Abstract
Cardiac mapping refers to the process of identifying the temporal and spatial distributions of myocardial electrical potentials during a particular heart rhythm. Mapping aims at elucidation of the mechanism or mechanisms of the cardiac rhythm, description of the propagation of activation from its initiation to its completion within a region of interest, and identification of the site of origin or a critical site of conduction to serve as a target for catheter ablation.
Cardiac mapping is a broad term that covers several modes of mapping such as body surface, endocardial, and epicardial mapping. Activation mapping involves the use of intracardiac and surface electrocardiogram (ECG) tracings for comparative timing of electrical events and to determine the location and direction of impulse propagation. Entrainment mapping is commonly used to approximate the location of a reentrant circuit and identify the critical isthmus of the reentry circuit to guide ablation. Pace mapping is a technique designed to help locate tachycardia sources by pacing at different endocardial sites to reproduce the ECG morphology of the tachycardia. The greater the degree of concordance between the morphology during pacing and that during tachycardia, the closer the catheter will be to the site of origin of the tachycardia.
Keywords
activation mapping, entrainment, pace mapping, intracardiac electrograms, mechanism of arrhythmias, focal tachycardias, macroreentry
Cardiac mapping refers to the process of identifying the temporal and spatial distributions of myocardial electrical potentials during a particular heart rhythm. Cardiac mapping is a broad term that covers several modes of mapping such as body surface, endocardial, and epicardial mapping, in order to characterize the timing and/or amplitude (voltage) of signals relative to each other. Mapping during tachycardia aims at elucidation of the mechanism or mechanisms of the tachycardia, description of the propagation of activation from its initiation to its completion within a region of interest, and identification of the site of origin or a critical site of conduction to serve as a target for catheter ablation.
Activation Mapping
Fundamental Concepts
Essential to the effective management of any cardiac arrhythmia is a thorough understanding of the mechanisms of its initiation and maintenance. Conventionally this has been achieved by careful study of the surface electrocardiogram (ECG) and correlation of the changes therein with data from intracardiac electrograms recorded by catheters at various key locations within the cardiac chambers (i.e., activation mapping). A record of these electrograms documenting multiple sites simultaneously is studied to determine the mechanisms of an arrhythmic event.
The main value of intracardiac and surface ECG tracings consists of the comparative timing of electrical events and the determination of the location and direction of impulse propagation. In addition, electrogram morphology can be of significant importance during mapping. Establishing electrogram criteria, which permit accurate determination of the moment of myocardial activation at the recording electrode, is critical for the construction of an area map of the activation sequence. Bipolar recordings are generally used for activation mapping. Unipolar recordings are used to supplement the information obtained from bipolar recordings.
Unipolar Recordings
Timing of local activation.
The major component of the unipolar electrogram allows for the determination of the local activation time, although there are exceptions. The point of maximum amplitude, the zero crossing, the point of maximum slope (maximum first derivative), and the minimum second derivative of the electrogram have been proposed as indicators of underlying myocardial activation ( Fig. 5.1 ). The maximum downslope (i.e., maximum change in potential, dV/dt) of the unipolar electrogram coincides best with the arrival of the depolarization wavefront directly beneath the electrode and is now considered the most accurate marker of local tissue activation. Using this fiducial point, errors in determining the local activation time as compared with intracellular recordings have typically been less than 1 millisecond. This is true for filtered and unfiltered unipolar electrograms.
Direction of local activation.
The morphology of the unfiltered unipolar recording indicates the direction of wavefront propagation. By convention, the mapping electrode that is in contact with the myocardium is connected to the positive input of the recording amplifier. In this configuration, positive deflections (R waves) are generated by propagation toward the recording electrode, and negative deflections (QS complexes) are generated by propagation away from the electrode ( Figs. 5.2 and 5.3 ). If a recording electrode is at the source from which all wavefronts propagate (at the site of initial activation), depolarization will produce a wavefront that spreads away from the electrode, thus generating a monophasic QS complex.
It is important to recognize that a QS complex can be recorded when the mapping electrode is floating in the cavity and not in contact with the myocardium. In that situation, the initial negative slope of the recording is typically slow, suggesting that the electrogram is a far-field signal, generated by tissue at some distance from the recording electrode.
