André Waleffe
University of Liège
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American Heart Journal | 1980
André Waleffe; L. Mary-Rabine; Victor Legrand; J.Cl. Demoulin; Henri Kulbertus
A combined mexiletine and amiodarone treatment was applied in nine cases with recurrent refractory ventricular tachycardia. During the first two days of treatment, mexiletine and amiodarone were perfused intravenously at a dose of 1,000 mg. and 1,500 mg. per 24 hours, respectively. Simultaneously amiodarone was also given orally at a dose of 600 mg. per 24 hours. From the third day onwards, the intravenous administration was interrupted and both drugs were continued orally at a dose of 600 mg. daily. The first three patients were very critically ill and had had at least five episodes of ventricular tachycardia per 24 hours during the last 10 days in the intensive care unit. The treatment resulted in total suppression of the tachycardic episodes within three days after initiation of therapy. In the remaining six cases, ventricular tachycardia was easily initiated by programmed electrical stimulation of the heart. No arrhythmia could be elicited by repeated testing on the seventh day of treatment. The mean follow-up period was 6 months. Two patients with poor left ventricular function died in intractable heart failure. Another one died suddenly 4-1/2 months after his release from the hospital. He had a large aneurysm and whether he continued his treatment is unknown. A fourth patient had an aneurysmectomy; he suffered a recurrence, and died at his second operation. All the others presently remain asymptomatic. The association of a class I (mexiletine) with a class III (amiodarone) agent is theoretically attractive for the treatment of refractory ventricular arrhythmias. The present findings corroborate this hypothesis, but show that this association is not able to protect individuals with severe underlying myocardial damage.
Pacing and Clinical Electrophysiology | 1984
Karel den Dulk; Michel Bertholet; Pedro Brugada; Frits W. Bär; Jean Claude Demoulin; André Waleffe; Noud Bakels; Fred W. Lindemans; Ivan Bourgeois; Henri Kulbertus; Hein J.J. Wellens
Pacing is becoming an accepted form of treatment for reentry tachycardias. The different pacing modalities available and experience with a patient‐activated antitachycardia pacemaker are presented in this paper. This system has bidirectional communication between pacemaker and pacemaker‐activator and between pacemaker and prescription formulator (which is a sophisticated portable stimulator used for non‐invasive electrophysiological evaluation of the system). This pacemaker was implanted in 18 patients with drug‐resistant tachycardias. Six patients had ventricular tachycardia, 3 had A‐V nodal reentrant tachycardia, 4 had the concealed accessory pathway, and 5 had the WPW syndrome. In the 3 months before implantation the mean number of admissions for termination of tachycardia was 2.1 per patient‐month. During a follow‐up period of 3–26 months only 6 patients were admitted once for termination of tachycardia (0.02 admissions per patient‐month). The reasons for admission of these 6 patients were: defective pacemaker activator in 2 patients, inadequate control of tachycardia in 2 patients, inappropriate use of the device in 1, and inadequate intake of medication in 1. All these problems were solved easily. Eight pacemaker activators required reprogramming, which was done in 5 patients on an out‐patient basis. The interval scanning mode was used in 9 patients. Nine patients required more than 2 stimuli for reproducible termination. A step‐wise increase in number of stimuli was used in 5 patients.
American Journal of Cardiology | 1983
Karel den Dulk; Michel Bertholet; Pedro Brugada; Frits W. Bär; David Richards; Jean Claude Demoulin; André Waleffe; Noud Bakels; Fred W. Lindemans; Ivan Bourgeois; Henri Kulbertus; Hein J.J. Wellens
Abstract Externally activated pacemaker systems were implanted in 13 patients to control their drug-resistant tachycardias. Four patients had ventricular tachycardia, 2 had atrioventricular nodal reentrant tachycardia, 3 had tachycardias due to a left-sided concealed accessory pathway and 4 had Wolff-Parkinson-White syndrome. Nine patients were paced from the right ventricle, 2 from the right atrium and 2 from the coronary sinus. The pacing system consisted of an implantable pacemaker, an external pacemaker activator and a prescription formulator. The pacemaker can signal sensing by way of radiofrequency signals to the pacemaker activator or prescription formulator. Either 1 of the latter 2 devices then determines whether the sensed rhythm fulfills the tachycardia detection criteria and, if so, controls the delivery of the selected stimulation treatment by the pacemaker. With this bidirectional radiofrequency coupling, tachycardias were noninvasively initiated by the prescription formulator after implantation and at follow-up visits to test and eventually reprogram the pacemaker activator. During a follow-up of 116 patient-months, 624 episodes of tachycardia were effectively terminated by the patients. Incidental failure to terminate occurred in 3 patients because of a defective activator, changes in the electrophysiologic substrate and inappropriate use of the device. These problems were solved by reprogramming, replacement of the activator and education of the patient. Hospital admissions for termination of tachycardia decreased from an average of 2.6 per patient-month (in the 3 months before implantation) to 0.03 per patient-month after implantation (follow-up 4 to 16 months). It is concluded that (1) this programmable externally activated pacemaker system effectively manages drug-resistant tachycardia; (2) this system has the advantage of easy testing, multiple pacing modes and ready reprogrammability; and (3) the marked reduction in hospital admissions makes the system cost-effective.
