Long-term results of electrophysiologically guided sotalol therapy for life-threatening ventricular arrhythmias.

The efficacy and safety of sotalol therapy for ventricular arrhythmias was evaluated in 133 patients with drug-refractory ventricular arrhythmias. All patients had baseline electrophysiologic studies before and after oral sotalol therapy. Sixty-six patients were discharged home, treated with sotalol (52 patients without inducible ventricular tachycardia or fibrillation and 14 patients with hemodynamically stable inducible ventricular tachycardia). The mean follow-up period was 41 +/- 27 months for the 14 patients with hemodynamically stable ventricular tachycardia. Sotalol was effective in 8 of these 14 patients. Recurrent nonlethal ventricular tachycardia occurred in 3 patients; 2 patients had sudden death; and 1 patient had adverse side effects. The 52 patients without inducible ventricular tachycardia were followed up for a mean period of 36 +/- 30 months. Thirty-five of 52 patients were successfully treated. Two patients had recurrent ventricular tachycardia; both of these episodes of ventricular tachycardia occurred within the first year. Four patients had sudden cardiac death; three of these deaths occurred within the first month, and the last episode of sudden death occurred after 8 years of sotalol therapy. The actuarial incidence of sotalol efficacy was 76% at 1 year, 72% at 2 years, 64% at 4 years, and 52% at 5 years. Approximately 46% of patients receiving long-term sotalol treatment reported side effects. Side effects severe enough to warrant withdrawal of sotalol occurred in 7 (11%) patients. The results of our study suggest that sotalol is effective for selected patients with drug refractory ventricular arrhythmias. Although the incidence of side effects are high, patients appear to tolerate long-term sotalol therapy well.

Radiofrequency catheter ablation of atriofascicular and nodoventricular Mahaim tracts.

BACKGROUND: Several mechanisms have been proposed to explain the pathogenesis of tachycardia in patients with Mahaim tracts. The tachycardia may involve antegrade conduction over an atriofascicular pathway with decremental properties or a nodofascicular pathway. METHODS AND RESULTS: We report six patients with recurrent episodes of preexcited tachycardia with findings consistent with "Mahaim tract" conduction. All patients exhibited decremental antegrade preexcited conduction with atrial pacing and a preexcited tachycardia with initial activation of the proximal right bundle branch. In four patients (group 1), atrial premature complexes (APCs) induced at the tricuspid annulus just after the inscription of the septal atrial electrogram and during left bundle branch block preexcited tachycardia advanced the next preexcited ventricular complex. In these patients, discrete Mahaim potentials were inscribed over the right anterolateral or lateral tricuspid annulus. Two patients (group 2) had evidence of dual atrioventricular nodal conduction. APCs during left bundle branch block tachycardia just after inscription of the septal atrial electrogram failed to advance the next ventricular complex with similar preexcited morphology, and no Mahaim potentials could be recorded from the tricuspid annulus. In group 1 patients, application of radiofrequency energy to sites recording the Mahaim potentials resulted in tachycardia cure. For patients in group 2, selective slow atrioventricular nodal pathway ablation in the midseptal region resulted in complete ablation of both the slow atrioventricular nodal pathway and Mahaim conduction in two patients. CONCLUSIONS: Mahaim tachycardia can be due to atriofascicular pathways, which may be ablated over the right tricuspid annulus, or to septal pathways, which may arise from the slow atrioventricular nodal pathway in patients with dual atrioventricular nodal physiology. In the latter circumstance, successful ablation is achieved by placing the lesion in the midseptal region.

Radiofrequency catheter ablation of atrial arrhythmias. Results and mechanisms.

