Impact of transesophageal electrophysiologic study to elucidate the mechanism of arrhythmia on children with supraventricular tachycardia and no preexcitation.

An electrophysiologic study (EPS) of children and teenagers with paroxysmal supraventricular tachycardia (SVT) and normal electrocardiography (ECG) in sinus rhythm was evaluated. Generally, EPS is performed only before paroxysmal SVT ablation in these patients. In this study, 140 patients (mean age, 15 ± 3 years) with normal ECG in sinus rhythm were studied for SVT by a transesophageal route in baseline state and after isoproterenol. Idiopathic left or right ventricular tachycardia was diagnosed in four patients (3 %). Anterograde conduction over an atrioventricular (AV) left lateral (n = 10) or septal (n = 9) accessory pathway (AP) was noted in 19 patients (13.5 %) at atrial pacing. Orthodromic AV reentrant tachycardia (AVRT) was induced in these children. Five of the patients had a high rate conducted over AP (>240 bpm in baseline state or >290 bpm after isoproterenol). Two of the patients (a 10-year-old girl with well-tolerated SVT and a 17-year-old with syncope-related SVT) had the criteria for a malignant form with the induction of atrial fibrillation conducted over AP at a rate exceeding 290 bpm in baseline state. Of the 140 patients, 74 (53 %) had typical AV node reentrant tachycardia (AVNRT), nine had atypical AVNRT (6 %), 1 had atrial tachycardia (0.7 %), and 33 (23.5 %) had AVRT related to a concealed AP with only retrograde conduction. Electrophysiologic study is recommended for children with paroxysmal SVT and normal ECG in sinus rhythm. The data are helpful for guiding the treatment. Ventricular tachycardia or atrial tachycardia can be misdiagnosed. Masked preexcitation syndrome with anterograde conduction through AP was present in 13.5 % of the patients, and 1.4 % had a malignant preexcitation syndrome.

[Significance of permanent atrial fibrillation in idiopathic dilated cardiomyopathy]. / Signification de la fibrillation auriculaire permanente dans la cardiomyopathie dilatée primitive.

UNLABELLED: The significance of atrial fibrillation (AF) in idiopathic dilated cardiomyopathy (IDCM) remains discussed. The purpose of the study was to evaluate the clinical significance of permanent atrial fibrillation in patients with IDCM. METHODS: Systematic noninvasive and invasive studies including Holter monitoring, measurement of left ventricular ejection fraction (LVEF), electrophysiological study and coronary angiography were performed in 323 patients with IDCM; all patients had a left ventricular ejection fraction (LVEF)<40%. The studies were indicated for spontaneous ventricular tachycardia (VT) in 69 patients, syncope in 103 patients and nonsustained VT on Holter monitoring in 151 asymptomatic patients. Sixty-five patients were in permanent AF (group I). Remaining patients were in sinus rhythm at the time of evaluation (group II). Programmed ventricular stimulation using up to 3 extrastimuli in control state and if necessary after isoproterenol was systematic. Patients were followed 3+/-2 years. RESULTS: Mean age was significantly older in group I (61+/-8 years) than in group II (52+/-12) (P<0.01). Syncope (31 vs 36%), spontaneous sustained VT (18 vs 23%); mean LVEF (28+/-9% vs 29+/-9%), VT induction (25 vs 35%) were similar in both groups. During the follow-up, there were no statistical differences between groups I and II concerning each event: sudden death occurred in 13 patients, 1.5% of group I patients and 5% of group II patients (NS); a death related to heart failure occurred 22 patients, 5% of group I patients and 7% of group II patients (NS); heart transplantation was performed in 13 patients, 8% of group I patients and 3% of group II patients (NS). CONCLUSIONS: An older age is the only significant clinical factor associated with the presence of a permanent atrial fibrillation in idiopathic dilated cardiomyopathy. The presence of permanent AF does not increase the induction of a sustained ventricular tachycardia and does not affect the general prognosis of IDCM.

Supraventricular tachyarrhythmia as a cause of sudden cardiac arrest.

