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TECHNIQUES OF ELECTROPHYSIOLOGIC EVALUATION
      
BY MASOOD AKKHTAR


The recording of intracavitary electrocardiographic signals and various forms of pacing programs have experienced enormous growth during the past 3 decades. Recordings of intracardiac signals from the region of the His bundle, initially made by Scherlag et al., were rapidly applied to clinical problems including atrioventricular (AV) blocks and supraventricular and ventncular tachyarrhythmias. Such recordings were then complemented by pacing to unmask sinus node dysfunction and AV conduction abnormalities as well as to initiate supraventricular tachycardias (SVTs). Intracardiac electrophysiologic studies (EPSs) have since found utility in a variety of cardiac arrhythmias, including sinus node dysfunction, intraventricular and AV conduction disturbances, SVTs, ventricular tachycardias (VTs), preexcitation syndromes, and ventricular fibrillation (VF). Such studies are now also employed as a prelude to correction of various arrhythmias and conduction defects. This chapter addresses recording and pacing techniques and their clinical utility.


TECHNIQUES OF INTRACARDIAC ELECTROPHYSIOLOGIC STUDIES


The exact type of electric signal recordings, specific equipment used, and pacing protocol depend upon the nature of the clinical problem, the type of electrophysiologic assessment, and the anticipated course of action. Routine cardiac EPSs are performed while patients are in a nonsedated postabsorptive state. Although some degree of sedation is advisable in apprehensive patients, the use of drugs that may alter the properties of the cardiac conduction system should be avoided. Antiarrhythmic drugs are usually stopped prior to these studies. In selected cases, antiarrhythmic drugs may be continued if a clinical event occurred while the patient was on a specific agent. Customarily, other cardioactive drugs that are necessary for nonarrhythmic cardiovascular problems such as hypertension, angina, and heart failure are continued.
The typical electrode catheters used for both recording and cardiac stimulation are multipolar (sizes varying from 4 to 8 F). Catheters can be inserted via peripheral veins such as the antecubital or femoral veins and, at times, the subclavian or internal jugular veins. When a catheter is intended to be left in place for several days, subclavian and internal jugular veins are preferable. After using local anesthesia, a guide wire is inserted percutaneously through a needle, and a sheath is advanced over the guide wire. A catheter is then guided fluoroscopically through the sheath to position in the appropriate cardiac chamber. For most electrophysiologic testing, the catheter is placed in the high right atrium, at the His bundle, or at the right bundle branch region across the tricuspid valve and right ventricular apex or outflow. For accessory pathways or AV junctional tachycardias, a catheter is placed in the region of the coronary sinus. Heparinization is recommended at approximately 1000 units per hour. For EPSs, good contact between the electrodes and the walls of the various chambers is critical. For His bundle and right bundle branch recording, the catheter is introduced via the femoral vein, advanced across the tricuspid valve, and gradually withdrawn until an appropriate recording from the right bundle and/or the His bundle is obtained (Fig. 206-1). A coronary sinus catheter can be placed via an arm, internal jugular, or subclavian vein. If necessary, coronary sinus catheterization can also be accomplished via a femoral approach. Right atrial catheter placement can be done via any of the larger peripheral veins. For a routine study, left-cases, antiarrhythmic drugs may be continued if a clinical event occurred while the patient was on a specific agent. Customarily, other cardioactive drugs that are necessary for nonarrhythmic cardiovascular problems such as hypertension, angina, and heart failure are continued.
The typical electrode catheters used for both recording and cardiac stimulation are multipolar (sizes varying from 4 to 8 F). Catheters can be inserted via peripheral veins such as the antecubital or femoral veins and, at times, the subclavian or internal jugular veins. When a catheter is intended to be left in place for several days, subclavian and internal jugular veins are preferable. After using local anesthesia, a guide wire is inserted percutaneously through a needle, and a sheath is advanced over the guide wire. A catheter is then guided fluoroscopically through the sheath to position in the appropriate cardiac chamber. For most electrophysiologic testing, the catheter is placed in the high right atrium, at the His bundle, or at the right bundle branch region across the tricuspid valve and right ventricular apex or outflow. For accessory pathways or AV junctional tachycardias, a catheter is placed in the region of the coronary sinus. Heparinization is recommended at approximately 1000 units per hour. For EPSs, good contact between the electrodes and the walls of the various chambers is critical. For His bundle and right bundle branch recording, the catheter is introduced via the femoral vein, advanced across the tricuspid valve, and gradually withdrawn until an appropriate recording from the right bundle and/or the His bundle is obtained (Fig. 206-1). A coronary sinus catheter can be placed via an arm, internal jugular, or subclavian vein. If necessary, coronary sinus catheterization can also be accomplished via a femoral approach. Right atrial catheter placement can be done via any of the larger peripheral veins.

