Joint Position Paper of the Working Group of Pacing and Electrophysiology of the French Society of Cardiology (SFC) and the Société française d'imagerie cardiaque et vasculaire diagnostique et interventionnelle (SFICV) on magnetic resonance imaging in patients with cardiac electronic implantable devices.

Magnetic resonance imaging (MRI) has become the reference imaging for the management of a large number of diseases. The number of MR examinations increases every year, simultaneously with the number of patients receiving a cardiac electronic implantable device (CEID). A CEID was considered an absolute contraindication for MRI for years. The progressive replacement of conventional pacemakers and defibrillators by MR-conditional CEIDs and recent data on the safety of MRI in patients with "MR-nonconditional" CEIDs have progressively increased the demand for MRI in patients with a CEID. However, some risks are associated with MRI in CEID carriers, even with "MR-conditional" devices because these devices are not "MR-safe". A specific programing of the device in "MR-mode" and monitoring patients during MRI remain mandatory for all patients with a CEID. A standardized patient workflow based on an institutional protocol should be established in each institution performing such examinations. This joint position paper of the Working Group of Pacing and Electrophysiology of the French Society of Cardiology and the Société française d'imagerie cardiaque et vasculaire diagnostique et interventionnelle (SFICV) describes the effect and risks associated with MRI in CEID carriers. We propose recommendations for patient workflow and monitoring and CEID programming in MR-conditional, "MR-conditional nonguaranteed" and MR-nonconditional devices.

[Non-valvular cardiac devices endocarditis]. / L'endocardite sur matériel de stimulation intracardiaque.

The risk of infective endocarditis on pacemaker or ICD is not negligible and has increased in recent years. Several host-related, procedure-related, or device-related risk factors have been recognized. Owing to its potential severity, the possibility of infective endocarditis should be envisaged in patients with repeated pulmonary infections or documented bacteremia and transesophageal echocardiography should then be used. The most common germs causing pacemaker endocarditis are staphylococci. Treatment requires prolonged antibiotic therapy and retrieval of the pacemaker and leads.

[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.

[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.

[Prevalence of sudden cardiac death during sports activities]. / Prévalence de la mort subite au cours du sport.

Sudden death during sport is a rare and unexpected event. It essentially affects young males, and a cardiomyopathy that had not been diagnosed during medical examinations is present in the majority of cases. In young subjects, there is generally hypertrophic cardiomyopathy or arhythmogenic right ventricular dysplasia. This is revealed during sporting activity, and sudden death is often the first symptom of the disease. Competitive sport increases the relative risk of sudden death to 2.5 compared to the risk in a non-sporting subject. The prevalence of sudden death during competitive sport is poorly understood. From the rare studies available, it could be estimated at 2.3/100,000 athletes per year. In Europe, it essentially occurs during football matches. However, the prevalence of sudden death during so-called 'recreational' sports is not precisely known. It could be much higher because these activities involve a larger number of people, and take place without supervision and usually without a medical examination beforehand. The participants are older, and coronary pathology is usually implicated.

[Implantable cardioverter defibrillators in pediatric patients: results in a series of 33 cases]. / Le défibrillateur automatique implantable chez l'enfant et l'adolescent: indications, complications et résultats à propos d'une étude multicentrique française de 33 cas.

UNLABELLED: Implantable defibrillator is the recognized treatment of sudden cardiac death. Miniaturization of the devices allows implantation in children. METHODS: This multicentric retrospective study analyzed data of 33 children aged 18 years and less who were implanted from 1990 to 2005. RESULTS: Age of patients are 10 to 18 years, 20 patients were implanted after a resuscitation of sudden death, 10 after a syncope, 2 after a ventricular tachycardia and 1 in a prophylactic way. Tachycardias on primary electrical disease are most frequent (46%). Hypertrophic cardiomyopathy accounts for 22%, DAVD for 14%, congenital cardiopathies for 12%. Seventeen patients received appropriate shocks and 14 patients had inappropriate shocks. There were two unexplained deaths. Five leads fractures and two device infections were noted. CONCLUSION: Implantable defibrillator is an effective treatment for children high-risk of sudden death. Occurrence of inappropriate shocks due to sinusal tachycardia, infections and leads fractures are frequent.