INTRODUCTION: Supraventricular tachyarrhythmias (SVTA) are an accepted cause of cardiac arrest in patients with Wolff-Parkinson-White syndrome (WPW) and hypertrophic cardiomyopathy but their participation in other conditions is less well understood. The purpose of the study was to examine the role of SVTA in sudden cardiac arrest (SCA) by comprehensive evaluation of patients successfully resuscitated from SCA. METHODS: A total of 169 survivors of SCA in the absence of acute myocardial infarction underwent systematic evaluation that included echocardiography, Holter monitoring, coronary angiography and electrophysiological study (EPS) with additional testing in selected cases using provocative drug testing with isoproterenol, ajmaline or ergonovine. RESULTS: SVTA was found as the only possible cause or as the cause facilitating SCA in 29 patients: (1) 3 had a WPW syndrome related to accessory pathway with short refractory period; (2) for 12 patients, SVTA was the cause of cardiovascular collapse; heart disease (HD) was present in 11 cases, but disappeared in two of four with dilated cardiomyopathy after the restoration of sinus rhythm; (3) in 14 patients, SVTA degenerated either in a VF or ventricular tachycardia (VT); HD was present in 12 cases, but disappeared in one; two had no HD and recurrent similar arrhythmia was documented by cardiac defibrillator in one of them. SVTA induced coronary ischemia was the main cause of SCA. CONCLUSION: Rapid SVTA was a cause of SCA, either by cardiovascular collapse or by the degeneration in VT or VF. The complication generally occurred in patients with advanced HD or with rapid SVTA-induced cardiomyopathy and rarely in patients without HD. The incidence of SVTA as the only cause or the facilitating cause of SCAs is probably underestimated, because it is difficult to prove.

[Significance of isuprel infusion in unexplained syncope after myocardial infarction]. / Intérêt de la perfusion d'Isuprel dans le bilan des syncopes inexpliquées après infarctus du myocarde.

UNLABELLED: The prognosis for patients with complications and syncope following myocardial infarction depends on the left ventricular ejection fraction (LVEF) and the mechanism of the syncope. The aim of this study was to evaluate the results of an electrophysiological study (EPS) following isoproterenol infusion in patients with a negative EPS under basal conditions. The population included 60 patients, aged 60 +/- 12 years, 5 of whom had syncope on effort or with stress. The EPS included measurement of AV conduction, with programmed atrial and ventricular stimulation. It was repeated following infusion of 2 to 4 microg/kg of isoproterenol. RESULTS: An arrhythmia was identified as preceding the syncope in 27 patients (45%): ventricular tachycardia (VT) n = 16, supraventricular tachycardia (n = 5), 2nd or 3rd degree AV block (n = 3), vaso-vagal reaction (n = 3): 3 subjects developed coronary ischaemia. The subjects with VT on Isuprel differed from those without VT, with a lower LVEF (34 +/- 8 vs 45 +/- 14%) (p < 0.05), a higher incidence of effort related syncope (4 vs 1) and a higher risk of cardiac death (6/16 vs 2/44) (p < 0.01). In conclusion, we recommend repeating the electrophysiogical test under Isuprel in patients with complications after MI and a negative EPS in the basal state whether or not they have exercise related syncope, which will reveal an arrhythmia in 45% of cases. Subjects with inducible VT are at high risk of cardiac death.

[Prevalence of supraventricular tachycardia and tachyarrhythmias in resuscitated cardiac arrest]. / Incidence des tachycardies et tachyarythmies supraventriculaires dans les morts subites récupérées.

Supraventricular arrhythmias are considered to be benign when the ventricular rate is slowed and treated by anticoagulants. The aim of this study was to determine the possible influence of these arrhythmias in resuscitated cardiac arrest. Between 1980 and 2002, 151 patients were admitted after a cardiac arrest. Supraventricular arrhythrmias were identified as a possible cause of the cardiac arrest in 21 patients. They underwent echocardiography, exercise stress test, Holter ECG monitoring , coronary angiography and electrophysiological investigation. After these investigations, three patients had a malignant form of the Wolff-Parkinson-White syndrome, two were asymptomatic and, in the third patient, ventricular fibrillation was induced by treatment with diltiazem. In 8 patients, a rapid supraventricular arrhythmia was considered to be the cause of cardiac arrest by cardiogenic shock; 2 patients had hypertrophic cardiomyopathy, 5 had severe dilated cardiomyopathy which regressed in one patient. In ten patients, cardiac arrest due to ventricular tachycardia or fibrillation was provoked by a rapid (> 220 beats/min) supraventricular arrhythmia; two patients had no apparent underlying cardiac pathology. In the others, myocardial ischaemia or acute cardiac failure were considered to be the cause of the cardiac arrest. The authors conclude that rapid supraventricular arrhythmias may cause cardiac arrest either by cardiogenic shock or degenerescence to ventricular tachycardia or fibrillation. Usually, this event occurs in patients with severe cardiac disease but it may occur in subjects without cardiac disease or by an arrhythmia-induced cardiomyopathy.