For a routine study, left-sided heart catheterization is seldom necessary. In patients with VT and/or left-sided accessory pathways, however, this is performed for diagnostic or therapeutic purposes. Continuous heparinization is desirable for left heart catheterization to avoid thromboembolic complications.

Electrophysiologic Recordings


Once the electrode catheters are placed appropriately, the connections are made via a junction box and isolation units to prevent excess current in the event of random electrical surges. All of the electrograms are displayed simultaneously on a multi-channel oscilloscopic recorder. In addition to the intracardiac signals, several unfiltered surface electrocardiographic leads (i.e., X, Y, and Z or leads I, II, or aVF and V1) are recorded. To reduce the noise generated with the low-frequency signals, the usual filtering frequency for intracardiac signals is between 30 and 40 Hz for the high-pass and 500 Hz for the low-pass filters. Although appropriately placed electrode catheters will record desired signals at any filtering frequency, filter settings between 30 to 40 and 500 Hz are best suited for sharp intracardiac signals such as those from the His bundle and accessorypathways (Fig. 206-2). Undesirable low-frequency signals can be reduced by a high-pass filter setting of more than 50 to 100 Hz. On the other hand, 60-cycle interference can be eliminated with a low-pass filter setting at 50 Hz. Alteration in the high-bandpass filter for surface electrocardiography can markedly alter the scalar electrocardiographic morphology. Amplification is frequently necessary to identify desirable signals from the specialized conduction system. This can lead to superimposition of the larger myocardial signals on various electrocardiographic tracings. In most recording equipment, however, limiting filters allow the adjustment of amplitude limits.


The main value of intracardiac! electrocardiographic tracings is timing of electric events and to determine the direction of impulse propagation. To acquire true local electrical activity, a bipolar electrogram with an interelectrode distance of less than 1 cm is desirable. When unipolar electrograms are obtained, a rapid intrinsic deflection will identify a point of local activation. For routine intracardiac electrocardiographic studies, unipolar electrograms provide relatively limited advantage over bipolar signals, and therefore the latter are more often utilized. The foregoing description relates to the routine diagnostic invasive EPSs. In other clinical situations, different types of diagnostic methods are employed. For example, during intraoperative mapping, direct placement of electrodes over the epicardium or endocardium is necessary to get appropriate signals for identifying the precise origin and route of impulse propagation. These electrodes can be in the form of either hand-held probes or plaques that can be placed or sutured over the myocardium. Socks and balloons incorporating several electrodes can also be used for epicardial and endocardial mapping techniques, respectively. All electrical signals can be recorded on either a disk or frequency-modulated tape for permanent storage.

More recently, several other types of mapping and recording equipment have emerged to locate the origin of cardiac arrhythmias more accurately. Two of the systems likely to find clinical utility in the mapping of arrhythmic origins are (1) nonfluoroscopic electromagnetic endocardial mapping (CARTO, Biosense (Cordis Webster) Marlton, NJ] and (2) noncontact mapping (EnSite, Endocardial Solutions, Saint Paul, MN).

1. The CARTO system consists of a magnetic field generator locator pad placed under the patient table, a sensor-mounted catheter and a reference catheter placed intracardially, a mapping system and a graphic computer. The catheter tip allows orientation in relation to the reference signal. The accuracy of catheter tip position is within a millimeter of arrhythmia location in this low magnetic field. By moving the sensor sequentially, one can generate a three-dimensional (3D) activation map. By color coding, both the earliest and the latest directions of electrical activation can be recorded. Once the initial fluoroscopy-guided placement of reference catheter and other catheters is satisfactory, several points are acquired. A 3D map is generated, and sensor-mounted catheters are manipulated further without the help of fluoroscopy.
Aside from creation of an accurate map guiding the origin and activation sequence, the CARTO system is also helpful in separating micro from macro reentry circuits. For example, in catheter and a reference catheter placed intracardially, a mapping system and a graphic computer. The catheter tip allows orientation in relation to the reference signal. The accuracy of catheter tip position is within a millimeter of arrhythmia location in this low magnetic field. By moving the sensor sequentially, one can generate a three-dimensional (3D) activation map. By color coding, both the earliest and the latest directions of electrical activation can be recorded. Once the initial fluoroscopy-guided placement of reference catheter and other catheters is satisfactory, several points are acquired. A 3D map is generated, and sensor-mounted catheters are manipulated further without the help of fluoroscopy.
Aside from creation of an accurate map guiding the origin and activation sequence, the CARTO system is also helpful in separating micro from macro reentry circuits. For example, in atrial flutter, by virtue of its large circuit, the impulse propagation along the entire route can be outlined. The atrial tachycardia, on the other hand, can be distinguished by its radial spread from an atrial focus. A typical map generated during this technique is shown in Fig. 206-3, Plate 75.