Filtering at higher corner frequencies (e.g., 30 Hz) alters the morphology of the signal, so that the morphology of the unipolar electrogram is no longer indicative of the direction of wavefront propagation, and the presence or absence of a QS complex cannot be used to infer proximity to the site of earliest activation ( Fig. 5.4 ).
Advantages of unipolar recordings.
One important value of unipolar recordings is that they provide a more precise measurement of the timing of local activation. This is true for filtered and unfiltered unipolar electrograms. In addition, unfiltered unipolar recordings provide information about the direction of impulse propagation. Furthermore, unipolar recordings allow pacing and recording at the same location while eliminating a possible anodal contribution to depolarization that is sometimes seen with bipolar pacing at high output. This generally facilitates the use of other mapping modalities—namely pace mapping.
Disadvantages of unipolar recordings.
The major disadvantage of unipolar recordings is that they have poor signal-to-noise ratio and contain substantial far-field signal generated by depolarization of tissue remote from the recording electrode. Therefore distant activity can be difficult to separate from local activity. This is especially true when recording from areas of prior myocardial infarction (MI), where the fractionated ventricular potentials are ubiquitous, and it is often impossible to select a rapid negative dV/dt when the entire QS potential is slowly inscribed—that is, cavity potential. Furthermore, a QS electrogram configuration has a low spatial resolution and relatively low specificity, being attainable in an area of more than 1 cm in diameter from the real site of origin of the arrhythmia or when the exploring electrode has poor contact with the myocardium. Another disadvantage is the inability to record an undisturbed electrogram during or immediately after pacing. This is a significant disadvantage when entrainment mapping is to be performed during activation mapping because the recording of the return tachycardia complex on the pacing electrode immediately after cessation of pacing is required to interpret entrainment mapping results. There is also some baseline drift of the unipolar recording in some recording systems that makes interpretation difficult.
Bipolar Recordings
Timing of local activation.
Algorithms for detecting local activation time from bipolar electrograms have been more problematic, partly because of generation of the bipolar electrogram by two spatially separated recording poles. In a homogeneous sheet of tissue, the initial peak of a filtered (30 to 300 Hz) bipolar signal coincides with depolarization beneath the recording electrode and appears to correlate most consistently with local activation time, corresponding to the maximal negative dV/dt of the unipolar recording (see Fig. 5.3 ).
A bipolar electrogram is the sum of two unipolar electrograms with a time delay due to the interelectrode distance. When a bipolar electrogram with an interelectrode distance is recorded in a homogeneous sheet of tissue, activation time delay between the two poles is usually minimal. In the setting of inhomogeneous conduction, however, a significant time delay can exist between two unipolar electrograms, resulting in a fractionated electrogram when converted to a bipolar electrogram ( Figs. 5.5 and 5.6 ).
In the setting of complex multicomponent bipolar electrograms, such as those with marked fractionation and prolonged duration seen in regions with complex conduction patterns (e.g., in regions of slow conduction in macroreentrant atrial tachycardia [AT] or ventricular tachycardia [VT]), determination of local activation time becomes challenging, and the decision about which activation time is most appropriate needs to be made in the context of the particular rhythm being mapped. Therefore, during mapping procedures, the onset (rather than the peak or nadir) of high-frequency components of a local bipolar electrogram is often used because it is easier to determine reproducibly, especially when measuring heavily fractionated, low-amplitude local electrograms. The onset of the bipolar electrogram likely precedes the maximal −dV/dt in unipolar electrogram by 15 to 30 milliseconds.
To acquire true local electrical activity, a bipolar electrogram with an interelectrode distance of less than 1 cm is desirable. Smaller interelectrode distances record increasingly local events (as opposed to far-field). Elimination of far-field noise is usually accomplished by filtering the intracardiac electrograms, typically at 30 to 500 Hz.
Direction of local activation.
The morphology and amplitude of bipolar electrograms are influenced by many factors, including (1) the orientation of the bipolar recording axis to the direction of propagation of the activation wavefront; (2) electrode size; (3) interelectrode distance; (4) electrode-tissue contact (i.e., the distance between the source of the potential and the recording electrode); (5) anisotropic conduction; and (6) intrinsic characteristics of the recorded medium (e.g., normal myocardial tissue versus scar). A wavefront that is propagating in the direction exactly perpendicular to the axis of the recording dipole produces no difference in potential between the electrodes and hence no signal.