The signal-averaged electrocardiogram is of limited value in patients with bundle branch block and dilated cardiomyopathy in predicting inducible ventricular tachycardia or death.

An abnormal signal-averaged electrocardiogram (SAECG) has predictive value for arrhythmic events in patients with idiopathic dilated cardiomyopathy and a normal conduction. The purpose of this study was to investigate whether the presence of a complete bundle branch block (BBB) affects prognostic information of the SAECG. We prospectively obtained SAECGs in 128 patients with idiopathic dilated cardiomyopathy. Forty-three of them had BBB and 85 had a normal QRS duration. According to their clinical history and results of ventricular programmed stimulation, patients were divided into 4 groups: (1) group IA with BBB and ventricular tachycardia (VT) (n = 18); (2) group IB with BBB but without VT (n = 25); (3) group IIA without BBB but with VT (n = 40); (4) group IIB without BBB and without VT (n = 45). Patients were compared with 129 patients without heart disease and without VT. Fifty-seven of them had BBB (group III) and 72 had normal conduction (group IV). The filtered QRS duration was longer in group IB than in group III (175 +/- 21 vs 149 +/- 16 ms, p <0.001), and in group IIB than in group IV (111 +/- 19 vs 96 +/- 12 ms, p <0.05). QRS duration was similar in groups IA and IB (176 +/- 24 vs 175 +/- 21 ms) but longer in group IIA than in group IIB (131 +/- 24 vs 111 +/- 19 ms, p <0.001). The low-amplitude signal duration (LAS) and the root-mean-square voltage (RMS) of the last 40 ms of the filtered QRS did not differ between groups IB and III and IA and IB. LAS and RMS were, respectively, longer (44 +/- 20 vs 31 +/- 13 ms, p <0.01) and lower (21 +/- 20 vs 43 +/- 33 microV, p <0.001) in groups IIA and IIB. In groups IA and IB the combination of 2 of the 3 available criteria: QRS duration >170 ms, RMS <20 microV, LAS >45 ms lead up to the best overall statistical result, with a sensitivity and specificity of 78% and 56%, respectively. In groups IIA and IIB, using conventional late potential criteria, the sensitivity and specificity of the SAECG for VT detection were 65% and 73%, respectively. The risk of sudden death was not predicted by the SAECG, and total cardiac mortality was only dependent on left ventricular ejection fraction. In conclusion, QRS duration was prolonged in all of the patients with a dilated cardiomyopathy compared with those without heart disease. BBB did not change the sensitivity but decreased the specificity of the SAECG to predict any VT risk in dilated cardiomyopathy. The risk of sudden death and total cardiac mortality could not be predicted by the SAECG.

Value of esophageal pacing in evaluation of supraventricular tachycardia.

Esophageal stimulation was performed in 40 patients who had spontaneous paroxysmal supraventricular tachycardias (SVTs). The purpose of this study was to look for the most sensitive stimulation protocol and criteria that would help to define the mechanism of reentry. In 20 patients (group I) atrial pacing up to second-degree atrioventricular block was performed under control conditions and isoproterenol, and SVT was induced in 14 patients (70%), 11 in the control state and 3 while receiving isoproterenol. In 20 patients (group II) atrial pacing and programmed atrial stimulation using 1 and 2 extrastimuli delivered at 2 cycle lengths (600 and 500 ms) was performed in the control state and while receiving isoproterenol. SVT was induced in all patients, in 13 patients in the control state and in 7 while receiving isoproterenol. Programmed stimulation always induced SVT and was the only method capable of tachycardia induction in 14 patients. The mechanism of SVT could be established in 91%. The measurement of the ventriculoatrial interval was the most useful sign to define the site of reentry. Occurrence of a bundle branch block helped to delineate the mechanism in 4 patients. When a positive P wave in V1 preceded the esophageal atrial electrocardiogram, it suggested that there was reentry through a left-sided accessory atrioventricular connection in 6 patients. SVT could always be induced by programmed atrial stimulation in the control state and under isoproterenol. The location of the P wave in V1 compared to the ventriculogram and the esophageal electrocardiogram helped to define the mechanism of tachycardia.

