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Biomedical subjects

R Cointe

Publications and source records attributed to R Cointe.

30 records · Page 2Linked to original sources
PubMed1987

Remote occurrence of high degree heart block following failure of transcatheter AV junctional ablation: incidence and clinical significance.

We report on two patients out of a series of 22 who underwent transcatheter ablation of the atrioventricular (AV) junction. The procedure failed to induce permanent complete heart block in 15 patients, 12 of whom were in sinus rhythm with 1:1 AV conduction before hospital discharge. Of the 12 patients, two (16.6%) were found to be in high degree heart block, one month later. We discuss the mechanism of late occurrence of high degree heart block and we emphasize the need for systematic implantation of permanent ventricular or dual chamber pacemakers, despite failure of transcatheter ablation of the AV junction.

Adult↗
PubMed1987

[Complex ventricular extrasystole. Value of technics of programmed electric stimulation].

The incidence and significance of ventricular arrhythmia induced by programmed electrical stimulation in subjects with complex ventricular ectopy were studied in 46 consecutive subjects: 34 with heart disease, 12 with an apparently normal heart. The procedure consisted of delivering on one spontaneous and 2 imposed rhythms one, two, then three extrastimuli. Significant arrhythmia with more than 6 ventricular complexes was induced in 17 patients (37%), including 6 (13%) with sustained ventricular tachycardia and 11 with unsustained ventricular tachycardia. Induction of ventricular arrhythmia was observed in 12 of the 14 patients with a history of myocardial infarction. At the end of a mean follow-up period of 12 +/- 4 months, there were 2 sudden deaths, and 3 patients had clinically sustained ventricular tachycardia. Clinical ventricular tachycardia occurred in the group of 17 patients inducible during programmed electrical stimulation. The patients who died suddenly belonged to the group of 29 patients without induced ventricular arrhythmia. This study shows a high proportion of significant stimulation-induced arrhythmia in patients who had suffered from myocardial infarction more than 3 months previously and who had complex ventricular ectopy. Owing to the good condition of this group of patients after a mean follow-up of 12 months, we were unable to determine the influence of stimulation-induced arrhythmia on mortality. However, it must be noted that spontaneous sustained tachycardia occurred in the group of patients with significant induced ventricular arrhythmia.

Adult↗
PubMed1987

[Reduction of ventricular tachycardia by programmed electric stimulation. Clinical implications].

The mode of termination by programmed electrical stimulation of sustained ventricular tachycardia (VT) (more than 30 seconds) and induced by stimulation was investigated in 33 patients. In 27 patients (82%) programmed stimulation was possible because VT did not require an immediate electric shock or did not terminate spontaneously, but constant reduction of VT was obtained with one extrasystole in only 1 patient (3%), with two extrasystoles in 5 patients (15%) and by overdrive stimulation in 12 patients (36%). The remaining 15 patients (45%) required an external electric shock either because VT was poorly tolerated clinically, or because stimulation had failed. In 8 of the 27 cases in whom stimulation was attempted (30%), acceleration of VT was observed. A significant correlation was found between the need for electrical shock and the VT cycle length. It is concluded that reduction of VT by programmed electrical stimulation can only be successful in a limited number of patients and carries a significant risk of acceleration. These data must be taken into account when temporary treatment of VT by stimulation is contemplated. They should incite to considerable caution in the use of implantable pacemakers for tachycardia termination.

Adult↗
PubMed1986

[Sinus dysfunction associated with catecholaminergic ventricular tachycardia. Therapeutic implications].

The presence of resting sinus bradycardia (less than or equal to 45 bpm) with junctional escapes in an 8 year old child with catecholamine induced ventricular tachycardia, raised the problem of an underlying sinus node dysfunction. This was an important consideration bearing in mind the potential risk of the high dose betablocker therapy aggravating the sinus bradycardia. Electrophysiological studies showed pathological sinus node recovery times. Betablocker therapy did not aggravate the bradycardia, even after 6 months' treatment. A review of the literature showed the association of sinus bradycardia and catecholamine-induced ventricular tachycardia to be relatively common (39 p. 100). However, no mention was found of aggravation of this sinus bradycardia by betablocker therapy.

Adrenergic beta-Antagonists↗
PubMed1986

[Total or partial electrical interruption of the atrioventricular pathway. Evaluation of clinical results and indications].