2. Noncontact mapping using the Endocardial Solutions EnSite 3000 system. The Endocardial Solutions EnSite 3000 is a new endocardial mapping system that takes a different approach to such mapping (Fig. 206-4, Plate 76). Like the CARTO system, the EnSite 3000 system also makes use of an amplifier and computer system with custom software. The EnSite catheter uses a balloon design with a 64-electrode array arranged over the outside of the balloon. This balloon is positioned in the center of the chamber and does not come in contact with the walls of the chamber being mapped. Using data from the 64-electrode array catheter, the computer uses sophisticated algorithms to compute an inverse solution to determine the activation sequence on the endocardial surface. Data from all points in the chamber are acquired simultaneously.

To create a map, the balloon catheter is positioned in the chamber and deployed. A conventional (roving) deflectable catheter is also positioned in the chamber and used to collect geometry information. A 5-kHz signal is emitted from the tip electrode of the conventional catheter, and the computer analyzes this signal to determine the position of the roving catheter relative to the position of the balloon. The roving catheter is moved throughout the chamber, and the location information is collected by the system. Using this information, the computer creates a model, called a convex hull, of the chamber during dastole. After the chamber geometry is determined, mapping can begin.the arrhythmia is induced, and data are acquired. The data acquisition Process is performed automatically by the system, and all data for the entire chamber are acquired simultaneously. The inverse-solution computations are performed by the system in real time and projected on to the surface of the convex-hull model, creating a 3D model showing the activation sequence within the chamber. Following this, the segment must be analyzed by the operator to find the early activation or vulnerable region of the reentry circuit. The locator technology that was used to collect the geometry information for the convex hull can then be used to guide an ablation catheter to the proper location in the heart.


Because data from the entire chamber are collected simultaneously with the EnSite 3000 system, it can be used to map nonsustained rhythms such as premature atrial complexes, irregular rhythms such as atnal fibrillation or polymorphic VT, and rhythms that are not hemodynamically stable. The system is highly useful for identifying focal arrhythmias (Fig. 206-4) and atrial flutter. Currently approved indications, however, are for the right atrium only. The other significant limitation of the system results from its reliance on the large-diameter balloon catheter with its current 9.5-F lumen.
These mapping systems, both of which are relatively new, provide electrophysiologists with new tools for diagnosing and treating what are often complex arrhythmias. They make use of state-ofthe-art technology to accomplish their objectives and improve the state of the art in arrhythmia management. Because these technologies are so new, further enhancements can be expected that will further the usefulness of advanced mapping techniques in the practice of electrophysiology.


Programmed Electrical Stimulation

After satisfactory placement of the electrode catheters, patches, or other forms of recording equipment, baseline recordings are made and programmed stimulation is initiated. The usual site of pacing is the right atrium or left atrium via the coronary sinus. For ventricular stimulation, the pacing sites are the right ventricular apex, outflow tract, and rarely some other right ventricular site. A variety of pacing programs can be utilized, depending upon the nature of the underlying arrhythmic problem under investigation. At least two formats of pacing protocol are common. The first is incremental pacing, which is pacing at a constant cycle length with gradual shortening until the occurence of a desireable event, such as induction of a tachycardia or production of AV block. Otherwise the incremental atrial pacing is continued until the onset of AV nodal Wenckebach's phenomenon: a physiologic response at faster pacing rates. Fixed-cycle-length ventricular pacing is also used for the induction of supraventricular tachyarrhythmias and study of ventriculoatrial conduction. Bursts of pacing at a constant cycle length are occasionally used to induce SVT, VT, or VF or for study of sinus node function and integrity of subsidiary pacemakers.