Provocation of supraventricular tachycardias by an intravenous class I antiarrhythmic drug.

Antiarrhythmic drugs may aggravate or induce ventricular arrhythmia. The induction of a supraventricular tachycardia or its facilitation has rarely been reported. The purpose of the study was to know whether the potential for supraventricular proarrhythmic effect of a class Ia intravenous antiarrhythmic drug can be exposed during electrophysiologic study. Ajmaline was chosen because of its short duration of action. The protocol of the study consisted of an electrophysiological study and programmed atrial stimulation using 1 and 2 extrastimuli on driven rhythm and atrial pacing up to second-degree atrioventricular block. Then 1 mg/kg of ajmaline was injected and atrial pacing was performed 3 minutes after its injection. Supraventricular proarrhythmic effect of ajmaline was defined as the spontaneous occurrence of a supraventricular tachycardia or the facilitation of its induction. Seventy patients among 1955 presented a proarrhythmic effect: 63 developed a supraventricular tachyarrhythmia (atrial flutter, fibrillation, tachycardia) and 7 an atrioventricular reentrant tachycardia, either spontaneously (n = 23) or during atrial pacing (n = 47). Risk factors were identified in most patients: old age, underlying heart disease, history of spontaneous supraventricular tachycardia and/or induction of a supraventricular tachycardia by 2 extrastimuli on driven rhythm in the control state (34 patients), sinus node dysfunction (22 patients). Compared with patients without proarrhythmic supraventricular effect only the history of spontaneous supraventricular tachycardia and the existence of a sinus node dysfunction were significantly more frequent (P less than 0.05) in patients with proarrhythmic effect of ajmaline. In conclusion, the supraventricular proarrhythmic effect of intravenous ajmaline exists and is related both to the electrophysiologic characteristics of the drug and to the arrhythmia substrate. The results indicate that a supraventricular tachyarrhythmia may be induced by a class I antiarrhythmic drug.

Predictors of atrial flutter with 1:1 conduction in patients treated with class I antiarrhythmic drugs for atrial tachyarrhythmias.

OBJECTIVES: The purpose of the study was to look for the predictor factors of atrial proarrhythmic effects of class I antiarrhythmic drugs. BACKGROUND: Class I antiarrhythmic drugs may induce or exacerbate cardiac arrhythmias. The predictors of ventricular proarrhythmia are known. The predictors of atrial flutter with 1:1 conduction are unknown. METHODS: Clinical history, EGG, signal-averaged EGG (SAECG) and electrophysiologic study were analysed in 24 cases of 1:1 atrial flutter with class I AA drugs and in 100 control patients without history of 1:1 atrial flutter with class I AA drugs. RESULTS: The ages of patients varied from 46 to 78 years. Underlying heart disease was present in nine patients. The surface EGG revealed the presence of a short PR interval (PR<0.13 ms), visible in leads V5, V6 in eight (35%) patients with normal P wave duration; in other patients with prolonged P wave duration, PR seemed normaL On SAECG recording, there was a pseudofusion between P wave and QRS complex. The electrophysiologic study revealed some signs indicating a rapid AV nodal conduction (short AH interval or rate of 2nd degree AV block at atrial pacing >200 beats/mm) in 19 of the 23 studied patients. All patients, except one, had at least one sign indicating a rapid AV nodal conduction (short PR and/or P wave-QRS complex continuity on SAECG). In the control group, seven patients (7%) had a short PR interval (P<0.01) and 11 (11%) had a pseudofusion between P wave and QRS complex on SAECG (P<0.001). The P wave-QRS complex pseudofusion on SAECG had a sensitivity of 100% and a specificity of 89% for the prediction of an atrial proarrhythmic effect with class I antiarrhythmic drug. CONCLUSION: We recommend avoiding class I AA drugs in patients with a short PR interval on surface EGG and to record SAECG in those with apparently normal PR interval to detect a continuity between P wave and QRS complex, which could indicate a rapid AV nodal conduction, predisposing to 1:1 atrial flutter with the drug.