Factors determining the occurrence of late potentials on the signal-averaged electrocardiogram after a first myocardial infarction: a multivariate analysis.

To determine the natural history of late potentials on the signal-averaged electrocardiogram (ECG), multivariate analysis was performed in 167 patients (138 men, 29 women) with a first anterior or inferior acute myocardial infarction. Seventy-four patients received thrombolytic therapy; the remaining 93 patients were treated conventionally. All patients underwent coronary angiography, left ventricular ejection fraction determination and signal-averaged ECG recording. Eight variables thought to be correlated with the presence of late potentials were studied; that is, age, infarct location, number of diseased coronary vessels, left ventricular ejection fraction, infarct-related coronary artery patency, treatment received, delay between admission and signal-averaged recording and delay between admission and coronary angiography. Statistical analysis showed that two independent factors (coronary artery occlusion and impaired left ventricular ejection fraction) were highly correlated with the incidence of late potentials. The occurrence of late potentials was multiplied by 5 in case of an occluded infarct-related vessel and by 1.75 each time the left ventricular ejection fraction value decreased by 0.10. This study suggests that coronary artery patency is the most important factor that decrease the rate of late potentials after a first acute myocardial infarction and it occurs independently of infarct location and left ventricular function.

Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: a multivariate analysis.

OBJECTIVES: This study sought to determine whether the reopening of the infarct-related vessel is related to clinical characteristics or cardiovascular risk factors, or both. BACKGROUND: In acute myocardial infarction, thrombolytic therapy reduces mortality by restoring the patency of the infarct-related vessel. However, despite the use of thrombolytic agents, the infarct-related vessel remains occluded in up to 40% of patients. METHODS: We studied 295 consecutive patients with an acute myocardial infarction who underwent coronary angiography within 15 days (mean [+/- SD] 6.7 +/- 3.2 days) of the onset of symptoms. Infarct-related artery patency was defined by Thrombolysis in Myocardial Infarction trial flow grade > or = 2. Four cardiovascular risk factors--smoking, hypertension, hypercholesterolemia and diabetes mellitus--and eight different variables-age, gender, in-hospital death, history of previous myocardial infarction, location of current myocardial infarction, use of thrombolytic agents, time interval between onset of symptoms, thrombolytic therapy and coronary angiography--were recorded in all patients. RESULTS: Thrombolysis in current smokers and anterior infard location on admission were the three independent factors highly correlated with the patency of the infarct-related vessel (odds ratios 3.2, 3.0 and 1.9, respectively). In smokers, thrombolytic therapy was associated with a higher reopening rate of the infard vessel, from 35% to 77% (p < 0.001). Nonsmokers did not benefit from thrombolytic therapy, regardless of infarct location. CONCLUSIONS: These observational data, if replicated, suggest that in patients with acute myocardial infarction, thrombolytic therapy may be most effective in current smokers, whereas nonsmokers and ex-smokers may require other management strategies, such as emergency percutaneous transluminal coronary angioplasty.

[Prevalence of Brugada syndrome among 35,309 inhabitants of Lorraine screened at a preventive medicine centre]. / Prevalence du syndrome de Brugada dans une population de médecine préventive en Lorraine a propos de 35,309 cas.

