Chapter 8. Electrophysiologic Mapping

The purpose of cardiovascular electrophysiologic mapping is to define the anatomic sequence of myocardial activation, both at baseline and/or with arrhythmia. There have been tremendous technologic advances in this area1 that have created fertile ground for the integration of multiple imaging modalities. High-level integration begins with preprocedural assessment of electrophysiologic properties revealed by the 12-lead surface electrocardiogram (ECG) viewed in the context of patient demographics and history.2,3 Further information is added during invasive electrophysiologic mapping with assessment of intracardiac electrograms viewed in the context of cardiac anatomy.4,5 The fusion of functional electrophysiologic data with anatomic data in the electrophysiology laboratory facilitates catheter navigation, data annotation, and direct visualization of target sites for therapy. Following an invasive electrophysiologic mapping procedure, there are likewise multiple imaging modalities useful for assessing response to therapy, excluding complications, and directing future diagnostic and therapeutic decisions.6

Baseline 12-Lead ECG and Patient History

The efficiency and effectiveness of an invasive electrophysiologic mapping procedure are dependent on the preprocedure evaluation. Patient demographics, history, and 12-lead surface ECG both at baseline and with arrhythmia help determine what diagnoses are possible and, among the possible, which are most likely. The 12-lead ECG is among the oldest and most useful imaging modalities for localizing arrhythmia origin and characterizing arrhythmia mechanism. The 12-lead ECG provides imaging by display of vectorial information contained in the body surface voltage pattern viewed from different leads, each viewing the heart from a different perspective or "angle." Tachycardia occurring in a female in her forties with a superior P wave axis, short RP interval, with a narrow QRS complex is most likely atrioventricular nodal re-entrant tachycardia.7 A younger male with tachypalpitations originally presenting in adolescence may have an ECG that looks similar; however, based on demographics, atrioventricular re-entrant tachycardia via an accessory pathway may be more likely8 (Fig. 8–1). A patient with a history of right atriotomy might have findings of typical right atrial flutter (ie, negative "sawtooth-shaped" flutter waves in the inferior leads and positive flutter waves in the anterior precordial leads) on the 12-lead ECG; however, the patient might also have right lateral wall atrial flutter encircling the atriotomy scar. These arrhythmias may present simultaneously or sequentially (Fig. 8–2). The probability of directing one's attention to the appropriate substrate is favored by a thoughtful preprocedure analysis.

Baseline 12-Lead ECG Compared with 12-Lead ECG in Arrhythmia

In addition to viewing the 12-lead ECG in arrhythmia in the context of patient history, it is likewise valuable to compare the 12-lead ECG in arrhythmia with the 12-lead ECG at baseline. Findings present on one but not the other can be helpful in elucidating arrhythmia mechanism. The presence of ventricular pre-excitation on a baseline ECG makes a narrow complex tachycardia most likely to be secondary to atrioventricular re-entrant tachycardia (orthodromic).9 The presence of a small retrograde P wave buried in the tail of the QRS in tachycardia that is absent at baseline would be suggestive of typical atrioventricular nodal re-entrant tachycardia. The presence of a "bump" in the T wave during tachycardia that is absent at baseline or a change in the P wave morphology with tachycardia may be suggestive of atrial depolarization with a focal atrial tachycardia. The P wave axis and duration give clues to the source of the tachycardia. Narrow complex arrhythmias originating from atria that have been incised or undergone extensive linear ablation will be more likely macro–re-entrant. Atria that are not scarred (with the exception of cavotricuspid isthmus–dependent right atrial flutter) will more often be focal, usually emerging from one of many known regions of increased arrhythmogenicity (crista terminalis, superior vena cava, tricuspid valve annulus, fossa ovalis, atrial septum, coronary sinus os/body, right atrial appendage, left atrial appendage, pulmonary veins, ligament of Marshall, mitral valve annulus, noncoronary cusp)10 (Fig. 8–3). Knowing prior to invasive electrophysiologic mapping whether a focal tachycardia is likely to be originating from the right atrium or left atrium assists in preprocedural planning from a technical, equipment planning standpoint, as well as in assessing risks and benefits of the mapping procedure for review with the patient undergoing the procedure. Likewise, analysis of baseline P wave characteristics, including P wave duration and axis, provides information about how electrical activity is initiated and propagated through the atria, adding information about atrial structure and function that may be relevant to arrhythmia mechanism.11

Other Features to Assist with Definition of Arrhythmia Substrate

A history of tachycardia termination with maneuvers that slow conduction through the atrioventricular node (ie, vagal maneuvers, carotid massage, adenosine, β-blockers, calcium channel blockers) suggests that the atrioventricular node may be a part of the tachycardia circuit. Assessment of the PR interval and QRS duration at baseline provides a noninvasive measure of conduction through the atrioventricular node and His-Purkinje system.12 The presence of baseline pathologic Q waves may be indicative of ischemic heart disease,13 making a wide complex tachycardia more likely to be a "scar-related" ventricular arrhythmia. Another finding suggestive of the presence of structural heart disease (making ventricular tachycardia more likely) is the presence of low limb lead voltage with preserved (or increased) precordial voltage on the baseline ECG. This finding is frequently seen with dilated cardiomyopathy secondary to a greater proportion of the thoracic cavity being occupied by myocardium and blood pool, thus producing a smaller voltage difference in the bipolar limb leads, but maintaining the voltage measured in the unipolar precordial leads.14,15 A prolonged QT interval (long QT syndrome), upward coved ST-segment elevation with T wave inversion in the anterior precordial leads (Brugada syndrome), epsilon waves (brief upward deflection at the J point) with T wave inversions across the anterior precordial leads (arrhythmogenic right ventricular cardiomyopathy), unexplained high voltage (hypertrophic cardiomyopathy), and frequent premature ventricular contractions with the same morphology as the clinical tachycardia (such as with an automatic or triggered ventricular tachycardia) are some of the many clues that may be seen on the baseline ECG and correlated with the ECG in tachycardia to help define the arrhythmia mechanism.

