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Author: Hongsheng M Guo, MD, Director of Cardiac Electrophysiology, Heart and Vascular Center, Park Nicollet Health System

Hongsheng M Guo is a member of the following medical societies: American College of Cardiology

Editors: Justin D Pearlman, MD, PhD, ME, MA, Director of Dartmouth Advanced Imaging Center, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine; Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital; Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital

Author and Editor Disclosure

Synonyms and related keywords: programmed electrical stimulation, electrophysiologic studies, electrophysiologic study, EPS, EP studies, electrophysiological studies, electrophysiological study, PES, noninvasive programmed electrical stimulation, NIPS, electrophysiology study, electrophysiology, cardiac electrophysiology, cardiac rhythm disturbance, rhythm disturbance, arrhythmia, acute myocardial ischemia, electrolyte disturbance, Wolff-Parkinson-White syndrome, WPW syndrome, long QT syndrome, MI, myocardial infarction, cardiac conduction system, cardiac workup, cardiac evaluation, heart workup, heart work up, cardiac work up

Although the history of cardiac electrophysiology (EP) dates to the mid- to late-19th century, when J. E. Purkinje and W. His, Jr, first described the special conduction tissues in the heart (see Key discoveries related to the cardiac conduction system), the infancy of modern cardiac EP did not arrive until more than a century later.

In 1969, from the cardiopulmonary laboratory at the US Public Health Service Hospital in Staten Island, NY, Scherlag and colleagues described a reliable, reproducible, and simple technique to record from and pace at the human His bundle with a catheter electrode. This discovery, along with systematic use of programmed electrical stimulation (PES) of the heart described by Drs Durrer and Wellens (Durrer, 1967; Wellens, 1971), became the basis and the major tool that allowed scientists and clinical electrophysiologists to investigate the mechanisms underlying different cardiac rhythm disturbances.

Based on a better understanding of the mechanisms, newer diagnostic and therapeutic techniques, such as detailed endocardial activation mapping (including 3-dimensional mapping); surgical and catheter ablation of supraventricular and ventricular tachyarrhythmias; and devices (eg, pacemaker, cardioverter defibrillator) for both bradyarrhythmias and tachyarrhythmias, were soon developed and have continued to be improved. By using these sophisticated techniques, electrophysiologists currently have more opportunities not only to better treat arrhythmias but also to cure some of the clinically common arrhythmias.

Key discoveries related to the cardiac conduction system include the following:

  • Purkinje fibers - J. E. Purkinje in 1845
  • Bundle of His - W. His, Jr, in 1893
  • Atrioventricular (AV) node - L. Aschoff and S. Tawara in 1906
  • Sinus node - A. B. Keith and M. W. Flack in 1907
  • Bachmann bundle - J. G. Bachmann in 1916

Modern EP testing is a multifaceted approach to assessing cardiac arrhythmias. The procedure involves (1) measurements of cardiac electrical activation and conduction; (2) assessment of electrical activation patterns, either spontaneous or induced (ie, mapping); (3) induction and termination of arrhythmias (with PES); (4) assessment of risk for malignant arrhythmias and sudden cardiac death; (5) treatment with ablation; and (6) assessment of the effects of drug and electric interventions, including device and ablative therapies. The approach can be either invasive or noninvasive.



A normal heart consists of both excitable tissues and nonexcitable tissues (eg, central fibrous body). The excitable tissues include the sinoatrial node (sinus node), the intra-atrial and interatrial conduction pathways, the atrioventricular junction (AV node), the His-Purkinje system, and the atrial and ventricular muscles (working tissues). Under normal conditions, all excitable tissues (except the atrial and ventricular muscles) have the capacity to spontaneously generate electric impulses (automaticity) and to excite the adjacent excitable tissues. However, the activation of the heart is normally controlled by the sinus node because it has the highest automaticity.