The second pacing format is premature (or extra) stimulation from atrial or ventricular sites. For the study of a physiologic phenomenon, refractory periods, and conduction characteristics, a single extra stimulus is usually applied after a series of beats with a constant cycle length (Fig. 206-5). The scanning is initiated late during electrical diastole, and the coupling interval is progressively decreased until the atrial and/or ventricular muscle is refractory.


For induction of SVTs, single, two, or more extra stimuli are delivered (Fig. 206-6). For the induction of VT, up to three ventricular extra stimuli are employed. The sensitivity of pacing protocols seems to be directly related to the number of extra stimuli utilized.This occurs, however, at the expense of specificity when polymorphic VT/VF can be induced at very short coupling intervals by using multiple extra stimuli. Regardless of the pacing protocol, the induction of sustained monomorphic VT constitutes a specific response and is seldom induced in patients not prone to such arrhythmias clinically. In contrast, the induction of polymorphic VT/VF with three extra stimuli at short coupling intervals can be nonspecific and does not provide a reliable guide for serial testing. Both polymorphic VT and VF can be avoided to a great extent at short coupling intervals (<200 ms) and the induction of latency between the stimulus artifact and the local ventricular electrograms is avoided.


During routine EPSs, a variety of electrophysiologic parameters are measured, including sinus node function and intraatrial, AV nodal, and His-Purkinje system conduction. Initiation of SVT and VT is attempted to determine the mechanisms, the site of origin (by pacing and mapping techniques), and the potential of overdrive termination as a therapy option. After baseline studies, intravenous drugs are frequently administered to facilitate either induction of tachycardias, aggravation of sinus node function, or production of AV block (Fig. 206-7), or to determine drug efficacy. At the completion of testing, the catheters are withdrawn, and gentle pressure is applied at the area of catheter insertion. Unless arterial catheterization is performed, patients are usually allowed to ambulate after 4 to 6h.The role of EPSs in patient management has evolved over the past decades from a purely diagnostic method to a frequently applied therapeutic tool. A brief outline of the value of clinical EPSs in various arrhythmia settings is outlined separately under diagnostic and therapeutic categories.


INVASIVE ELECTROPHYSIOLOGIC STUDIES FOR DIAGNOSIS

Sinus Node Dysfunction

EPSs are generally performed to detect suspected sinus node dysfunction in patients with dizziness, presyncope, syncope, etc., in whom the diagnosis cannot be made noninvasively. The most frequently performed test is that of sinus node suppression by using overdrive atnal pacing. After pacing at several basic cycle lengths for a period of approximately 30 s or longer, the pacing is interrupted. The resultant escape interval, which is called sinus node recovery time, is measured. By deducting the predominant sinus cycle length from this interval, one can obtain the so-called corrected sinus node recovery time. In one study, sinus node recovery time in patients with sinus node disease averaged 3087 ms, and averaged 1073 ms in normal individuals. In another series, the value for corrected sinus node recovery time was less than 525 ms in normal individuals and exceeded those values in patients with overt sinus node dysfunction. Direct sinus node recordings have been obtained by amplification of recording from catheters placed in close proximity to the sinus node, where both the sinus node automaticity and sinoatrial conduction can be determined more accurately.
In the vast majority of patients with true sinus node disease,sinoatrial conduction abnormalities are the predominant reason for sinus node dysfunction.The sinoatrial conduction time in the absence of obvious sinus node disease is less than 100 ms. The sensitivity of sinus node recovery time for the detection of sinus node dysfunction is 54 percent, whereas that of sinoatrial conduction time is 51 percent, with a combined sensitivity of the two tests of around 64 percent. Poor sensitivity of such testing relates in part to the fact that, in previous studies, documented episodes of sinus bradycardia or sinus arrest due to neurocardiogenic mechanisms may have been included as examples of sinus node dysfunction. The specificity of the two tests combined is approximately 88 percent. It is important to test the AV conduction in patients with sinus node dysfunction, since the former is also frequently abnormal. In patients with bradycardia/ tachycardia syndrome, tachycardias are frequent, particularly those arising in the atrium, and testing may also be necessary for the proper diagnosis and therapy of the concomitant tachyarrhythmia.