Wide QRS Complex Tachycardia

When there is lack of clarity as to whether an arrhythmia is atrial or ventricular, evidence of ventricular pre-excitation at baseline (particularly if multiple accessory pathways are present) makes an atrioventricular reciprocating mechanism more likely. The absence of an anterograde conducting accessory pathway combined with notation of a typical bundle branch block appearance with or without presence of a "long-short" (Ashman) phenomenon prior to the onset of a wide QRS tachycardia (right bundle branch block occurring more frequently than left bundle branch block) may indicate aberrant conduction. If the wide QRS complex is not a typical bundle branch block pattern and particularly if diagnostic features such as atrioventricular dissociation or fusion/capture beats can be identified, then attention can be focused on the ventricular chambers. The presence of a left bundle branch block pattern and inferior axis in a patient without history of structural heart disease suggests a right ventricular outflow tract origin. However, if the precordial transition occurs at V3 or earlier, then the right coronary cusp or left ventricular outflow tract is also a possible site of origin. If a right bundle branch block morphology with inferior axis is present in the absence of structural heart disease, then the left coronary cusp, left ventricular outflow tract, aortic-mitral continuity, or superior mitral valve annulus is a likely site of origin. Left coronary cusp ventricular tachycardias often have an "M-shape" QRS complex in V1, whereas the aortic-mitral continuity frequently demonstrates qR in V1; are negative in V2; and then are positive in V3. Ventricular arrhythmias from the mitral valve annulus should have positive concordance across all precordial leads. As the site of origin moves away from the center of the heart, the QRS width should increase because it will take longer to complete ventricular depolarization moving from one side of the heart to the other rather than starting in the middle and traveling both to the left and the right simultaneously (similar to the finding of P waves in atrioventricular nodal re-entrant tachycardia being narrower than in sinus rhythm secondary to the shorter time required to activate both atria from the center of the heart).

Transthoracic Echocardiography

Beyond clues provided by the history and surface ECG, transthoracic echocardiography is a useful tool to evaluate cardiac structure and function. Two-dimensional and three-dimensional echocardiography is capable of assessing chamber size, myocardial function, and valve function. Additional information relevant to electrophysiologic mapping is the ability of the transthoracic echocardiogram to exclude the presence of left ventricular thrombus as a relative contraindication to left ventricular endocardial mapping (Fig. 8–4). Transthoracic echocardiography with Doppler can also be used to estimate right ventricular systolic pressures. The presence of significant pulmonary hypertension may predict poor tolerance of sustained tachycardia and therefore may modify plans for the electrophysiologic mapping approach. Two-dimensional echocardiography findings of unexpected wall motion abnormalities or worse than expected valvular heart disease may also raise points requiring further investigation prior to consideration of electrophysiologic mapping. Electrophysiologic mapping may require the use of isoproterenol and/or rapid burst pacing for arrhythmia induction. Exclusion of significant obstructive coronary artery disease may be important prior to performance of an electrophysiologic mapping procedure to avoid inducing a significant amount of ischemia with attempts at arrhythmia induction. Presence of a previously unrecognized atrial septal defect or patent foramen ovale may also be important to recognize in order to minimize risks for paradoxical embolus with right-sided procedures that would otherwise not be present with an intact atrial septum.

Transesophageal Echocardiography

Although transthoracic echocardiography is useful for the analysis of many cardiac structures, patients with rhythms of atrial flutter or atrial fibrillation require transesophageal echocardiography for exclusion of left atrial appendage thrombus. In the case of right atrial flutter, arrhythmia duration <48 hours or therapeutic anticoagulation (ie, warfarin with international normalized ratio ≥2.0) for ≥4 weeks is usually adequate prior to right atrial mapping and ablation. However, for patients with atrial fibrillation who require mapping catheter instrumentation of the left atrium, a more thorough investigation with transesophageal echocardiogram may be warranted to exclude the presence of left atrial appendage thrombus16 (Fig. 8–5).

Cardiac Magnetic Resonance Imaging and Computed Tomography

Regarding left atrial mapping specifically, there may be much to be gained from preprocedural imaging of the left atrium and surrounding structures by either magnetic resonance imaging (MRI)17 or computed tomography (CT).18 Preprocedural left atrial imaging provides a road map of pulmonary vein anatomy (normal and variant) and identifies esophageal position (Fig. 8–6). Other potential left atrial structures of interest that may be imaged with these techniques include left atrial diverticula or accessory left atrial appendices.19 These structures have the potential to be arrhythmogenic and to be sites of increased perforation risk. MRI has the benefit of image acquisition without the use of ionizing radiation or the use of iodinated contrast. The former is of particular interest to younger patients and women. The latter is of particular interest to those with a history of iodine/contrast/shellfish allergy or renal insufficiency. In either case, both CT and MRI are able to create data sets that accurately depict left atrial anatomy in a way that can facilitate left atrial electrophysiologic mapping.

In addition to left atrial anatomy, cardiac MRI is also able to evaluate left ventricular myocardial function and obtain data regarding tissue characteristics in this region (Fig. 8–7). Although history, ECG, and echocardiogram detect the majority of patients with structural heart disease, there are patients who have myocardial abnormalities that may not be identified by techniques other than MRI,20 particularly when the underlying disease process is in its early stages. Examples of this can be found in patients with previously unrecognized myocarditis (acute, chronic, or resolved) (Fig. 8–8), sarcoidosis,21 hypertrophic cardiomyopathy,22 hemochromatosis,23 amyloidosis,24 arrhythmogenic right ventricular cardiomyopathy,25 or Chagas disease.26

In addition to anatomic and functional data, cardiac MRI is also able to obtain physiologic data including stress perfusion imaging and flow-velocity data. Both MRI and CT angiography can be useful for assessment of proximal coronary arterial anatomy, assessing systemic and pulmonary arterial and venous connections, although the ability of MRI to acquire data in a multiplanar fashion can be particularly useful in patients with complex anatomy such as patients with some forms of congenital heart disease (Fig. 8–9). The MRI information obtained in this patient population can be useful not only for roadmapping anatomic regions of interest, but also for treatment planning (ie, exclusion of need for interventions such as baffle stenting or surgical repair that might affect the plan for electrophysiologic mapping and arrhythmia treatment).