The normal conduction pattern can be disrupted by different causes. In many cases, particularly those of acute and transient causes, including acute myocardial ischemia, electrolyte disturbances, and medication toxicity, EP testing is probably not warranted. On the other hand, EP testing may provide imperative insights into many other conduction disturbances, especially those related to significant symptoms, such as results of derangement in normal pacemaker activity, damage to the myocardium due to infarction, abnormal cardiac channel activity (eg, long QT syndrome, Brugada syndrome), and abnormal electrical pathways (eg, Wolff-Parkinson-White [WPW] syndrome). EP testing can help evaluate the integrity of the cardiac conduction system and the components that create cardiac arrhythmias. EP testing is the definitive study presently available to assess the mechanism, cause, and treatment of many cardiac arrhythmias.

Common mechanisms of arrhythmogenesis (abnormal impulse formation) and clinical examples are as follows:

  • Automaticity
    • Normal automaticity - Sinus tachycardia or bradycardia
    • Abnormal automaticity - Accelerated ventricular tachycardia
    • Combined - Modulated parasystole
  • Triggered activity
    • Early after-depolarizations - Ventricular tachycardia associated with long QT syndromes
    • Delayed after-depolarization - Digitalis-induced arrhythmias
  • Abnormal impulse conduction
    • Conduction block - Any level in conduction system, sinoatrial node, AV node, His-Purkinje system, others
    • Reentry - Atrial flutter, AV nodal reentry, bundle-branch reentry, and other types of ventricular tachycardias

Common electrophysiological concepts and definitions are as follows:

  • Automaticity - Initiation of an impulse spontaneously without the need for prior stimulation
  • Triggered activity - Activation initiated by depolarizing oscillation induced by preceding action potentials either before (early after-depolarization) or after (delayed after-depolarization) the preceding action potentials reach full depolarization
  • Reentry - Circular impulse conduction along a fixed circuit with repetitive activation to the adjacent tissues
  • Refractoriness - Inability to be excited in a period during and immediately after activation



A modern electrophysiological laboratory needs proper equipment in order to optimize performance. The equipment should include a recording system that accommodates multiple intracardiac and body surface ECGs. The signals are displayed on oscilloscopes (computer screens) and stored. In addition, the laboratory should have a programmable impulse generator (stimulator), a high-resolution fluoroscopy system, and 2 external defibrillators (one for emergency backup).

Before the procedure, patient preparation involves a thoughtful discussion, including the associated risks and benefits, with the electrophysiologist responsible for the examination. Informed consent also should be obtained. The patient should receive adequate control for anxiety, discomfort, and pain. Finally, the venous and arterial sites should be prepared with antiseptic agents and drapes.

Insertion sites commonly include the femoral, jugular, and, occasionally, subclavian and cephalic veins. If necessary, the femoral arteries are used to gain access to the left side of the heart and for continuous direct blood pressure monitoring.

The purpose of a particular EP study (EPS) dictates the number and type of electrode catheters used. In general, a high right atrium, a His bundle, and a right ventricular apex catheter are often needed for the initial study. A coronary sinus catheter is frequently required during a supraventricular tachyarrhythmia study and ablative therapy

(see Images 1-2). Before addressing specific questions, the following baseline data are normally obtained:

  • Stimulation thresholds
  • Sinus node function - Sinus node recovery time (SNRT), sinoatrial conduction time (SACT)
  • AV node function - Dual AV node pathways, Wenckebach cycle length
  • Refractoriness
  • Inducibility of arrhythmias (when indicated) (see Image 7)

PES delivered during an EPS uses electrical stimulation of the heart delivered in a specific pattern to assess bradyarrhythmias and tachyarrhythmias (see Image 4). Less frequently, PES is used to assess the efficacy of antiarrhythmic drug therapy in patients at high risk for ventricular arrhythmias and sudden cardiac death. Consider EP testing to assess the following:

  • Mechanistic insights of arrhythmias, including tachyarrhythmias, bradyarrhythmias, and supraventricular and ventricular arrhythmias
  • Risk for malignant ventricular tachycardia and sudden cardiac death
  • Application of treatments and evaluation of those treatments, including drug therapy, device therapy (eg, pacemaker, implanted cardioverter/defibrillator [ICD], biventricular pacing device), and ablative therapy (see Image 3 and Images 5-6)
  • Potential of an arrhythmic etiology for syncope

Commonly used protocols

Although stimulation protocols are generally governed by clinical indications and the purpose of the study, they vary significantly from laboratory to laboratory and from operator to operator. The sensitivity and specificity of test results are greatly dependent on many factors, including underlying conditions, the aggressiveness of the protocol, and the different endpoints used. Commonly used protocols are listed in the following table, and the numbers listed are largely based on the author's interpretation of available literature (often limited) and personal experience.

