CLINICAL RESEARCH
Substrate Mapping to Detect Abnormal Atrial Endocardium With Slow Conduction in Patients With Atypical Right Atrial Flutter
Jin Long Huang, MD, PhD*, ,
Ching-Tai Tai, MD*, ,
Yenn-Jiang Lin, MD*,,
Bien-Hsien Huang, MD*,,
Kun-Tai Lee, MD*,,
Satoshi Higa, MD*,,
Yoga Yuniadi, MD*,,
Yi-Jen Chen, MD, PhD*,,
Shih-Lin Chang, MD*,,
Li-Wei Lo, MD*,,
Wanwarang Wongcharoen, MD*,,
Chih-Tai Ting, MD, PhD*, and
Shih-Ann Chen, MD*,,*
* Institute of Clinical Medicine and Cardiovascular Research Institute, National Yang-Ming University, Taipei, Taiwan
Cardiovascular Center, Taichung Veterans General Hospital, Taichung, Taiwan
Division of Cardiology, Department of Medicine, Veterans General Hospital-Taipei, Taipei, Taiwan
Manuscript received January 6, 2006;
revised manuscript received March 3, 2006,
accepted March 8, 2006.
* Reprint requests and correspondence: Dr. Shih-Ann Chen, Division of Cardiology, Veterans General Hospital-Taipei, 201 Sec. 2, Shih-Pai Road, Taipei, Taiwan (Email: epsachen{at}ms41.hinet.net).
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Abstract
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OBJECTIVES: The purpose of this study was to investigate the relationship between the abnormal substrate and peak negative voltage (PNV) in the right atrium (RA) with atypical flutter.
BACKGROUND: The impact of a local abnormally low voltage electrogram on the local activation pattern and velocity of atrial flutter (AFL) remains unclear.
METHODS: Twelve patients with clinically documented AFL were included to undergo noncontact mapping of the RA. The atrial substrate was characterized by the: 1) activation mapping; 2) high-density voltage mapping; and 3) conduction velocity along the flutter re-entrant circuit. The normalized PNV (i.e., the relative ratio to the maximal PNV) in each virtual electrode recording was used to produce the voltage maps of the entire chamber. The protected isthmus was bordered by low voltage zones.
RESULTS: Atypical AFL of the RA was induced by atrial pacing in 12 patients, including 10 upper loop re-entry and 2 RA free wall re-entry flutter. These protected isthmuses were located near the crista terminalis. The mean width of the protected isthmus was 1.7 ± 0.3 cm and mean voltage at the isthmus was –0.91 ± 0.39 mV. The conduction velocities within these paths were significantly slower than outside the path (0.30 ± 0.18 m/s vs. 1.14 ± 0.41 m/s, respectively; p = 0.004). The ratiometric PNV of 37.6% of the maximal PNV had the best cut-off value to predict slow conduction, with a high sensitivity (92.3%) and specificity (85.7%).
CONCLUSIONS: Characterization of the RA substrate in terms of the unipolar PNV is an effective predictor of the slow conduction path within the critical isthmus of the re-entrant circuit.
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Abbreviations and Acronyms
| | AFL = atrial flutter | | CS = coronary sinus | | CTI = cavotricuspid isthmus | | LAL = low anterolateral | | LVZ = low voltage zone | | MEA = multielectrode array | | NCM = noncontact mapping | | PNV = peak negative voltage | | RA = right atrium | | 3D = 3-dimensional |
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The understanding of the relationship between voltage mapping and myocardial disease is based on the investigation of the animal and human infarction models. These studies indicated that regions of a contiguous reduction in the electrogram voltage represented the diseased myocardium (1–3). Our laboratory demonstrated that high-density unipolar voltage mapping offered a unique electrophysiologic description of the atrial substrate in patients with atrial flutter (AFL) (4). However, the impact of the local abnormally low electrogram voltage on the local activation pattern and velocity remains unclear. Therefore, the present study investigated the relationship between the conduction delay and abnormal substrate detected by the high-density noncontact unipolar peak negative voltage (PNV) in the right atrium (RA) with atypical AFL.