Although the direction of wavefront propagation cannot be reliably inferred from the morphology of the bipolar signal, a change in morphology can provide important clues about the activation pattern of the propagating wavefront. The change in polarity in bipolar electrograms recorded across an ablation line is consistent with complete line conduction block. For example, when recording from the lateral aspect of the cavotricuspid isthmus (CTI) during pacing from the coronary sinus (CS), a reversal in the bipolar electrogram polarity from positive to negative at the ablation line indicates complete isthmus block. Similarly, if bipolar recordings are obtained with the same catheter orientation parallel to the atrioventricular (AV) annulus during retrograde bypass tract (BT) conduction, an RS configuration electrogram will be present on one side of the BT, where the wavefront is propagating from the distal electrode toward the proximal electrode, and a QR morphology electrogram will be present on the other side, where the wavefront is propagating from the proximal electrode toward the distal electrode ( eFig. 5.1 ).
Furthermore, the “bipolar” electrogram can be considered as a “mini-unipolar” recording with the proximal electrode simulating the indifferent remote electrode in the unipolar electrogram configuration, and thus the bipolar electrogram morphology may also be helpful in localizing the site of origin of focal arrhythmias. Hence, when the distal electrode of the mapping catheter is positioned at the site of origin of a focal tachycardia (e.g., premature ventricular contractions [PVCs]), an early negative deflection in the initial component of the bipolar electrogram reflects the wavefront propagation opposite to the recording dipole vector (i.e., depolarization reaches electrode 1 before electrode 2). A recent report found that a negative concordance in the initial forces of both unipolar and bipolar electrograms (in addition to the electrogram temporal relationship assessment) may be considered a reliable criterion to identify the site of origin of focal ventricular arrhythmias.
Advantages of bipolar recordings.
Bipolar recordings provide an improved signal-to-noise ratio. In addition, high-frequency components are more accurately seen, which facilitates the identification of local depolarization, especially in abnormal areas of infarction or scar.
Disadvantages of bipolar recordings.
In contrast to unipolar signals, the direction of wavefront propagation cannot be reliably inferred from the morphology of a single bipolar signal; however, with two adjacent bipolar recordings, the recording that occurs first is closer to the wavefront source. Furthermore, bipolar recordings do not allow simultaneous pacing and recording from the same location. To pace and record simultaneously in bipolar fashion at endocardial sites as close together as possible, electrodes 1 and 3 of the mapping catheter are used for bipolar pacing, and electrodes 2 and 4 are used for recording. The precision of locating the source of a particular electrical signal depends on the distance between the recording electrodes, because the signal of interest can be beneath the distal or proximal electrode (or both) of the recording pair.
Mapping Procedure
Several factors are important for the success of activation mapping, including inducibility of tachycardia at the time of electrophysiology (EP) testing, hemodynamic stability of the tachycardia, and stable tachycardia morphology. In addition, determinations of an electrical reference point, of the mechanism of the tachycardia (focal vs. macroreentrant), and subsequently of the goal of mapping are essential prerequisites.
Selection of the Electrical Reference Point
Local activation times must be relative to some external and consistent fiducial marker (such as the onset of the P wave or QRS complex on the surface ECG) or a reference intracardiac electrode. For VT, the QRS complex onset should be assessed using all surface ECG leads to search for the lead with the earliest QRS onset. This lead should then be used for subsequent activation mapping. Similarly, the P wave during AT should be assessed using multiple ECG leads, choosing the one with the earliest P onset. However, determining the onset of the P wave can be impossible if the preceding T wave or QRS is superimposed. To facilitate visualization of the P wave, a ventricular extrastimulus (VES) or a train of ventricular pacing can be delivered to anticipate ventricular activation and repolarization and permit careful distinction of the P wave onset ( Fig. 5.7 ). After determining P wave onset, a surrogate marker, such as right atrial (RA) or CS electrogram indexed to the P wave onset, where it is clearly seen, can be used rather than the P wave onset.