Commonly Used Stimulation Protocols

Stimulation SitePurpose of TestStimuli UsedIsoproterenol InfusionSensitivity*, %Specificity*, %
Right atriumSinus Node Assessment
SNRTS1-50-6080
SACTS1S2-50-6090
AV Node Assessment
AH interval (ie, AV nodal conduction time)
-

Wenckebach cycle lengthS1-10060
ERP† (slow and fast pathway)S1S2 -

Accessory Pathways
LocalizationS1(S2)->95>95
ERPS1S2With or without

Antegrade Intraventricular Conduction
His-Purkinje conduction (with or without procainamide infusion)S1(S2)->95>95
Induction of Arrhythmia
AV nodal reentry tachycardiaS1S2(S3)
Burst
With or without
(with or without atropine)
>95>90
Accessory pathways>95>95
Atrial tachycardia>95>95
Reentrant70-80>90
Triggered60-70>90
Automatic40-5090
Atrial flutter>90~80
Atrial fibrillation40-6040-60
Right ventricle (apex with or without outflow tract)Retrograde AV conductionS1(S2)-

Accessory Pathway
LocalizationS1(S2)
>95>95
ERPS1S2


Induction of Arrhythmia
Supraventricular tachycardiaS1S2(S3)
Burst
With or without
(with or without atropine)


Ventricular Tachycardia
In Conjunction With CAD‡
MMVT§S1S2S3(S4)
Burst
With or without if no severe structural heart disease, but none in severe CAD>95>90
NSVT|| and VF¶ (CHF#)3350
Idiopathic cardiomyopathy

BBRT**5090
NSVT2030-40
Cardiac arrest6090
Valvular or other heart disease with NSVT2030

*All sensitivity and specificity percentages are approximations. No data are available for all of these conditions.

†ERP - Effective refractory period

‡CAD - Coronary artery disease

§MMVT - Monomorphic ventricular tachycardia

||NSVT - Nonsustained ventricular tachycardia

¶VF - Ventricular fibrillation

#CHF - Congestive heart failure

**BBRT - Bundle-branch reentrant tachycardia

Mapping techniques

During EPS, mapping techniques are frequently used to elucidate the mechanism and to localize the substrate of rhythm disturbance. In general, 4 types of mapping are used: activation sequence mapping, voltage amplitude mapping, pacing morphology mapping, and entrainment mapping.

Activation sequence mapping can be achieved by either simultaneous mapping or sequential mapping.

The most commonly used simultaneous activation sequence mapping is multipolar electrode mapping, such as multipolar coronary sinus electrode and multipolar atrial/ventricular electrode mapping using, for example, a Halo catheter (see Image 2 and Image 6) and basket catheter (see Image 3). A noncontact mapping system (EnSite, Endocardial Solutions; St. Paul, Minn) is able to construct a 3-dimensional activation map using virtual electrograms sensed from a single heartbeat. It is a new diagnostic tool that enables electrophysiologists to rapidly and comprehensively map arrhythmias and facilitate the selection of therapeutic options, including curative ablation.

Sequential mapping, also known as point-to-point mapping, is also a frequently used activation sequence mapping technique during diagnostic EPS and therapeutic intervention. During the procedure, after a fixed reference point is chosen, a mapping catheter is then moved from point to point in the area of interest. The activation pattern is analyzed. A 3-dimensional activation map can be constructed by a sophisticated computer system (CARTO, Biosense Webster; Diamond Bar, Calif).

Voltage amplitude mapping can be achieved using any of the aforementioned mapping techniques except virtual electrogram mapping (EnSite). EnSite is mainly used to localize the low-amplitude scar tissue in the diagnosis and treatment of ventricular tachycardia and, sometimes, atrial tachycardia.