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Methods
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Patient population.
Between July 2002 and March 2004, 12 patients (6 men, age 66 ± 15 years, range 32 to 80 years) with clinically documented atypical AFL were included in this study. None of the patients had a previous history of an RA atriotomy. Six patients had cardiovascular disease, including 6 with hypertension, 2 with hypertrophic cardiomyopathy, and 1 with coronary artery disease.
Electrophysiologic study.
All patients were studied in the postabsorptive nonsedated state after giving written informed consent to the electrophysiologic study and catheter ablation, and the details of the noncontact mapping study were explained to all patients. All antiarrhythmic drugs were discontinued for >5 half-lives. In all patients, three multipolar electrode catheters (Daig Corp., Minnetonka, Minnesota) were positioned, respectively, in the high RA, His-bundle area, and right ventricle via the femoral veins. A 7-F deflectable decapolar catheter with 5 pairs of electrodes separated by 5 mm and an interelectrode spacing of 2 mm (Daig Corp.) was also inserted into the coronary sinus (CS) via the internal jugular vein. The position of the proximal electrode pair at the ostium of the CS was confirmed with a contrast injection. In the patients with AFL, a 7-F 20-pole deflectable Halo catheter with 10 mm paired spacing (Cordis-Webster, Baldwin Park, California) was positioned around the tricuspid annulus to simultaneously record the RA activation in the lateral wall and the lower RA isthmus simultaneously. A 9-F sheath placed in the left femoral vein was used to introduce the noncontact mapping catheter. All patients presented into the laboratory in sinus rhythm. The techniques used to induce different types of tachycardias in our laboratory have been described previously (4–11). Conventional multicatheter mapping and noncontact mapping of the RA were performed simultaneously during sinus rhythm, atrial pacing (the low anterolateral [LAL] wall and CS ostium with cycle lengths of 500 and 300 ms), and the tachycardia.
Noncontact mapping (NCM) system.
The use of NCM system in our laboratory has been previously described in detail (4–11). In brief; the system consisted of a catheter (9-F) with a multielectrode array (MEA) surrounding a 7.5-ml balloon mounted at the distal end. Raw data detected by the MEA was amplified and digitally transferred to a computer workstation.
The MEA catheter was deployed in the RA over a 0.035-inch guidewire, which was advanced 5 cm into the superior vena cava. The system located the 3-dimensional (3D) position of the electrodes on any desired catheter relative to the MEA using a navigation signal. Navigation provided the means to define a model of the chamber anatomy and to track the position of standard contact catheters within the chamber relative to labeled points of interest, such as anatomic structures or critical zones of conduction. Simultaneous virtual unipolar electrograms were mathematically reconstructed and displayed on the anatomic model, producing isopotential or isochronal color maps. Signals for both electrograms were filtered with a bandwidth of 2 to 300 Hz. Virtual electrograms could also be selected and displayed from any site of interest on the anatomic model using the mouse pointer.
Atrial substrate analysis.
The atrial substrate was characterized by the: 1) activation mapping; 2) high-density voltage mapping; and 3) conduction velocity along the flutter re-entrant circuit, using the NCM system (EnSite 3000 System, ESI, St. Paul, Minnesota). The details of these measurements have been previously described (4–11).
Activation mapping
Activation mapping was performed during atypical AFL. During a review of the recorded data during the tachycardia, we began the analysis with a default high-pass filter setting of 2 Hz to preserve the components of the slow conduction on the isopotential map. Color settings were adjusted so that the color range matched 1:1 with the millivolt range of the electrogram deflection of interest. We also interactively placed virtual electrodes on the map's color contours to analyze the corresponding unipolar virtual electrograms. Occasionally, conduction through gaps in a line of block was sufficiently slow that we moved the high-pass filter down to 1.0 to 0.5 Hz. If the atrial electrograms overlapped with the T wave, we delivered ventricular extrastimuli to block 1 ventricular beat and eliminate the associated QRS and T waves. This typically revealed more than 1 full cycle of the re-entrant circuit without far-field interference (8,9).
