Efficacy of midodrine hydrochloride in neurocardiogenic syncope refractory to standard therapy.

INTRODUCTION: Some patients with neurocardiogenic syncope continue to have recurrent syncope or presyncope despite the use of currently available drug therapy. The purpose of this study was to determine whether midodrine hydrochloride, a selective adrenergic agonist, could be effective in patients resistant to, or intolerant of, currently used medications in the treatment of neurocardiogenic syncope. METHODS AND RESULTS: Eleven patients with a history of recurrent syncope or presyncope in whom hypotension with syncope or presyncope could be provoked during head-up tilt testing were included. There were 4 men and 7 women with a mean age (+/-SD) age of 34 +/- 13 years. In all patients, standard therapy with beta-adrenergic receptor blocking agents, ephedrine, theophylline, disopyramide, fludrocortisone, and sertraline hydrochloride, was either ineffective, poorly tolerated, or contraindicated. Midodrine was initially administered orally at a dose of 2.5 mg three times daily. After adjustment of dosage over 2 to 4 weeks, patients were followed-up clinically. Midodrine was discontinued in one patient because of side effects. Frequency of syncope or presyncope during the 3 months prior to starting treatment was compared during a mean follow-up of 17 +/- 4 weeks after starting treatment with midodrine. There was significant (P < 0.01) reduction in syncopal and presyncopal episodes on midodrine. Five patients had complete resolution of symptoms, while four patients had significant improvement. Symptoms did not improve in one patient. CONCLUSIONS: Midodrine hydrochloride can be effective in preventing recurrent symptoms in selected patients with neurocardiogenic syncope unresponsive to, or intolerant of, standard drug therapy.

Ventricular tachycardia in valvular heart disease: facilitation of sustained bundle-branch reentry by valve surgery.

BACKGROUND: The clinical characteristics of sustained monomorphic ventricular tachycardia (SMVT), when it develops after valve surgery, have not been described. METHODS AND RESULTS: Between 1985 and 1996, 31 patients (30 men and 1 woman) who had undergone valve surgery were found to have inducible SMVT. Nine patients (29%) had sustained VT due to bundle-branch reentry (BBR) (group 1). Four of these patients had normal left ventricular function, and VT with a right bundle-branch morphology was inducible in 4 patients. Group 2 included 20 patients with inducible myocardial (ie, non-BBR) VT. Coronary artery disease was present in 15 group 2 patients (75%) due to atherosclerotic (n=12) and nonatherosclerotic (n=3) causes. Two patients had both inducible sustained BBR and myocardial VT (group 3). Sustained BBR VT occurred significantly earlier after valve surgery (median, 10 days) than the onset of postoperative myocardial VT (median, 72 months; P<.005). CONCLUSIONS: Myocardial VT was the most common type of inducible SMVT in patients with valvular heart disease. The majority of these patients had underlying coronary artery disease and significant left ventricular dysfunction. However, in almost one third of the patients, sustained BBR VT was the only type of inducible SMVT. This type of VT was facilitated by the valve procedure occurring within 4 weeks after surgery in most patients. In these patients, left ventricular function was relatively well preserved, and the right bundle-branch block type of BBR was frequently induced. Because a curative therapy can be offered to these patients (ie, bundle-branch ablation), BBR should be seriously considered as the mechanism of VT in patients with valvular heart disease, particularly if the arrhythmia occurs soon after valve surgery.

Relevance of asystole during head-up tilt testing.

The prognosis of patients manifesting prolonged asystole during head-up tilt testing is unclear. In 209 consecutive patients with a history of syncope and positive head-up tilt tests, 19 had asystole lasting > 5 seconds (mean duration 15 +/- 10) (group 1a). When compared with patients without asystole (group 1b), group 1a patients were younger (32 +/- 12 vs 47 +/- 21 years, p < 0.005), but clinical manifestations were not any more dramatic (the number of episodes of syncope [7 +/- 5 vs 8 +/- 6 episodes, p = NS] and injury during syncope [2 vs 13 patients, p = NS] were similar). During follow-up (mean 2 +/- 1 year), with the patient taking pharmacologic therapy such as beta blockers, ephedrine, theophylline, or disopyramide, the recurrence rate was 11% and 8% in groups 1a and 1b (p = NS). No patient in the asystole group underwent pacemaker implantation. Additionally, of 75 normal volunteers (group 2) with no history of syncope undergoing tilt tests to define its specificity, 3 had asystole (mean duration 10 seconds). During > 1 year of follow-up, despite no treatment, all 3 are symptom free. Thus, asystole during head-up tilt testing does not predict either a more malignant outcome or a poor response to pharmacologic therapy. Moreover, an asystolic response does not enhance the specificity of the head-up tilt test because it may be present in asymptomatic "normal" volunteers.