UNLABELLED: Brugada syndrome is a recently identified cause of sudden death. Its primary prevention remains controversial, and epidemiology poorly defined. PATIENT POPULATION AND METHODS: Electrocardiograms (ECG) of 35,309 individuals (mean age = 37.2 years, 47% men) recorded over a 1-year period were reviewed and classified as (1) typical, (2) suspicious, and (3) negative. Subjects whose ECG was suspicious were offered a provocative test with flecainide, 2 mg/kg, i.v., and individuals whose ECG was typical were advised to undergo programmed ventricular stimulation (PVS). RESULTS: In 14 men and 6 women between the ages of 24 and 77 years (mean =47.5), ECGs were typical (n=6) or suspicious (n=14). Among 6 subjects with typical ECGs, 3 underwent PVS, which was positive in 1, who received an implantable cardioverter defibrillator (ICD). Among 14 subjects whose ECGs were suspicious, 5 declined further investigations and 5 developed typical ECG characteristics of Brugada syndrome after flecainide administration. PVS was negative in 4 subjects who consented to the procedure. Overall, among 35,309 individuals screened, 11 had ECG findings consistent with Brugada syndrome and, over a follow-up of 30 months, all had remained free of adverse cardiac event. CONCLUSIONS: we estimated a prevalence of Brugada syndrome of 0.3% in Lorraine. A single patient received an ICD for inducible ventricular tachyarrhythmia during PVS, representing a potential 30 per million asymptomatic adult rate of ICD implantation for this indication.

Prognostic value of thrombolysis, coronary artery patency, signal-averaged electrocardiography, left ventricular ejection fraction, and Holter electrocardiographic monitoring for life-threatening ventricular arrhythmias after a first acute myocardial infarction.

Prognostic studies after acute myocardial infarction (AMI) have mainly been performed in the prethrombolytic era. Despite the fact that modern management of AMI has reduced mortality rates, the occurrence of malignant ventricular arrhythmias in the late phase of AMI remains an important issue. We prospectively studied 244 consecutive patients (97 treated with thrombolytics) who survived a first AMI. All patients underwent time domain signal-averaged electrocardiography (vector magnitude: measurements of total QRS duration, terminal low [<40 microV] amplitude signal duration, and root-mean-square voltage of the last 40 ms of the QRS complex), Holter electrocardiographic monitoring, and cardiac catheterization. Late life-threatening ventricular arrhythmias were recorded. Eighteen arrhythmic events occurred during a mean follow-up period of 57 +/- 18 months. Three independent factors were associated with a higher risk of arrhythmic events: (1) left ventricular ejection fraction (odds ratio 1.9/0.10 decrease), (2) terminal low-amplitude signal duration (odds ratio 1.5/5 ms increase), and (3) absence of thrombolytic therapy (odds ratio 3.9). Low-amplitude signal duration sensitivity for sudden cardiac death was low (30%). Left ventricular ejection fraction had the highest positive predictive value for sudden cardiac death (10%). Thus, thrombolysis decreases both the incidence of ventricular tachycardia and sudden cardiac death with a higher reopening rate of the infarct-related vessel. Signal averaging predicts the occurrence of ventricular tachycardia and an impaired left ventricular ejection fraction predicts the occurrence of sudden cardiac death.

Adult presentation of MCAD deficiency revealed by coma and severe arrythmias.

We report the case of a 33-year-old man who presented with headaches and vomiting. Soon after admission he became drowsy and agitated, developed ventricular tachycardia and his neurological state worsened (Glasgow coma score 6). Blood analysis showed respiratory alkalosis, hyperlactacidemia (8 mmol/l), hyperammonemia (390 micro mol/l) and hypoglycaemia (2.4 mmol/l). Subsequently, he developed supraventricular tachycardia, ventricular tachycardia and ultimately ventricular fibrillation resulting in cardiac arrest, which was successfully treated. A CT scan of the head revealed cerebral oedema. Whilst in the intensive care unit, he developed renal failure and rhabdomyolysis. The metabolic abnormalities seen at the time of admission normalised within 48 h with IV glucose infusion. Biological investigations, including urinary organic acids and plasma acylcarnitines, showed results compatible with MCAD deficiency. Mutation analysis revealed the patient was homozygous for the classical mutation A985G. This is one of only a few reports of severe cardiac arrhythmia in an adult due to MCAD deficiency. This condition is probably under-diagnosed in adult patients with acute neurological and/or cardiac presentations.