[Signal averaged ECG and mechanisms of sudden death]. / ECG haute amplification et mécanisme de la mort subite.

The aim of signal averaged electrocardiography is to detect late potentials (LP) which are markers of ventricular tachycardia. As sudden death is often due to ventricular fibrillation which can complicate ventricular tachycardia, some workers have suggested that the presence of LP may increase the risk of sudden death. We analysed the results of signal averaged ECG in 17 subjects who died suddenly and compared them with 8 patients who died from ventricular tachycardia. These two groups of patients were part of a general population of 450 subjects who underwent programmed ventricular stimulation and signal averaged ECG by Simson's method (25 Hz filter). Three parameters of this ECG were analysed: total QRS duration (Dur QRS), amplitude of the signal 40 ms before its termination (V 40), and the duration of the terminal activity less than 40 microV (Dur LP). The criteria of diagnosis of Lp were: Dur QRS greater than or equal to 120 ms, V 40 less than or equal to 20 microV, Dur LP greater than or equal to 40 ms. The results of signal averaged ECG of patients who died suddenly were different to those of patients who died from VT: Dur QRS 116 +/- 40 vs 140 +/- 25 ms, V 40 27 +/- 24 vs 7 +/- 8 microV, Dur LP 39 +/- 27 vs 59 +/- 14 ms. Only 8 patients who died suddenly had LP (47%) whereas all patients who died of VT had LP. A correlation was observed between the presence of LP and 2 factors: the LV ejection fraction which was significantly lower in patients with LP (28 +/- 8 vs 46 +/- 19%) and the results of programmed ventricular stimulation: patients with induced sustained VT less than 270/mn usually had LP (15/16). LP were usually absent (4/6) in cases of ventricular flutter (VT greater than or equal to 270/mn) or induced VF. The presence of LP in 2 patients could signify a risk of developing VT later on. In conclusion, 9/17 patients who died suddenly did not have LP. The risk of sudden death due to primary VF or V flutter cannot be predicted. Other causes of VF are even harder to identify.

[Changes in high amplitude ECG during hospitalization for myocardial infarction]. / Evolution de l'ECG haute amplification en phase hospitalière d'infarctus du myocarde.

The aim of this study was to determine the optimal time for recording the signal averaged electrocardiogram in order not to miss cardiac events after acute myocardial infarction. Three signal averaged electrocardiograms were recorded by Simson's method in the early post infarction period at Day 1 (24 to 48 hours after the onset of symptoms) at Day 8 (8 days after the onset) and Day 15 (2 weeks after the onset) in 66 patients. The results showed late potentials in only 18% of patients at Day 1 and that this was not related to a greater risk of ventricular arrhythmia in the acute phase. Late potentials were recorded in 34.8% of patients on Day 8 and 28.7% at Day 15. We suggest that signal averaged electrocardiography be performed one to two weeks after the onset of myocardial infarction; 13 of 66 patients had abnormalities at Day 8 but not on Day 1.

[Changes in high amplification ECG during the 2 years following the acute phase of myocardial infarction]. / Evolution de l'ECG haute amplification sur deux ans après la phase aiguë d'un infarctus du myocarde.

Late potentials have been reported 1 to 15 days after the onset of myocardial infarction but the evolution during long-term follow-up is not so well known. In order to determine if the signal averaged electrocardiogram remained stable or if it was necessary to repeat the investigation during a period of 2 years, 90 patients underwent 2 recordings on average 3 weeks after the onset of the infarct and then 2 years later. After the first recording, 16 patients (18%) had late potentials. The second recording was performed under the same conditions by the same operator. Globally, the signal averaged electrocardiogram recorded by Simson's method remained remarkably stable (83/90). It was rare to observe late potentials occurring for the first time after the initial recording (4 cases, 5%) in this study. It was more common to observe their disappearance (3 cases, 19%). No explanation could be found except in one case. These possible long-term changes in the signal averaged electrocardiogram suggest that the investigation should only be repeated in patients with abnormalities on the initial recording. Some authors have reported a better prognosis in patients in whom late potentials disappeared but this was not verified in this study.

[Characteristics and prognosis of ventricular tachycardia induced by atrial fibrillation]. / Caractéristiques et pronostic des tachycardies ventriculaires induites par stimulation auriculaire.