Pacing mapping is also frequently used to locate the foci of arrhythmias. A pacing catheter is moved from point to point in the area of concern, and the electrocardiographic morphologies from pacing are compared with those of clinically significant arrhythmias. It has been used to facilitate curative ablation of both supraventricular and ventricular tachyarrhythmias.

Entrainment mapping is another mapping technique frequently used in EP laboratories in the diagnosis and therapeutic intervention of arrhythmias with a reentrant mechanism, such as atrial or ventricular tachycardia, atrial flutter, and tachycardia due to accessory pathways.



Although no absolute contraindications exist, EPS, in general, should be performed only on patients who are medically stable and have no acute medical condition that could compromise safety during the study. The following conditions are generally considered contraindications to invasive EPS:

  • Critical aortic stenosis
  • Severe hypertrophic obstructive cardiomyopathy
  • Unstable angina
  • Acute myocardial infarction within the past 48 hours
  • Severe and extensive coronary artery disease, including left main artery disease
  • Acute exacerbations of heart failure
  • Severe respiratory distress
  • Recent thromboembolic events
  • Acute metabolic or electrolyte disturbances
  • Systemic infection
  • Compromised hemodynamics of any cause



Electrophysiological laboratories are equipped with the most advanced cardiac support systems. A reasonable claim is that electrophysiological laboratories, particularly those with adequate procedure volume, are the best places for the worst (sometimes even lethal) arrhythmic events to occur. Therefore, an EPS is a safe procedure, especially in well-established laboratories. However, most studies are still invasive and are associated with the following complications (although uncommon):

  • Hypotension - 1%
  • Vascular problems (eg, hemorrhage, arterial injury, thrombophlebitis) - 0.7%
  • Thromboembolism - 0.2%
  • Cardiac perforation - 0.15%
  • Death - 0-0.6%



Although guidelines are available, whether an EPS is clinically indicated is sometimes unclear (American College of Cardiology/American Heart Association Task Force, 1995). Two general rules usually apply. First, rhythm disturbances (particularly bradyarrhythmias) rarely mandate testing when associated with no symptoms in patients without obvious structural heart disease. Second, an EPS is not indicated to confirm the causal relationship of a rhythm disturbance when a relationship has already been established based on results from ECG or other noninvasive approaches.

Bradyarrhythmias

Sinus node dysfunction

PES can be used to evaluate sinus node functions, including automaticity and sinoatrial conduction. Sinus node ECG tracings are not recorded during a routine EPS, and no direct measurement of sinus node function occurs.

A measurement of SNRT after overdrive suppression and an estimation of SACT by atrial stimuli are often performed during an EPS. Although SNRT and SACT values are frequently abnormal in symptomatic patients with intrinsic sinus node disease, the sensitivity and specificity are suboptimal. When SNRT was measured in a group of 75 subjects, significant overlap was observed between those with known sinus node disease and normal control subjects, although the patient group had a significantly longer SNRT. The reported false-negative rate to detect sinus node disease using SNRT is greater than 30% and the false-positive rate is 5%.

In patients with near syncope or syncope, an EPS is almost never indicated to evaluate pure sinus node function. However, when a causal relationship cannot be established despite repeated ambulatory ECG monitoring and stress tests or if arrhythmic mechanisms (eg, ventricular tachycardia) and sinus dysfunction are considered the cause of symptoms, an EPS may be very informative. AV nodal and His-Purkinje function must be evaluated in patients with sinus nodal dysfunction because 8-10% of these patients also may exhibit impaired AV conduction over 3 years if it does not already exist.

Patients who are not considered candidates are those who have asymptomatic bradycardia or those whose symptoms have clearly been related causally to sinus node dysfunction. Transient bradycardia with clearly correctable causes (eg, acid-base or electrolyte disturbances, autonomic disturbance, bradycardia and sinus pauses during sleep) does not require an EPS.

Impaired AV conduction and block

Generally, 12-lead and ambulatory ECG monitoring provide enough information to diagnose AV conduction abnormalities. Ambulatory ECG monitoring, with or without stress tests, also helps establish an existing causal relationship between ECG findings and patient symptoms. However, a surface ECG does not pinpoint the exact level of block, and, untreated, chronic second-degree AV block below the His bundle is associated with a high risk to progress to a higher degree of block and become symptomatic with syncope.