Ventilatory response to fatiguing and nonfatiguing resistive loads in awake sheep.

To study the changes in ventilation induced by inspiratory flow-resistive (IFR) loads, we applied moderate and severe IFR loads in chronically instrumented and awake sheep. We measured inspired minute ventilation (VI), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory cycle time (TT), tidal volume (VT), mean inspiratory flow (VT/TI), and respiratory duty cycle (TI/TT)], transdiaphragmatic pressure (Pdi), functional residual capacity (FRC), blood gas tensions, and recorded diaphragmatic electromyogram. With both moderate and severe loads, Pdi, TI, and TI/TT increased, TE, TT, VT, VT/TI, and VI decreased, and hypercapnia ensued. FRC did not change significantly with moderate loads but decreased by 30-40% with severe loads. With severe loads, arterial PCO2 (PaCO2) stabilized at approximately 60 Torr within 10-15 min and rose further to levels exceeding 80 Torr when Pdi dropped. This was associated with a lengthening in TE and a decrease in breathing frequency, VI, and TI/TT. We conclude that 1) timing and volume responses to IFR loads are not sufficient to prevent alveolar hypoventilation, 2) with severe loads the considerable increase in Pdi, TI/TT, and PaCO2 may reduce respiratory muscle endurance, and 3) the changes in ventilation associated with neuromuscular fatigue occur after the drop in Pdi. We believe that these ventilatory changes are dictated by the mechanical capability of the respiratory muscles or induced by a decrease in central neural output to these muscles or both.

DDD pacing in hypertrophic cardiomyopathy: a multicentre clinical experience.

BACKGROUND: DDD pacing has been advocated as an effective treatment for drug refractory obstructive hypertrophic cardiomyopathy. This study reports the outcome of pacing in 56 patients with refractory symptoms referred to four tertiary centres. METHODS: Core data on symptoms, drug burden, and left ventricular outflow tract gradient were recorded. Patients underwent a temporary pacing study with optimisation of the atrioventricular (AV) delay for greatest gradient reduction without haemodynamic compromise. Patients were assessed after implantation in terms of changes in symptoms, drug load, and outflow tract gradient. RESULTS: 56 patients underwent pacing assessment. The mean (SD) left ventricular outflow tract gradient before pacing was 78 (31) mm Hg. At temporary study the mean (SD) left ventricular outflow tract gradient was 38 (24) mm Hg with a median (range) optimised sensed AV delay of 65 (25-125) ms. Fifty three patients were implanted and followed up for a mean (SD) of 11 (11) months. The median (range) programmed sensed AV delay was 60 (31-200) ms. Left ventricular outflow tract gradient at follow up was 36 (25) mm Hg. Forty four patients had improved functional class. Although a correlation (r = 0.69) was shown between acute and chronic left ventricular outflow tract gradient reduction, there was no correlation between magnitude of gradient reduction and functional improvement, and no appreciable change in pharmacological burden. CONCLUSION: This series confirms symptomatic improvement after DDD pacing in hypertrophic cardiomyopathy. There remains, however, a discrepancy between perceived symptomatic benefit and modest objective improvement. Furthermore, the optimal outcome has been achieved only with continued pharmacological treatment. Current methods of temporary evaluation do not predict functional outcome which seems to be independent of the magnitude of gradient reduction.

Conversion from intravenous to oral slow-release disopyramide in acute myocardial infarction.