High-density voltage mapping
In this study, the mean voltage of the global RA was analyzed from the negative portion of the unipolar electrograms, which were obtained simultaneously from 256 virtual mapping sites equally distributed throughout the RA; off-line software was used to analyze the voltage data (4). The normalized PNV (i.e., the relative ratio to the maximal PNV) in each virtual electrogram was used to produce the voltage maps of the entire chamber (Fig. 1). The protected isthmus was bordered by the low-voltage zones (LVZs). At the border, the convergence of voltage lines was observed (Fig. 2). Once the protected isthmus was found, concealed entrainment pacing was performed to further prove the isthmus in the re-entry circuit. The post pacing interval was defined as the time interval from the last stimulus artifact to the beginning of the first rapid electrogram deflection of the first tachycardia cycle after cessation of the pacing (12).
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Figure 1 Definition of a normalized low-voltage zone: ratio of the local peak negative voltage (PNV) of the unipolar electrogram to the maximal PNV of a selected atrial cycle of the entire right atrium.
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Figure 2 A schematic example of the protected isthmus bordered by the low-voltage zones (LVZs). Convergence of a voltage gradient was found on both sides of the isthmus.
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Conduction velocity
The conduction velocity was also analyzed along the re-entrant circuit of the atypical AFL. The NCM system displayed the Cartesian coordinates relative to the MEA center of points on the virtual endocardium. Therefore, we calculated the distance between two points using the mathematical formula:
where: d = distance
x1, y1, z1 = the Cartesian coordinates at 3D surface point 1
x2, y2, z2 = the Cartesian coordinates at 3D surface point 2
The time it took the wavefront to pass across a distance was determined by observing the propagation of the leading edge of the wavefront on the isopotential map and confirmed by the time interval between the fastest down slope (maximum – dV/dt) of the electrograms at the start and end of the distance measured. The conduction velocity was measured within the path of the protected isthmus and outside of the isthmus, respectively.
Ablation strategy and defining the protected isthmus.
We identified the critical isthmus in the RA via activation mapping and guided the radiofrequency ablation (8,9), for which we used a 4-mm electrode-tipped ablation catheter connected to an EPT-1000 generator (Boston Scientific Corp., Natick, Massachusetts). Sequential point-by-point energy applications (50 W, 50°C to 55°C, 20 to 40 s) were performed to produce a linear lesion. The conduction block of the protected isthmus was confirmed with atrial pacing from the LAL wall and CS ostium. Successful ablation was defined as termination and noninducibility of the targeted tachycardia.
Statistical analysis.
All continuous data were presented as the mean value ± standard deviation. Comparisons of the parametric data (voltage data inside and outside isthmus) were made by paired Student t test and nonparametric data (conduction velocity inside and outside isthmus) by Mann-Whitney rank test. Receiver-operating characteristic (ROC) curves were constructed to identify the optimal decision threshold for the slow conduction zone in the derivation sets (a fixed PNV or normalized voltage), defined as the value on the ROC curve with the best sensitivity-specificity trade-off. A p value of <0.05 was considered to be statistically significant.
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Results
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Atrial substrate analysis.
Activation and voltage mapping
Before the induction of the AFL, NCM revealed slow preferential conduction paths through LVZs in the posterolateral RA in all patients. Atypical AFL in the RA was clinically documented and inducible by atrial pacing in 12 patients, including 10 patients with upper loop re-entry (Fig. 3) and 2 patients with RA free wall re-entry flutter. The wavefronts passing through the cavotricuspid isthmus (CTI) were bystanders and did not involve the atypical AFL circuits. The mean conduction velocity of CTI was 0.86 ± 0.43 m/s. The mean cycle length of the AFL was 200 ± 45 ms. Forty-eight rhythms were retrospectively analyzed from the RA (all 4 rhythm types, including sinus rhythm, atrial pacing from the CS ostium and the LAL wall, and AFL in each of 12 patients). These isthmuses were located predominantly near the region of the crista terminalis (Fig. 4). During atypical AFL, the wavefront passed through the same preferential path with a local fragmented electrogram, indicating slow conduction. Concealed entrainment could be obtained at the isthmus with a post-pacing interval within the tachycardia cycle length +20 ms in all patients.