Defining the Goal of Mapping
Determination of the mechanism of the tachycardia (focal vs. macroreentrant) is essential to define the goal of activation mapping. For focal tachycardias, activation mapping entails localizing the site of origin of the tachycardia focus. This is reflected by the earliest presystolic activity that precedes the onset of the P wave (during focal AT) or QRS (during focal VT) by an average of 10 to 40 milliseconds because only this short amount of time is required after the focus discharges to activate enough myocardium and begin generating a P wave or QRS complex ( Fig. 5.8 ). For mapping macroreentrant tachycardias, the goal of mapping is identification of the critical isthmus of the reentrant circuit, as indicated by finding the site with a continuous activity spanning diastole or with an isolated mid-diastolic potential (see Fig. 5.8 ). One caveat is that focal tachycardias can occur in patients with scar, and the focus can be imbedded in scar tissue; in this setting, propagation from the source to a site at which enough atrium (or ventricle) is activated to generate a P (or QRS complex) can be significantly delayed, such that the timing of the earliest site may be considerably longer than 50 milliseconds.
Epicardial Versus Endocardial Mapping
Activation mapping is predominantly performed endocardially. Occasionally, epicardial mapping is required because of an inability to ablate some VTs, ATs, or AV BTs by using the endocardial approach. Limited epicardial mapping can be performed with special recording catheters that can be steered in the branches of the CS. This technique has been used for mapping VTs and AV BTs, but its scope is limited by the anatomy of the coronary venous system.
A more common epicardial mapping technique utilizes the subxiphoid percutaneous approach for accessing the epicardial surface. This technique has become an important adjunctive strategy to ablate a diverse range of cardiac arrhythmias, especially in patients with scar-related VT, in whom more reentrant circuits with vulnerable isthmuses are on the epicardial surface. The same fundamental principles of activation mapping are used for both endocardial mapping and epicardial mapping.
Mapping Catheters
The simplest form of mapping is achieved by moving the mapping catheter sequentially to sample various points of interest on the endocardium to measure local activation. The precision of locating the source of a particular electrical signal depends on the distance between the recording electrodes on the mapping catheter. For ablation procedures, recordings between adjacent electrode pairs are commonly used (e.g., between electrodes 1 and 2, 2 and 3, and 3 and 4), with 1- to 5-mm interelectrode spacing. In some studies, wider bipolar recordings (e.g., between electrodes 1 and 3 and 2 and 4) have been used to provide an overlapping field of view. For bipolar recordings, the signal of interest can be beneath the distal or the proximal electrode of the recording pair. As noted, this is germane in that ablation energy can be delivered only from the distal (tip) electrode ( Fig. 5.9 ). Because of this, many operators display the unipolar recordings from each component of the distal bipole, in order to determine which electrode is actually recording the earliest activity.
Mapping Focal Tachycardias
The goal of activation mapping of focal-appearing tachycardias (automatic, triggered activity, or microreentrant) is identifying the site of origin, defined as the site with the earliest presystolic bipolar recording in which the distal electrode shows the earliest intrinsic deflection and QS unipolar electrogram configuration ( Figs. 5.10 and 5.11 ). Local activation at the site of origin precedes the onset of the tachycardia complex on the surface ECG by an average of 10 to 40 milliseconds. Earlier electrograms occurring in mid-diastole, as in the setting of macroreentrant tachycardias, are not expected and do not constitute a target for mapping.
Endocardial activation mapping of focal tachycardias can trace the origin of activation to a specific area, from which it spreads centrifugally. There is generally an electrically silent period in the tachycardia cycle length (TCL) that is reflected on the surface ECG by an isoelectric line between tachycardia complexes. Intracardiac mapping shows significant portions of the TCL without recorded electrical activity, even when recording from the entire cardiac chamber of tachycardia origin. However, in the presence of complex intramyocardial conduction disturbances, activation during focal tachycardias can extend over a large proportion of the TCL, and conduction spread can follow circular patterns suggestive of macroreentrant activation.
Technique of activation mapping of focal tachycardias.