Journal of Electrocardiology | 1978
André Waleffe; Patrick Bruninx; Henri Kulbertus
Summary The atrio-ventricular and ventriculo-atrialconduction times as well as the mechanism of tachycardia were studied by programmed electrical stimulation, before and after the intravenous injection of 300 mg of amiodarone, in 12 patients with paroxysmal reentrant supraventricular tachycardia (PSVT). Four subjects had, at least intermittently, electrocardiographic evidence of the Wolff-Parkinson-White syndrome. In four patients, a concealed accessory pathway was present. In the remaining four cases, the tachycardia circuit was confined to the A-V node. Amiodarone lengthened the effective andfunctional refractory periods of the A-V node, the A-V nodal conduction time and the refractory period of the atrial muscle. Administered intravenously during PSVT,amiodarone terminated the tachycardia in five out of six patients. It also slowed the heart rate during the tachycardic episodes. In two of four subjects with intranodal tachycardia, no arrhythmia could be initiated after amiodarone administration. In three patients, atrial fibrillation was induced during positioning of the catheters at the beginning of the procedure. Amiodarone was injected intravenously in those cases; sinus rhythm was restored in two instances and, in the third, the arrhythmia could be interrupted by a DC shock which had been unsuccessful prior to drug administration.
American Journal of Cardiology | 1980
André Waleffe; Luc Mary-Rabine; Henri Kulbertus
Moxaprindine, a new derivative of aprindine, possesses antiarrhythmic properties and is significantly less toxic than its parent compound on hematopoietic cells in culture. Its electrophysiologic effects were studied with programmed electric stimulation of the heart in 19 patients with recurrent episodes of reentrant tachyarrhythmias (atrioventricular nodal tachycardia, 8 cases; circus movement tachycardia involving an accessory pathway, 6 cases; ventricular tachycardia, 4 cases; ventricular tachycardia and atrioventricular nodal tachycardia, 1 case). Moxaprindine was perfused intravenously at a dose of 0.15 (10 cases) or 0.2 mg/kg per min (9 cases) during 15 minutes. Moxaprindine lengthened the conduction time along the His-Purkinje system as well as the refractory periods of right atrial and ventricular muscle. Depressing effects on the atrioventricular node were also seen, especially at the larger dose. The effects of the drug on accessory pathways used in anterograde manner were measurable in three cases. Complete blockade along the bypass was seen in two and prolongation of the effective refractory period in the remaining one. After moxaprindine, five of six patients showed retrograde blockade along the accessory pathway, whereas the last subject had prolongation of the refractory period of the bypass used in a ventriculoatrial direction. Perfused intravenously during episodes of tachycardia (atrioventricular nodal tachycardia, eight cases; circus movement tachycardia using an accessory pathway, six cases; ventricular tachycardia, three cases), the drug interrupted the rhythm disorder in all 17 instances. No tachycardia could be elicited after moxaprindine in 11 of the 19 patients. Among the six in whom sustained tachycardia could still be initiated, five had received the smaller dose. It is concluded that moxaprindine is a potent antiarrhythmic agent whose long-term efficacy and toxicity in patients deserve further investigation.
American Journal of Cardiology | 1979
André Waleffe; Patrick Bruninx; Luc Mary-Rabine; Henri Kulbertus
The electrophysiologic effects of tocainide were studied with programmed electrical stimulation of the heart in two patients with atrioventricular (A-V) nodal tachycardia, five patients with reentrant tachycardia involving an accessory pathway and two patients with paroxysmal ventricular tachycardia. The measurements were made before and after a 15 minute perfusion of tocainide at a dose of 0.75 mg/kg per min in the first seven patients and of 0.5 mg/kg per min in the last two. At the end of perfusion, the drug plasma level ranged from 2.0 to 10.2 μg/ml (mean 6). During the subsequent 60 minutes, the plasma level decreased extremely slowly, its mean value remaining constantly between 3 and 4 μg/ml. Tocainide failed to achieve statistically significant effects on the functional properties of the A-V node. However, an increase of A-H time (two patients), prolongation of nodal refractory period (one patient) and lengthening of the cycle length producing a second degree A-V block (four patients) were observed in isolated cases. The H-V interval increased by 20 msec in three of the eight cases in which its measurement was not hampered by the constant presence of a preexcitation wave. No systematic effect on the refractory periods of the atrial and ventricular muscle was noted. In six patients, tocainide was perfused during sustained episodes of tachycardia (A-V nodal tachycardia, two patients; circus movement tachycardia using an accessory pathway, three patients; and paroxysmal ventricular tachycardia, one patient). Sinus rhythm was restored in all six patients. The drug prevented reinitiation of tachycardia in four of the eight patients in whom it could easily be triggered during the control period; it lengthened the tachycardia cycle length in the remaining four. No side effects were noted. These results, obtained with low plasma levels of tocainide, allow one to consider this drug a promising antiarrhythmic agent.
