[Bi-tachycardia and ischemic cardiopathy (following myocardial infarction)]. / Bitachycardies et cardiopathies d'origine ischémique (antécédent d'infarctus du myocarde).

OBJECTIVE: The association of supraventricular tachycardia (SVT) and ventricular tachycardia (VT) is not common. The aim of this study was to evaluate its incidence and possible predisposing factors in patients with a history of myocardial infarction (MI), in order to correct them. METHODS: Out of 359 patients consecutively recruited for spontaneous VT occurring at least one month after the acute phase of an MI, 33 were noted to have a possible association of SVT with VT. These patients underwent the following investigations: Holter recording, left ventricular ejection fraction (LVEF) measurement, and electrophysiological studies including programmed atrial and ventricular pacing. RESULTS: The LEVF was 37.5+/-11%. An SVT was induced in 21 patients and a VT in 31 patients. Following investigation, the presumed factor predisposing to the two tachycardias was considered to be initiation of an SVT associated with rapid nodal conduction to the ventricle (Wenckebach point 210+/-23/mn) in 12 patients, branch to branch re-entry in 4 patients, reversible rhythmic dilated cardiomyopathy in 4 patients, an ischemic factor in 8 patients, post-operative period in 1 subject, infundibular VT in 1 subject, and an undetermined mechanism in 3 patients. The specific treatment of each of the identified etiologies usually prevented the recurrence of VT with the exception of one patient who had further VT during defibrillator recording, independent of any SVT. CONCLUSION: The association of SVT with VT is rare because it was only noted in 9% of subjects who presented with spontaneous VT following myocardial infarction; This incidence is debatable, and could be an underestimate due to the fact that diagnosis is difficult. Several presumed predisposing factors are implicated and should be actively sought.

[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.

[Complete electrophysiological study remains necessary in symptomatic advanced cardiomyopathy]. / Une étude électrophysiologique complète reste nécessaire dans une cardiopathie évoluée symptomatique.

Multiple mechanisms can explain a tachycardia associated or not with a heart disease. It is important to establish its origin, particularly if advanced heart disease is present, for the treatment. Complete electrophysiological study remains an important means of diagnosis. We report the case of a 39-year old man, who had a dilated cardiomyopathy since the age of 25 years and who complained of tachycardia. These symptoms were shown to be related to atrioventricular nodal re-entrant tachycardia at electrophysiological study and a specific treatment was indicated.

[Comparison of patients with paroxysmal junctional tachycardia and syncope with those without syncope]. / Comparaison des sujets ayant des tachycardies jonctionnelles paroxystiques et des syncopes avec des sujets sans syncopes.

INTRODUCTION: The purpose of the study was to determine the possible mechanisms of presyncope in patients who have paroxysmal junctional tachycardias (PJT) and a normal surface ECG between tachycardias. METHODS: Among 419 patients consecutively recruited for PJT, aged from 10 to 88 years (47+/-19), 78 of them had presented at least one syncope; they had a normal ECG in sinus rhythm. Transesophageal programmed atrial stimulation was performed using one and two atrial extrastimuli delivered in control state and if necessary after infusion of 20-30 microg of isoproterenol; arterial blood pressure was monitored; vagal maneuvers and tilt test (n=25) were performed; echocardiogram was systematic. RESULTS: Age, sex, method of induction, tachycardia mechanism and the mean heart rate in tachycardia were similar in patients with and without syncope. Syncope was related to a vagal reaction induced by the PJT in 31 patients, to a fast rate during PJT in 15 patients, to a sinus node dysfunction in six patients, to a coronary ischemia in five patients, to a tetany induced by PJT in three patients, to an advanced age in three patients, to multiple causes in three patients and remained unexplained in eight patients. Radiofrequency ablation of reentrant circuit, performed in 28 patients, suppressed syncope in 26 of them. CONCLUSION: Presyncope or syncope occurred in 18% of patients who had a history of paroxysmal junctional tachycardia. Several mechanisms were implicated; the most frequent causes were coronary ischemia or sick sinus syndrome in old patients, vasovagal reaction or fast rate in tachycardia or tetany in patients of all ages.