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Biomedical subjects

J L Tonet

Publications and source records attributed to J L Tonet.

At least 37 records · Page 2Linked to original sources
PubMed1986

[Treatment of resistant ventricular tachycardia with endocavitary ablation combined with anti-arrhythmia agents].

Catheter ablation was used in 26 consecutive cases of high risk ventricular tachycardia (VT) resistant to antiarrhythmic therapy. Seven patients were in permanent VT at the time of catheter ablation, three of them were moribund. There were 10 cases of arrhythmogenic right ventricular dysplasia, 9 cases of VT complicating chronic myocardial infarction, 4 cases of dilated cardiomyopathy, 2 cases of idiopathic VT and one congenital cardiac malformation. Ten patients required 2 or more sessions of catheter ablation to treat their arrhythmia. Three of the 4 early deaths (less than 1 month) were due to technical problems. Combined with antiarrhythmic drugs in 8 cases, catheter ablation brought the VT under control in the 22 remaining patients. The follow-up period ranges from 10 to 28 months (average follow-up longer than 17 months). Catheter ablation is a technique which is currently under evaluation. The very encouraging results obtained in this series suggest that it may replace surgery in the treatment of chronic refractory VT.

Adolescent↗
PubMed1986

[Anti-tachycardia radiofrequency pacemakers. Experience with 44 cases].

Programmed cardiac stimulation may be performed externally using implanted radiofrequency receiving capsules. Between 1979 and 1984, 44 patients underwent implantation of these devices, 12 with atrial leads for supraventricular tachycardias (8 orthodromic reciprocating tachycardias, 1 intranodal junctional tachycardia and 3 atrial tachycardias), and 32 with ventricular leads for ventricular tachycardias. In the first case the transmitter was given to the patients so that they could terminate the tachycardias themselves. In the second case, the transmitter was kept in the cardiology department. All patients were also prescribed prophylactic antiarrhythmic drugs. The radiofrequency method was effective in 11 out of 12 cases of supraventricular tachycardia with a follow-up period ranging from 24 to 65 months (average 45 +/- 11 months). In the ventricular tachycardia group, the device was used in 11 patients to terminate ventricular tachycardia and in all patients to evaluate the efficacy of the antiarrhythmic therapy by provocative programmed stimulation with a follow-up ranging from 2 to 81 month (average 24 +/- 20 months). This palliative therapeutic method has reduced the number of hospital admissions in these patients. The indications are relatively few because of the efficacy of currently available antiarrhythmic agents and the possibility of radical treatment of tachyarrhythmias by surgery or catheter ablation.

Adult↗
PubMed1985

[Effect of oral propafenon on accessory pathways of atrioventricular conduction].

Fifteen consecutive patients with accessory AV pathways comprising 12 cases of the Wolff-Parkinson-White syndrome and 3 cases with exclusively retrograde conduction diagnosed by endocavitary electrophysiological investigation were studied. 5 patients had paroxysmal atrial fibrillation and the other 10 had reciprocating orthodromic tachycardia. 12 patients underwent electrophysiological investigation to measure the refractory periods and anterograde and retrograde conduction times in sinus rhythm and induced reciprocating tachycardia treatment with oral propafenone at a dose of 900 mg/day for 3 to 6 days. The refractory periods of anterograde conduction and the conduction times were then measured using an endocavitary atrial recording electrode left in position after the initial investigation. The anterograde Wenckebach point decreased from 259 +/- 35/min to 158 +/- 13/min (p less than 0.001). The refractory periods were increased from 270 +/- 45 ms to 371 +/- 100 ms (p less than 0.05). Atrial fibrillation could only be initiated in 2 cases with a mean rate which had decreased from 258 to 130/min. Reciprocating tachycardia could only be initiated in 5 cases and then with a slower rate (average cycle length increasing from 352 +/- 52 ms to 430 +/- 41 ms). Eight of these patients continued the treatment for over one year without recurrence of their arrhythmias, confirming the long-term efficacy of propafenone in the prevention of arrhythmias complicating accessory AV conduction pathways.

Administration, Oral↗
PubMed1985

[Emergency treatment of chronic ventricular tachycardia after myocardial infarction by endocavitary fulguration].

Endocavitary catheter ablation consists of delivering an impulse of 160 to 240 joules via a catheter used for electrophysiological investigation resulting in an electrical discharge which, in addition to its thermal effects may alter the arrhythmogenic substrate mechanically. This method was used in 2 patients with resistant and recurrent VT after myocardial infarction complicated by ventricular aneurysm. Two sessions of catheter ablation were necessary in both patients, but in the second one a single shock was successful in critically ill patients with VT. The first patient has been followed up for 20 months and the second for 13 months. Under prophylactic antiarrhythmic therapy, neither patient has had recurrence of the ventricular arrhythmias which had previously led to their hospitalisation. Catheter ablation is therefore presented as a technique which may be performed in the electro-physiological laboratory and repeated in cases of incomplete efficacy. This method may be used successfully in the treatment of chronic VT after myocardial infarction complicated by ventricular aneurysm.

