Alan B. Schwartz

Long-term follow-up of patients with recurrent unexplained syncope evaluated by electrophysiologic testing.

Electrophysiologic testing was performed in 53 patients with recurrent syncope that remained unexplained despite a thorough neurologic and noninvasive cardiac evaluation. Fifteen patients had no structural heart disease, 9 had mitral valve prolapse and 29 had structural heart disease other than mitral valve prolapse. Nonsustained ventricular tachycardia was induced in 15 patients (28%), sustained ventricular tachycardia was induced in 9 (17%), ventricular fibrillation was induced in 4 (8%) and sinus node function was abnormal in 2 (4%). Female sex and lack of structural heart disease were independently associated with a negative electrophysiologic study (p less than 0.001). Patients with inducible ventricular tachycardia or ventricular fibrillation were treated with drugs selected on the basis of the results of electropharmacologic testing. The recurrence rate of syncope was 43% over a 31 +/- 10 month period (mean +/- standard deviation) of follow-up in patients with a negative electrophysiologic study, 40% over a 22 +/- 6 month period in patients with inducible nonsustained ventricular tachycardia, 0% over a 30 +/- 12 month period in patients with inducible sustained ventricular tachycardia and 25% over a 21 +/- 10 month period in patients with inducible ventricular fibrillation. In patients with recurrent unexplained syncope undergoing electrophysiologic testing, a potential cause of syncope is least likely to be found in women without structural heart disease. The results of programmed ventricular stimulation must be interpreted with regard to the method of induction of ventricular tachycardia and the type of ventricular tachycardia induced. The excellent response rate in patients with inducible sustained ventricular tachycardia whose therapy is guided by the results of electropharmacologic testing suggests that sustained ventricular tachycardia is a clinically significant response.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation.

Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.

Electrophysiologic testing in bundle branch block and unexplained syncope

Thirty-two patients with bundle branch block and unexplained syncope underwent electrophysiologic testing, including programmed ventricular stimulation with up to triple extrastimuli. The infranodal conduction time (HV) was 70 ms or greater in 12 patients. Pathologic infranodal block during atrial pacing occurred in 2 patients. Unimorphic ventricular tachycardia (VT) was induced in 9 patients (28%) and polymorphic VT in 5 (16%). A permanent pacemaker was implanted in patients with infranodal block during atrial pacing and, generally, in patients with an HV of 70 ms or more. Patients with inducible unimorphic or sustained polymorphic VT were treated with an antiarrhythmic drug. The mean follow-up period was 19 +/- 14 months (+/- standard deviation). Three patients died suddenly: a noncompliant patient with inducible sustained VT; a patient with a normal electrophysiologic study treated empirically with quinidine for premature ventricular complexes; and a patient with an HV of 70 ms and no inducible VT treated with a permanent pacemaker. The actuarial incidence of sudden death was 10% at 45 months of follow-up. Only 2 patients had recurrent syncope; both had a normal electrophysiologic study. Approximately 50% of patients with bundle branch block and unexplained syncope who undergo electrophysiologic testing are found to have a clinically significant abnormality (HV of 70 ms or more, infranodal block during atrial pacing and inducible unimorphic VT), and some patients have more than 1 abnormality. Long-term management guided by the results of electrophysiologic testing generally is successful in preventing recurrent syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic effects of intravenous amiodarone in patients with depressed left ventricular function and recurrent ventricular tachycardia

The systemic hemodynamic effects of intravenously administered amiodarone were evaluated in patients with depressed left ventricular function and recurrent sustained ventricular tachycardia. Heart rate decreased linearly up to 1 hour after amiodarone infusion (5 mg/kg). Cardiac index varied in a cubic fashion, diminishing at 10 minutes and returning to baseline by 60 minutes (p less than 0.05). Stroke work index also showed a similar decrease at 10 minutes, which was transient (p less than 0.005). These changes occurred without any significant change in systemic vascular resistance and with slight or no increase in pulmonary capillary wedge pressure, indicating a negative inotropic effect of amiodarone. The depression of left ventricular function in these patients, however, was mild and transient, and intravenously administered amiodarone was tolerated by the vast majority of patients. In two patients with overt heart failure and severely depressed left ventricular ejection fraction and marked hemodynamic abnormalities, profound hypotension occurred during amiodarone therapy; in such patients, therefore, hemodynamic monitoring is preferable. Limited data are available on the hemodynamic effects of orally administered amiodarone, but the determination of left ventricular ejection fraction by radionuclide ventriculography before and during long-term amiodarone administration has shown no reduction of function even in patients with severely reduced myocardial performance.