Atrioventricutar Block


In asymptomatic patients with first-degree AV block (prolonged PR interval), electrophysiologic assessment is unnecessary, regardless of the QRS morphology of the conducted beats. In asymptomatic individuals with second-degree AV block, electrophysiologic assessment is used to find the site of the block (Fig. 206-8 below).


Figure 206-8
click to enlarge

Patients with intra-Hisian or infra-Hisian block tend to have a more unpredictable course, and permanent pacing is desirab1e. On the other hand, asymptomatic patients with AV nodal block generally do not require permanent pacing. Even though the intranodal block usually presents as Wenckebach's phenomenon or Mobitz type I, it is not uncommon to see Wenckebach phenomena within the HisPurkinje system or within the His bundle. There is no difference in prognosis regardless of how the infra- or intra-Hisian second-degree block manifests itself, i.e., type I versus type II (Fig. 206-8 above). On occasion, intranodal blocks are preceded by no discernible change in PR interval and from a surface electrocardiogram may appear as forms of Mobitz type II. The absolute length of the PR interval is usually quite diagnostic in that it is markedly prolonged (i.e., >300 ms), and there is a PR shortening exceeding 100 ms following the block beat (Fig. 206-8 ). In symptomatic patients with second-degree AV block, the role of EPS is limited because permanent pacing is the appropriate intervention. On the other hand, if the patient's symptoms cannot be explained on the basis of AV block and may be related to another arrhythmia, such as VT, EPSs should be considered. In patients with third-degree or complete AV block, EPSs are seldom required, and permanent pacing is the obvious option in symptomatic patients.
For EPSs to determine the site of AV block, it is critical to have the catheter across the AV junction that records the His bundle. A discernible His bundle recording enables one to determine the exact site of AV conduction abnormality, i.e., proximal to, within, or distal to the His bundle region. This, in combination with surface electrocardiographic morphology of conducted beats, enables one to identify precisely the location of conduction abnormality. The normal atrial to His bundle activation time (A-H) is approximately 50 to 140 ms, whereas the His to ventricular myocardial depolarization interval (H-V) measures 35 to 55 ms.
If 1:1 AV conduction is noted during EPSs in patients suspected of intermittent AV block, incremental atrial pacing should be done to see whether AV block can be reproduced. AV block in the His-Purkinje system is abnormal during incremental atrial pacing but is a physiologic response during atrial extrastimulation (see Fig. 206-5A) or with abrupt acceleration of atrial pacing rate. First- and second degree blocks in the Av nodeare considered physiologic responses during incremental atrial pacing or atriai extrastimuiauon (see Fig. 206-5B).


Wide QRS Tachycardia

Wide QRS tachycardia occurs due to a variety of electrophysiologic mechanisms, both from supraventricular and ventricular mechanisms in the presence and absence of accessory pathways (Fig. 206-9). The underlying nature of the wide QRS tachycardia is critical for both prognosis and therapy. EPSs have proven invaluable in distinguishing the various etiologies (Fig. 206-10). With few exceptions, when the nature of the arrhythmic problem is not known and the direction of therapy is not clear, patients with wide QRS tachycardia should undergo EPS. This is particularly true in situations where nonpharmacologic therapy is the desired goal.


Unexplained Syncope

Unexplained syncope is predominantly due to cardiovascular mechanisms. The two most common reasons for cardiovascular syncope are cardiac arrhythmias and neurocardiogenic dysfunction, often referred to as vasodepressor syncope. Electrophysiologic evaluation constitutes an integral part of the evaluation of patients with unexplained syncope. During such studies, all arrhythmic possibilities such as sinus node dysfunction, AV conduction abnormalities, SVT, and VT should be excluded. Neurocardiogenic mechanisms constitute the most common causes of syncope in patients without structural heart disease, and incomplete assessment of these patients may lead to inappropriate therapy (Fig. 206-11). The possibility of neurocardiogenic dysfunction should always be considered in younger patients (<50 years of age) with syncope and documented bradycardia (sinus arrest or AV block) and can be unmasked on a tilt table. The triage of patients toward one or the other, i.e., electrophysiologic testing versus head-up tilt, is fairly simple and predicted by clinical history and the presence or absence of structural heart disease? Patients with underlying structural heart disease, such as old myocardial infarction, primary myocardial disease, or poor left ventricular function, generally have underlying VT to explain the symptoms of syncope (Fig. 206-12). When arrhythmias occur in patients without overt structural heart disease, sinus node dysfunction, AV block (particularly intra-Hisian block), or SVTs are likely. Less frequently, VT can occur in the absence of an overt structural heart disease.

