[Syncope in patients with normal EKG and without cardiac disease: value of ambulatory esophageal electrophysiology in determining etiology]. / Syncopes chez des patients avec ECG normal sans cardiopathie: intérêt étiologique d'une étude électrophysiologique par voie oesophagienne en ambulatoire.

The aim of this study was to determine whether ambulatory oesophageal electrophysiological recordings are valuable in identifying the cause of syncope in patients with a normal ECG and without cardiac disease. One hundred and forty-five patients aged 16 to 88 years of age, without cardiac disease, and with a normal ECG without a documented arrhythmia, were examined for unexplained syncope: 55 patients complained of palpitations at the time of syncope. The electrophysiological study was carried out in the clinic with oesophageal recordings using a classical protocol: Wenckebach point and sinus node recovery time were determined; programmed atrial stimulation was used with delivery of 1 and 2 extra-stimuli on the basal rhythm and with 20/30 micrograms infusion of isoprenaline; blood pressure was monitored. The study was negative in 41 patients (28%). Sinus node dysfunction was observed in 9 patients (6%). A vaso-vagal reaction reproducing the symptoms was induced by isoprenaline in 21 patients (14.5%); a conduction defect was revealed in 2 cases (1%). Atrial fibrillation or tachycardia > 1 minute was induced in 22 patients (15%). Paroxysmal junctional tachycardia was induced in 50 patients (35%). Patients with a negative study were younger than those with sinus node dysfunction or atrial fibrillation (44 +/- 21, 71 +/- 9 and 63 +/- 14 years respectively). Treatment was guided by these results: cardiac pacing, antiarrhythmic therapy or radiofrequency ablation of the reentrant pathway were indicated and suppressed syncope in all but two patients. The authors conclude that electrophysiological studies in the out-patient clinic with oesophageal recordings is a safe, rapid and economic method of detecting arrhythmias (sinus node dysfunction or supraventricular tachycardia) in 60% of patients with syncope, especially if they have symptoms of palpitations.

[Doppler tissue imaging of the myocardium and right ventricle]. / Doppler tissulaire myocardique et ventricule droit.

Doppler tissue imaging is a technique of analysis of myocardial wall motion. It may easily be used for the right ventricular walls, especially in the apical 4-chamber view, from which the velocities of the RV free wall can be measured from the tricuspid annulus to the apex. The regional velocities of the right ventricle in its long axis and the excursion of the tricuspid annulus are higher than those of the left ventricle but the velocities of circumferential fibre shortening are lower. Moreover, the time interval between the end of the Sm wave and the onset of the Em wave (equivalent to the isovolumic relaxation time) is almost virtual in the right ventricle. The parameters of deformation (strain rate, strain) are also higher in the right than in the left ventricle and are variably distributed. Several studies have examined the clinical value of Doppler tissue imaging of the right ventricle. In cardiac failure, a significant correlation between the systolic velocity of the tricuspid annulus displacement and right ventricular ejection fraction has been reported. The ratio of tricuspid E wave velocity to the tricuspid annulus B wave allow assessment of right ventricular filling pressures. The measurement of tricuspid annulus velocities could be diagnostic of right ventricular extension of an inferior wall infarct. The recording of a "rebound" positive wave just after the E wave in the RV and LV free walls (and in the interventricular septum) is a diagnostic sign of constrictive pericarditis. Doppler tissue imaging is therefore a promising technique for evaluating right ventricular function.

[Treatment with lepirudin in heparin-induced thrombocytopenia. A case report]. / Traitement par lépirudine au cours d'une thrombopénie à l'héparine. A propos d'un cas.

We report the case of a 71 old woman presenting a bilateral massive pulmonary embolism with intraventricular right thrombus complicating heparin induced thrombocytopenia (HIT) persistent after one month of conventional anticoagulant processing. We underline the effectiveness of lepirudin (Refludan) in the curative processing of pulmonary embolism allowing here to avoid a complex surgical thromboembolectomy. We evoke the place of this molecule in the curative therapeutic strategy of HIT with thrombotic phenomena.

Influence of age on the potential risk of sudden death in asymptomatic Wolff-Parkinson-White syndrome.

Sudden death might be the first event in patients with asymptomatic WPW. The purpose of the study was to know if the age of the patient modifies the electrophysiological characteristics of asymptomatic WPW. Transesophageal stimulation was performed on 92 asymptomatic WPW patients from the following age groups: 10-69 years (n = 14), 20-29 years (n = 33), 30-39 years (n = 15), 40-49 years (n = 17), and 50-69 years (n = 13). The procedure consisted of atrial pacing up to the second AV block, programmed atrial stimulation using one and two extrastimuli delivered on two driven rhythms in the control state, and after infusion of isoproterenol. In thefive age groups, paroxysmal junctional tachycardia occurred, respectively, in 1 (7%), 1 (3%), 2 (13%), 2 (12%) patients, and not at all in the oldest group. AF > 1 minute occurred, respectively, in 3 (21%), 9 (27%), 5 (33%), 3 (18%), and 4 (31%) patients. The dangerous form of WPW (rapid conduction in the Kent bundle > 240/min in the control state or > 300/min after isoproterenol + AF induction) occurred, respectively, in 3 (21%), 9 (27%), 4 (27%), 1 (6%), and 3 (23%) patients. In conclusion, electrophysiological data of asymptomatic WPW are not modified by age of the patient. Elderly patients remain at risk of a dangerous form of WPW; systematic evaluation of WPWis recommended in patients with an active life independent of age.

