Mechanism of syncope in patients with isolated syncope and in patients with tilt-positive syncope.

BACKGROUND: Because of its episodic behavior, the correlation of spontaneous syncope with an abnormal finding can be considered a reference standard. METHODS AND RESULTS: We inserted an implantable loop recorder in 111 patients with syncope, absence of significant structural heart disease, and a normal ECG; tilt-testing was negative in 82 (isolated syncope) and positive in 29 (tilt-positive). The patients had had >/=3 episodes of syncope in the previous 2 years and were followed up for 3 to 15 months. Results were similar in the isolated syncope group and the tilt-positive group: syncope recurred in 28 (34%) and 10 patients (34%), respectively, and electrocardiographic correlation was found in 24 (23%) and 8 (28%) patients, respectively. The most frequent finding, which was recorded in 46% and 62% of patients, respectively, was one or more prolonged asystolic pauses, mainly due to sinus arrest, preceded for a few minutes by progressive bradycardia or progressive tachycardia-bradycardia. Bradycardia without pauses was observed in 8% and 12% of cases, respectively. The remaining patients had normal sinus rhythm or sinus tachycardia, except for one, who had ectopic atrial tachycardia. In the tilt-positive group, an asystolic syncope was also recorded when the type of response to tilt-testing was vasodepressor or mixed. Presyncopal episodes were never characterized by asystolic pauses; normal sinus rhythm was the most frequent finding. CONCLUSIONS: Homogeneous findings were observed during syncope. In most patients, the likely cause was neurally-mediated, and the most frequent mechanism was a bradycardic reflex. In the other cases, a normal sinus rhythm was frequently recorded. Presyncope was not an accurate surrogate for syncope in establishing a diagnosis.

Long-term follow-up after atrioventricular nodal ablation and pacing: low incidence of sudden cardiac death.

Sudden cardiac death (SCD) has been reported in patients with drug refractory AF who underwent AV nodal ablation and pacing. However, whether SCD in these patients is related to the underlying heart disease or to the ablating and pacing procedure remains uncertain. Between May 1987 and January 1997, AV nodal ablation was performed in 585 patients (mean age 66 +/- 11 years) with drug-resistant, paroxysmal (n = 308) or chronic (n = 277) AF in 12 Italian centers. Lone AF was present in 133 patients. After AV junction ablation, patients underwent VVIR (454 patients) or DDDR (131 patients) pacemaker implantation. At a follow-up of 33.6 +/- 24.2 months, 80 (13.7%) deaths were recorded: 40 noncardiac, 23 nonsudden, and 17 sudden cardiac death (3%, 1.04% per year). Among five variables, including age. NYHA functional class, presence of heart disease, paroxysmal or chronic AF, previous embolic events, and LVEF, the presence of heart disease (P = 0.007) and a LVEF < 0.45, (P = 0.003) were associated with a higher risk of SCD. Analysis of SCD-free survival by log-rank test showed a higher incidence of SCD in patients with LVEF < 0.45 (P = 0.0001) and with coronary artery disease (P = 0.005). In this large cohort, a low incidence of long-term SCD after AV nodal ablation and pacing for drug-refractory AF was observed. The presence of underlying heart disease and the extent of baseline LV dysfunction were associated with an increased likelihood of SCD.

[A case of atrial paralysis during the use of intravenous flecainide acetate]. / Un caso di paralisi atriale durante impiego di flecainide acetato per via venosa.

The aim of the present study is to describe a case of complete temporary atrial standstill, following iv administration of flecainide during the course of an endocavitary electrophysiologic study (EES). The patient, 79 years old, with frequent anamnestic periods of flutter and atrial fibrillation, which was followed by heart failure and with conductory disturbances to the surface ECG (first degree A-V block and left axis deviation), underwent EES in order to evaluate the functional reserve of cardiac eccito-conduction. With electric programmed stimulation, during EES, we induced atrial flutter, with a cycle length of about 300 ms. The administration of flecainide, dosage 1.5 mg/Kg in 15 min, determined the complete disappearance of every atrial electric activity, confirmed by right and left (coronary sinus) atrial mapping, also after electrical stimulation, and the emergency of substitutional ventricular rhythm, to a frequency of about 30-40/min. After atropine, dosage 0.02 mg/Kg iv, we noted an increase in the frequency of added focus up to the value of about 110 b/min, without any evidence of atrial electric activity. With sulfate isoprenaline in venous infusion, dosing 2 gamma/min, we noted firstly a ventricular-atrial back-leading 1:1; and after an ectopic atrial rhythm, with a frequency of about 130 b/min. After 5 hours a sinusal rhythm appeared.

[Flecainide acetate in the acute and medium-term prophylactic treatment of 2 cases of ectopic atrial tachycardia]. / Trattamento acuto e profilassi a medio termine con flecainide acetato in 2 casi di tachicardia atriale ectopica.

The aim of this study is to evaluate the efficacy of flecainide acetate, which was administered intravenously, to induce cardioversion in 2 female patients of 48 and 76 years, with ectopic atrial tachycardia. Besides the clinical examination, ECG monitoring by radiotelemetry, chest x-ray, echocardiographic examination, thyroid tests and other routine hematochemical tests, we carried out an endocavitary electrophysiologic study, followed by pharmacologic tests in series: propranolol (5 mg/5 min iv), verapamil (5 mg/5 min iv) and flecainide (1.5 mg/kg/15 min iv). We confirmed the presumptive diagnosis of ectopic atrial tachycardia and that, among all the drugs tested, flecainide acetate was the only one restoring the sinus rhythm. In a medium-term follow-up, during which the patients were treated with flecainide, 100 mg twice-a-day, we didn't notice relapse of the tachycardia and the patients tolerated the drug well.