Conventional Intracardiac Mapping Techniques

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Chapter 5 Conventional Intracardiac Mapping Techniques

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. 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 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. Additionally, electrogram morphology can be of significant importance during mapping. Interpretation of recorded electrograms is fundamental to the clinical investigation of arrhythmias during electrophysiological (EP) studies. Establishing electrogram criteria, which permit accurate determination of the moment of myocardial activation at the recording electrode, is critical for 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. The differences in unipolar and bipolar recordings can be used to assist in mapping by simultaneously recording bipolar and unipolar signals from the mapping catheter.1

Unipolar Recordings

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 also important to recognize that a QS complex can be recorded when the mapping electrode is not in contact with the myocardium, but is floating in the cavity. 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 some distance from the recording electrode.1 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 an indication 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).2

Bipolar Recordings

Direction of Local Activation

The morphology and amplitude of bipolar electrograms are influenced by the orientation of the bipolar recording axis to the direction of propagation of the activation wavefront. 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.1,2 However, the direction of wavefront propagation cannot be reliably inferred from the morphology of the bipolar signal, although a change in morphology can be a useful finding. For example, when recording from the lateral aspect of the cavotricuspid isthmus 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 (Fig. 5-5).

Mapping Procedure

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 and 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. 5-6). After determining P wave onset, a surrogate marker, such as a 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 versus 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. 5-7). 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. 5-7).

Mapping Focal Tachycardias

The goal of activation mapping of focal 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. 5-8 and 5-9). 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.1

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 (CL) that is reflected on the surface ECG by an isoelectric line between tachycardia complexes. Intracardiac mapping shows significant portions of the tachycardia CL 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 tachycardia CL, and conduction spread can follow circular patterns suggestive of macroreentrant activation.2,4

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 ventricular 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.1

Subsequently, a single mapping catheter is moved under the guidance of fluoroscopy 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). The distal pole of the mapping catheter should be used for mapping the earliest activation site because it is the pole through which RF energy is delivered. 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. 5-6). Using the onset (rather than the peak or nadir) of a local bipolar electrogram is preferable because it is easier to determine reproducibly, especially when measuring heavily fractionated, low-amplitude local electrograms.4

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.2 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. 5-8 and 5-9). However, the size of the area with 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. The presence of ST elevation on the unipolar recording and the ability to capture the site with unipolar pacing are used to indicate good electrode-tissue contact.4

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 the macroreentrant circuit.8 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 represents 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 both, 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 activity spanning diastole or with an isolated mid-diastolic potential. 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 (Figs. 5-10 and 5-11; see also Fig. 5-7).2,4

However, identification of critical isthmuses is often challenging. The abnormal area of scarring, where the isthmus is located, is frequently large and contains false isthmuses (bystanders) that confound mapping. Additionally, 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, despite the limitations of bipolar recordings, these 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. 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.1

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.4,8