After checking on the efficacy and innocuity of catheter ablation of the His bundle in an experimental study in the sheep, 22 patients with supraventricular tachycardia resistant to an average of 5.5 +/- 1.7 antiarrhythmic drugs per patient underwent this procedure. The most common arrhythmias were atrial fibrillation or flutter (poorly tolerated in 14 cases), and reciprocating tachycardia (8 cases, including 3 with accessory atrioventricular pathways). In 3 of the 5 patients with intranodal tachycardia, an initial attempt was made to modify one of the two AV nodal conduction pathways. Although complete atrioventricular block was obtained in all patients, atrioventricular conduction returned in 15 patients between the 30th minute and 4th day after the procedure. A second attempt at His bundle ablation was carried out in 9 patients. During follow-up ranging from 1 to 38 months, complete or an advanced degree of atrioventricular block persisted in 5 patients, the other patients being in sinus rhythm (12 cases) or slow atrial fibrillation (2 cases). The remaining patient who was in complete atrioventricular block died of septicaemia 2 months after the procedure. The clinical results were evaluated by electrophysiological investigation, exercise testing and Holter monitoring. There were 15 satisfactory clinical results (83.3 p. 100) and 3 poor results. This series shows that interruption or modification of the normal atrioventricular conduction pathway may be performed at low risk and with good results in a high percentage of cases. It is a valuable therapeutic option in patients with supraventricular tachycardia resistant to antiarrhythmic therapy.

Adult↗
PubMed1986

[Intravenous sotalol in the acute treatment of supraventricular tachycardias].

The effects of intravenous sotalol (0.5 mg/kg in 6 minutes) were studied in 23 patients with supraventricular tachycardia (ventricular rate greater than 120 bpm) after failure of placebo (isotonic dextrose). Thirteen patients had atrial flutter or fibrillation and 10 a junctional tachycardia of recent onset. Sinus rhythm was restored in 4 of the patients with atrial flutter or fibrillation and the ventricular rate was slowed significantly in 3 patients (less than 100 bpm). In 3 other patients the ventricular rate decreased (31 to 35 p. 100) but remained above 100 bpm. Sinus rhythm was restored in 3 of the 10 patients with a junctional tachycardia five to twelve minutes after beginning the injection. A slight slowing of the heart rate (13 to 27 p. 100) was observed in the other 7 patients but the frequency remained over 100 bpm. Overall, a satisfactory result was obtained in 10 patients (43 p. 100) including 7 cases in which sinus rhythm was restored. Sotalol was well tolerated in 21 patients; one patient complained of cold in the legs and one patient developed asymptomatic bradycardia (46 bpm). This study shows that intravenous sotalol may be useful in the emergency treatment of supraventricular tachycardia.

Adolescent↗
PubMed1985

Alternate ventriculo-atrial Wenckebach conduction during ventricular tachycardia.

Although pacing-induced ventriculo-atrial (VA) Wenckebach conduction has been previously described, the occurrence of this phenomenon during ventricular tachycardia has received little attention. The latter is defined as 2:1 VA block in which the conducted beats show progressive lengthening of VA conduction until the sequence is terminated by two or three blocked ventricular beats. This phenomenon was observed in a 16-year-old boy who underwent electrophysiologic study for ventricular tachycardia as a late complication of surgical correction of tetralogy of Fallot. During pacing-induced ventricular tachycardia with a morphology similar to that of the spontaneous tachycardia, 8:4 alternating VA block was observed. This sequence suggested that the AV node was the site of block, the 2:1 block being located at the upper level, and the VA Wenckebach block at the lower level. Alternate VA Wenckebach conduction appears as a possible cause of variation in atrial depolarization intervals during ventricular tachycardias with short cycle lengths.

Adolescent↗
PubMed1985

[Treatment of recurrent ventricular tachycardia with hydroquinidine. Evaluation of its efficacy with electrophysiological technics].

Electrophysiological investigations were used to test the efficacy of dihydroquinidine chlorhydrate (600 or 1 200 mg/day) in a prospective study of 18 patients with recurrent ventricular tachycardia documented by electrocardiography. These patients did not respond to an average of 3.1 +/- antiarrhythmic drugs, including amiodarone in 12 patients. Hydroquinidine was well tolerated in 17 patients but had to be withdrawn in 1 patient because of hypotension. The effect of hydroquinidine on ventricular tachycardia induced by programmed pacing was evaluated after a 48 to 72 hours treatment, 3 to 5 hours after the last dose. After hydroquinidine it was not possible to induce ventricular tachycardia in 10 patients (58.8%). In the other 7 patients, it was possible to induce a ventricular tachycardia under treatment. In one case, hydroquinidine aggravated the arrhythmia as the induced tachycardia had a shorter cycle. In the other patients, hydroquinidine lengthened the tachycardia cycle by an average of 94 +/- 79 ms. The right ventricular refractory period increased cycle by 44 +/- 23 ms. Long-term hydroquinidine was prescribed for 7 patients, twice in association with amiodarone. Relapse was observed in 2 patients, 1 and 5 months after the onset of treatment. Five patients were well controlled by the treatment. The results of this study demonstrate the efficacy of hydroquinidine for the prevention of tachycardia induced by stimulation and underline its value in the treatment of sustained, recurrent ventricular tachycardia. This study illustrates the illustrates the importance of electrophysiological techniques for the identification of patients likely to benefit from a given antiarrhythmic treatment.