The aim of this study was to evaluate the clinical significance of ventricular tachycardia (VT) induced by atrial pacing. A group of 145 patients with spontaneous and induced VT was studied. Twenty-four VTs were induced by atrial stimulation (Group I) and 121 by ventricular stimulation (Group II). The underlying cardiac disease was comparable in the two groups (ejection fraction 32 +/- 14% versus 34 +/- 17%). Spontaneous bi-tachycardias, syncope and VT induced by exercise testing were more common in Group I. The prognosis was worse with 7 cardiac deaths in Group I versus 23 in Group II; recurrences of VT were commoner in group I. In this group, an electrophysiological (branch to branch or fascicular reentry) or clinical mechanism (ischaemia or poor haemodynamic status) could usually be demonstrated. Some cases of idiopathic VT were also observed in young patients. These results suggest that atrial stimulation should be performed routinely during electrophysiological studies of VT because the induction of VT by this method is not uncommon (16%). In addition, these cases of VT usually have a precise mechanism and a poor prognosis and, therefore, an appropriate treatment should be given.

[Paroxysmal atrial fibrillation: main cause of syncope in hypertrophic cardiomyopathy]. / La fibrillation auriculaire paroxystique: principale cause de syncope dans la cardiomyopathie hypertrophique?

The aim of this retrospective study was to determine the mechanism of syncope in idiopathic hypertrophic cardiomyopathy (HCM). An electrocardiographic study was undertaken in 43 patients with HCM: 27 (Group I) had a history of syncope and 16 (Group II) had no history of syncope but were investigated for conduction defects (n = 7) or unsustained ventricular tachycardia (VT) (n = 9). The stimulation protocol used programmed atrial pacing with 1 and 2 extrastimuli and ventricular pacing using up to 3 extrastimuli delivered at 2 sites. The following results were obtained: sustained atrial fibrillation (AF) (> 1 min) was induced in 21 patients in Group I (78%), 4 in Group II (25%); VT was induced in 3 patients in Group I (11%), and 3 in Group II (19%); infra-Hisian block was detected in 1 patient in Group I. The mechanism of syncope was elucidated in 23 patients in Group I (85%): one atrioventricular block 1 sinus node dysfunction, 18 atrial fibrillations, 2 associations of AF-VT and 1 VT. The authors conclude that the prevalence of inducible AF was higher in patients with HCA and syncope than in controls and HCM without syncope: this was the only detectable difference in 67% of patients with unexplained syncope. Paroxysmal AF could therefore explain malaise or syncope in up to 2/3 of cases of HCM.

[Arrhythmogenic effect of ajmaline on the atrial level]. / Etude de l'effet arythmogène de l'ajmaline à l'étage auriculaire.

The aim of this study was to determine whether an antiarrhythmic, Ajmaline, could have proarrhythmic effects on the atrium and to compare the results with those of other antiarrhythmic drugs. A total of 1950 patients without cardiac failure or recent (less than 6 weeks) myocardial infarction were given 1 mg/kg of Ajmaline intravenously during electrophysiological investigation. A proarrhythmic effect was defined as the occurrence of supraventricular tachycardia (SVT) in a patient without this arrhythmia before the test or the facilitation of its induction. Fifty five patients developed SVT (mainly atrial tachyarrhythmias: 48 cases, and some junctional tachycardia: 7 cases) which occurred spontaneously in 22 patients and during fixed atrial pacing in 33 patients. Fifteen patients developed ventricular tachycardia (VT). The predisposing factors for the development of SVT were: a previous history suggesting spontaneous SVT (28 patients; 51 p. 100); sinoatrial block (14 patients--the only abnormality in 10 cases). Seventeen patients had none of these factors but 8 had known cardiac pathology and the other 9 were relatively elderly patients (79 years). Twelve of the patients developing VT had known cardiac disease, bundle branch block in 12 cases and previous VT in 6 cases. In conclusion, proarrhythmic effects of Ajmaline are infrequent if its contraindications are respected, but they do exist at both atrial (2.8 p. 100) and ventricular levels (0.8 p. 100): the risk factors are comparable: previous spontaneous arrhythmias or ECG changes (SA block at the atrial and bundle branch block at the ventricular level).

[Should the Isuprel test be performed systematically in Wolff-Parkinson-White syndrome?]. / Le test à l'Isuprel doit-il être systématique dans le syndrome de Wolff-Parkinson-White?