Cardiac MRI with Implanted Cardiac Devices

Cardiac MRI is useful for identifying the myocardial scar that is the substrate for ischemic ventricular tachycardia. However, most ischemic ventricular tachycardia mapping procedures are done in patients with implantable cardioverter defibrillators. The absence of a completely MRI-compatible implantable cardioverter defibrillator (or the presence of other contraindication to MRI) is a significant barrier to the routine use of cardiac MRI in this setting. This barrier, however, does not completely exclude the possibility of performing cardiac MRI with a defibrillator in situ. MRI protocols for some implanted cardiac devices have been published with documentation of points of concern as well as statements that MRIs can be obtained without prohibitive image compromise and without adverse effects to the patient or the device (devices implanted on or after the year 2000).27 In the study by Nazarian and Halperin,27 emphasis was placed on the preprocedural review of the chest x-ray to assess all used and abandoned hardware. Lead length and loops were noted to increase current and therefore create heat. A specific absorption rate (SAR) of ≤2.0 W/kg was recommended with the noted caveat that the SAR-to-heat correlation is not consistent among different MRI scanners. Recommendations were also made for the use of the largest acceptable field of view, longest repetition time, minimal flip angle, and minimal acquisition bandwidth. There was notation that magnetic fields can flip reed switches, which may affect the function of certain devices. A full device interrogation was recommended before MRI scanning (checking battery voltage, sensing, impedance, pacing threshold, and programmed parameters) and after MRI scanning to assure stability. Tachycardia detection and tachycardia therapy were programmed off prior to MRI to prevent filling tachycardia counters with noise and to prevent inappropriate tachycardia therapies for electromechanical interference associated with performance of the cardiac MRI. For pacemakers, pacing parameters were programmed to an asynchronous mode (if pacemaker dependent) or VVI/DDI (if underlying rhythm was stable) to avoid inhibition of pacing or tracking of noise, respectively (MRI scanning was not recommended for implantable cardioverter-defibrillator patients if pacemaker dependent). All magnet response features were disabled. Recommendations were made for blood pressure, ECG, oxygen saturation, and symptom monitoring with physicians and advanced cardiac life support equipment present. Imaging planes perpendicular to the device generator with shortened echo time and use of spin-echo and fast spin-echo spoiled gradient recall echo cine were used to reduce qualitative device artifacts. Implantable loop recorders are MRI safe; however, the data recorded on these devices must be downloaded prior to MRI and the memory must be cleared after MRI to avoid overwriting previous useful electrogram data with electromechanical interference and to avoid maintaining arrhythmia logs filled with electromechanical interference, respectively. Temporary pacing wires, abandoned leads, and epicardial leads are not MRI safe. MRI should not be performed within the first 6 weeks after device implant. Although the total number of patients in this study was relatively small, the combination of imaging success and absence of adverse outcomes is encouraging. Underreporting of adverse consequences, however, remains a concern; therefore, prior to attempting MRI with a pacemaker or defibrillator in situ, consideration must be given to the risk-benefit analysis of this endeavor. For further investigation of questions regarding MRI compatibility, useful information can be obtained from the following Website: http://www.mrisafety.com/.

Cardiac MRI for Left Ventricular Scar Mapping

Incorporation of cardiac MRI–defined ventricular scar-specific data into a three-dimensional electroanatomic map has been described.28 Although Desjardins et al28 showed a good correlation between MRI scar data and information obtained electroanatomically, the transfer of scar data from the MRI to the electroanatomic map was somewhat laborious, and when imported into the electroanatomic mapping system, the ventricular scar was not able to be represented with the level of detail achievable on the original MRIs. Nevertheless, this basic concept shows great potential. Most of the technology required to bring these MRIs into the electrophysiologic mapping laboratory is available. When defibrillators become fully MRI compatible to ease the safety concerns and logistic challenges of performing cardiac MRI in patients with implantable cardioverter-defibrillators, it is likely that preprocedural scar imaging data will make a rapid leap into the electrophysiologic laboratory. Bringing these multiple imaging modalities together in a three-dimensional, merged/fused fashion will likely facilitate efficiency, safety, and efficacy in the treatment of ischemic ventricular tachycardia.

Cardiac Positron Emission Tomography

In addition to cardiac MRI and CT, cardiac positron emission tomography (PET) may hold promise for the assessment of metabolic abnormalities relevant to arrhythmogenesis.29 Evaluating abnormalities of metabolism, such as those that occur with inflammation, may provide insight into the status of myocardium not measurable by other techniques. The ability to visualize these abnormalities may be particularly useful in the investigation of cardiac sarcoidosis or myocarditis. In these disease processes, systemic markers of disease activity may be variably present and may not accurately represent disease activity in the myocardium. Identification of cardiac-specific metabolic abnormalities may be one area where cardiac PET can provide useful information (Fig. 8–10). At times of active myocardial inflammation, treatments targeting the suppression of inflammation30 (or consequences of inflammation) may be more effective for improving long-term outcomes than using mapping and catheter-based therapies on a dynamic substrate.

Electrophysiologic mapping of complex arrhythmias requires integration of multiple imaging techniques to achieve the best possible safety and efficacy profile. Multiple techniques for assessing static and real-time representations of cardiac anatomy and myocardial electrical activity are displayed simultaneously, in digital, two-dimensional, three-dimensional, and merged formats to provide well-validated information about target anatomy and target electrophysiology.

The Electrophysiology Laboratory

A typical electrophysiologic laboratory is divided into two rooms, the control room and the patient room. The control room contains displays for real-time electrograms (EGMs), a review screen for assessment of static EGMs, fluoroscopy displays, an electronic stimulator display, three-dimensional electroanatomic mapping display, and additional monitor screens as needed for viewing real-time echocardiography, preprocedure studies, and/or a procedure room camera display. Lead glass and a doorway separate the control room from the patient room. The patient room is equipped with multiple monitor booms to display the multiple imaging modalities needed for guiding catheter manipulation during the electrophysiologic mapping procedure (Figs. 8–11 and 8–12).

EGM Recording

Within the electrophysiologic laboratory, the EGM recording system measures and displays electrical signals from both surface leads and intracardiac catheters. The timing and morphology of surface ECG leads provide the starting point for EGM interpretation and arrhythmia analysis. Three or four surface ECG leads are displayed at the top of the live EGM recording screen. The leads selected are most frequently orthogonal in the frontal plane (ie, leads I and aVF) with one or two precordial leads, usually including V1 (V1 is particularly useful to differentiate right bundle branch block and left bundle branch block QRS morphologies). Displayed below the surface ECG leads are the intracardiac EGMs (Fig. 8–13). Intracardiac EGMs are amplified and filtered to produce sharp deflections used to indicate timing of local electrical activity. The presentation of these EGMs on the live screen scrolls from left to right at an adjustable speed depending on operator preference (eg, 100 mm/s or 200 mm/s). There is also an audible beep that can be programmed to sound for ventricular sensed events that changes in tone for paced events in order to alert all in the electrophysiologic laboratory to the heart rate without looking at the EGM screen. Next to the live EGM screen is most frequently a review screen. When a pacing train is complete, the EGM screen shot at the end of the train is directed to the review screen for analysis. If there is a spontaneous event of interest, a single-button stroke can transmit the EGMs from the live screen to the review screen for analysis. The EGM recording screens (live and review) are displayed in the control room, as well as at the bedside in the patient room to allow for EGM analysis during catheter manipulation.

The Electronic Stimulator and Fluoroscopy

The EGM recording system monitors (live and review) in the control room are positioned next to the stimulator. The electronic stimulator is used to deliver pacing signals from the control room to intracardiac catheters for the purpose of electrophysiologic study and mapping. The indwelling catheters are placed in strategic positions in and around the cardiac chambers. Fluoroscopy is used to guide diagnostic catheter placement (Fig. 8–14). One limitation of fluoroscopy is its two-dimensional nature. For this reason, use of orthogonal views to represent three-dimensional anatomy is important (Fig. 8–15). In addition to the use of orthogonal views to assess location in three-dimensional space, intravascular contrast can be used to provide more detailed information about the vascular structure in question. Contrast may also be required to assist with visualizing structures such as the interatrial septum in preparation for transseptal puncture (Fig. 8–16) or epicardial tenting in preparation for epicardial access, for defining coronary anatomy that may be in close proximity to an arrhythmogenic focus (Fig. 8–17), for identifying coronary sinus diverticula that may mark the site of an accessory pathway,31 for opacifying structures to clarify catheter position (Fig. 8–18), or for identifying right ventricular wall motion abnormalities in patients with suspected arrhythmogenic right ventricular cardiomyopathy.

