhythmias. In a preliminary report, the authors give several examples of this concept; they have obtained their material by using a computerised magnetic tape recording of the electrocardiogram during a 24 hour period.

Adult↗
PubMed1977

Wolff-Parkinson-White syndrome type A obscured by left bundle branch block.

2 patients are presented whom the presence of left bundel branch block obscured the signs of the Wolff--Parkison--White syndrome expected with a bypass on the left side of the heart. While it was possible to infer the presence of both disorders from the surface ECGS, electrophysiological studies proved invaluable in defining the precise situation in both cases. When atypical electrocardiographic appearances are observed in the Wolff-Parkinson-White syndrome, careful investigation may reveal the cause to be bundle branch block on the same side of the hear as the anomalous pathway. In both patients there was in addition evidence of sinoatrial disease, which was associated with the occurrence of arrythmias, and this was also confirmed with intracardiac studies.

Adult↗