Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.

To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of note, verapamil completely suppressed VT inducibility in these three patients. These observations lead us to suggest that verapamil does not affect VT caused by reentry and catecholamine-sensitive automaticity but is effective in suppressing VT caused by triggered activity related to delayed afterdepolarizations in humans.

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 patient's 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.

Coexistent Mahaim and Kent accessory connections: diagnostic and therapeutic implications.

Six patients with coexistent Mahaim and Kent accessory connections are described. Two had left nodoventricular Mahaim connections, the first reported cases demonstrating these findings. In neither were the left-sided Mahaim connections components of a tachycardia and their presence was incidental. In two of four with nodoventricular connections, associated atrioventricular (AV) node conduction and coexistent posteroseptal accessory pathways were found. One of these had the unusual finding of a right-sided Mahaim connection arising from a "fast" AV node pathway. In only one patient did the tachycardia incorporate the Mahaim connection. In this patient, anterograde conduction during tachycardia occurred over a right nodoventricular connection whereas retrograde conduction occurred through a concealed right free wall Kent connection. Two patients had fasciculoventricular connections that were associated with either septal (one patient) or left free wall (one patient) Kent connections. The latter also had evidence of enhanced AV node conduction. This report is unique in that it describes in detail two patients with left nodoventricular connections (Mahaim) inserting in or near the left posterior fascicle. Combined Kent and Mahaim connections, present in the six patients, appear to occur in approximately 5% of patients with the Wolff-Parkinson-White syndrome. Precise identification of bypass connections critical for reentrant circuits is essential for intelligent application of treatment options.

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.

Electrophysiologic mechanism of exercise-induced sustained ventricular tachycardia.

To elucidate electrophysiologic mechanism of exercise-induced ventricular tachycardia (VT), electrophysiologic studies were performed in 12 patients in whom sustained VT had developed during treadmill exercise testing. Six patients had arteriosclerotic coronary heart disease, 3 had cardiomyopathy, and 3 had no clinical evidence of organic heart disease. All patients had had documented episodes of sustained VT related to exertion and had experienced dizziness, syncope, or both. In addition, 3 patients had had nonfatal cardiac arrest. Electrophysiologic studies provoked paroxysms of sustained VT identical to those observed during treadmill exercise testing in 10 patients and provoked ventricular flutter/fibrillation in 1. Seven patients had VT suggestive of a reentrant mechanism, as the VT could be readily initiated with programmed ventricular extrastimulation or terminated by ventricular overdrive pacing, or both. Three patients had VT suggestive of catecholamine-sensitive automaticity. The VT could not be initiated with programmed electrical stimulation, but it could be provoked by intravenous isoproterenol infusion; furthermore, the VT could not be terminated with ventricular overdrive pacing, but it could be abolished by discontinuing isoproterenol infusion. Reproduction of VT in these 10 patients allowed serial pharmacologic testing in selecting an effective antiarrhythmic regimen. Thus (1) exercise-induced VT can be caused by either reentry or catecholamine-sensitive automaticity, and (2) electrophysiologic studies are of use in defining the underlying mechanism of exercise-induced sustained VT.

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)

Ventricular tachycardia with congenital ventricular diverticulum.

A 24-year-old man presented with symptomatic, recurrent, sustained ventricular tachycardia (VT). He was found to have a basal inferior left ventricular diverticulum. His sustained VT was reproduced by programmed electrical stimulation and was unresponsive to procainamide, tocainide, propafenone, and flecainide. Endocardial mapping followed by resection and cryoablative surgery was performed. The patient had only one recurrence after 18 months, with subsequent control with procainamide for over 14 months.

Radiofrequency catheter cure of idiopathic ventricular tachycardia--first experience in Hawaii.

Radiofrequency catheter ablation is a well-established technique in the therapy of many forms of supraventricular tachyarrhythmias. Its usage in ventricular arrhythmias is little known. This is a report of its first usage in Hawaii in the treatment of 2 specific forms of ventricular tachycardia in 5 patients without structural heart disease. A cure was achieved in 4 of the 5 patients.

Low predictive value of an elevated prothrombin time for bleeding on oral anticoagulation.

This study is a retrospective analysis of 39 consecutive patients who had a prothrombin time of over 25 seconds with respect to the bleeding complications. This study finds that the overall risk of bleeding is low, 2/39 (5.1%), that there is no statistical difference in the values of the patients who bled when compared to those who did not, and that patients who bled tended to have a clearly identifiable precipitating event.

Radio-frequency catheter cure of re-entrant supraventricular tachycardias: report of the first experience in Hawaii.

Other than atrial fibrillation-flutter, the majority of supraventricular tachyarrhythmias involve either a macro-re-entry circuit utilizing an atrioventricular (AV) accessory pathway or a micro-re-entry circuit inside or around the AV node. The traditional form of therapy has been medical, with suppression by antiarrhythmic agents, most of which carry a heavy side-effect profile. The established alternative for medical therapy has been surgery, with open-chest excisional ablation of the accessory pathway or cryo-modification of the AV node. Even though, as opposed to medical therapy, surgery promises cure, it requires thoracotomy and cardiopulmonary bypass with significant associated morbidity and even mortality, as well as high cost. Ten years ago, the technique of "fulguration" was first introduced, which involved the delivery of an electrical charge through specialized catheters. Our first experience with this technique was reported in this Journal. Unfortunately, despite being a much better tolerated curative procedure involving a very brief hospitalization, the use of high-energy direct current (DC) shocks is associated with a low but significant incidence of serious complications including cardiac perforation, hypotension, coronary artery spasm, and late occurrence of ventricular fibrillation. Concerns about these potential complications have markedly limited the application of the catheter technique. In the past 2 years, adoption of radio-frequency (RF) current as the energy source has allowed the ablation to be performed in a very efficacious and much safer fashion. We would like to report the first experience with this technique in Hawaii.