The isoprenaline (Is) test was designed by Wellens et al. in 1982 to evaluate the effect of catecholamines on the effective refractory period (ERP) of Kent's bundle (K). The purpose of our study was to assess the value of this test in the prognosis of Wolff-Parkinson-White syndrome (WPW), to define its criteria of severity and to determine the usefulness of the test. Out of 33 patients with WPW syndrome, 10 (group I) had a clinical history of severe arrhythmia and 23 (group II) were asymptomatic or had paroxysmal nodal tachycardia. The prognosis of WPW syndrome was evaluated by measuring Kent's bundle ERP under coupled atrial stimulation (S1 S2) and the shortest cycle conducted by K during induced atrial fibrillation (AF) and atrial pacing (AP) both in the basal state (B) and under a 20-30 micrograms Is infusion. (table; see text). Analysis of the results showed constant shortening of ERP in group I and reproduction of the clinical tachycardia in 6 cases. In group II patients isoprenaline unmasked the WPW syndrome in 3 cases and reproduced the clinical tachycardia in 5 cases. The ERP of Kent's bundle evaluated by S1 S2 became smaller or equal to 220 ms in 70 p. 100 of the cases, and this shortening was not specific. The shortest cycle in AF or AP became inferior of equal to 220 ms in only 6 cases, the history being concordant with clinical findings in 4 of them. Altogether, the most reliable and simplest way of evaluating the severity of WPW syndrome is the highest frequency conducted by Kent's bundle in atrial pacing during the Is test which should be performed in all patients in view of its specificity, simplicity and safety.

[Correlation between late surface potentials and inducible ventricular arrhythmias. Apropos of 115 cases]. / Corrélations potentiels tardifs de surface et arythmies ventriculaires déclenchables. A propos de 115 cas.

Programmed ventricular stimulation and a search for late surface potentials (LP) by means of signal-averaging and quantification by Simson's method were performed in 115 patients divided into five groups: group I (n = 50) with no myocardial infarction (MI) and no clinical or induced ventricular tachycardia (VT); group II (n = 28) with MI and no clinical or induced VT; group III (n = 8) with MI, no clinical VT but induced non sustained VT (NSVT); group IV (n = 19) with MI, no clinical VT but induced sustained VT (SVT); group V (n = 15) with clinical and induced VT. The terminal portion of the averaged signal (AS) was analyzed by three parameters: duration of AS terminal portion less than 40 microvolts (Dur TP), AS amplitude 50 and 40 ms before its end (Amp 50, Amp 40). The presence of TP was defined in two ways: criterion A = Amp 40 less than 25 mcv, criterion B = at least two sub-criteria: Dur TP greater than 40 ms, Amp 50 less than 25 mcv, Amp 40 less than 15 mcv. Compared to groups I and II, the AS of group V was characterized by a prolonged and low amplitude terminal portion (p less than 0.001). Groups III and IV were intermediate. The incidence of TP in groups I to V was 20, 28, 37, 56 and 80% respectively with criterion A, and 4, 4, 0, 28 and 66% respectively with criterion B. The lower incidence of TP in group IV as compared to group V was probably due to the induction of purely artefactual SVT's, notably those with rapid cycle (greater than 270 cps/min) which are remarkable on several accounts.(ABSTRACT TRUNCATED AT 250 WORDS)

[Factors predicting the response to an antiarrhythmic during an electrophysiologic study for ventricular tachycardia]. / Facteurs prédictifs de réponse à un anti-arythmique au cours d'une étude électrophysiologique pour tachycardie ventriculaire.