If noninvasive test results are inconclusive, EPS with His bundle ECG recording is indicated in symptomatic patients in whom His-Purkinje block is thought to be the cause of symptoms. If patients with advanced AV block remain symptomatic after pacemaker implantation, an EPS is also indicated to search for other explanations. As in patients with bradycardia due to sinus dysfunction, asymptomatic patients with AV block or with clearly transient correctable causes for conduction block should not be tested.

Intraventricular conduction defect

Patients with complete right bundle-branch block and either a left anterior or a left posterior fascicular block (bifascicular block) on surface ECG tracings may progress to complete heart block and have a higher risk for sudden cardiac death when a prolonged His-ventricle (HV) interval (>70 millisecond) is also evident. Therefore, EPS is indicated in symptomatic patients in whom the cause of symptoms is not established. In addition, intraventricular conduction defects are frequently associated with structural heart diseases.

Sudden cardiac death in patients with bifascicular block may not be caused by the development of complete heart block, but rather by ventricular tachyarrhythmias. For this reason, an electrophysiological evaluation of patients with intraventricular conduction defects and unexplained symptoms should include a study of the AV conduction system, an evaluation of sinus node function, and programmed atrial and ventricular stimulation to assess the potential for the development of both bradyarrhythmias and tachyarrhythmias in an attempt to induce tachyarrhythmias.

Tachyarrhythmias

Narrow QRS complex tachycardias

Narrow QRS complex (QRS duration <120 millisecond) tachycardias include the following:

  • Sinus tachycardia
  • Sinus or sinoatrial reentrant tachycardia
  • Accelerated trial tachycardia and multifocal atrial tachycardia
  • Atrial flutter (see Image 2 and Image 6)
  • Atrial fibrillation (see Image 3)
  • Accelerated AV junctional tachycardia
  • AV nodal reentrant tachycardia
  • Orthodromic AV reentrant tachycardia (see Images 4-5)
  • Fascicular tachycardia

In general, consider performing an EPS in patients with narrow QRS complex tachycardias when reentry is considered the underlying mechanism and when patients have a condition for which curative catheter ablation has a high success rate (eg, AV nodal reentrant tachycardia, typical atrial flutter, tachycardia related to an accessory pathway). Also consider an EPS in patients with poorly tolerated symptoms, frequent recurrences, no response to drug therapy, or a preference for ablative therapy over pharmacological treatment.

Recent advances in the understanding of mechanisms and ablation techniques have made curative therapy possible for more narrow QRS complex tachycardias with mechanisms other than macroreentry (eg, atrial fibrillation, atrial tachycardia). Results have been promising.

Wide QRS complex tachycardias

Both ventricular tachycardia and supraventricular tachycardia with intraventricular aberrancy or preexcitation can manifest as wide QRS complex tachycardia. Although uncommon, some patients with ventricular tachycardias may have narrow QRS complexes. Distinguishing between the two remains a clinical challenge, despite numerous proposed ECG criteria, and often requires invasive EPS, particularly in patients with known structural heart diseases. (See Images 8-11). The clinical significance of EPS results in these patients is 3-fold and consists of (1) understanding the mechanism of arrhythmia, (2) determining the need for and type of therapy, and (3) assessing the efficacy of therapy.

Myocardial infarction, malignant ventricular arrhythmias, and sudden cardiac death

EPS is not indicated in patients with ventricular tachycardia and cardiac arrest during the acute phase of myocardial infarction (<48 h). An EPS might be indicated in patients with prior infarction, particularly those with a depressed left ventricular systolic function (ejection fraction [EF] £40%), nonsustained ventricular tachycardia, and a history of near syncope or syncope.

After having a myocardial infarction (Q wave or non–Q wave), patients, especially those with depressed left ventricular function, have significantly higher risk for ventricular tachyarrhythmias and sudden cardiac death. PES has been used widely for risk stratification, assessment of the need for and type of therapy, and assessment of the response and efficacy of therapy (see Image 7).