Closed-chest electrical ablation (fulguration) of atrioventricular accessory pathway in the Wolff-Parkinson-White syndrome: report of the first case in Hawaii.

Wolff-Parkinson-White (WPW) syndrome is a condition characterized by the presence of an atrioventricular (AV) accessory pathway or bypass tract, which is an extraneous piece of muscular tissue connecting atrium to ventricle. This pathway leads to characteristic findings on the electrocardiogram (EKG). Patients with this syndrome are often asymptomatic, but many frequently have various forms of tachyarrhythmias, some of which may be life-threatening. The conventional therapy is medical, by suppression with antiarrhythmic agents. The established alternative to medical therapy has been surgery, with open-chest excisional ablation of the accessory pathway. In experienced centers, this has a high success rate and holds the promise of cure. Unfortunately, it requires thoracotomy, with its not insignificant associated surgical morbidity.

Coronary atherectomy: report of the first experience in Hawaii.

Since Andreas Gruentzig first introduced percutaneous transluminal coronary angioplasty (PTCA) in 1977, the ability to revascularize occluded coronary vessels with a catheter has enjoyed an explosive and unimaginable growth. As the equipment and operator experience improved, the possibilities appeared boundless. However, balloon angioplasty is hampered by a significant restenosis rate in the dilated vessel (approximately 30%), which is higher in selected locations (up to 60% in the proximal left anterior descending artery), even in the best of hands. This fundamental limitation may in part be due to the actual nature of the technique itself--stretching the vessel and fissuring the plaque causing remodeling without removal. The uneven, exposed vessel surface post-plaque rupture may contribute to activation of the hemostatic system, with acute thrombosis and release of various platelet and endothelial-derived growth factors, leading to long-term tissue proliferation and restenosis. Atherectomy, the mechanical removal of plaque from the vessel wall, appears to be an answer. This process actually debulks the culprit tissue and leaves behind a smoother, presumably less thrombogenic surface. We wish to report our first experience with a specific form of this technique in 4 consecutive patients, with a brief discussion of its promises and limitations.

Automatic implantable cardioverter defibrillator: report of the first two implants in Hawaii.

Sudden cardiac death is the major cause of death in the United States today, claiming over 400,000 victims each year, or one per minute. In the majority of cases, the underlying mechanism is malignant ventricular tachyarrhythmia, with the common substrate being abnormal myocardium from ischemic heart disease or congestive cardiomyopathy.

Intraoperative transesophageal echocardiography.

Intraoperative echocardiography in patients undergoing cardiac surgery was first described in 1972. Interest in intraoperative echocardiography has grown in recent years due to the extensive information provided by 2-dimensional (2-D) and color-flow Doppler imaging via the transesophageal approach. The value of this technique also has been verified in large clinical studies involving patients undergoing cardiac surgery. Intraoperative transesophageal echocardiography (TEE) is very useful in preoperative formulation of surgical plans and in immediate post-operative assessment of surgical results in patients undergoing valve surgery.

Clinical symptoms in patients with sustained ventricular tachycardia.

We questioned 113 patients with subsequently diagnosed sustained ventricular tachycardia (VT) regarding the symptoms that prompted their seeking hospital treatment, eliciting the following: 15% of patients had lost consciousness, 15% had near syncope, 35% had mild lightheadedness and 35% had no cerebral symptoms. Patients with preexisting congestive heart failure or a VT rate of 200 beats per minute or greater more often lost consciousness. Other symptoms included palpitations in 57% of patients, chest pain in 27%, dyspnea in 25%, weakness in 6%, nausea or diaphoresis in 3% each and flushing in 2%. In approximately 50% of patients who had mild lightheadedness or no cerebral symptoms, their condition was incorrectly diagnosed as supraventricular tachycardia based on the absence of severe symptoms during the tachycardia. In some patients, VT may be associated with mild or atypical symptoms. The differentiation of supraventricular from ventricular tachycardia should be based on electrocardiographic criteria and should not be influenced by the nature or severity of a patient's symptoms. The severity of cerebral symptoms is at least partially related to the VT rate and a patient's underlying heart disease.

Intravenous propafenone for termination of reentrant supraventricular tachycardia. A placebo-controlled, randomized, double-blind, crossover study.

To assess the antiarrhythmic efficacy of intravenous propafenone, 20 patients with inducible sustained supraventricular tachycardia received propafenone, 2 mg/kg body weight, or placebo in a double-blind, randomized, crossover study. Three patients had intra-atrial reentrant tachycardia, 3 had atrioventricular nodal reentrant tachycardia, and 14 had atrioventricular reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. Termination of supraventricular tachycardia occurred in 15 of the 20 patients receiving propafenone but 0 of the 11 patients receiving placebo (p less than 0.01). Propafenone prolonged refractoriness and slowed conduction of the atrium, the atrioventricular node, and accessory atrioventricular bypass tracts, and these effects provided antiarrhythmic action to halt tachycardia. No adverse effects were observed in any patient. We conclude that intravenous propafenone is safe and effective in the acute treatment of various forms of reentrant supraventricular tachycardia.