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Biomedical subjects

J F Leclercq

Publications and source records attributed to J F Leclercq.

At least 91 records · Page 5Linked to original sources

[Mobitz type II suprahisian atrioventricular block : block in the subnodal-suprahisian (NH) zone?].

The electrophysiological properties of the atrioventricular node differ from those of the His bundle. Nodal conduction is always decremential; this is its principal physiological characteristic, and accounts for the fact that almost the only form of block found at this level is Wenckebach block. The His bundle is characterised by an all-or-nothing response and usually blocks in the Mobitz II mode. Wenckebach phenomena have been described in the His Purkinje system, but Mobitz II block has not been reported in the atrioventricular node. Similarly, phase IV paradoxical block is found in the His Purkinje system but has not been described in the atrioventricular node in the absence of vagal phenomena. In addition, the atrioventricular node is very sensitive to the influence of the autonomic nervous system, the His bundle much less so. The first patient had a normal resting electrocardiogram showing sinus rhythm; second degree atrioventricular block was observed when the atrial rhythm was increased by exercise, atropine or atrial pacing. His bundle recordings showed the block to be suprahisian; the blocked atrial potentials were not followed by a His potential, whilst the conducted atrial activity was followed by a normal His potential and a normal HV interval. However, this atrioventricular block was of the Mobitz II and not the expected Mobitz I type, conduction to the ventricles suddenly blocking (with a 3/2 or 2/1 response) when the atrial rate was increased, without obvious lengthening of the PR or AH intervals before the blocked atria.(ABSTRACT TRUNCATED AT 250 WORDS)

Electric Stimulation↗

[Polymorphic familial incessant ventricular rhythm disorders with ventricular repolarization abnormalities: borderline form of the congenital long QT syndrome?].

Two cases of polymorphic ventricular tachycardia (VT) are reported in siblings: the elder sister (18 years) was admitted to hospital because of syncope and ECG showed incessant attacks of VT. There was no obvious cardiac disease on echocardiography or cardiac catheterisation. A second syncopal attack occurred during Holter monitoring: this showed prolonged torsades de pointe which terminated spontaneously after a few minutes. Both syncopal attacks occurred at moments of intense emotional stress. Concomitantly, the duration of ventricular repolarisation was also observed to be increased. The attacks of polymorphic VT disappeared when the atrial rhythm accelerated, for example during exercise of isoprenaline infusion. It was not possible to induce VT by ventricular extrastimulation. The arrhythmia was controlled by nadolol and propafenone or flecainide. A familial investigation revealed that a younger brother had attacks of incessant VT with a long QT interval. The mother had frequent polymorphic ventricular extrasystoles and abnormal ST-T wave changes. The association of familial ventricular arrhythmias and long QT interval is suggestive of the Romano-Ward syndrome, but in this condition the intercritical ECG is normal except for the long QT. Conversely, in benign VT, the arrhythmia disappears during atrial pacing and exercise but there have been a few reports of sudden death. Our two cases could represent an intermediary form between these two pathological entities.

Adolescent↗

[Anti-arrhythmic effect of oral propafenone. Apropos of 70 cases].