Analysis of Data from Electrophysiologic Mapping Catheters

With diagnostic catheters in place, the electrophysiologic substrate can be characterized before and after arrhythmia induction to help define arrhythmia mechanism. Diagnostic and mapping catheters are positioned to obtain as much information as possible with the minimum number of catheters. A four-catheter setup such as that displayed in Figure 8–14 can be used to investigate supraventricular tachycardia. From these four catheters, information can be obtained regarding patient-specific electrophysiologic characteristics. These catheters (along with surface ECG analysis) provide information about the relative location of the tachycardia origin (ie, right or left, high or low, anterior or posterior) by EGM timing (ie, right atrial catheter is RIGHT, distal coronary sinus catheter is LEFT, the atrial EGM on the His bundle is HIGH and ANTERIOR in the middle of the heart, the proximal coronary sinus catheter is LOW and POSTERIOR in the middle of the heart). Additional multipolar catheters and mapping systems may be applied to further assist in tachycardia localization; however, the principle of using EGM location and time-specific information to define arrhythmia mechanism is the same. The likely arrhythmia mechanism is suggested by analysis of the surface ECG and baseline conduction properties and is confirmed with mapping and pacing maneuvers in tachycardia.

Tachycardia Mechanism and Location

Tachycardias are generally either focal (emerging from a discrete location, spreading out in a centrifugal manner in all available directions) or macro–re-entrant (following a head-meets-tail propagation) (Fig. 8–19). The origin is either supraventricular (right atrial vs left atrial vs atrioventricular node vs coronary sinus vs noncoronary cusp) or ventricular (right ventricular vs left ventricular [endocardial vs epicardial, scar related vs non–scar related] vs pulmonary artery vs left/right coronary cusps) or dependent on an accessory pathway between the atrium and ventricles that allows for atrioventricular reciprocating tachycardia.

EGM Interpretation

Morphologic analysis of intracardiac EGMs is useful for such things as distinguishing atrial EGMs from ventricular EGMs when obtaining electrical information near the atrioventricular groove, distinguishing far-field from near-field signals, and analysis of low-amplitude high-frequency aspects of EGM signals that may be suggestive of tissue anisotropy at an arrhythmogenic focus; otherwise, the majority of the information obtained from diagnostic catheters is from EGM timing. For this reason, EGM recording systems time-synchronize intracardiac EGMs and surface ECGs. Electronic calipers can then be used to quickly and accurately perform conduction interval measurements that are reproducible to within a few milliseconds.

Conduction Intervals, Activation Sequence, and Refractory Periods

An electrophysiologic study begins with the measurement of baseline conduction intervals. In addition to the standard surface PR, QRS, QT, and RR intervals, intracardiac EGMs allow for the measurement of the AH (time from the local atrial EGM on the His catheter to the onset of the His EGM on the His catheter) and HV (time from the onset of the His EGM on the His catheter to the first sign of ventricular activation, usually with the imitation of the QRS complex on the surface ECG). While measuring conduction intervals, Wenckebach cycle lengths, and refractory periods, parameters such as ventriculoatrial activation can also be assessed. Ventriculoatrial activation is determined by pacing from the ventricular catheter and observing the timing of atrial signals on diagnostic catheters in the right atrium, His bundle region, and throughout the length of the coronary sinus. Normal ventriculoatrial conduction in the absence of an accessory pathway should only occur through the atrioventricular node and therefore should be concentric (earliest at the center of the heart with earliest atrial EGMs on the His bundle catheter). Although this does not exclude a septal accessory pathway, it makes the presence of a rapidly conducting lateral (eccentric) accessory pathway less likely. If there is no ventriculoatrial conduction at baseline, then there is no retrogradely conducting accessory pathway, and the diagnosis of orthodromic reciprocating tachycardia is excluded. If there is suspicion of a septal accessory pathway, additional diagnostic maneuvers can be performed to evaluate this possibility (ie, parahisian pacing and/or comparing ventriculoatrial conduction times when pacing from the ventricular base vs the ventricular apex).

Following the assessment of ventriculoatrial conduction, assessment of atrioventricular conduction can be made. This provides information about atrioventricular node function and allows for assessment of atrioventricular conduction at rapid rates that might uncover anterograde conduction across a previously unrecognized accessory pathway as atrioventricular nodal conduction becomes decremental. If ventricular pre-excitation is suspected, additional maneuvers such as differential pacing (pacing from different locations in the atria in an attempt to identify ventricular pre-excitation by comparing QRS morphology pacing close to vs far away from the location of the suspected accessory pathway) can be used to support this hypothesis. Likewise, administration of adenosine can be used to block atrioventricular nodal conduction, noting that some accessory pathways (particularly slowly conducting accessory pathways with decremental "atrioventricular node–like" properties) may also block with adenosine. Following these pacing maneuvers, programmed electrical stimulation can then be performed in the atrium. The presence of an "AH jump" (defined as a prolongation of the AH interval >50 ms with an S1/S2 coupling interval decrease of only 10 ms) implies the presence of dual atrioventricular nodal physiology, with fast pathway (fast conduction velocity, but relatively long effective refractory period) and slow pathway (slow conduction velocity, but relatively short effective refractory period) inputs to the atrioventricular node creating the substrate for atrioventricular nodal re-entrant tachycardia. Additional extra stimuli may be applied (ie, atrial for supraventricular tachycardia and ventricular for ventricular tachycardia) or rapid burst pacing may be pursued with and without pharmacologic agents such as the adrenergic agonist isoproterenol (burst pacing during isoproterenol initiation, upward titration, plateau, and washout) to increase automaticity/triggered activity, increase conduction velocity, shorten refractory periods, and/or increase the dispersion of refractoriness in hopes of creating suitable substrate for tachyarrhythmia initiation and maintenance.

Catheter Mapping of Tachycardia

In addition to the four cardiac chambers (right atrium, right ventricle, left atrium, and left ventricle), there are additional regions surrounding these chambers relevant to electrophysiologic mapping (ie, coronary sinus, coronary cusps, epicardial space). It is important to consider each of these regions as a potential site for arrhythmia origin. For example, a ventricular tachycardia may be identifiable as emerging from the right ventricular outflow tract region using only the surface ECG. This arrhythmia may be mapped in great detail positioning the mapping catheter in numerous regions throughout the right ventricular outflow tract; however, if the true origin is from the right coronary cusp, this region cannot be assessed from the right ventricle. Likewise, an atrial tachycardia may have points of earliest activation mapped from the right atrium, as well as the left atrium along the anterior interatrial septum; however, if the arrhythmia is from the noncoronary cusp, the true origin cannot be confirmed with the mapping catheter anywhere other than the proximal aorta.

