Role Of Electrophysiologic Testing Research Articles

Role of electrophysiological testing in the diagnosis of atypical retinitis pigmentosa

Retinitis pigmentosa (RP) is not a single entity but rather a disease spectrum. The classical triad of waxy disc pallor, bony spicules in the fundus, and arteriolar attenuation may not be found in all of the patients. In this series of seven atypical RP cases, we provide an overview of its varied clinical presentations and the role of electroretinogram in its diagnosis.

Mechanisms and clinical management of inherited channelopathies: Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, and short QT syndrome

The following briefly reviews features and management of long QT syndrome (LQTS), Brugada Syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), and short QT syndrome (SQTS). LQTS is marked by QT prolongation, syncope and sudden death due to torsades de pointes. Risk stratification is based on age, gender, history of symptoms, QT interval, and genetic subtype of LQTS. In addition to avoidance QT-prolonging drugs and high intensity sports, standard treatment for LQTS involves anti-adrenergic therapy, with implantable cardioverter-defibrillator (ICD) use in high risk subgroups. Brugada Syndrome is associated with right ventricular conduction delay and ST elevation in the right precordial leads, syncope, and sudden death from ventricular fibrillation. The electrocardiographic abnormality can be accentuated by sodium channel blocker, vagal stimulation or fever. Patients with aborted cardiac arrest and those with syncope and a spontaneous or sodium channel blocker-inducible type I Brugada ECG pattern are at high risk and should receive an ICD. The role of electrophysiologic testing is controversial. Although there is no reliable drug therapy for Brugada Syndrome, quinidine, which suppresses I(to) current, can reduce the incidence of arrhythmias. Patients with CPVT present with exercise-induced syncope and sudden cardiac death but normal resting electrocardiograms. Exercise or isoproterenol infusion may cause increased ventricular ectopy or bidirectional ventricular tachycardia. Treatment modalities include anti-adrenergic therapy and ICD implantation. Congenital SQTS is a relatively recently described disorder characterized by a very short QT interval and by susceptibility to atrial and ventricular fibrillation. ICD implantation is the primary therapy; quinidine may be a useful adjunctive therapy.

Role of Electrophysiological Testing in the Evaluation and Management of Idiopathic Ventricular Tachyarrhythmias

Role of Electrophysiological Testing in the Evaluation and Management of Idiopathic Ventricular Tachyarrhythmias

Role of electrophysiologic testing and coronary spasm provocation test in survivors of cardiac arrest.

Twenty-one patients were successfully resuscitated from cardiac arrest. Electrocardiograms (ECG) during cardiac arrest were recorded in 14 patients with ventricular fibrillation in 7, ventricular tachycardia in 4, cardiac standstill in three, Torsade de Points in one and atrial fibrillation with rapid ventricular response in 1. Thirteen patients (group I) had structural heart disease or primary ECG abnormality and 8 patients (group II) had no apparent heart disease. Electrophysiologic study (EPS) was performed in 12 patients of group I and 5 of group II. In group I, ventricular tachycardia was induced in 7, and His-ventricular conduction disturbance was demonstrated in 2, and 2 patients with Wolff-Parkinson-White (WPW) syndrome had an effective refractory period of the antegrade accessory pathway less than 250 msec. No patients in group II showed abnormal EPS findings. Spasm provocation test was performed in 8 patients (2 in group I and 6 in group II). Coronary spasm was induced in 5 patients (1 in group I and 4 in group II). Two patients in group II had positive results of upright-tilt testing. During the follow-up period, 2 patients died suddenly in group I and 1 patient whose cause of cardiac arrest was unknown had a recurrence of cardiac arrest. In group II, all patients whose etiology could be demonstrated by serial examinations had good prognosis. In conclusion, EPS is useful in evaluation of the cause of cardiac arrest especially when patients have structural heart disease, and coronary spasm may be involved in patients with cardiac arrest without apparent heart disease.