Aged↗
PubMed1984

Arrhythmogenic right ventricular dysplasia: a clinical model for the study of chronic ventricular tachycardia.

Arrhythmogenic right ventricular dysplasia (ARVD) is a recently individualised clinical entity which sometimes presents with episodes of ventricular tachycardia (VT). These attacks may be resistant to anti-arrhythmic therapy and new therapeutic approaches have been developed for the treatment of this condition. These new methods are mainly surgical, based on the analysis of the electrical activation of the heart in sinus rhythm and during VT. This approach has increased our understanding of the physiopathology of VT, not only in the context of ARVD, but also in the most commonly encountered clinical setting of VT, after myocardial infarction. Electrophysiological study of the epicardial activation of the dysplastic zones has demonstrated the presence of delayed potentials recorded after the end of the QRS complex. This can be explained by the histopathology of these tissues. ARVD is characterised histologically by partial degeneration of the myocardial wall. Most of the muscle fibers are replaced by fatty tissue in the middle of which some healthy fibers survive. These changes are mainly observed in the intramyocardial and subepicardial layers, the subendocardium being almost normal. Strands of isolated muscle fibers within the non-conducting fatty degeneration may lead to very delayed activation with respect to the adjacent healthy tissues. The propagation of activation is delayed as it passes through this plexiform structure and in the zones adjacent to healthy muscle were reentry phenomena may arise. In ARVD, these changes are mainly located over the right ventricle, so explaining the right ventricular origin of most forms of VT observed in this condition. However, we have also observed a case which suggested an isolated arrhythmogenic left ventricular dysplasia. Epicardial mapping localizes the point of origin of VT in zones situated between the slow and normally conducting tissues. Simple ventriculotomy, a full thickness section of the ventricular wall, at the point of epicardial breakthrough of the VT prevents recurrence in the great majority of patients. The same pathophysiological concepts may be applied to VT complicating myocardial infarction but in this situation the myocardial fibers capable of slowly conducting the activation are isolated within the fibrous tissue in the border zone of the infarct. The point of origin of VT is usually within the interventricular septum with a point of epicardial breakthrough which could be located some distance away. Different surgical techniques have been developed to deal with this condition. Encircling endocardial ventriculotomy isolates the arrhythmogenic zone from the rest of healthy tissues by tracin

Adult↗
PubMed1984

[Endocavitary electric shock. Problems related to equipment].

Endocavitary catheter ablation is a new method of treating cardiac arrhythmias. It may be used indirectly, interrupting conduction through the His bundle in supraventricular arrhythmias, or directly by altering the arrhythmogenic substrate to prevent ventricular tachycardia or fibrillation. We have observed, together with other workers, that changes in the electrical properties of the catheters used to deliver the endocavitary electrical discharge. This was unexpected as the shock was delivered through a unipolar electrode with the indifferent electrode placed on the patient's back. An analysis of the morphology of the discharge impulse in intensity and voltage at increasing energy values showed that the unconnected electrodes of the multi-electrode catheter were raised to approximately the same voltage as the indifferent electrode. The change in electrical properties of some catheters was therefore the result of an insulation defect between the conducting wires leading to the electrodes. A study of the rupturing voltage of 32 USCI endocavitary catheters showed that 5 were able to sustain repeated shocks of 2 Kv and that 3 were able to sustain 3.5 Kv. The insulation of Cordis catheters was good but problems were encountered due to the resistance of the wires leading to the electrodes which dissipated an abnormally high amount of energy, so reducing the energy actually reaching the myocardium. These observations may explain the inconsistency of results obtained by different groups performing endocavitary catheter ablation with material not designed specifically for this purpose.

Arrhythmias, Cardiac↗
PubMed1984

[Endocavitary fulguration. A new method of treating arrhythmia?].

Endocavitary diathermy consists of transmitting the energy of a defibrillator shock to the tip of an intracardiac catheter. The circuit is completed via a neutral plate placed under the patient's back. Energies in the order of 200 to 300 joules produce an electric arc at the catheter tip which causes an abrupt variation in pressure and the creation of a shock wave which modifies the myocardial structures directly in contact with the catheter. This method, which was originally used to treat supraventricular arrhythmias by interrupting the conduction in the His bundle, has recently been extended to the treatment of resistant ventricular tachycardia, and has even been used to interrupt the accessory pathway in certain cases of Wolff-Parkinson-White syndrome. The authors report the basic experimental data and the clinical results obtained with this method in the treatment of 20 cases of arrhythmia, especially in various types of ventricular tachycardia. The very promising results obtained, particularly in cases of ventricular tachycardia, suggest that this is a radical method which can be extended to patients unable to support a surgical operation. Although the follow-up period is only short, these results are encouraging. They confirm the basic principle of diathermy in the treatment of supraventricular tachycardia by interruption of the conduction in the His bundle and for the radical treatment of chronic ventricular tachycardia unresponsive to medical treatment. However, a longer follow-up period is required before we can demonstrate the long term effectiveness of this new therapeutic method.