During a 3 year period, seventy patients aged 53 +/- 16 years with a total of 73 arrhythmias were treated over a mean period of 6.8 months (maximum 27 months) with oral propafenone, the usual dose being 900 mg/day. The study covered the whole spectrum of cardiac arrhythmias (32 supraventricular, 41 ventricular), and their relation to the autonomic nervous system. The efficacy was scored from 1 (no effect) to 5 (complete control) as judged by the clinical response, the results of Holter monitoring (175 control and 133 test recordings on therapy), and a comparison was made between the effects of propafenone and other antiarrhythmics: quinidine-like drugs, beta-blockers and amiodarone. With respect to supraventricular arrhythmias: 9 cases of vagally-induced atrial flutter and fibrillation were unaffected by propafenone (mean score = 1.1). On the other hand, the drug was very effective (mean score = 4.1) in 8 cases of adrenergic atrial arrhythmias. In 12 arrhythmias with more varied mechanisms (extrasystoles, tachysystole, paroxysmal atrial fibrillation) an intermediate score was obtained (2.8). Three cases of resistant junctional tachycardia due to reentry were improved. At ventricular level, 5 cases of extrasystole sensitive to quinidine were also improved by propafenone (4.6); the difference was more clearcut in 8 cases of benign idiopathic tachycardia (propafenone: 4.1, and quinidine: 2.4). This was more marked in 13 cases of more severe arrhythmia in diseased hearts in which the effect of propafenone (4.1) was superior even to that of amiodarone. However, propafenone was less effective (3.3) than amiodarone in 4 cases of severe polymorphic idiopathic ventricular tachycardia closely related to the autonomic nervous system. The antiarrhythmic effect of propafenone was appreciable in 10 cases of resistant post-infarction ventricular tachycardia, eventually in association with amiodarone. Slowing of the sinus rhythm (-11.6%) with no change in the day/night ratio was due to beta-inhibition. However, in toxic doses this may progress to sinoatrial block (9 cases). A lengthening of the PR interval and duration of QRS was common, but this was not complicated by torsade de pointes, one case of which was successfully treated by propafenone. Secondary gastro-intestinal effects and vertigo were rarely severe enough to warrant stopping therapy. In conclusion, these results show that the introduction of propafenone is a valuable therapeutic advance in the treatment of arrhythmias, especially in those with a favoring adrenergic mechanism.

Administration, Oral↗

[How and why treat ventricular hyperkinetic arrhythmias].

The Authors present their experience, based on 180 patients, concerning the treatment of chronic ventricular tachycardia. According to the underlying etiology, about 1/3 of the cases were considered idiopathic (most of all in form of salvos), 1/3 were ischemic with a prior myocardial infarction (ventricular tachycardias in the setting of acute myocardial infarction were not considered) and 1/3 had miscellaneous cardiac diseases. Prophylactic treatment of ventricular tachycardia recurrences was divided in three steps: classic antiarrhythmic drugs used in monotherapy (Quinidine or Quinidine-like, betablockers, Verapamil); Amiodarone or recent class I antiarrhythmics (Flecainide, Propafenone); drug combinations. The results of medical treatment were different according to the underlying etiology: the first two steps achieved control of the arrhythmia in 2/3 of patients with idiopathic ventricular tachycardia, in 45% of ventricular tachycardia due to miscellaneous cardiopathy and only in 35% of cases with post-myocardial infarction ventricular tachycardia. Four patients were referred for antiarrhythmic surgery and 3 received a palliative electrical device. During a mean follow-up period of 5 years, there were no deaths in the group with idiopathic ventricular tachycardia, 10% of deaths in the group with miscellaneous cardiopathy and 17% in the group with post-myocardial infarction ventricular tachycardia. Idiopathic ventricular tachycardias seem to bear a minimal risk, and the need to treat them depends only on the severity of functional signs and on the frequency of arrhythmic episodes. In patients with severe underlying cardiopathy, particularly ischemic heart disease, active search for an effective treatment is mandatory, due to the high risk of death.

Anti-Arrhythmia Agents↗

[The implantable automatic defibrillator. Preventive treatment of sudden death caused by ventricular arrhythmia].

The material and implantation technique of the implantable defibrillator developed by M. Mirowski and used by the authors in 3 patients are described. Through lateral thoracotomy, 4 electrodes are installed, including one patch on the apex of the heart. In case of sustained ventricular arrhythmia the instrument delivers, after less than 30 seconds, a 25 joules shock increased to 30-35 joules if this fails. The results were very encouraging since conversion of severe ventricular arrhythmia was obtained in all 3 patients after the first shock. There was no false detection or inappropriate start. The limitations and indications of the technique are discussed and compared with other treatments of ventricular arrhythmia.

Arrhythmias, Cardiac↗

Circadian changes in heart rate in unanesthetized normotensive and spontaneously hypertensive rats.