The role of electrophysiologic testing in the selection of amiodarone therapy.

The role of electrophysiologic testing in the selection of amiodarone therapy.

Evaluation of the Patient with Syncope

Evaluation of the patient who has experienced spontaneous, transient loss of consciousness requires a comprehensive consideration of many disease etiologies. Syncope may be a relatively benign condition with a good prognosis or may be a precursor of subsequent cardiac arrest and sudden death. In this article, the cardiovascular causes of syncope and the role of electrophysiologic testing in the diagnostic evaluation of patients with syncope are discussed.

Ventricular Tachycardia: Mechanisms, Diagnosis, and Management

This article discusses ventricular tachycardia with reference to the various proposed mechanisms, diagnosis, and management. Criteria for the diagnosis of ventricular tachycardia caused by reentry, automaticity, and triggered activity are presented. The use of various drugs as well as the role of electrophysiologic testing is discussed.

Electropharmacology of nonsustained ventricular tachycardia: Effects of class I antiarrhythmic agents, verapamil and propranolol

Forty-seven patients with spontaneous and inducible nonsustained ventricular tachycardia (VT) underwent serial electrophysiologic studies to evaluate the effects of antiarrhythmic agents on inducible arrhythmias, the role of electrophysiologic testing in the evaluation of pharmacologic therapy for these arrhythmias, and potential mechanisms underlying these arrhythmias. Type I antiarrhythmic agents prevented induction of VT by programmed stimulation in 18 of 37 patients and by isoproterenol in 9 of 11 patients. Verapamil and propranolol did not prevent or alter the mode of induction of VT by programmed stimulation, nor did they slow the induced tachycardias. Propranolol prevented induction of VT by isoproterenol in all 14 patients tested. Type I antiarrhythmic agents converted nonsustained into sustained VT in 2 of 37 patients. Inducible VT was prevented in 88% of patients without underlying heart disease, in contrast to only 38% of patients with associated cardiac disease (p < 0.02). This study demonstrates that electrophysiologic studies may be used to identify antiarrhythmic agents with both beneficial and potentially harmful effects in patients with nonsustained VT. The responses of inducible tachycardias to antiarrhythmic agents in this group of patients with spontaneous nonsustained VT are similar to those previously observed in patients with sustained VT. Finally, the results suggest that VT induced by isoproterenol may frequently respond to type I antiarrhythmic agents in addition to beta blockers.

The Clinical Significance of Ventricular Arrhythmias After Myocardial Infarction

Based on a sound foundation of data in thousands of patients who underwent ambulatory ECG recording after myocardial infarction, it is clear tht ventricular arrhythmias are harbingers of sudden cardiac death. Ambulatory electrocardiography, usually performed for 24 hours, continues to be the standard by which clinicians can identify patients at risk for sudden cardiac death after acute myocardial infarction. Ideally, this test should be performed in the late hospitalization phase of acute myocardial infarction, usually 1 to 2 days prior to discharge from the hospital, and the results made known to the clinician prior to the patient's departure from the hospital. Although performed less frequently, low-level exercise testing prior to discharge from the hospital has been shown in some studies to be of prognostic value in defining a group at high risk for sudden cardiac death. This test offers the additional benefit of allowing the clinician to more knowledgeably prescribe an exercise regimen after hospitalization. The specific role of electrophysiologic testing is presently under clinical investigation. At present, only patients with documented spontaneous sustained ventricular tachycardia or sudden cardiac death after myocardial infarction should be candidates for this study. Although it may be possible in the future that electrophysiologic testing will also be used in patients with high-risk arrhythmia detected on ambulatory electrocardiography, at present this is the subject of clinical investigation in academic medical centers and is not recommended as part of standard therapy.