Endothelial nitric oxide synthase limits left ventricular remodeling after myocardial infarction in mice.

Background- To investigate the role of endothelial nitric oxide synthase (NOS3) in left ventricular (LV) remodeling after myocardial infarction (MI), the impact of left anterior descending coronary artery ligation on LV size and function was compared in 2- to 4-month-old wild-type (WT) and NOS3-deficient mice (NOS3(-/-)). Methods and Results- Two days after MI, both strains of mice had a similar LV size, fractional shortening, and ejection fraction by echocardiography. Twenty-eight days after MI, both strains had dilated LVs with decreased fractional shortening and lower ejection fractions. Although the infarcted fraction of the LV was similar in both strains, LV end-diastolic internal diameter, end-diastolic volume, and mass were greater, but fractional shortening, ejection fraction, and the maximum rate of developed LV pressure (dP/dt(max)) were lower in NOS3(-/-) than in WT mice. Impairment of diastolic function, as measured by the time constant of isovolumic relaxation (tau) and the maximum rate of LV pressure decay (dP/dt(min)), was more marked in NOS3(-/-) than in WT mice. Mortality after MI was greater in NOS3(-/-) than in WT mice. Long-term administration of hydralazine normalized blood pressure in NOS3(-/-) mice, but it did not prevent the LV dilatation, impaired systolic and diastolic function, and increased LV mass that followed MI. In WT mice, capillary density and myocyte width in the nonischemic portion of the LV did not differ before and 28 days after MI, whereas in NOS3(-/-) mice, capillary density decreased and myocyte width increased after MI, whether or not hydralazine was administered. Conclusions- These results suggest that the presence of NOS3 limits LV dysfunction and remodeling in a murine model of MI by an afterload-independent mechanism, in part by decreasing myocyte hypertrophy in the remote myocardium.

Influence of age on the electrophysiological mechanism of paroxysmal supraventricular tachycardias.

The purpose of this study was to evaluate the influence of age on the mechanism of paroxysmal supraventricular tachycardia (PSVT). Previous studies have shown age and sex differences between certain arrhythmias and especially changes in electrophysiological characteristics of Wolff-Parkinson-White syndrome. Four hundred and eighty five patients aged 9-86 years, with PSVT and without Wolff-Parkinson-White syndrome in sinus rhythm, were studied. The esophageal or intracardiac electrophysiological study used a standardized atrial pacing protocol. Paroxysmal junctional tachycardia was induced in 475 patients. The mechanism of tachycardia was not influenced by age and atrioventricular nodal reentrant tachycardia (AVNRT) was found as the main cause of PSVT in all ranges of age. Atrioventricular reentrant tachycardia (AVRT) using a concealed accessory pathway (AP) had a similar incidence from youth to elderly. The ratio male/female (M/F) and the inducibility of other arrhythmias (atrial flutter/fibrillation) (AF/AFl) were also found to be similar in all ranges of age. The age of the patients did not influence the mechanism of the tachycardia. Most of PVST were related to a AV nodal reentrant tachycardia. Concealed accessory pathway was identified with a similar incidence in young and old patients.

[Contribution of the transesophageal electrophysiologic study to the etiologic diagnosis of wide QRS tachycardia]. / Apport de l'étude électrophysiologique par voie transoesophagienne dans le diagnostic étiologique des tachycardies à QRS larges.

INTRODUCTION: A wide-QRS complex tachycardia is suggestive of a ventricular tachycardia (VT). Its diagnosis requires an intracardiac electrophysiological study. That study is sometimes difficult to indicate in old or very young patients. The purpose of the study was to evaluate the interest of a rapid and noninvasive study by transesophageal route for the evaluation of the nature of a wide-QRS complex tachycardia. PATIENTS AND METHODS: Forty patients, aged from 16 to 85 years, without bundle branch block (BBB) in sinus rhythm, were admitted for documented wide-QRS tachycardia. Transesophageal electrophysiologic study (EPS) using one and two extrastimuli was performed in control state and after infusion of 20/30 micrograms of isoproterenol. Intracardiac EPS was performed in a second time in 38 of them. RESULTS: The study was negative six patients; intracardiac EPS remained negative in four of them, induced a VT in one and a Mahaim-reentrant supraventricular tachycardia in another one. Clinical tachycardia was induced in remaining patients: in 27 of them, the diagnosis of SVT with aberrancy was assessed; in other patients, the diagnosis of VT was assessed; The VT was a verapamil-sensitive VT or a bundle branch reentry (n = 7). The diagnosis was confirmed by intracardiac study. CONCLUSION: Esophageal EPS was a means to reproduce the clinical tachycardia in 34 of 40 patients and to evaluate the mechanism of wide-QRS tachycardia in 33 of 34 patients; this technique easy to perform should be indicated in patients in whom intracardiac study is debatable to avoid to diagnose by excess a VT or in the opposite to miss this diagnosis.