Serial PES testing to guide antiarrhythmic agent use, although once considered the most advanced approach, is now rarely indicated because (1) clear proarrhythmic effects of almost all antiarrhythmic agents, particularly in post–myocardial infarction patients with impaired left ventricular function, have been shown in many clinical trials since the landmark Cardiac Arrhythmia Suppression Trial in 1989 (Echt, 1991) and (2) the significant survival benefits of ICDs have been demonstrated repeatedly in all but one large, prospective, multicenter randomized trial.

The published Multicenter Automatic Defibrillator Implantation Trial II study suggests that all patients with evidence of myocardial infarction (based on ECG, echocardiogram, ventriculogram, or nuclear scan findings) and with an EF of 30% or less benefit from prophylactic defibrillator implantation, without performing an EPS (Moss, 2002).

The Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), a recent multicenter, prospective, randomized study, shows that when compared with placebo and amiodarone, prophylactic use of an ICD is associated with a 23% decrease in the risk of death (a 7.2% absolute decrease in mortality rate in patients with high risks). Based on these recently published data from both the Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial (Kadish, 2004) and the SCD-HeFT (Bardy, 2005), the Centers for Medicare and Medicaid Services (CMS) has extended coverage for prophylactic use of ICDs, without performing an EPS, for Medicare beneficiaries with New York Heart Association class II or class III congestive heart failure due to ischemic or nonischemic cardiomyopathy with a left ventricular EF of 35% or less.

The following is a summary of multicenter trials in which EPS was used in patients with coronary heart disease and impaired left ventricular function to assess the need for an ICD:

  • Multicenter Automatic Defibrillator Implantation Trial I 1996 (Moss, 1996)
    • Clinical presentation - Asymptomatic nonsustained ventricular tachycardia, not suppressible with procainamide therapy
    • EF - 35%
  • Multicenter Nonsustained Tachycardia Trial Investigators 1999 (Buxton, 1999)
    • Asymptomatic nonsustained ventricular tachycardia
    • EF - 40%



Patients with WPW syndrome

See Images 4-5. An EPS is indicated in a patient being evaluated for curative ablation of an accessory pathway. Also, patients with ventricular preexcitation who have survived cardiac arrest or who have unexplained syncope should undergo an EP evaluation. Finally, an EPS is indicated for symptomatic patients in whom a determination of the mechanism of arrhythmia or knowledge of the electrophysiological properties of the accessory pathway and normal conduction system would help therapeutic decision making. However, some investigators have recently advocated prophylactic catheter ablation for patients with asymptomatic WPW syndrome. (Pappone, 2003; Pappone, 2004)

Patients with unexplained syncope

EPS is indicated only in patients with probable or known structural heart disease and syncope that remains unexplained after appropriate evaluation.



In the past few decades, exciting advances have occurred in the field of clinical cardiac EP. PES has played a key role in the development of modern cardiac EP and provides a unique tool to uncover mechanistic insights into arrhythmias, including tachyarrhythmias, bradyarrhythmias, and supraventricular and ventricular arrhythmias. PES also helps better assess risks for malignant ventricular tachycardia and sudden cardiac death, especially in patients with structural heart disease.

PES is an essential tool to assess the efficacy of electrophysiological therapy, including drug therapy, device therapy (eg, pacemaker, ICD, biventricular pacing device), and curative therapy with catheter ablation or surgery. However, serial PES testing to guide antiarrhythmic agent therapy has become archaic as a result of findings provided by large, randomized clinical trials.