Role of Electrophysiologic Testing in the Therapy of Ventricular Arrhythmias

The past decade has witnessed important advances in the understanding of the mechanism underlying ventricular arrhythmias. It has become clear that sustained ventricular arrhythmias can generally be reproduced with programmed ventricular stimulation in the clinical electrophysiology laboratory. False positive results may, however, occur with very vigorous stimulation techniques, particularly in patients without documented arrhythmias. False negative results are not infrequent in victims of cardiac arrest. Ability or inability to initiate ventricular tachycardia during acute and chronic drug testing has predicted clinical failure or success, at least for conventional antiarrhythmics. Patients with sustained ventricular tachycardia and cardiac arrest occurring outside the peri-infarction period are those most likely to benefit from study. Conventional antiarrhythmic agents are successful in about one-third of patients with a high degree of concordance among these drugs. Amiodarone is frequently effective in patients with drug-refractory ventricular arrhythmias. However, its efficacy cannot be predicted by programmed stimulation. This is in striking contrast to Type 1A anti-arrhythmic agents.

Role of electrophysiologic testing in managing patients who have ventricular tachycardia unrelated to coronary artery disease

This study examined the usefulness of programmed electrical stimulation in managing 83 patients who had ventricular tachycardia not due to coronary artery disease. Among 39 patients with a history of sustained ventricular tachycardia, programmed stimulation induced ventricular tachycardia in 14 of 14 patients with mitral valve prolapse or primary electrical disease (arrhythmias without evidence of structural heart disease) and in 13 of 25 with cardiomyopathy (total 27 of 39, 69 percent). Programmed stimulation induced nonsustained ventricular tachycardia in 15 (34 percent) of 44 patients with a history of nonsustained tachycardia (5 of 13 with mitral valve prolapse, 6 of 19 with primary electrical disease and 4 of 12 with cardiomyopathy). Seventy-three of the 83 patients were treated with antiarrhythmic drugs and then followed up for 14.4 ± 11.4 months (mean ± standard deviation). Drug therapy was determined with serial electrophysiologic testing in 31 patients. Twenty-four of these 31 patients had a history of sustained ventricular tachycardia, and drugs prevented induction of ventricular tachycardia in 9 (none of whom manifested symptomatic events) but did not prevent it in 15 (6 of whom had symptomatic events). Among seven patients with a history of nonsustained ventricular tachycardia, drugs prevented induction of ventricular tachycardia in five (none of whom had symptomatic events) and did not prevent it in two (none of whom had symptomatic events). Forty-two patients were treated using the results of noninvasive testing. Drugs suppressed spontaneous ventricular tachycardia in 15 of 15 patients with a history of sustained tachycardia (7 of whom had symptomatic events including one sudden death), and in 26 of 27 with a history of nonsustained tachycardia (6 of whom had symptomatic events including one sudden death). Thus, in patients with ventricular tachycardia unrelated to coronary artery disease: (1) programmed electrical stimulation induced ventricular tachycardia less often than in patients whose tachycardia was due to coronary artery disease; (2) programmed stimulation induced ventricular tachycardia less often in patients with a history of nonsustained versus sustained tachycardia; and (3) suppression of inducible ventricular tachycardia appeared to predict effective drug therapy but drug therapy predicted with noninvasive testing appeared to be unreliable.

Role of electrophysiologic testing in the diagnosis and treatment of patients with known and suspected bradycardias and tachycardias

Electrophysiologic testing has made possible more accurate diagnosis and treatment of recurrent tachycardias and syncopal episodes. The rapid expansion in clinical electrophysiology is reflected both in the number of reports in the literature and in the texts, monographs, and reviews appearing in recent years. 1–8 The challenge for the 1980s will be the continued refinement of present studies and the identification of high-risk patients for the development of bradycardias or tachycardias who warrant prophylactic treatment. Over the last decade, a battery of tests has been developed to assess the electrophysiologic function of cardiac tissues. The details of these tests vary among investigators. Occasionally, differences in investigator's assumptions, experience, or definitions may result in marked differences in viewpoints or conclusions, much to the consternation of the unwary reader. This article will review some fo the electrophysiologic tests and procedures currently in use, their applications, and reliability.