Adolescent↗
PubMed1983

[Torsades de pointes initiated by slow ventricular stimulation].

The authors report a case of isolated and probably congenital complete heart block with spontaneous torsades de pointes preceded by an increase in the QT interval. During positioning of a temporary pacing catheter mechanically induced extrasystoles were observed, which seem to favor ventricular extrasystoles and unsustained runs of torsades de pointes. When the basal rhythm showed no extrasystoles, electrical stimulation delivered late in diastole captured the ventricle normally and was then followed in reproducible fashion by episodes of torsades de pointes or minor equivalents. The mechanism of this phenomenon is thought to be related to a concealed phase 4 intramyocardial block. It may have important practical consequences in paced patients predisposed to torsades de pointes. If the pacemaker is programmed at too slow a rate, with stimulation falling late in diastole, torsades de pointes could occur, some attacks of which are known to degenerate to true ventricular fibrillation.

Cardiac Pacing, Artificial↗
PubMed1983

[Evaluation of the response to the ajmaline test in the diagnosis of paroxysmal atrioventricular blocks].

Between October 1973 and December 1981, 31 symptomatic patients who underwent pacemaker therapy on the results of a positive Ajmaline test alone, showing infrahisian AV block, were followed up clinically and electrocardiographically. The mean follow up from the date of implantation was 30 months. Two groups of patients were identified according to the results of electrophysiological investigations and clinical and electrocardiographic follow-up: --group I: 13 patients with either infrahisian AV block or an HV interval greater than or equal to 120 ms after Ajmaline; --group II: 18 patients with an HV interval less than 120 ms after Ajmaline. During follow-up, the 5 AV blocks observed out of the 7 documented at inhibition of the pacemaker and the only two cases of deterioration of the intraventricular conduction during sinus rhythm occurred in Group I. The only discriminating variable between the two groups before the implantation of a pacemaker was the response to the Ajmaline test. The difference of the results of the electrical outcome between the two groups was statistically significant (p less than 0,03). During the same study period this critical value was observed in 49 other patients with a basal HV greater than or equal to 70 ms. In this group, 20 developed infrahisian AV block after Ajmaline, 26 had a HV interval greater than or equal to 120 ms and only 3 cases had HV intervals of 100 ms. These results suggest that a HV interval greater than or equal to 120 ms after Ajmaline has the same significance as infrahisian block produced by the drug.

Aged↗
PubMedDate not supplied

[Ventricular dysplasia. Nosology and sudden death].

The arrhythmia generating dysplasia of the right ventricle is a congenital anomaly suggesting a hereditary substratum. It usually manifests itself as follows: a young patient, with recurrent episodes of ventricular tachycardiac. There is no "pathognomonic sign" of dysplasia. The latter may only be determined by anatomical examination of the heart, macroscopically as well as microscopically. The most difficult differential diagnosis concerns minor or localized forms of dilated idiopathic myocardiopathy or sequelae of myocarditis with ventricular tachycardia originating in the right ventricle. It seems, currently, more appropriate to talk about "arrhythmia generating syndrome of the right ventricle" rather than arrhythmia generating dysplasia of the right ventricle, in these particular cases. The arrhythmia generating syndrome of the right ventricle could cause a sudden death in these young patients, especially during a violent physical exercise or practise of sports. The current nosological classification is based on an experience acquired by comparing a few isolated cases. The search for late potentials by summation-mean measurements and nuclear magnetic resonance could provide a new diagnostic approach.

Death, Sudden↗
PubMedDate not supplied

[Sudden death of a patient with a pacemaker caused by heart rupture in a "cloisonné" pericardium].

Myocardial infarction is sometimes accompanied by bradycardia requiring either temporary or permanent cardiac pacing. In addition an MI reduces the amplitude of endocardial action potentials which produces the conditions for defective detection of spontaneous ventricular complexes by the pacemaker. In this particular condition, the competing cardiac rhythm which arises frequently causes malignant arrhythmias which are potentially fatal. This danger is increased even further by endocardial stimulation of the right ventricle with myocardial infarction of the right ventricle. We have reported in this paper the instructive case of a patient with coronary heart disease, hospitalized for third degree AV block with syncope which developed following a massive postero-diaphragmatic MI, but with few symptoms. After secondary extension of the necrotic area, the artificial pacemaker implanted manifested defective firing which resulted in development of ventricular fibrillation. The latter was controlled by cardioversion, but the patient died from disordered conduction after 30 seconds of complete asystole. For one minute, the pacemaker did not stimulate the ventricle because of "electrical stunt to the myocardium", caused by the shock from the defibrillator. Anatomical examination (at autopsy) confirmed the cardiac rupture.

Aged↗