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Figure 3 Voltage maps (A), isopotential maps (B), and unipolar electrograms along the re-entry circuit (C) in a patient with atypical flutter. (A) Normalized peak negative voltage (PNV) distribution of the right atrium (RA) in a posterolateral view. Note that the protected isthmus was found between 2 low voltage zone (LVZ) areas, where the normalized PNV was from 0% to 30%. (B) Activation wavefront of atypical flutter (clockwise upper loop re-entry flutter) passing through the protected isthmus identified by the voltage maps. CT = crista terminalis; IVC = inferior vena cava; SVC = superior vena cava. (C) Unipolar electrograms (Eg) within the isthmus exhibit fragmented electrograms (virtual 3 and 4), indicating there is slow conduction; whereas the unipolar electrograms outside the isthmus exhibit an rS pattern (virtual 1, 2, and 5).
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Figure 4 The normalized unipolar voltage maps, conduction block, and activation circuit of atypical atrial flutter (white lines) in 6 patients. Note that the most protected isthmuses were at the posterolateral right atrium near the location of the crista terminalis. LVZ = low voltage zone; PNV = peak negative voltage.
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Characteristics of the protected isthmus
The protected isthmus could be identified during CS pacing in 11 patients (93%), during LAL pacing in 10 patients (77%), and during AFL in 12 patients (100%). The mean width of the protected isthmus was 1.7 ± 0.3 cm (1.2 to 2.3 cm), and the mean voltage at the isthmus was –0.91 ± 0.39 mV (–0.33 to –1.69 mV) (Fig. 5A), which was equivalent to 43 ± 14% of the maximal PNV (23% to 58%). The mean distance from the center of the slow conduction area to the center of the MEA was 2.0 ± 0.2 cm (Table 1). The conduction velocities within these paths were significantly lower than outside the path (0.30 ± 0.18 m/s vs. 1.14 ± 0.41 m/s, respectively; p = 0.004) (Fig. 5B).
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Figure 5 Characteristics of the protected isthmus. (A) Mean peak negative voltage (PNV) inside and outside the isthmus. The PNV is lower inside the isthmus than outside. (B) Conduction velocity was slower inside the isthmus than outside.
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Prediction of slow conduction in the protected isthmus
Fragmented electrograms were frequently observed when the conduction velocity was <1 m/s, and we defined it as a slow conduction velocity. Forty-eight rhythms were retrospectively analyzed from the posterolateral wall (all 4 rhythm types in each of 12 patients). A fixed PNV (–0.54 mV) was the best cut-off value to detect the slow conduction within the isthmus (sensitivity = 61.5%; specificity = 85.7%). On the other hand, if the PNV was normalized by the maximal PNV of the selected atrial cycle, a ratiometric PNV of 37.6% of the maximal PNV had a higher sensitivity (92.3%) and specificity (85.7%) (Fig. 6).
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Figure 6 Receiver-operating characteristic (ROC) curve analysis predicting the slow conduction of the isthmus using the normalized voltage threshold.
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Radiofrequency ablation.
Delivery of ablation energy across the path was successful (8.8 ± 2.6 pulses), suggesting that it represented the critical isthmus of the re-entrant circuit. After the ablation, the voltage mapping exhibited a significant reduction in the unipolar negative voltage at the protected isthmus and double potentials, which indicated conduction block. The activation propagated around the upper end of the crista terminalis, instead of conducted through the protected isthmus. No more sustained atypical AFL could be induced in these patients.
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Discussion
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Major findings.
Noncontact mapping in patients with atypical AFL in the RA consistently demonstrated slow conduction between the LVZs of the posterolateral RA near the crista terminalis. High-density mapping of the RA substrate was performed by using the reconstructed unipolar PNV. Areas with slow conduction were identified along the re-entrant circuit of the atypical AFL. Because of a large overlap of the PNV between the areas with slow conduction and those without, a fixed unipolar voltage to differentiate that distinction was not very accurate. A ratiometric threshold, which was normalized by the maximum PNV, improved the diagnostic accuracy over a fixed amplitude threshold.