Electrophysiologic and hemodynamic effects of intravenous propafenone in patients with recurrent ventricular tachycardia.

Electrophysiologic and hemodynamic studies were performed before and after intravenous infusion of a new antiarrhythmic agent, propafenone, in 28 patients with recurrent ventricular tachycardia. Propafenone was given at a loading dose of 2 mg/kg in all patients. Subsequently, group A, the first 14 patients, received 1 mg/min and group B, the second 14 patients, received 2 mg/min continuous infusion. Propafenone exerted no effect on sinus nodal recovery time and sinoatrial conduction time, but significantly prolonged atrioventricular (AV) nodal and His-Purkinje conduction time and the QRS duration (respectively, 95 +/- 19, 48 +/- 10 and 120 +/- 23 ms before, and 110 +/- 28, 53 +/- 10 and 135 +/- 27 ms after; p less than 0.001). Propafenone did not change the mean arterial blood pressure but slightly increased right atrial, pulmonary artery and capillary wedge pressures resulting in mild depression of the cardiac index (2.6 +/- 0.8 liters/min per m2 before and 2.3 +/- 0.7 liters/min per m2 after; p less than 0.001). None of the patients were symptomatic from these changes. In group A, propafenone did not affect the inducibility of ventricular tachycardia except for one patient whose arrhythmia was sustained before and become nonsustained after propafenone. In group B, sustained ventricular tachycardia became noninducible in three patients and nonsustained in two patients, and nonsustained ventricular tachycardia became noninducible in one patient after propafenone. Therefore, an appropriate loading dose of intravenous propafenone such as 2 mg/kg followed by 2 mg/min infusion may be given safely and may suppress ventricular tachycardia. Propafenone may be a useful addition to currently available antiarrhythmic agents.

Catheter-induced his bundle ablation in a patient with reentrant tachycardia associated with a nodoventricular tract

A patient with refractory tachycardia associated with a nodoventricular tract in whom tachycardia was successfully controlled with catheter-induced ablation of the His bundle is reported. Tachycardia was always initiated by ventricular impulses that blocked retrogradely in the nodoventricular tract and conducted by way of the His-Purkinje system. The His bundle ablation was successfully accomplished by delivering two direct current countershocks of 400 J each in the region of the His bundle. Postablation, the patient manifested stable 1:1 anterograde conduction via the atrioventricular (AV) node-nodoventricular fiber over a wide range of heart rates (50 to 180 beats/min). A permanent pacemaker was not implanted at the patients request. During 16 months of follow-up, the patient has had stable sinus rhythm with no sustained tachycardia. Brief asymptomatic episodes of ectopic atrial tachycardia have been recorded on ambulatory electrocardiographic monitoring. This case 1) demonstrates the potential role of ablation of the His bundle in patients with refractory tachycardia associated with a nodoventricular tract provided that the His bundle is a critical component in the initiation of the tachycardia or a part of the tachycardia circuit; 2) reveals stable 1:1 AV conduction over a nodoventricular tract; and 3) emphasizes the utility of the phase image technique for diagnosis of a Mahaim tract.