The purpose of this study was to search for factors correlated with the absence of reinduction of a clinical ventricular tachycardia (VT) by stimulation in patients under anti-arrhythmic treatment. Repeated stimulations were performed in 41 patients with spontaneous VT and sustained, monomorphous ventricular arrhythmia induced by stimulation. The stimulation included 1 or 2 extrastimuli delivered into the right ventricle in sinus rhythm, then in imposed ventricular rhythm (600-400 ms). At least 4 anti-arrhythmic drugs were tested. In 16 patients (group I) of mean age 51 +/- 11 years VT was no longer reinducible under anti-arrhythmic treatment. In 25 patients (group II) of mean age 57 +/- 12 years no anti-arrhythmic drug was able to prevent VT induction. The characteristics of spontaneous and induced VT and of isotopic left ventricular ejection fraction (LVEF) were compared in both groups. The absence of reinduction of VT was obtained more easily in patients with: spontaneous, frequently unsustained VT; VT requiring 2 ventricular extrastimuli delivered in imposed rhythm to be induced; rapid initial induced VT (cycle 233 +/- ms vs 297 +/- 63 ms); less advanced underlying heart disease (LVEF 38 +/- 18 vs 27 +/- 13%). The subsequent history of the patients showed that the absence of reinduction of VT was correlated with a low risk of recurrence of VT (12.5 vs 48%) and with a lower risk of mortality (6% vs 32%) than in patients whose VT was always inducible under anti-arrhythmic treatment.

[Influence of the duration of myocardial infarction on QRS duration measured by signal averaged electrocardiography]. / Influence de l'ancienneté de l'infarctus du myocarde sur la durée de QRS mesurée à l'ECG haute amplification.

The aim of this study was to determine the influence of the chronicity of myocardial infarction on QRS duration. The signal-averaged electrocardiogram (SA ECG) was recorded with a 40 Hz filter in 239 patients with a history of myocardial infarction. The infarction was recent (up to 6 weeks) in 105 patients (group A) and chronic (> 1 year) in the other 134 cases (group B). In group A, 35 patients had inductible sustained ventricular tachycardia (VT) at less than 270/mn; 40 had negative electrophysiological investigations and 30 had inducible ventricular flutter or fibrillation (VF). In group B, 58 had inducible VT, 54 had negative investigations and 22 had inducible VF. The three SA ECG parameters (QRS duration, amplitude of RMS 40 and duration of LAS) differed significantly in subjects with VT with respect to those with negative investigations and inducible VF, irrespective of the chronicity of infarction. On the other hand, only QRS duration differentiated patients with recent infarction from those with chronic infarction, irrespective of the results of programmed pacing, QRS duration being longer in group B. The best diagnostic value of QRS duration for identifying subjects with VT < 270/mn and negative investigations was 110 ms in group A and 120 ms in group B (sensitivity 46% and 77.5% respectively). In chronic infarction, the increase in QRS duration was significantly correlated to the decrease in left ventricular ejection fraction. The authors conclude that the criteria of abnormality of QRS duration are dependent on the chronicity of myocardial infarction. Although a duration of 110 ms is abnormal in the early post-infarction period, after a period of one year, a value of 120 ms should be considered to be pathological, especially when the sequellae of infarction are important.

[Can signal-averaged electrocardiograms be interpreted in cases of complete bundle branch block?]. / Peut-on interpréter un électrocardiogramme haute amplification en cas de bloc de branche complet?

The aim of this study was to evaluate the results of signal-averaged (SA) ECG in cases of complete right (RBBB) or left bundle branch block (LBBB). One hundred and seven patients had RBBB; 42 without cardiac disease (0), 56 with chronic myocardial infarction (MI) and 9 with primary cardiomyopathy (CMP). Seventy-four patients had LBBB: 20 without cardiac disease, 26 with chronic myocardial infarction and 28 with primary cardiomyopathy. A SA ECG (Cardionics, Fidelity) was performed with a 40 Hz band pass and compared with the recordings of 72 healthy controls without bundle branch block. The duration of the averaged QRS (QRS dur), the voltage of the last 40 milliseconds (RMS40) and duration of terminal activity < 40 microV (LAS) were measured. The analysis of results showed that QRS dur was significantly longer in subjects with ventricular tachycardia (VT) (p < 0.05) and in those with advanced cardiac disease (p < 0.05), whatever the type of bundle branch block, and that only the RMS40 distinguished patients with VT from those without VT, irrespective of the underlying cardiac disease and the type of bundle branch block. However, the study of the diagnostic value of each parameter showed very mediocre results: RMS 40 < 20 microV in myocardial infarction and < 17 microV in cardiomyopathy had sensitivities and specificities in RBBB of 73% and 50% respectively, incalculable in CMP, in LBBB 70% and 33%, 77% and 60% respectively; the LAS was unusable. The authors conclude that it is hazardous to interprete SA ECG in bundle branch block, especially in advanced cardiac disease where the specificity of the criteria becomes very low (< 50%).