[Can the supraventricular proarrhythmic effects of class 1C antiarrhythmic drugs be prevented with the association of beta blockers?]. / Les effets proarythmiques supraventricúlaires des antiarythmiques de classe IC sont-ils prévenus par l'association avec des bêtabloquants?

Due to their electrophysiological characteristics, class 1 antiarrhythmic drugs can induce an auricular flutter with a 1/1 response. In addition to antiarrhythmic treatment, several authors have therefore considered using drugs capable of slowing auriculoventricular nodal conduction and preventing the 1/1 response. Beta-blockers have been proposed as candidate drugs. In this study, two patients were treated with an association of class 1 antiarrhythmic drugs (cibenzoline in one case, flecainide in the other) and beta-blockers. The administration of these drugs resulted in an atrial proarrhythmic response, and wide QRS tachycardia. Although both subjects had underlying heart disease, the tachycardia was relatively well tolerated in both instances. It was concluded that although beta-blockers may not suppress the risk of atrial proarrhythmia, they at least permit an improved tolerance to this complication.

[Paroxysmal junctional tachycardia and normal ECG in sinus rhythm. Is their mechanism influenced by the age of the patient at the time of the study?]. / Tachycardies jonctionnelles paroxystiques et ECG intercritique normal. Leur mécanisme est-il influencé par l'âge d'exploration du patient?

At the time of the curative treatment of paroxysmal junctional tachycardias, to determine the mechanism of the tachycardia is important. Five-hundred forty intracardiac or esophageal electrophysiological studies were performed in patients aged from 9 to 86 years and then revieved. There was no preexcitation syndrome on surface ECG. Programmed atrial stimulation was performed in basal state and if necessary repeated after infusion of isoproterenol. Atrioventricular nodal reentrant tachycardia was the most frequent cause of junctional tachycardia (72%) since childhood and in all stages of life. Concealed accessory pathway reentrant tachycardias were identified in 22% of tachycardias with a stable incidence during the course of life. Various mechanisms of tachycardia were identified in the remaining patients. In conclusion, the mechanism of paroxysmal junctional tachycardia is not correlated with the age of the patient.

[Does patient age influence the indications for investigating asympatomatic Wolff-Parkinson-White syndrome?]. / L'âge du sujet modifie-t-il les indications d'exploration du syndrome de Wolff-Parkinson-White asymptomatique?

Sudden death may be the presenting symptom of a Wolff-Parkinson-White syndrome. Electrophysiological investigation is the best method of identifying high risk cases. The aim of this study was to determine whether this investigation should be proposed to all patients, irrespective of age. Transoesophageal stimulation was performed in 85 asymptomatic patients with the Wolff-Parkinson-White syndrome. Of the 85 subjects, 13 were under 20 years of age, 30 under 30 years, 15 under 40 years, 16 under 50 years and 11 between 50 and 69 years of age. A protocol of incremental stimulation until 2nd degree AVB was attained and programmed atrial stimulation with one or two extrastimuli delivered on 2 paced cycles (600 and 400 ms) was used under basal conditions and with Isoprenaline. A malignant form of the condition was defined as the demonstration of two abnormalities: rapid conduction in the bundle of Kent (over 240/min) under basal conditions or over 300/min after Isoprenaline, and if it induced sustained atrial fibrillation (> 1 min). The results were: [table: see text] In conclusion, the number of malignant forms of the Wolff-Parkinson-White syndrome is exactly the same, irrespective of age. Elderly patients remain at risk of malignant WPW syndrome because of the increased incidence of atrial fibrillation. Therefore, the authors recommend systematic evaluation of this syndrome if the patient has an active life-style especially with regard to sporting activities.

Bradycardia-induced polymorphic ventricular tachycardia after radiofrequency catheter modification of atrioventricular junction.

We report the case of a 59-year-old man with a dilated nonischemic cardiomyopathy who had chronic rapid atrial fibrillation despite several therapies. Radiofrequency modification of the atrioventricular (AV) junction slowed the mean ventricular rate from 120 beats per minute (bpm) to 60 bpm. Five hours after the procedure and during the following 1 week, despite ventricular pacing at 90 bpm, the patient developed nonsustained or sustained polymorphic ventricular tachycardias. Finally, pacing at 90 bpm was successfully used in this patient. In conclusion, patients who have undergone modification of AV conduction may be at high risk of life-threatening ventricular arrhythmias in the first week following the procedure.