 

Survivors of Sudden Cardiac Death

In most patients with documented episodes of cardiac arrest from the onset, VF can be documented. Patients dying suddenly generally have underlying structural heart disease (usually coronary artery disease or primary myocardial disease) and are prone to VT/VF due to electrical instability. It seems prudent to investigate both the nature and extent of organic heart disease and also to assess vulnerability to recurrent VT/VF. At present, EPS is considered a routine part of the overall patient assessment in this group of individuals.

EPSs in survivors of VT/VF are desirable for a variety of reasons. Some are listed here:

1. Not infrequently, the underlying VT leading to cardiac arrest is bundle branch reentry or BBR (Fig. 26-13). Almost 40 percent of patients with monomorphic VT in association with idiopathic dilated cardiomyopathy and valvular heart disease have BBR as the underlying mechanism. This arrhythmia is preferably managed with bundle branch ablation, which is curative, rather than with an implantable cardioverter defibrillator (lCD) alone.

2. Several VT morphologies or other types of tachycardia may be induced in addition to VT. Lack of awareness of such arrhythmias may complicate patient management. For example, the presence of rapid SVT may require separate attention to prevent unnecessary lCD shocks.

3. In some cases, supraventricular arrhythmia may trigger VT/VF. This may happen in patients with severe coronary artery disease, congestive heart failure, Wolff-Parkinson-White syndrome, etc. Elimination of the underlying causes is a more rational therapeutic approach in such cases.

4. Patients with VT/VF often have underlying sick sinus syndrome or AV block, which can be further aggravated with antiarrhythmic drugs and may require permanent pacing. Assessment for this eventuality can be done during the conduct of an EPS and may help selection of a particular device. Because of the increasing flexibility of these devices this need for EPS may be less relevant in the future.

INVASIVE CARDIAC ELECTROPHYSIOLOGIC STUDIES FOR THERAPEUTIC INTERVENTION


Because of the episodic nature of most cardiac arrhythmias, the efficacy of any therapeutic intervention is difficult to assess unless the arrhythmia in question can be replicated. Diagnostic EPS provides that opportunity,and it seems logical to use the same tool to assess therapeutic interventions.This method to assess efficacy can be applied for both pharmacologic and non- pharmacologic therapy.

Pharmacologic Therapy

It is arguable whether the assessment of pharmacologic intervention is essential in patients with relatively benign cardiac arrhythmias. The clinical course can be observed to determine whether control has been achieved. With life-threatening tachycardias, such as VT/VF, or with severe manifestations of cardiac arrhythmias, such as syncope or presyncope, it is desirable to assess efficacy of pharmacologic intervention (Fig. 26-14). The technique of drug testing has been developed whereby the elimination of inducibility of a given tachycardia is assessed following a drug administration. Both the drug efficacy or inefficacy can be evaluated by this method. When drug therapy does eliminate induction of a previously inducible tachycardia, the addition of isoproterenol will frequently demonstrate reversal of therapeutic drug effect. This is helpful in considering additional beta-blocker therapy. The latter can be accomplished with ease in patients with good left ventricular function, whereas the addition of beta blockers may pose a problem in patients with VT and poor left ventricular function. Failure of serial drug testing is associated with a significant recurrence rate and a strong incidation for nonpharmacologic intervention.

Some controversy has arisen regarding the valuee of EPS for prediction of drug efficacy in comparison to ambulatory monitoring. However,because of the infrequency of spontaneous VT/VF in most patients with life-threatening ventricular arrhythmias, ambulatory monitoring is an impractical approach. At present, serial drug studies with multiple oral antiarrhythmic agents are seldom carried out for SVT or VT.


Nonpharmacologic Therapy


Nonpharmacologic intervention has become an integral part of patient management in cardiac arrhythmias. With documented cardiac arrest from VF, implantation of an automatic lCD is fairly common, and electrophysiologic assessment before such therapy is routine. Both preoperative and postimplant electrophysiologic evaluation can be done through permanent leads of an lCD through a wand and programmer. Pacing, antitachycardia function, low-energy cardioversion, and cardiac defibrillation can all be programmed with newer devices. When problems are encountered following discharge of a patient with an lCD, electrophysiologic reassessment via lCD is frequently necessary, both for reprogramming and for the detection of any unexplained events. For assessment of certain other electrophysiologic parameters (e.g., AV conduction and mechanism of SVTs), however, transvenous catheterization may be necessary.