Twelve patients with acute myocardial infarction were given 1.5 mg/kg/5 min bolus +0.4 mg/kg/hr 6 hr IV infusion of disopyramide followed by 250 mg twice daily of a slow-release oral formulation of this drug. Plasma concentrations of total disopyramide rapidly reached steady-state within the therapeutic margins. The plasma steady-state concentrations of the major metabolite mono-N-dealkyl-disopyramide (MND) showed large intra-individual variations. There was no correlation between plasma levels of either disopyramide or MND and the occurrence of anticholinergic side effects. The drug had no significant effect on mean blood pressure, heart rate, or ECG intervals. This therapeutic regimen, including conversion from the IV form to oral slow-release tablets, could be recommended in myocardial infarction.

Reproducibility of bipolar endocavitary electrogram measurements at sites of radiofrequency energy delivery in patients with the Wolff-Parkinson-White syndrome.

BACKGROUND: Radiofrequency ablation of atrioventricular accessory pathway is widely used to cure patients with the Wolff-Parkinson-White syndrome. The site of successful ablation is determined using electrophysiological parameters, endocavitary bipolar electrogram measurements being the most commonly used. Interobserver reproducibility of these measurements may limit the reliability of ablation criteria based upon bipolar measurements only but, to our knowledge, this reproducibility has not been evaluated so far. Such was the aim of this study. METHODS: Three independent observers reviewed the bipolar electrograms recorded at sites were radiofrequency energy was delivered (successfully or not) in 28 consecutive patients with the Wolff-Parkinson-White syndrome. In each tracing, 4 intervals were measured: (1) A0V0 (onset of the atrial electrogram to onset of the ventricular electrogram), (2) AaVa (activation time of the atrial electrogram to activation time of the ventricular electrogram), (3) V0-QRS (onset of the ventricular electrogram to onset of delta wave on the surface ECG) and (4) Va-QRS (activation time of the ventricular electrogram to onset of delta wave on the surface ECG). RESULTS: The interobserver reproducibility was low since only 50% of A0V0 intervals were measured with an interobserver difference lower than 10 ms and up to 43% of Va-QRS intervals were measured with an interobserver difference greater than 30 ms. The reproducibility of interval measurement was graded from the highest to the lowest as follows: A0V0, AaVa, V0-QRS and Va-QRS (Chi-square statistic, chi 2 = 71.72, p < 0.0001). Kappa values were lower than 0.40, indicating a poor interobserver reproducibility. CONCLUSIONS: Our study suggests that interobserver reproducibility of only bipolar electrograms interval measurements at sites of radiofrequency ablation of atrioventricular accessory pathway is poor, which limits the reliability of bipolar criteria to predict a successful ablation site.

Effects of radiofrequency catheter ablation on patients with permanent pacemakers.

The objective of this study was to assess the effects of radiofrequency energy application on implanted pacemaker functions. Radiofrequency (RF) catheter ablation may cause pacemaker dysfunction due to electromagnetic interferences. The effects of RF on pacemaker behavior were studied in a series of 38 pacemakers, implanted 18 +/- 26 months prior to a RF procedure using either a right ventricular approach (AV node ablation, n = 35) or a left ventricular approach (left concealed accessory pathway ablation, n = 1; VT ablation, n = 2). The 38 patients (mean age 65 +/- 9 years) included 20 men and 18 women. Before energy applications, the 23 different pacemaker models were programmed to the VVI mode at the lowest available rate. The continuous surface ECG was recorded throughout the procedure. Thorough testing of the devices was performed before and after each RF delivery. Unusual pacemaker responses occurred in 20 of the 38 cases studied (53%). The impact of RF delivery was unpredictable, and variable dysfunctions were observed at different times for a given patient or could vary for a given model. Unusual pacemaker responses included pacemaker inhibition (n = 8), untoggled backup mode (n = 3), electromagnetic interference noise mode (n = 3), temporary RF-induced pacemaker tachycardia (n = 2), erratic behavior (n = 1), oversensing of RF onset and offset (n = 8), and transient loss of ventricular capture, (n = 1). Postablation, most devices automatically toggled back to full functionality. The three devices in the untoggled backup mode had to be reprogrammed to obtain normal operations. At the end of the procedure, pacing thresholds remained unchanged in all but one patient, in whom the increase in ventricular threshold was due to a nicked lead. In conclusion, implanted pacemakers frequently exhibit transient, unpredictable responses to RF energy application. Although all pacemaker functions were restored postablation, some devices had to be reset manually. The anomalies observed during the RF application argue for the simultaneous use of an external pacemaker in pacing-dependent patients.