Feasibility of concomitant implantation of permanent transvenous pacemaker and defibrillator systems.

In 17 patients (14 men and 3 women aged 69 +/- 10 years), a transvenous pacemaker was implanted before (8 patients), following (7 patients), or simultaneously (2 patients) with the insertion of a transvenous defibrillator. Indications included malignant ventricular arrhythmias and symptomatic bradycardia in all patients. All patients had structural heart disease. All pacemakers were non-programmable bipolar, either single chamber (n = 7) or dual chamber (n = 10). Eleven pacemakers were rate responsive. The Transvene system was implanted in 7 patients (Pacer-Cardioverter-Defibrillator in 6 patients and the Cadence defibrillator in 1). The Endotak lead system was implanted in 10 patients (Ventak in 7 patients and the Cadence in 3). The mean defibrillation threshold was 16 +/- 5 J. Repositioning of the pacemaker leads eliminated undersensing of ventricular fibrillation by the defibrillator, which occurred during asynchronous pacing in 2 patients. During a mean follow-up of 11 +/- 6 months, 2 patients died because of pump failure and 7 patients received defibrillator therapy for ventricular arrhythmias. No significant complications were noted. Successful concomitant implantation of transvenous pacemakers and defibrillators was thus accomplished in 17 patients, which suggests that insertion of a second transvenous device can be safely accomplished.

Control of supraventricular tachycardia with transcatheter ablative technique using radio frequency as the energy source.

Supraventricular tachycardia constitutes a significant clinical problem, frequently requiring medical intervention. We analyzed data in 413 consecutive patients with supraventricular tachycardia treated at our center with the catheter ablative technique and found the following outcome. Among 272 patients who had regular narrow QRS tachycardia without ventricular pre-excitation during sinus rhythm (Group I), control was achieved in all but one case (success rate 99.6%). Patients in Group II had ventricular pre-excitation during sinus rhythm and narrow or wide QRS tachycardia. Elimination of ventricular pre-excitation and control of the tachycardia was achieved in 104 of the 106 cases in this group (a success rate of 98%). Group III patients had atrial flutter-fibrillation as the predominate arrhythmia and control of rapid ventricular response was successfully achieved with atrioventricular junctional ablation in all 35 cases. Serious complications were related to anticoagulation and were seen in less than 2% of the cases. There were no instances of thromboembolic phenomena or death related to these procedures. It is concluded that the catheter ablative technique with radio frequency as the energy source is a highly effective means for control of supraventricular tachycardia with minimal associated risk of serious complications.

Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations.

BACKGROUND: Atrioventricular (AV) nodal reentry is a relatively common cause of regular, narrow QRS tachycardia. The underlying basis for this arrhythmia is functional (and anatomic) duality of pathways in the region of the AV node, although the exact boundaries of the reentrant circuit have not been convincingly defined. During the more common type of AV nodal reentry (seen in approximately 90% of cases), a slow conducting pathway is used in the anterograde direction, and a fast pathway is operative in the retrograde direction. In the uncommon form, the direction of impulse propagation within the reentrant circuit is reversed. In this article, the clinical, ECG, and electrophysiological features of AV nodal reentry as well as approaches to therapy are discussed. METHODS AND RESULTS: Clinical diagnosis may be made from the surface ECG. In the common type of AV nodal reentry, the P wave is obscured by the QRS or may be present in its terminal portion. The P wave in the uncommon form occurs late (i.e., in or after the T wave), producing a pattern of long RP and short PR. Both forms of AV nodal reentry are controllable with various therapeutic modalities. For acute termination, adenosine is probably the ideal agent. Prevention of recurrences can be achieved with several pharmacological agents, including beta-blockers, calcium channel blockers, and class Ia, Ic, and III antiarrhythmic agents. Curative therapy is now available with a variety of nonpharmacological methods. However, the most promising therapy at the present time is catheter modification of the AV node by ablation of either the fast or slow pathway, using radiofrequency energy. Ablation of the fast pathway carries a higher risk of second- or third-degree AV block. Slow pathway ablation, by providing a high rate of success and minimal risk of AV block, seems to be a more acceptable initial approach. CONCLUSIONS: AV nodal reentry is a common cause of paroxysmal supraventricular tachycardia, and a precise diagnosis can be made with intracardiac electrophysiological evaluation. Although the arrhythmia responds to a variety of antiarrhythmic agents, curative therapy can now be offered with catheter modification of the AV node using radiofrequency energy. At the time of this writing, it seems that catheter modification of the AV node is rapidly becoming the therapy of initial choice in patients with symptomatic AV nodal reentrant tachycardia requiring treatment.