American Heart Journal | 1985
Michel Bertholet; J. C. Demoulin; André Waleffe; Henri Kulbertus
Sixteen patients with recurrent, drug-resistant supraventricular (13 patients) or ventricular (3 patients) tachycardia were treated chronically by programmable extrastimulus pacing; either a fully automatic device (Telectronics PASAR 4151: eight patients with supraventricular tachycardia) or a patient--activated device (Medtronic Interactive Tachy System) was used. During a follow-up period of 5 to 30 months, five of the subjects treated with the fully automatic device showed successful results, one had recurrent tachycardia, and two had their units explanted for system-related problems. The patients treated with the externally activated device were, on the whole, very well controlled. This mode of treatment, if applied in well-selected cases, is promising; it seems safe and considerably reduces the number of hospital admissions.
Pacing and Clinical Electrophysiology | 1989
Veronique Mahaux; André Waleffe; Henri Kulbertus
Sensolog 703 is a new single chamber activity sensing rate modulated pacemaker that offers an automatic adjustment of settings called Autoset. Units were implanted in 11 patients (mean age: 67 years) for atrioventricular block (two patients), sinoatrial block (three patients), sick sinus syndrome (four patients), chronotropic incompetence (one patient), and atrial fibrillation with slow ventricular response (one patient). The devices were programmed in VVIR mode using Autoset. The accuracy of the settings was verified by the built‐in histogram function. In 6/11 patients, these settings were not satisfactory. Autoset was repeated at 6 months (nine patients) and 10 months (five patients) after implantation. External telemetric recordings daring daily life activities, Holter monitoring, bicycle or treadmill stress tests helped in the evaluation of the rate response obtained with the automatic programming. The following problems were encountered: maximum pacing rate for a low level of exercise (four patients), insufficient rate increase (four patients), higher pacing rate daring low than daring heavy exercises (four patients). A time‐consuming (15 to 48 minutes) manual programming was necessary in eight out of nine patients (6 months) and five out of five patients (10 months). In our study, Sensolog 703 algorithm tended to behave as an on/off system; automatic programming was time consuming and only indicative.
Pacing and Clinical Electrophysiology | 1992
Veronique Mahaux; Yves Verboven; André Waleffe; Henri Kulbertus
A sensor driven algorithm limiting ventricular pacing rate during supraventricular tachycardia (SVT) is included in a dual chamber rate modulated pacemaker sensitive to acceleration forces (Relay, 294‐03, Intermedics Inc.). According to the intensity of concomitant exercise, the ventricular pacing rate is limited either to the programmed maximum pacing rate (MPR) or to an interim lower limit, called “conditional ventricular tracking limit” (CVTL). The MPR prevails over the CVTL when the sensor calculated pacing rate exceeds the minimal rate by more than 20 beats/mm. The purpose of the study is to determine the clinical safety and efficacy of this algorithm in patients with intermittent SVT. Method: a Relay was implanted in four patients with a bradycardia/tachycardia syndrome and in four patients with complete atrioventricular block (CAVB). All had episodes of paroxysmal atrial tachycardia. The units were programmed in DDDR: rate responsive parameters were adjusted by simulating the rate response during three levels of exercise to let the MPR override the CVTL only during strenuous exercise. Holter monitors and exercise testings were performed at 3‐month follow‐up. Results: in seven patients, Holter recordings showed Supraventricular arrhythmias at rest with a ventricular pacing rate limited to the CVTL. Appropriate rate increases during exercise testings were also demonstrated. Three devices had to be reprogrammed in DDIR tone patient suffering from nearly permanent atrial flutter and two patients not tolerating the CVTL pacing rate at rest). Conclusion: the CVTL algorithm is effective in protecting against high ventricular pacing rates during Supraventricular arrhythmias. It allows the selection of the DDDR mode even with a high MPR in patients with intermittent SVT.
Acta Clinica Belgica | 1988
Luc Jordaens; André Waleffe; Derom F; Luz Marie Rodriguez; Denis Clement; Henri Kulbertus
SummaryFive patients received the automatic implantable cardioverter-defibrillator (AICD-B) for °ut-of-hospital cardiac arrest.The primary clinical arrhythmia was ventricular fibrillation in two patients, recurrent mnornorphic ventricular tachycardia in another and polymorphic ventricular tachycardia in another last one. The defibrillation threshold for ventriular fibrillation was 15 Joules in all patients. The rate cut-off criterion was choscn between and 174 beats/min. During a mean follow-up period of sixteen months (range 6 to 35), the five Patients received 60 discharges. Nine shocks were given for arrhythmias induced in the laboratory and 51 were given in clinical conditions. We documented twenty-nine shocks.Sinus rhythm triggered the device once, atrial fibrillation twice and short lasting ventricular tachycardia two times. These unwanted discharges never resulated in ventricular arrhythmias. Assocciated treatment consisted of antiarrthymic drugs in four patients and a maker for bradycardia and tac...