Initially one should seek the general region of the origin of the tachycardia as indicated by the surface ECG. In the EP laboratory, additional data can be obtained by placing a limited number of catheters within the heart in addition to the mapping catheter or catheters; these catheters are frequently placed at the right ventricle (RV) apex, His bundle region, high RA, and CS. During initial arrhythmia evaluation, recording from this limited number of sites allows a rough estimation of the site of interest. Mapping simultaneously from as many sites as possible greatly enhances the precision, detail, and speed of identifying regions of interest.
Subsequently, a single mapping catheter is moved under fluoroscopic guidance over the endocardium of the chamber of interest to sample bipolar signals. Using standard equipment, mapping a tachycardia requires recording and mapping performed at several sites, based on the ability of the investigator to recognize the mapping sites of interest from the morphology of the tachycardia on the surface ECG and baseline intracardiac recordings.
Local activation time is then determined from the filtered (30 to 300 Hz) bipolar signal recorded from the distal electrode pair on the mapping catheter; this time is determined and compared with the timing reference (fiducial point). Activation times are generally measured from the onset of the first rapid deflection of the bipolar electrogram to the onset of the tachycardia complex on the surface ECG or surrogate marker (see Fig. 5.7 ). Using the onset (rather than the peak or nadir) of a local bipolar electrogram is often preferable because it is easier to determine reproducibly, especially when measuring heavily fractionated, low-amplitude local electrograms.
Once an area of relatively early local activation is found, small movements of the catheter tip in the general target region are undertaken until the site is identified with the earliest possible local activation relative to the tachycardia complex. Recording from multiple bipolar pairs from a multipolar electrode catheter is helpful in that if the proximal pair has a more attractive electrogram than the distal, the catheter may be withdrawn slightly to achieve the same position with the distal electrode.
Once the site with the earliest bipolar signal is identified, the unipolar signal from the distal ablation electrode should be used to supplement bipolar mapping. The unfiltered (0.05 to 300 Hz) unipolar signal morphology should show a monophasic QS complex with a rapid negative deflection if the site was at the origin of impulse formation (see Figs. 5.10 and 5.11 ). However, the size of the area from which a QS complex can be larger than the tachycardia focus, exceeding 1 cm in diameter. Thus a QS complex should not be the only mapping finding used to guide ablation. Successful ablation is unusual, however, at sites with an RS complex on the unipolar recording because these are generally distant from the focus (see Fig. 5.2 ). Concordance of the timing of the onset of the bipolar electrogram with that of the filtered or unfiltered unipolar electrogram (with the rapid downslope of the S wave of the unipolar QS complex coinciding with the initial peak of the bipolar signal) helps ensure that the tip electrode, which is the ablation electrode, is responsible for the early component of the bipolar electrogram. A tissue contact force measuring 10 to 20 g, as well as the presence of slight ST elevation on the unipolar recording and the ability to capture the site with unipolar pacing, are used to indicate good electrode-tissue contact.
Furthermore, a negative concordance of the vector of the initial (first 20 milliseconds) forces of both unipolar and bipolar electrograms (both being negative deflections), in conjunction with electrogram temporal relationship assessment, further improves the accuracy of conventional mapping to localize the site of origin of PVCs ( Fig. 5.12 ). In a recent report, the presence of this criterion (“negative concordance”) at sites fulfilling other conventional criteria used to guide focal PVC ablation highly predicted the acute success rate of radiofrequency ablation with a sensitivity and specificity of 94% and 95%, respectively. Furthermore, its positive predictive value was significantly superior to those of all other conventional criteria (76% vs. 33% to 43%).
Mapping Macroreentrant Tachycardias
The main goal of activation mapping of macroreentrant tachycardias (e.g., post-MI VT, macroreentrant AT) is identification of the isthmus critical for maintenance of the macroreentrant circuit. The site of origin of a tachycardia is the source of electrical activity producing the tachycardia complex; although this is a discrete site of impulse formation in focal rhythms, during macroreentry it can represent the exit site from the diastolic pathway (i.e., from the critical isthmus of the reentrant circuit) to the myocardium that gives rise to the ECG deflection. During macroreentry, an isthmus is defined as a corridor of conductive myocardial tissue bounded by nonconductive tissue (barriers) through which the depolarization wavefront must propagate to perpetuate the tachycardia. These barriers can be scar areas or naturally occurring anatomical or functional (present only during tachycardia, but not in sinus rhythm) obstacles. The earliest presystolic electrogram closest to mid-diastole is the most commonly used definition for the site of origin of the reentrant circuit. However, recording continuous diastolic activity or bridging of diastole at adjacent sites, or mapping a discrete diastolic pathway, is more specific. Therefore the goal of activation mapping during macroreentry is finding the site, or sites, with continuous electrical activity spanning diastole or with an isolated mid-diastolic potential; once such a site has been located, further testing should be done to ensure that the tissue generating that electrogram is in fact integral to the tachycardia rather than a bystander. Unlike focal tachycardias, a presystolic electrogram preceding the tachycardia complex by 10 to 40 milliseconds is not adequate in defining the site of origin of a macroreentrant tachycardia (see Figs. 5.8, 5.13, and 5.14 ).