Circadian changes in heart rate and heart rate variability were measured in spontaneously hypertensive (SHR) and normotensive (WKY) rats. Electrocardiograms (ECG) were continuously recorded, over a 24 hour period from freely moving conscious rats via three small metallic subcutaneous electrodes which were positioned a week before the recording period. The findings reported here show: 1/ Mean heart rate calculated over 24 hours were lower in both strains than previously reported. This difference probably reflects the lack of anesthesia and minimal stress in the present study. 2/ The timing of the circadian variations in both strains were the same, suggesting that were both entrained to the light-dark cycle. 3/ The 24 hours mean heart rate variability was significantly higher in SHR than in WKY but in each strain it was similar throughout the 24 hours. This suggests that the vagal tone in SHR was higher by a fairly constant amount throughout the light-dark cycle.

Animals↗

Long-term prevention of vagal atrial arrhythmias by atrial pacing at 90/minute: experience with 6 cases.

Six patients (5 men, 1 woman) with a history ranging from 3-16 years of resistant vagal atrial arrhythmias were treated by atrial pacing at a rate of 90/Min. These patients have been followed up for an average of 5.5 years (range 2-11 years) with favorable results. The arrhythmias were characterized by daily or weekly attacks of typical atrial flutter and atrial fibrillation occurring mainly or exclusively at night, at rest, or in the digestive periods in otherwise normal hearts of middle-aged patients (first attack between 25 and 54, mean 40). The arrhythmias were resistant to quinidine, and were usually aggravated by digitalis, beta-blockers and verapamil. Amiodarone is usually the only effective drug in this syndrome, but was not used before pacing in the 2 first cases, and was ineffective in the other 4 cases. Electrophysiologic studies confirmed the absence of sick sinus syndrome, and the close relationship between relative bradycardia and the onset of the arrhythmia. Atrial pacing alone totally controlled the arrhythmia in 1 patient; amiodarone was used in conjunction with pacing in 3 patients. In 1 patient the improvement was clear but incomplete, and in 1 patient permanent atrial fibrillation occurred shortly after pacemaker implantation.

Adult↗

[Antidromic reciprocating rhythm in Wolff-Parkinson-White syndrome precipitated by a ventricular extrasystole arising at the emergence of the preexcitation pathway].

A 9 year old child was investigated for attacks of wide QRS complex tachycardia occurring exclusively during the daytime and favoured by exercise or stress, with ventricular extrasystoles of the same form occurring between attacks. Endocavitary investigation showed a concealed atrioventricular accessory pathway during sinus rhythm with anterograde 1/1 conduction up to 270/min; retrograde conduction was not so good with block occurring at 175/min. The spontaneous tachycardia was reproduced by catecholamine infusion: it was an antidromic reciprocating rhythm triggered by a ventricular extrasystole of identical form to that of a pure preexcitation complex and to that of the tachycardia complexes. Spontaneous termination of attacks always occurred when conduction from the ventricle to the atria stopped. The attacks could be induced by ventricular extrastimuli when they caused an increment in retrograde conduction time resulting from retrograde conduction up the nodohisian pathway and not the Kent bundle. The tachycardia could also be initiated by atrial extrastimuli providing pure pre-excitation could be obtained. In both cases, retrograde conduction of the nodohisian pathway had to be improved by catecholamines. When the patient was given betablocker therapy the attacks of tachycardia completely disappeared. The association of ventricular extrasystoles and antidromic reciprocating rhythm and their morphological identity suggest that these extrasystoles were in fact automatic activity of the Kent bundle. Escape phenomena as signs of passive automatism have been described in this conditions but, to our knowledge, extrasystoles suggesting an active automatic process have not been previously reported.

Cardiac Complexes, Premature↗

[Flecainide: a new antiarrhythmic agent].