BACKGROUND: Radio frequency catheter ablation is accepted therapy for patients with paroxysmal supraventricular tachycardia and has a low rate of complications. For patients with atrial arrhythmias, catheter ablation of the His bundle has been an option when drugs fail or produce untoward side effects. Although preventing rapid ventricular response, this procedure requires a permanent pacemaker and does not restore the atrium to normal rhythm. Therefore, we evaluated the safety and efficacy of radiofrequency ablation directed at the atrial substrate. METHODS AND RESULTS: Thirty-seven patients with 42 atrial arrhythmias (mean +/- SD age, 41 +/- 24 years) who had failed a median of three drugs were enrolled. Diagnoses were automatic atrial tachycardia in 12, atypical atrial flutter in 1, typical atrial flutter in 18, reentrant atrial tachycardia in 8, and sinus node reentry in 3 patients. Sites for atrial flutter ablation were based on anatomic barriers in the floor of the right atrium. For automatic atrial tachycardia, the site of earliest activation before the P wave was sought. All with reentrant atrial tachycardia had previous surgery for congenital heart disease and reentry around a surgical scar, anatomic defect, or atriotomy incision and our goal was to identify a site of early activation in a zone of slow conduction. At target sites, 20 to 50 W of radiofrequency energy was delivered during tachycardia between the 4- or 5-mm catheter tip and a skin patch, except in 4 patients with atrial flutter, in whom a catheter with a 10-mm thermistor-embedded tip was used. Procedure end point was inability to reinduce tachycardia. Acute success was achieved in 11 of 12 (92%) with automatic atrial tachycardia, 17 of 18 (94%) with typical atrial flutter, 7 of 8 (88%) with reentrant atrial tachycardia, and 3 of 3 (100%) with sinus node reentry but not in the patient with atypical atrial flutter. For tachycardia involving reentry (reentrant atrial tachycardia and atrial flutter), successful ablation required severing an isthmus of slow conduction. For those with atrial flutter, this was between the tricuspid annulus and the coronary sinus os (10) or posterior (4) or posterolateral (3) between the inferior vena cava (2) or an atriotomy scar (1) and the tricuspid annulus. Deep venous thrombosis occurred in 1 patient. At mean follow-up of 290 +/- 40 days, the ablated arrhythmia recurred in 1 (9%) with automatic atrial tachycardia, 5 (29%) with atrial flutter, and 1 (14%) with reentrant atrial tachycardia, all of whom had successful repeat ablation. Previously undetected arrhythmias occurred in 2 patients who are either asymptomatic or controlled with medication. CONCLUSIONS: Ablation of automatic and reentrant atrial tachycardia and atrial flutter had a high success rate and caused no complications from energy application. Repeat procedures may be required for long-term success, especially in patients with atrial flutter. The mechanism by which ablation is successful is similar for atrial flutter and other forms of atrial reentry and involves severing a critical isthmus of slow conduction bounded by anatomic or structural obstacles. Automatic arrhythmias are abolished by directing lesions at the focus of abnormal impulse formation.

Evaluation and management of patients with polymorphic ventricular tachycardia.

This article reviews the current understanding of the mechanisms for polymorphic VT, its clinical manifestation, and therapies. The various idiopathic long QT syndromes and acquired forms of this entity are addressed, and a new syndrome of polymorphic VT associated with a normal heart and normal QT interval is emphasized.

Advances in evaluating and treating Wolff-Parkinson-White syndrome.

Interest has increased in the use of new noninvasive modalities, particularly body surface mapping, for localizing accessory pathways in Wolff-Parkinson-White syndrome. New data from invasive studies reviewed here include evidence of decremental conduction and the linking phenomenon in patients with accessory pathways. Risk factors for sudden death, including syncope and atrial fibrillation, are reviewed. The most notable advances involve our ability to offer patients catheter ablation, which has proven to be safe and effective. Both direct current and radiofrequency catheter ablation are discussed.

Enhanced detection of intracardiac sources of cerebral emboli by transesophageal echocardiography.

We performed transesophageal echocardiography in 50 consecutive hospitalized patients with recent transient ischemic attack or stroke of embolic origin to determine whether transesophageal echocardiography is more sensitive than transthoracic echocardiography in detection of possible intracardiac sources of embolism. Twenty-six of 50 patients with a negative transthoracic echocardiogram for potential source of emboli had a transesophageal echocardiography study that demonstrated at least one intracardiac abnormality. Abnormalities noted by transesophageal echocardiography included five of 50 patients with either a left atrial or left atrial appendage clot, four patients with a patent foramen ovale, and nine patients with spontaneous echocardiographic contrast. In 11 of 50 patients with no other source of embolism, we found highly mobile filamentous strands on the mitral valve, which have not been described previously. These mitral valve echo strands may represent a fissured surface or fibrosis that can serve as a nidus for thrombus formation. We detected no unexpected left ventricular thrombus or left atrial myxoma. Factors significantly associated with a greater likelihood of a positive transesophageal echocardiography study included left atrial enlargement, atrial fibrillation, and a calcified or thickened mitral valve. Our study suggests that transesophageal echocardiography is a valuable addition to transthoracic echocardiography in investigating potential intracardiac sources of embolism.