Programmed ventricular stimulation in mitral valve prolapse: Analysis of 36 patients

Programmed ventricular stimulation with 3 extrastimuli was performed in 36 patients with mitral valve prolapse (MVP). Among 11 patients without transient cerebral symptoms, none had inducible ventricular tachycardia (VT) or ventricular fibrillation (VF), whether or not nonsustained VT or ventricular premature complexes (VPC) were present during ambulatory electrocardiographic recordings. These patients remained well without antiarrhythmic drug therapy for 6 to 57 months (mean 23) of follow-up. Two patients with recurrent unexplained syncope and no documented ventricular arrhythmia during electrocardiographic monitoring also had no inducible VT or VF. Among 20 patients with syncope or presyncope and documented nonsustained VT or VPCs during electrocardiographic monitoring, polymorphic nonsustained VT was induced in 8, sustained unimorphic VT in 2, and VF in 3. In 1 patient who had inducible polymorphic nonsustained VT, electrocardiographic monitoring during syncope showed sinus rhythm. Among 3 patients with a history of sustained VT or VF, unimorphic VT was induced in each. Patients with MVP who have asymptomatic ventricular ectopic activity and no inducible VT may have a benign prognosis without treatment. In patients who have transient cerebral symptoms and documented nonsustained VT or VPCs, VT or VF is inducible in 65%, most often polymorphic VT. It is unclear in which patients this finding is clinically significant and in which it is a nonspecific response to programmed stimulation.

Myocardial blood flow in patients with dilated cardiomyopathy: quantitative assessment with velocity-encoded cine magnetic resonance imaging of the coronary sinus.

To quantify global myocardial perfusion using magnetic resonance imaging (MRI) in patients with heart failure due to idiopathic dilated cardiomyopathy (IDC) and to compare myocardial perfusion and microvascular reactivity with healthy subjects.

Variability in coronary hemodynamics in response to ergonovine in patients with normal coronary arteries and atypical chest pain

Because an increase in coronary vascular resistance in response to ergonovine maleate has been suggested as a possible diagnostic aid for variant angina, changes were evaluated in coronary hemodynamics and serial myocardial thallium-201 perfusion scans in 15 patients without angina and with normal coronary arteries in response to ergonovine (0.05, 0.10 and 0.20 mg intravenously). For the group, heart rate-blood pressure product increased significantly (p less than 0.001) without any change in coronary sinus flow, coronary vascular resistance, myocardial oxygen extraction, arterial-coronary sinus oxygen difference and lactate extraction. In 7 of 15 patients, however, coronary vascular resistance increased (mean 39%, range 11 to 75%, probability [p] less than 0.001), and coronary sinus flow decreased (14%, p less than 0.001), despite an increase in heart rate-blood pressure product (36%, p less than 0.02). No electrocardiographic, metabolic or thallium-201 scan abnormalities occurred. Therefore, significant increases in coronary vascular resistance in response to ergonovine may occur in patients with normal coronary arteries and atypical chest pain.

Myocardial blood flow in patients with dilated cardiomyopathy: Quantitative assessment with velocity-encoded cine magnetic resonance imaging of the coronary sinus

PURPOSE To quantify global myocardial perfusion using magnetic resonance imaging (MRI) in patients with heart failure due to idiopathic dilated cardiomyopathy (IDC) and to compare myocardial perfusion and microvascular reactivity with healthy subjects. MATERIALS AND METHODS A total of 19 subjects (healthy volunteers (N = 12) and IDC patients (N = 7)) were studied using cine MRI to measure left ventricular (LV) mass and a velocity-encoded cine MRI technique to measure coronary sinus flow at rest and after dipyridamole-induced hyperemia. Absolute values of total myocardial blood flow (MBF) were calculated from coronary sinus flow and LV mass. RESULTS At baseline, MBF was not significantly different in patients with IDC (0.48 +/- 0.07 mL/minute/g) and healthy subjects (0.55 +/- 0.19 mL/minute/g, P= 0.41). After dipyridamole administration, MBF in IDC patients increased to a level significantly less than that in normal volunteers (1.05 +/- 0.35 mL/minute/g vs. 1.99 +/- 1.05 mL/minute/g, P < 0.05). Consequently, MBF reserve was impaired in patients with IDC (2.19 +/- 0.77) compared to that in healthy subjects (3.51 +/- 1.29, P < 0.05). A moderate correlation was found between MBF reserve and LV ejection fraction (r = 0.48, P < 0.05). CONCLUSION MBF reserve is reduced in patients with IDC, indicating that coronary microcirculatory flow is impaired. This integrated MRI approach allows quantitative measurement of global MBF in humans and may have the potential to study the effects of pharmacological interventions on myocardial perfusion.