Adult↗
PubMed1985

[Treatment of recurrent ventricular tachycardias using oral propafenone].

The effect of oral propafenone on prevention of pacing-induced ventricular tachycardia (VT) was studied in 11 patients. All patients experienced documented sustained VT refractory to 4.1 +/- 2 antiarrhythmic agents per patient including amiodarone in 8. Programmed electrical stimulation was performed before and 48-72 hours after oral propafenone (900 mg/day) 2-3 hours after the last dose. Two patients developed spontaneous incessant VT before the scheduled date of the study on propafenone, and were classified as aggravation. Propafenone prevented pacing-induced VT in 2 patients (successful results). In 3 additional patients the results were partial, as non-sustained VT was induced on propafenone whereas sustained VT could be provoked during the control study. In the remaining 4 patients, oral propafenone failed to prevent pacing-induced VT. Tachycardia cycle length increased in 3 (C = 284 +/- 129 P = 450 +/- 202 ms) and was shorter in 1 aggravation. The 5 patients with successful or partial results (45.4 p. cent), underwent long-term therapy with a mean follow up of 5.6 +/- 4 months. Recurrence of VT occurred in 2. The remaining 3 are well controlled. This study demonstrates that propafenone is able to prevent pacing-induced VT in a limited number of patients. Stimulation techniques are useful in order to detect patients with potential pro-arrhythmic effect.

Administration, Oral↗
PubMed1985

[Oral and intravenous bepridil in the treatment of recurrent sustained ventricular tachycardias. Electropharmacological study].

The antiarrhythmic properties of bepridil on ventricular tachycardia (VT) termination and prevention were studied in 16 patients using programmed electrical stimulation techniques. All patients were admitted for documented sustained VT resistant to 3.5 +/- 2.4 antiarrhythmic agents. Intravenous bepridil (2 mg/kg) successfully terminated 4 out of 8 and prevented 3 out of 8 patients with hemodynamically well tolerated sustained VT. Oral bepridil (800 mg day 500-600 mg the following days) prevented successfully pacing-induced VT in 7 patients (43.7 p. cent) and a partial result was obtained in additional 3 (18.7 p. cent). In 6 patients bepridil failed to prevent pacing-induced VT including 2 patients with a shorter cycle length on bepridil (classified as aggravation). Tachycardia cycle length lengthened in the remaining 4 a mean of 11 +/- 12 p. cent. One of the 7 patients with a good result presented on bepridil evidence of sinus node dysfunction. The remaining 6 underwent long-term therapy (600 mg/24 h). During a mean follow up of 19 +/- 4 months, 4 patients are well controlled, 1 presented a side-effect (paralytic ileus) and 1 a recurrence. This study emphasizes the antiarrhythmic properties of bepridil at the ventricular level and provides evidence of its usefulness in patients with recurrent sustained VT.

Administration, Oral↗
PubMed1984

Bepridil for recurrent sustained ventricular tachycardias: assessment using electrophysiologic testing.

Bepridil was found to possess electrophysiologic properties common to class I and IV antiarrhythmic agents. Intravenous and oral bepridil were evaluated using serial electrophysiologic studies in a selected group of 9 patients with recurrent sustained ventricular tachycardia (VT) unresponsive to usual therapy, including amiodarone therapy in 15 patients. Intravenous bepridil treatment terminated sustained, well tolerated, pacing-induced VT in 3 of 6 patients and prevented the initiation of VT in 2 of these and in a patient in whom the drug failed to restore sinus rhythm. Oral bepridil was administered at a loading dose of 800 mg on day 1, and 500 to 600 mg the following days, and programmed electrical stimulation was repeated 2 to 6 days after initial study. Oral bepridil therapy prevented VT initiation in 6 patients (66%). The tachycardia cycle length was prolonged (30 to 105 ms) in 2 patients in whom VT remained inducible. In 1 patient the tachycardia cycle length significantly shortened after bepridil and prompt cardioversion was required. Five of the 6 patients with successful results underwent long-term oral treatment with bepridil. VT recurred in 1 patient during the hospitalization period and an adverse effect (paralytic ileus) in another patient required drug discontinuation. Three patients remain symptom-free over a follow-up of 4 to 13 months. These data suggest that bepridil may be useful in patients with recurrent, sustained VT.

Administration, Oral↗