Media file 1:  Fluoroscopic position (in right anterior oblique view) of catheters used for atrial fibrillation ablation. The catheters are positioned at the right atrium appendage (RAA), His bundle (His), and coronary sinus (CS). An intracardiac ultrasound probe (ICE) is also introduced and positioned in the right atrium to guide transseptal catheterization and pulmonary vein isolation during atrial fibrillation ablation.
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Media type:  Image

Media file 2:  Fluoroscopic position (in left anterior oblique view) of catheters used for an atrial flutter ablation. The catheters are positioned in the right atrium (Halo), at the His bundle (His), and at the coronary sinus (CS). In addition, a catheter is positioned on the cavotricuspid annulus isthmus for both entrainment pacing and linear isthmus ablation.
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Media type:  Image

Media file 3:  Pulmonary vein (PV) potentials are recorded in the left superior pulmonary vein during distal coronary sinus (CS) pacing (panel A) using a basket mapping catheter (Constellation, Boston Scientific; Natick, Mass). These pulmonary vein potentials disappear after segmental radiofrequency applications and the vein is completely disconnected from the left atrium (panel B).
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Media type:  ECG

Media file 4:  A programmed ventricular stimulus (arrow) is delivered during a tachycardia in the refractory period of the His bundle. It captures the ventricle and advances atrial activation (*) in a retrograde fashion through the accessory pathway. This maneuver confirms that the mechanism of the tachycardia is atrioventricular reentry using an accessory pathway. The numbers are measured AA intervals in milliseconds. HRA is high right atrial, His is His bundle, CSp is proximal coronary sinus, CSd is distal coronary sinus, Abl is proximal ablation (distal electrodes were used for radiofrequency energy delivery), and RV is right ventricle.
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Media type:  ECG

Media file 5:  Surface ECG (I, aVF, V1 and V5) and endocardial electrogram recording during an accessory pathway ablation. High right atrial (HRA) pacing was used to demonstrate maximal preexcitation. Ventricular preexcitation is evident on the first 2 beats (arrows), but it disappeared after a few seconds of radiofrequency energy application to a right posterior septal site. A sudden change in His-ventricle (HV) intervals is also apparent on the His bundle recording (His). CSp is proximal coronary sinus, CSd is distal coronary sinus, Abl is proximal ablation (distal electrodes were used for radiofrequency energy delivery), and RVA is right ventricle apex.
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Media type:  ECG

Media file 6:  Bidirectional conduction block across the cavotricuspid annulus isthmus is demonstrated by pacing at the lower anterolateral right atrium (H1) and coronary sinus ostium (CSm). H1-H8 is the Halo catheter, His is His bundle, CSp is proximal coronary sinus, CSm is middle coronary sinus, CSd is distal coronary sinus, and RVA is right ventricle apex.
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Media type:  ECG

Media file 7:  Monomorphic ventricular tachycardia with a right bundle-branch block pattern is induced during ventricular pacing (S1) at the right ventricle outflow tract (RV). Atrioventricular dissociation is clearly shown on His recordings. Hisp is proximal His bundle, Hisd is distal His bundle, and Stim is stimulation.
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Media type:  ECG

Media file 8:  Images 8-11 show simultaneous ventricular tachycardia (VT) and supraventricular tachycardia (SVT) in a 49-year-old woman during a treadmill exercise stress testing. Baseline 12-lead ECG shows sinus rhythm with right bundle-branch block and left anterior fascicular block.
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Media type:  ECG

Media file 9:  Less than 2 minutes into exercise, the woman developed a sustained wide complex tachycardia with a left bundle-branch block morphology and inferior axis at a rate of 220 beats per minute (same patient as in Images 8 and 10-11).
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Media type:  ECG

Media file 10:  The tachycardia in Image 8 changed into a completely different morphology (right bundle-branch block), but the rate remained at 220 beats per minute (same patient as in Images 8-9 and 11).
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Media type:  ECG

Media file 11:  Programmed electrical stimulation provokes no tachycardia. A ventricular tachycardia, however, occurs spontaneously with left bundle-branch block morphology during isoproterenol infusion with intermittent ventricular arrhythmia conduction, which triggers a supraventricular tachycardia with right bundle-branch block (RBBB) morphology. While the rate remains unchanged, the tachycardia switches into an RBBB morphology with superior axis, which is similar to but still significantly different from baseline. Endocardial recordings from the right atrial appendage (RA) and the right ventricular outflow tract (RV) are displayed along with surface ECG leads aVF, V1, and V5 (same patient as in Images 8-10).
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Media type:  ECG



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Programmed Electrical Stimulation excerpt

Article Last Updated: Nov 13, 2006