Patients with coronary artery disease and mappable VT are also candidates for VT surgery when it cannot be managed with lCD, antiarrhythmic drugs and for catheter ablation. Preoperative EPS assessment for this possibility is important. Surgery for VT in the form of endocardial resection or cryoablation can be performed very effectively and relatively safely in patients with a left ventricular ejection fraction greater than 20 percent. This curative procedure provides effective control in approximately 75 percent of the patients who have monomorphic VT that can be appropriately mapped, and it may be considered when other forms of therapies are ineffective.


Surgery for SVT has gone through a significant evolution. The introduction of catheter ablative techniques has made it rare for patients to undergo surgery for Wolff-Parkinson-White syndrome and/or AV nodal reentrant tachycardia. Some individuals with resistant atrial fibrillation and flutter and those who fail catheter ablative therapy may still be considered candidates for such a procedure, but this is now becoming exceedingly less frequent.


CATHETER ABLATION TECHNIQUES

The realization that the origin of VT and SVT can be effectively mapped has made the catheter ablative technique a rational approach. The radiofrequency form of energy delivered through a catheter has permitted controlled trauma to cardiac tissue to abolish or modify reentrant circuits. This is true for both SVT and VT. Unifocal atrial tachycardia, AV nodal reentry of all varieties, and accessory pathways including atriofascicular fibers can be cured in over 90 percent of patients with radiofrequency catheter ablation. Among the VTs, BBR tachycardia seen in association with dilated cardiomyopathy (both ischemic and nonischemic) and valvular disease is an ideal substrate for catheter ablation. Patients with monomorphic VT associated with myocardial scarring or other substrates can also be considered candidates, particularly when they are not suitable for VT surgery and have failed drug therapy. Additionally, in patients with incessant VT or frequency VT with inadequate control despite ICD therapy, VT ablation should be considered. By using the electromagnetic mapping, the scarred area can be mapped during sinus rhythm and ablation of this substrate can effectively eliminate VT. Noncontact mapping techniques outlined earlier are likely to further help improve ablation success rate with unifocal or possibly multifocal tachycardias.


IATROGENIC PROBLEMS ENCOUNTERED DURING ELECTROPHYSIOLOGIC STUDIES

Mechanical irritation from catheters during placement and even when not being manipulated can cause a variety of arrhythmias and conduction disturbances. These include induction of atrial, junctional, and ventricular ectopic beats and right bundle branch block and thus AV block in the His-Purkinje system in patients with preexisting left bundle branch block during right ventricular catheterization. Obviously, AV block in the His-Purkinje system can occur in patients with preexisting right bundle branch block during left ventricular catheterization. Ventricular stimulation can also occur from physical movement of the ventricular catheter coincident with atrial contraction, producing electrocardiographic patterns of ventricular preexcitation. Recognition of all these iatrogenic patterns is important for avoiding misinterpretation of electrophysiologic phenomena and the significance of findings in the laboratory.


Certain types of arrhythmias must be avoided at all costs, such as atrial and VF. Atnal fibrillation will obviously not permit study of any other form of SVT, and VF will require prompt cardioversion, making it difficult to continue the EPS. If atrial fibrillation must be initiated for diagnostic purposes (i.e., to assess ventricular response over the accessory pathway in Wolff-Parkinson-White syndrome), it should be done at the end of the study. Patients with a prior history of atrial fibrillation are more prone to the occurrence of sustained atrial fibrillation in the laboratory. Frequently, this will occur during initial placement of catheters, and excessive manipulation of catheters in the atria should therefore be avoided. Catheter trauma resulting in abolition of accessory pathway conduction or reentrant pathway may make the curative ablation difficult or impossible.


Risks and Complications

The complication rate is relatively low when only right heart catheterization is done, with almost negligible mortality. Other complications include deep venous thrombosis, pulmonary embolism, infection at catheter sites, systemic infection, pneumothorax, and perforation of a cardiac chamber or coronary sinus. Potentially lethal arrhythmias such as rapid VT or VF are common in the laboratory. These are not necessarily counted as complications, however, but are often expected and anticipated. Nonetheless, their common occurrence makes the electrophysiology laboratory a place for only highly trained personnel equipped to handle such problems.