If mapping of a focal tachycardia is not performed in the correct location, the origin of the arrhythmia will not be discovered, and attempts at treatment will be frustrating. The importance of mapping in the correct location is also seen with macro–re-entrant arrhythmias. Left atrial flutters that encircle the mitral annulus often use muscular bands residing in the coronary sinus. Effective linear ablation of the mitral isthmus frequently requires ablation in the coronary sinus to achieve conduction block in the tissue between the inferolateral mitral valve annulus and the inferolateral aspect of the left lower pulmonary vein.32 Likewise, accessory atrioventricular pathways residing in the coronary sinus or middle cardiac vein will not be detected unless the mapping catheter is placed in these structures. The presence of a negative delta wave in lead II on the surface ECG suggests an epicardial location of a posteroseptal accessory pathway.33 When evaluating ventricular arrhythmias, consideration may also need to be given to whether the focus of the arrhythmia is epicardial or endocardial. There are some clues identifiable prior to invasive mapping that indicate that the source of a ventricular arrhythmia may be epicardial such as the underlying disease process (eg, sarcoidosis, Chagas, arrhythmogenic right ventricular cardiomyopathy), and surface ECG QRS morphology (eg, slurred upstroke to a late peaking QRS, more than one negative to positive QRS transition in the anterior precordial leads).34 However, in many cases, requirement for epicardial access may not be apparent until subendocardial approaches have failed. With requirement for epicardial access, the need for multiple imaging modalities becomes apparent because fluoroscopy, EGMs, and three-dimensional electroanatomic maps may require additional information from intravenous contrast injection and coronary angiography to ensure that the epicardium is entered safely and to confirm that ablation energy is delivered at a safe distance from the coronary arterial tree, as illustrated in Figure 8–17.

Characterizing Macro–Re-Entrant Arrhythmias

If tachycardia can be initiated and maintained, additional diagnostic maneuvers can be performed to define the mechanism of the arrhythmia. The primary pacing maneuver used to define a re-entrant mechanism is entrainment. By pacing from a given sight at a paced cycle length that is slightly faster than the tachycardia cycle length (ie, entrainment pacing cycle length = tachycardia cycle length – 20 to 30 ms) and then measuring the time it takes for the local EGM in tachycardia to return to the pacing electrode after cessation of pacing, the return cycle length or postpacing interval (PPI) can be measured. Likewise, additional information can be obtained by looking for diastolic potentials, assessing EGM timing, and comparing the surface ECG morphology both while pacing and in tachycardia. Among other cardinal features, entrainment is heralded by acceleration of the tachycardia to the paced cycle length prior to cessation of pacing without termination of tachycardia. Entrainment can be attempted from any region of paceable myocardium; however, success will depend on the ability of the pacing stimulus to enter the excitable gap of the re-entrant arrhythmia (excitable gap = tachycardia cycle length – effective refractory period) without extinguishing tachycardia. If entrainment is successful, a shorter PPI will indicate that the pacing catheter is closer to the tachycardia circuit. The longer the PPI, the further away the pacing catheter is from the circuit. When the PPI equals the tachycardia cycle length (without change in EGM activation sequence or change in surface ECG morphology), the pacing catheter is in the circuit.

Additional information is obtained by incorporation of known anatomic structures serving as portals of conduction (ie, the atrioventricular node, the His-Purkinje system, accessory pathways) and areas of conduction block (ie, atrioventricular valves, the eustachian ridge, the crista terminalis) and knowledge of relatively narrow regions of conducting tissue between structures of known anatomic block (eg, the cavotricuspid isthmus lying between the eustachian ridge and the tricuspid valve annulus). Which of these structures are relevant to the tachycardia circuit needs to be determined, and these hypotheses can be tested with assessment of EGM timing, use of pharmacologic agents such as adenosine to produce atrioventricular block, and pacing maneuvers designed to test participation of a given chamber or pathway in tachycardia (ie, pacing from the ventricle during narrow complex tachycardia to produce tachycardia termination at a time of His refractoriness demonstrating participation of the ventricle in the tachycardia circuit with orthodromic reciprocating tachycardia). A single observation or response to a pacing maneuver may not be adequate to determine arrhythmia mechanism conclusively; however, reproducible observations during multiple pacing maneuvers are usually able to clarify arrhythmia mechanism.9

Characterizing Focal (Automatic or Triggered) Arrhythmias

For tachyarrhythmias that do not have a re-entrant mechanism (eg, focal atrial tachycardia or focal right ventricular outflow tract tachycardia secondary to increased automaticity or triggered activity), entrainment is not possible. Pacing at rates faster than the tachycardia cycle length results in overdrive suppression of these arrhythmias however, stable manifest fusion will not be achievable, and the return cycle length or PPI analysis will often yield variable results that will not provide reliable information about the proximity of the pacing catheter to the focus of the arrhythmia. One pacing tool that can be useful for defining the origin of an automatic or triggered ventricular arrhythmia is pacemapping. Pacemapping is achieved by positioning the mapping catheter in a region of suspected arrhythmia origin and pacing the local myocardium at 1.5 to 2 times the pacing threshold and then comparing the paced 12-lead surface ECG to the 12-lead surface ECG morphology of the clinical arrhythmia (Fig. 8–20). The presence of a "12-out-of-12" lead pacemap match is supportive of the catheter position being at the origin of the tachycardia. Additional information of critical importance to include with information obtained by maneuvers such as pacemapping is assessment of the local EGMs at the suspected site of arrhythmia origin. Whether the arrhythmia is atrial or ventricular, the local EGM at the site of arrhythmia origin should precede the surface ECG deflection by 25 to 45 ms. If the local EGM is not sufficiently early, then additional mapping will usually be required to identify the true origin of the arrhythmia. In addition to timing of this EGM, features such as low-amplitude, highly fractionated (high-frequency) bipolar EGMs and a QS pattern (indicative of all electrical activity moving away from the catheter tip) on unipolar EGMs are usually present at the origin of a focal arrhythmia. As with integration of multiple imaging modalities to achieve an accurate depiction of cardiovascular anatomy, the accuracy of electrophysiologic mapping is improved when multiple ways of identifying arrhythmia mechanism and/or arrhythmia origin are all supportive of the same conclusion.