[Electric stability of the heart after myocardial infarction: role of anti-arrhythmia agents during postinfarction]. / La stabilité électrique du coeur après infarctus du myocarde: place des antiarythmiques dans le postinfarctus.

Electrical instability of the heart after myocardial infarction threatens surviving patients with sudden death from a severe ventricular arrhythmia. These arrhythmic complications are usually the result of several factors: an arrhythmogenic substrate corresponding to the ischaemic myocardium, a trigger factor (usually a ventricular extrasystole) and other predisposing factors (autonomic nervous system, electrolyte imbalance, activation of the renin-angiotensin system). Risk stratification of electrical instability combines noninvasive (Holter, exercise testing, signal averaged electrocardiography, study of the variability of the heart rate, radionuclide or echocardiographic evaluation of the left ventricular ejection fraction) and invasive investigations (coronary angiography and even programmed ventricular stimulation). The presence of late ventricular potentials, a low ejection fraction and/or a ventricular arrhythmia on Holter monitoring identifies a high risk subgroup. Although the assessment of electrical instability is better than it used to be, pharmacological prevention remains disappointing. Class I antiarrhythmics are ineffective or dangerous. The efficacy of Class III antiarrhythmics is uncertain and only the betablockers seem to have any beneficial effects on this post-infarction electrical instability.

[Interferences in the everyday life of the patient with a cardiac pacemaker or an implantable defibrillator]. / Interférences de la vie quotidienne chez le patient avec stimulateur cardiaque ou défibrillateur implantable.

The electromagnetic sources of interferences being able to deteriorate the operation of cardiac pacemakers or implantable defibrillators are numerous. This potential risk has been known since the release, 40 years ago, of pacemakers incorporating a detection circuit. Many papers, reviewed in this article, have been published about these conflicts. In daily practice, the risk of dangerous interference is weak, but it seems obvious that the implantable defibrillators are much more sensitive to the external environment than the cardiac pacemakers. With some precautions to eliminate manifest risk situation, it is possible to carry out a strictly normal life. Diagnostic memories increasingly sophisticated included in the new prostheses make possible the identification of asymptomatic conflicts, and the specification of the mechanism of a real problem. Provided information may also be useful to find solutions (adjustment, precautions) to decrease, even to remove the risks.

[Primary ventricular fibrillation]. / Les fibrillations ventriculaires primitives.

In the absence of autopsy studies, the etiological diagnosis of this form of ventricular fibrillation (VF) depends on the exclusion of cardiac disease by all available invasive and non-invasive diagnostic methods. Primary VF is rare and affects young adults. There are few clinical markers and published electrophysiological data indicates that sustained ventricular tachycardia or VF is unlikely to be induced by programmed ventricular stimulation. The underlying mechanism of the arrhythmia is poorly understood. However, a possible arrhythmogenic substrate has been suggested in small zones of fibrosis within normal Purkinje tissues, as encountered in some minor forms of arrhythmogenic right ventricular dysplasia. Also, the role played by the autonomic nervous system in triggering VF seems to be particularly important. Some described cases resemble curiously "torsades de pointes" with a short coupling interval. The "cardiac" prognosis of resuscitated patients is usually good. However, arrhythmic recurrences are common, and, classically, antiarrhythmic drugs are usually ineffective. The indication for implantation of an automatic defibrillator is therefore justified in patients surviving primary VF. The lack of understanding of this condition is an argument in favour of setting up a French register of patients with primary VF in order to establish its clinical features.