The authors report their clinical experience with flecainide, a new Class I antiarrhythmic drug, in 44 patients classified into three groups. The first group (7 cases) comprised patients with a wide range of arrhythmias sensitive to the usual antiarrhythmic agents. The second (17 cases) were atrial arrhythmias resistant to the usual antiarrhythmic agents and were mainly vagal atrial arrhythmias. The last group (20 cases) comprised patients with resistant VT, 14 of whom had underlying cardiac disease (8 chronic infarcts). The results obtained were analysed by a score test because of the wide range of arrhythmias and the wide variations in their spontaneous recurrent rate. The antiarrhythmic effect was checked by repeated Holter monitoring correlated with the results of interrogation. Provocative pacing studies were performed in 5 cases of inducible VT under therapy. The results with flecainide were compared with those obtained with reference Class I antiarrhythmics: quinidine, 700 to 1100 mg/day or disopyramide, 600 mg/day. Amiodarone was often associated with each Class I antiarrhythmic because of the resistant nature of these arrhythmias. In group I the results with flecainide were equivalent to those of quinidine. In the other two groups the results were significantly better than those of the reference antiarrhythmic: mean scores: group II 3,20 +/- 0,5 compared to 1,9 +/- 0,4 (p less than 0,01); group III 3,70 +/- 0,37 compared to 1,85 +/- 0,22 (p less than 0,001). Tolerance was good apart from neurosensory side effects (loss of accomodation, vertigo) which were dose dependent and which led to the withdrawal of therapy in only 4 cases. Four types of cardiac side effects were observed: aggravation of existing sinoatrial block (1 case); aggravation of existing intraventricular block (2 cases); aggravation of contractile function which was very poor before therapy (2 cases); and sudden death during therapy in patients with ischemic heart disease in cardiac failure and with incessant resistant VT (2 cases). In these instances the role of the drug cannot be confirmed. These complications were observed with doses of more than 5 mg/kg/day and in patients with cardiac failure. Two of these patients had serum flecainide levels which were very high. It may therefore be possible to reduce the incidence of these complications by adapting dosage to the patient's clinical state and to the serum drug levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Role of sympathetic nervous system in non-ischaemic ventricular arrhythmias.

Propranolol and nadolol were used in two groups of patients having ventricular arrhythmias. The two groups were characterised by differences in sympathetic drive. The 10 non-adrenergic patients had idiopathic, monomorphic extrasystoles (isolated with fixed coupling or in pairs or salvoes) arising from the right ventricle or the septum. These extrasystoles were chronic and benign, with a slightly increased daytime frequency (day:night = 1.6). They disappeared on exercise. The nine adrenergic patients had less frequent but more complex polymorphic ventricular extrasystoles, and rapid and irregular tachycardias which were resistant. They occurred predominantly during the day and were associated particularly with stress and exercise. They were either idiopathic, or coexisted with mitral valve prolapse (three cases) or hypertrophic subaortic stenosis (one case) in young patients (mean age, 32 years) who did not have coronary heart disease. Nadolol was more effective than propranolol in controlling the arrhythmia, heart rate, and variations in sinus rhythm in the adrenergic group, while the arrhythmia was not controlled in the non-adrenergic group. Using clinical variables, comparison of the frequency of extrasystoles by day and night, and assessment of the antiarrhythmic effect of beta-blockers, the role of the sympathetic tone in non-ischaemic ventricular arrhythmias may be elucidated.

Adolescent↗

[Traumatic tricuspid insufficiency with right-left atrial shunt].

A particular form of traumatic tricuspid incompetence with a right-to-left interatrial shunt through a patent foramen ovale is reported. This case and six similar previously published reports have the following features in common: clinically, tricuspid incompetence is associated with cyanosis and raised jugular venous pressure, pulsatile hepatomegaly and a systolic murmur in the subxiphoid region in about haĺf the cases. The ECG showed incomplete or complete right bundle branch block in six of the seven cases, associated with left anterior hemiblock in four cases. The right cardiac chambers were dilated in all cases. Diagnosis may be confirmed by cardiac catheterisation and selective angiocardiography. The outcome and tolerance of the condition depend on the underlying tricuspid lesions. Papillary muscle rupture imposes early surgical intervention. Rupture or elongation of the chordae is compatible with good tolerance over a number of years.

Bundle-Branch Block↗