Ablation and Impedance Mapping

In addition to pacing maneuvers and EGM characteristics, delivery of radiofrequency energy itself can be useful for mapping. Whether the ablation catheter is on a critical isthmus of a re-entrant circuit or the origin of an automatic or triggered focal tachycardia, delivery of radiofrequency energy to this area that results in termination (usually preceded by prolongation of the tachycardia cycle length if the mechanism is macro-reentrant or tachycardia acceleration if mechanism is automatic or triggered) and subsequent noninducibility of that arrhythmia provides further proof of mechanism. Additional data provided by the ablation catheter include impedance information.35 When mapping in pulmonary veins and/or other cardiac vascular structures, marked increase in impedance may indicate catheter position that lacks myocardial tissue and therefore lacks the substrate to serve as a source for arrhythmia. During pulmonary vein isolation for the treatment of atrial fibrillation, catheter position is viewed under fluoroscopy, compared with fluoroscopic road maps from pulmonary venograms, and combined with analysis of local EGMs and catheter impedance to help direct catheter position out of the pulmonary vein and to the pulmonary vein antrum (Fig. 8–21). By ablating and isolating antral tissue, procedural efficacy is improved. By preventing delivery of radiofrequency energy outside of the pulmonary vein, complications such as pulmonary vein stenosis are reduced.

Three-Dimensional Transesophageal Echocardiography

In addition to EGM, fluoroscopic, and impedance data, information during electrophysiologic mapping can be obtained by the use of echocardiography. Three-dimensional transesophageal echocardiography (TEE) can guide mapping and ablation in regions of the left atrium where complex left atrial topography may present challenges in achieving reliable, reproducible, and predictable catheter position.36 Three-dimensional TEE produces heat as well as some degree of mechanical compression between the mid esophagus and posterior wall of the left atrium, and therefore, TEE is relatively contraindicated if radiofrequency energy is being delivered to the posterior wall of the left atrium. In regions of complex anatomy, however, that are more anterior, such as the ligament of Marshall region, three-dimensional TEE provides high-resolution images of both the mapping catheter and intracardiac contours to guide catheter positioning (Fig. 8–22).

Intracardiac Echocardiography

Intracardiac echocardiography (ICE) has taken a central role in numerous aspects of electrophysiologic mapping. For procedures where transseptal access of the left atrium is required, ICE allows direct visualization of the interatrial septum, access needle, and sheath apparatus to confirm a crossover point in the region of the fossa ovalis, as well as to provide real-time visualization of the passage of this equipment into the left atrium (Fig. 8–23). In addition to use during transseptal access, ICE can also be used to assess cardiac anatomy, confirming absence of pericardial fluid before, during, and after the procedure. The ICE catheter can also be passed directly into the left atrium for visualization of catheter position and its relation to important structures such as the pulmonary vein (to confirm good catheter-tissue contact at the pulmonary vein antrum) and esophageal tissue (Fig. 8–24). ICE can also play an important role in electrophysiologic mapping through its use in the three-dimensional electroanatomic mapping system CARTO-sound (Biosense Webster, Diamond Bar, CA) (Fig. 8–25). One frontier in electrophysiologic mapping assisted by multiple imaging modalities is pending the development of real-time, multiplanar three-dimensional ICE. If such imaging can be achieved in a probe of acceptable size, the current requirements for mental integration of multiple sources of information (eg, biplane fluoroscopy, pulmonary venogram road maps, mapping catheter impedance data, EGMs) to reliably identify catheter position and tissue contact may be greatly simplified.

Cardiac MRI and CT

In lieu of three-dimensional real-time multiplanar ICE, the most detailed representations of intracardiac anatomy are provided by integration of images obtained by cardiac MRI or CT with imaging data obtained using a three-dimensional electroanatomic mapping system. The integration of these imaging modalities has been most useful for electrophysiologic mapping of the left atrium.

Three-Dimensional Contact Mapping

The application of imaging data obtained by CT or MRI is more fully appreciated in the electrophysiologic laboratory when integrated with a three-dimensional electroanatomic mapping system. The two contact mapping systems used most commonly are ESI (Endocardial Solutions Incorporated, St. Paul, MN) and CARTO (Biosense Webster). The mapping catheter (and additional diagnostic catheters) is viewed under fluoroscopy in the most basic electrophysiologic mapping setup; however, additional information can be obtained by annotating EGM characteristics and catheter tip position in three-dimensional space by use of a three-dimensional electroanatomic mapping system. Annotation of points where catheter contacts myocardium can then be used to create an anatomic shell representing the walls of the cardiac chamber of interest. This three-dimensional electroanatomic image can then be combined with other forms of imaging, such as that obtained by CT or MRI, to improve the depiction of target the anatomy (Fig. 8–26). In addition to creation of an anatomic shell, analysis of the EGMs obtained at tissue contact points can be used to provide information about the electrophysiologic properties of the tissue at that point to create voltage maps and activation maps.

Voltage Mapping (Three-Dimensional Contact Mapping System)

Local EGM amplitude (measured in millivolts in regions where myocardial contact is unimpeded by fat or other barrier to myocardial tissue contact) can be assessed to provide information about tissue viability. Voltage measurements >1.5 mV are indicative of viable myocardium. Low-voltage measurements (ie, <0.3 mV) are more indicative of myocardium with limited viability or scar tissue. Tissue with low-amplitude (or absent) EGMs that cannot be paced even with high output (ie, 10 mA) may represent dense scar or "electrically unexcitable scar." Assigning various colors to represent variations in EGM voltage allows for creation of a voltage map (Figs. 8–27 and 8–28). Macro–re-entrant scar-related ventricular arrhythmias, for example, frequently use heterogeneous regions of limited viability at the border zone of myocardial scar or regions of viable tissue between electrically unexcitable scar to create a critical isthmus of slowed conduction that allows for arrhythmia perpetuation.37 These regions are of particular interest because they often represent the therapeutic target for elimination of the arrhythmia circuit.38

Activation and Propagation Mapping (Three-Dimensional Contact Mapping System)

In addition to voltage data, additional useful information can be obtained using a three-dimensional electroanatomic mapping system by annotating local EGM timing. By comparing the timing of EGMs detected at the tip of a mapping catheter to a stable reference and representing the difference with a colorimetric scale to highlight the area of earliest activation (such as that which would be of interest with a focal tachycardia) or to identify points where early activation meets late activation (such as that which would be of interest with a macro–re-entrant circuit), the arrhythmia mechanism can be displayed anatomically. This activation data can likewise be viewed dynamically to demonstrate wave-front propagation (Fig. 8–29).