However, identification of critical isthmuses is often challenging. The abnormal area of scarring, where the isthmus is located, is frequently large and contains side branch pathways (bystanders) that confound mapping. In addition, multiple potential reentry circuits can be present, giving rise to multiple different tachycardias in a single patient. Furthermore, in abnormal regions such as infarct scars, the tissue beneath the recording electrode can be small relative to the surrounding myocardium outside the scar; thus a large far-field signal can obscure the small local potential. For this reason, bipolar recordings are preferred in scar-related VTs because the noise is removed and high-frequency components are more accurately seen. Unipolar recordings are usually of little help when mapping arrhythmias associated with regions of scar, unless the recordings are filtered to remove far-field signal; even so, signal amplitude in the unipolar recording is often extremely small and may be difficult to distinguish from noise. Much of the far-field signal in a unipolar recording consists of lower frequencies than the signal generated by local depolarization because the high-frequency content of a signal diminishes more rapidly with distance from the source than the low-frequency content. Therefore high-pass filtering of unipolar signals (at 30 or 100 Hz) is generally used when mapping scar-related arrhythmias to reduce the far-field signal and improve detection of lower amplitude local signals from abnormal regions.
Although activation mapping alone is usually inadequate for defining the critical isthmus of a macroreentrant tachycardia, it can help guide other mapping modalities (e.g., entrainment or pace mapping, or both) to the approximate region of the isthmus.
Continuous electrical activity.
Theoretically, if reentry were the mechanism of the tachycardia, electrical activity should occur throughout the tachycardia cycle. For example, in macroreentrant AT, the recorded electrical activity at different locations in the atrium should span the TCL (see Fig. 5.13 ).
For macroreentrant VT, conduction during diastole is extremely slow and is in a small area so that it is not recorded on the surface ECG. The QRS complex is caused by propagation of the wavefront from the exit of the circuit from that isthmus to the surrounding myocardium. After leaving the exit of the isthmus, the circulating wavefront propagates through a broad path (loop) along the border of the scar, back to the entrance of the isthmus (see Fig. 5.8 ). Continuous diastolic activity is likely to be recorded only if the bipolar pair records from a small circuit; if a large circuit is present (i.e., the reentrant circuit is larger than the recording area of the catheter, or the catheter is not covering the entire circuit), non-holodiastolic activity will be recorded. In such circuits, repositioning of the catheter to other sites may allow visualization of what is termed bridging of diastole ; electrical activity in these adjacent sites spans diastole.
All areas from which diastolic activity is recorded are not necessarily part of the reentrant circuit. Such sites can reflect late activation of sites that may not be related to the tachycardia circuit. Analysis of the response of these electrograms to spontaneous or induced changes in TCL is critical in deciding their relationship to the tachycardia mechanism. In addition, electrical signals that come and go throughout diastole should not be considered continuous ( eFig. 5.2 ). For continuous activity to be consistent with reentry, it must be demonstrated that such electrical activity is required for initiation and maintenance of the tachycardia, so that termination of the continuous activity, either spontaneously or following stimulation, without affecting the tachycardia, would exclude such continuous activity as requisite for sustaining the tachycardia. It is also important to verify that an electrogram that extends throughout diastole is not just a broad electrogram whose duration equals the TCL. This can be achieved by analyzing the local electrogram during pacing at a pacing cycle length (PCL) comparable to TCL; if pacing produces continuous diastolic activity in the absence of tachycardia, the continuous electrogram may have no mechanistic significance. Furthermore, the continuous activity should be recorded from a circumscribed area, and motion artifact should be excluded.