Comparison with previous studies.
Atypical right AFL could be either CTI-dependent or non–CTI-dependent (13). The non–CTI-dependent atypical right AFL does not necessarily depend on the activation through the CTI. Atypical right AFL could arise from single-loop or double-loop figure-of-eight re-entry (8,10,14). Conventional mapping, concealed entrainment pacing, and local fragmentation electrograms were used to find the critical circuit for ablation (12,13). However, entrainment mapping may result in termination of the tachycardia or transformation into nonclinical arrhythmias (14). Using the 3D mapping system, the re-entry circuit could be identified and facilitate the radiofrequency ablation (8,10,14–18). However, the critical isthmus of the re-entrant circuit would still be difficult to identify in cases of unmappable or nonsustained tachycardia.
The critical isthmus or slowest conduction of the circuit of the typical AFL was located around the CTI region (9,15). On the other hand, the critical isthmus was different in each type of atypical AFL. Della et al. (16) demonstrated that the optimal target sites were at the right atrial free wall, septum, left atrium, and coronary sinus. An electroanatomic study by Horlitz et al. (18) showed that there was an abnormal atrial substrate in terms of a low-voltage area in patients with atypical AFL. The optimal ablation sites in those patients were between the LVZs and the anatomic barriers. Tai et al. (10) used NCM to show that there was an activation wave front propagating around the central obstacle in the anterolateral wall with conduction through the channel between the central obstacle and the crista terminalis in atypical right AFL. Radiofrequency ablation of the free-wall channel and/or crista terminalis gap was effective in eliminating those AFLs.
Electrical voltage in diseased atrial myocardium.
In the present study, we used the peak negative voltage as a recording technique for the voltage mapping of the RA substrate (4). An atrial substrate characterized by an abnormally low PNV could predict areas with slow conduction during AFL, which would predispose the substrate to sustained AFL. Our studies further demonstrated that individual normalization with a maximal PNV improved the accuracy of predicting the slow conduction region compared with the fixed value of the PNV. This is compatible with the previous experience in the ventricle (19).
It had been shown that diseased myocardium could be diagnosed and distinguished from normal myocardium by a reduction in the unipolar electrical voltage (2,3). Dysfunctional myocardium may be comprised of fibrous tissue and less viable myocardium. The mean voltage reduction of the unipolar voltage was 37% in the contact unipolar recordings and 68% in the contact bipolar recordings in human infarction areas compared with areas remote from the infarction (2,3). Our observation suggested that a 37% preservation of the maximal PNV throughout the entire RA reflected the presence of partly viable tissue in that area which allowed slow conduction during AFL.
Prediction of slow conduction in the protected isthmus..
The ROC curve plots the true-positive rate (sensitivity) against the false positive rate (1 – specificity) over a range of cut points. The points along the diagonal indicate results that are no better than chance. When comparing tests, the test with the largest area under the ROC curve is preferred, assuming that the goal is to balance the sensitivity and specificity. In this study, a fixed PNV (–0.54 mV) was the best cut-off value for predicting slow conduction within the isthmus, but it had a low sensitivity (61.5%). That is because of the large overlap in the PNV between the area with slow conduction and that without, and the fixed unipolar voltage to differentiate that distinction is not very accurate. A ratiometric threshold (37.6% of the maximal PNV), which was normalized by the maximum PNV, had the largest area under the ROC curve, with a higher sensitivity (92.3%) and specificity (85.7%). That provided us with a useful predictor of the slow conduction path within the protected isthmus of atypical right AFL.
Conclusions.
Noncontact mapping in patients with atypical right AFL consistently demonstrated slow conduction within the LVZs in and around the crista terminalis. Characterization of the RA substrate in terms of the unipolar PNV is an effective predictor of the slow conduction path within the critical isthmus of the re-entrant circuit. A ratiometric threshold, normalized by the maximum PNV, provided diagnostic accuracy over a fixed amplitude threshold.
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Footnotes
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Supported in part by grants from Taichung Veterans General Hospital (TCVGH-, 933104C, 943103C, 953107C), Taiwan.
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References
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Abstract
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