Putting It All Together

Invasive electrophysiologic mapping often requires a combination of the following processes: fluoroscopy for catheter positioning to allow safe and effective catheter manipulation; EGMs for determination of electrical activity at tissue contact points (timing: early vs late diastolic potentials; morphologic: amplitude, frequency); three-dimensional electroanatomic maps to allow data annotation for creating a multipoint anatomic shell with or without merged/fused images from other modalities (CT angiography/MRI) incorporating voltage (surrogate marker for determining myocardial viability) and activation/propagation data (timing sequence); validating data with techniques such as extrainment and pacemapping; and using tools such as ICE to survey anatomy and assist with catheter navigation.

Limitations of Contact Mapping

One limitation of activation mapping using the contact mapping method described earlier is a requirement for sustained (or at least frequently recurring) arrhythmia to provide activation data. This limitation can prevent successful characterization of nonsustained or infrequently occurring arrhythmias, such as may be the case with many automatic or triggered tachycardias, which may have a tendency to occur in bursts that are symptomatic outside the electrophysiology laboratory but occur less frequently under conditions in the electrophysiology laboratory (eg, in the presence of sedation, alteration in environmental stimuli). Despite efforts to minimize sedation and specifically to avoid sedative agents known to suppress automatic tachyarrhythmias, and even with the addition of provoking agents such as isoproterenol or atropine, a paucity of arrhythmia may be a significant limitation to the point-by-point contact mapping approach discussed earlier. An additional limitation of contact mapping may be experienced if the clinical arrhythmia has a tendency to degenerate into a disorganized rhythm, such as atrial tachycardia degenerating into atrial fibrillation or ventricular tachycardia degenerating into ventricular fibrillation. Point-by-point mapping is also limited if the clinical arrhythmia is not hemodynamically tolerated, such as with rapid ventricular tachycardia in the setting of poor left ventricular function. Unless a perfusing blood pressure can be maintained in tachycardia with the addition of vasopressors, hemodynamic support with an intraaortic balloon pump, or ventricular assist device, activation mapping using a contact mapping system in this scenario may not be possible.

Three-Dimensional Electroanatomic Mapping (Three-Dimensional Noncontact Mapping System)

Some of the limitations of contact mapping described earlier can be overcome by use of a noncontact mapping system. The EnSite multielectrode array (MEA; Endocardial Solutions) uses a 7.5-cc balloon to expand a woven braid of 64 wires mounted on a 9-French catheter to detect far-field electrical potentials from the cardiac chamber of interest. These far-field electrical potentials are used to reconstruct "virtual" unipolar endocardial EGMs over more than 3000 points. This reconstruction is accomplished by using inverse-solution mathematics to create an instantaneous endocardial isopotential map superimposed onto a computer-simulated model of the endocardium during a single heartbeat. Electrodes are created at specified regions of disrupted insulation in the woven braid of wires. There is a ring electrode on the proximal shaft to serve as a reference. While moving the mapping catheter around the endocardial surface, the MEA detects and determines locator signal angles to create a three-dimensional computer model of the endocardium. The inverse-solution method considers how a signal detected at a remote point would have appeared at its source by noting how the potential field at any one electrode is influenced to a degree by potentials from the entire endocardium. The degree of influence is inversely proportional to the distance between the electrode and each endocardial point. Accuracy of this mapping system decreases with distance from the endocardial source and with increasing chamber complexity39,40 (Fig. 8–30). To assure accurate mapping data, the array position must be stable and ideally within 1.5 cm of the substrate being assessed. Movement of the MEA will invalidate previously obtained data.41 An additional limitation of this technique is the large size of the balloon, which may limit maneuverability of the balloon itself as well as the mapping catheter being used in concert with the balloon. Additionally, when mapping relatively small regions, such as the right ventricular outflow tract, the MEA may contact endocardium, producing ectopy that can be confused with the clinical arrhythmia. The balloon may be partially deflated to assist with some of these limitations. The MEA also has potential thrombogenicity that must be abrogated with concurrent use of intravenous heparin.

Remote Catheter Navigation Systems

In addition to mechanistic challenges of mapping complex arrhythmias, there are also logistic challenges presented by long procedure times, radiation exposure, and operator standing time while wearing lead. The toll of these undesirable aspects of electrophysiologic mapping accumulate with time and may significantly reduce the number of procedures a single operator may perform in his or her lifetime.42 In hopes of addressing these issues as well as aiming to continue improvements in safety, effectiveness, and reproducibility of electrophysiologic mapping procedures, there has been interest in the development of automated electrophysiologic mapping techniques.

The first step in this process has been the development of remote catheter navigation systems. Remote catheter navigation systems using MRI-like large magnets to manipulate catheter position have been developed and continue to be refined (Stereotaxis, St. Louis, MO).43 Limitations of this system have included room requirements to safely accommodate the Stereotaxis magnets (ie, large size of magnets requires large room size, large weight of magnets requires floor reinforcement, and powerful magnetic fields require magnetic shielding and nonmagnetic ancillary equipment). Additional limitations have included mapping catheter compatibility (special catheter construction required to respond to magnetic field manipulation). Specific benefits of the Stereotaxis system have included a theoretical reduction in perforation risk due to a decreased likelihood of a calculable magnetic pull leading to perforation as opposed to mechanical push that may be less able to perceive force at the tissue contact interface. An unfortunate consequence of decreased tissue contact force occurs with attempts at arrhythmia treatment, as force of tissue contact is a key determinant of ablation lesion depth.44 Inadequate lesion depth may prevent procedural success.

A second commercially available remote catheter navigation system has been created using a mechanical/robotic platform rather than magnetic force to manipulate catheter position (Hansen Medical, Mountain View, CA).45 Attributes of the Hansen remote catheter navigation system include compatibility with a broad range of catheters and improved catheter-tissue contact pressure. The improved catheter-tissue contact pressure requires management to minimize risk of perforation; however, it provides significant benefits in maintaining catheter stability and increasing ablation lesion depth. To provide operator feedback to facilitate safe and effective catheter navigation, tissue contact pressure is displayed for the operator both graphically and via tactile feedback provided by the Intellisense algorithm (Sensei; Hansen Medical).42,46 Whether the remote catheter navigation system is magnetic or mechanical, an attribute of both is the creation of a workstation environment that concentrates multiple imaging modalities in a relatively compact area (Fig. 8–31).47 Level I multimodal imaging (MMI) is demonstrated by adding information from one two-dimensional fluoroscopic view to a second orthogonal fluoroscopic view. Level II MMI is seen when comparing the fluoroscopic view of catheter position in the pulmonary venogram to the ICE image to assure catheter position with good tissue contact at the pulmonary vein antrum. Level III MMI is represented by both the three-dimensional electroanatomic map and the three-dimensional MRI image of the left atrium and proximal pulmonary veins. Level IV MMI is achieved when the images in two dimensions are represented side by side. Level V MMI is achieved when the three-dimensional electroanatomic image is merged/fused with the three-dimensional MRI (or CT) image.