Mid-diastolic activity.
An isolated mid-diastolic potential is defined as a low-amplitude, high-frequency diastolic potential separated from the preceding and subsequent electrograms by an isoelectric segment ( Fig. 5.15 ). Sometimes these discrete potentials provide information that defines a diastolic pathway, which is believed to be generated from a narrow isthmus of conduction critical to the reentrant circuit. Localization of this pathway is critical for guiding catheter-based ablation.
Detailed mapping usually reveals more than one site of presystolic activity, and mid-diastolic potentials can be recorded from bystander sites attached to the isthmus. Therefore, regardless of where in diastole the presystolic electrogram occurs (early, middle, or late), its timing and appearance on initiation of the tachycardia, although necessary, does not confirm its relevance to the tachycardia mechanism. One must always confirm that the electrogram is required to maintain, and cannot be dissociated from, the tachycardia. Thus, during spontaneous changes in the TCL or those produced by programmed stimulation, the electrogram, regardless of its timing in diastole, should show a fixed relationship with the subsequent tachycardia complex (and not the preceding one). Very early diastolic potentials (in the first half of diastole) can represent an area of slow conduction at the entrance of a protected isthmus. These potentials remain fixed to the prior tachycardia complex (exit site from the isthmus), and a delay between this complex and the subsequent tachycardia complex would reflect a delay in entering or propagating through the protected diastolic pathway. Although such potentials that are related to the prior QRS complex can in fact be integral to the tachycardia (e.g., if the variability in cycle length [CL] is due to varying delay in the diastolic corridor “downstream” from the recording site), this is not guaranteed as it is when the electrogram is tightly related to the subsequent QRS complex.
If after very detailed mapping the earliest recorded site is not at least 50 milliseconds presystolic, this suggests that the map is inadequate (most common), the mechanism of tachycardia is not macroreentry, or the diastolic corridor is deeper than the subendocardium (in the midmyocardium or subepicardium).
Limitations
Standard catheter endocardial mapping, as performed in the EP laboratory, is limited by the number, size, and type of electrodes that can be placed within the heart. Therefore these methods do not simultaneously cover a vast area of the endocardial surface. Time-consuming, point-by-point maneuvering of the catheter is required to trace the origin of an arrhythmic event and its activation sequence in the neighboring areas.
The success of roving point mapping depends on the sequential beat-by-beat stability of the activation sequence being mapped and the ability of the patient to tolerate sustained arrhythmia. Therefore it can be difficult to perform activation mapping in poorly inducible tachycardias, in hemodynamically unstable tachycardias, and in tachycardias with unstable morphology. Sometimes poorly tolerated rapid tachycardias can be slowed by antiarrhythmic agents to allow for mapping. Alternatively, mapping can be facilitated by starting and stopping the tachycardia after data acquisition at each site. In addition, newer techniques (e.g., basket catheter, electroanatomic mapping, and noncontact mapping) can facilitate activation mapping in these cases by simultaneous multipoint mapping.
Although activation mapping is adequate for defining the site of origin of focal tachycardias, it is insufficient by itself in defining the critical isthmus of macroreentrant tachycardias, and adjunctive mapping modalities (e.g., entrainment mapping, pace mapping) are required. Moreover, the laborious process of precise mapping with conventional techniques can expose the electrophysiologist, staff, and patient to undesirable levels of radiation from the extended fluoroscopy time.
Using conventional activation mapping techniques, it is difficult to conceive the three-dimensional orientation of cardiac structures because a limited number of recording electrodes guided by fluoroscopy is used. Although catheters using multiple electrodes to acquire data points are available, the exact location of an acquired unit of EP data is difficult to ascertain because of inaccurate delineation of the location of anatomical structures. The inability to accurately associate the intracardiac electrogram with a specific endocardial site accurately also limits the reliability with which the roving catheter tip can be placed at a site that was previously mapped. This results in limitations when the creation of long linear ablation lesions is required to modify the substrate, as well as when multiple isthmuses or channels are present. The inability to identify, for example, the site of a previous ablation increases the risk of repeated ablation of areas already dealt with and the likelihood that new sites can be missed.
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