Catheter Guidance Without Exposure to Ionizing Radiation

Additional opportunities for multimodal imaging in electrophysiologic mapping may be present with use of MRI, rather than fluoroscopy, to guide catheter manipulation.48,49 Catheter guidance with MRI has several benefits over fluoroscopy. One benefit is the decreased radiation exposure for the operator and the patient. In addition, cardiac MRI has the ability to represent three-dimensional anatomy with particular imaging sequences used to depict tissue characteristics such as tissue viability; cardiac MRI also has the ability to provide detailed display of cardiac structures such as heart valves and papillary muscles that are not visible with fluoroscopy. There are several barriers to the use of MRI-guided techniques, including image acquisition speed and resolution, as well as requirement for MRI-compatible catheters effective for mapping and ablation with imaging characteristics allowing catheter visibility without marked distortion. Patient physiologic stability and tolerance of prolonged procedure times in the bore of a magnet are also important issues; however, many of these patient-related challenges may be overcome with use of anesthesia support. Development of MRI-compatible pacemakers and defibrillators will also facilitate this process by broadening the population of candidates for MRI.

Ultrasound has been shown to be a useful tool to guide catheter manipulation for the purpose of electrophysiologic mapping.50 Currently, ultrasound use is primarily as an adjunct to images obtained using conventional fluoroscopy. However the absence of radiation exposure with ultrasound imaging makes it an attractive candidate for reducing procedural radiation exposure. As three-dimensional ultrasound technology improves, the possibility of ultrasound-only guided catheter navigation may become a viable strategy.

The requirement for multimodal imaging continues beyond the completion of the electrophysiologic mapping procedure. The ICE probe is useful for a survey of cardiac structures to confirm stable function and anatomy. Specifically, analysis to exclude an unexpected pericardial fluid collection prior to removal of catheters from the heart may be useful. Following departure from the electrophysiologic laboratory, telemetry analysis is used for monitoring heart rate and rhythm. Postprocedure 12-lead ECGs are useful for establishment of electrophysiologic properties after the procedure and for investigation of any concerns regarding ischemia for cases involving myocardium with ablation performed in close proximity to coronary vasculature.

Esophageal Evaluation

For patients who have undergone ablation along the posterior left atrial wall, there may be concern about thermal esophageal injury. Features concerning for risk of atrioesophageal fistula may be investigated early with esophagogastroduodenoscopy without insufflation (noting that absence of insufflation may limit endoscopic visualization within the esophagus); however, if it is more than 48 hours after the procedure, overt atrioesophageal connection is best evaluated by imaging modalities such as chest CT and, to a lesser extent, echocardiography.51,52

Pulmonary Vein Evaluation

Imaging modalities that have been particularly useful for evaluation after pulmonary vein procedures include both CT and cardiac MRI. Cardiac MRI in particular allows not only depiction of the pulmonary vein in three dimensions, but also en-face analysis of pulmonary vein ostia for direct measurement and flow-velocity analysis. In addition to flow-velocity information, the variation in circumference at the pulmonary vein os can also be observed throughout the cardiac cycle. A significant reduction in pulmonary vein contraction after circumferential pulmonary vein isolation may correlate with electrical isolation of the pulmonary vein (Fig. 8–32). Likewise, notation of pulmonary vein contraction that is not significantly reduced following an attempt at pulmonary vein isolation may correlate with absence of electrical isolation.

Cardiac MRI for Assessment of Ablated Tissue

Additional magnetic resonance–based techniques are being developed to assist with imaging regions of ablated tissue after percutaneous arrhythmia treatment. Ablated myocardium, including regions of delayed gadolinium enhancement, and acute changes such as "no reflow" (regions of contrast void secondary to vasculature disruption preventing tissue delivery of gadolinium contrast) can be clearly seen in cases of focal ventricular tachycardia ablation (Fig. 8–33). Barriers to imaging atrial myocardium in this same manner can be attributed to the relatively thin nature of the atrial myocardium, surrounded on both sides by bright structures such as blood pool or fat. Development of dark blood delayed-enhancement images may provide promise in overcoming some of these issues. Additional means that may improve imaging in the thin-walled atria include use of techniques to track respiratory motion and adjust image analysis so that gated images can be obtained for times greater than could be achieved by breath-holding techniques alone. Successful depiction of delayed enhancement in the thin-walled atrium not only has applications for follow-up of electrophysiologic procedures, but also has the potential to be applied to other regions of the heart where identification of small regions of delayed enhancement might have substantial clinical relevance (ie, arrhythmogenic right ventricular cardiomyopathy).

Cardiac PET

Additional imaging modalities under investigation in arrhythmia management include use of cardiac PET. Metabolic markers of arrhythmogenic substrate are incompletely defined; however, cardiac PET has found a useful role in individual cases. An example of cardiac PET utility after left atrial ablation was found after an initial successful treatment of atrial fibrillation with pulmonary vein isolation was followed by recurrent, incessant, drug-refractory atrial fibrillation. Antiarrhythmic medications that before the procedure had been at least partially efficacious were no longer able to maintain sinus rhythm even for a short period of time with or without electrical cardioversion. Transesophageal echocardiographic images performed for the purpose of excluding left atrial appendage thrombus were notable for marked thickening of the left atrial wall. This was evaluated in greater detail with cardiac MRI, which confirmed the presence of extensive left atrial thickening having the appearance of a rind around the left atrium. Cardiac PET imaging found this rind to be metabolically active, consistent with inflammatory tissue. The patient had no history or current evidence of malignancy. There was no lymphadenopathy or mass on chest CT. The patient was treated empirically with steroids for left atrial pericarditis reactive to the ablation process. Following steroid taper, a repeat cardiac PET scan revealed resolution of left atrial inflammation. Reinstitution of antiarrhythmic medication followed by cardioversion resulted in sustained sinus rhythm (Fig. 8–34).

For successful electrophysiologic mapping to be achieved, all available information must be integrated to explain arrhythmia mechanism. The multiple imaging modalities obtained by two-dimensional techniques such as fluoroscopy and ultrasound must be incorporated with three-dimensional representations of cardiac anatomy obtained both by preprocedure cardiac CT and cardiac MRI, as well as data obtained in the electrophysiologic laboratory with the use of three-dimensional electroanatomic mapping systems. At times, there are automated techniques to bring these imaging modalities together (eg, CARTO-merge, Biosense Webster; NavX Fusion, Endocardial Solutions); however, much of the coalescence of information required to achieve level V MMI integration is still done mentally by the primary operator of the electrophysiology mapping procedure. As real-time, multiplanar, three-dimensional imaging modalities that do not depend on registration for accurate depiction of anatomy are developed, the level of mental processing to provide an understanding of the relationship between cardiovascular electrophysiology, cardiac anatomy, and catheter position will be decreased and relevant procedural outcomes of safety, efficacy, and reduced procedure times will likely follow.