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. 2023 Jul 10;25(9):euad195. doi: 10.1093/europace/euad195

Detailed analysis of tachycardia cycle length aids diagnosis of the mechanism and location of atrial tachycardias

Masateru Takigawa 1,2,3,4,, Tsukasa Kamakura 5,6, Claire Martin 7,8,9, Nicolas Derval 10,11, Ghassen Cheniti 12,13, Josselin Duchateau 14,15, Thomas Pambrun 16,17, Frederic Sacher 18,19, Hubert Cochet 20, Meleze Hocini 21,22, Miho Negishi 23, Tasuku Yamamoto 24, Takashi Ikenouchi 25, Kentaro Goto 26, Takatoshi Shigeta 27, Takuro Nishimura 28, Susumu Tao 29, Shinsuke Miyazaki 30,31, Masahiko Goya 32, Tetsuo Sasano 33, Michel Haissaguierre 34,35, Pierre Jais 36,37,2
PMCID: PMC10403248  PMID: 37428890

Abstract

Aims

Although the mechanism of an atrial tachycardia (AT) can usually be elucidated using modern high-resolution mapping systems, it would be helpful if the AT mechanism and circuit could be predicted before initiating mapping.

Objective

We examined if the information gathered from the cycle length (CL) of the tachycardia can help predict the AT-mechanism and its localization.

Methods

One hundred and thirty-eight activation maps of ATs including eight focal-ATs, 94 macroreentrant-ATs, and 36 localized-ATs in 95 patients were retrospectively reviewed. Maximal CL (MCL) and minimal CL (mCL) over a minute period were measured via a decapolar catheter in the coronary sinus. CL-variation and beat-by-beat CL-alternation were examined. Additionally, the CL-respiration correlation was analysed by the RhythmiaTM system. : Both MCL and mCL were significantly shorter in macroreentrant-ATs [MCL = 288 (253–348) ms, P = 0.0001; mCL = 283 (243–341) ms, P = 0.0012], and also shorter in localized-ATs [MCL = 314 (261–349) ms, P = 0.0016; mCL = 295 (248–340) ms, P = 0.0047] compared to focal-ATs [MCL = 506 (421–555) ms, mCL = 427 (347–508) ms]. An absolute CL-variation (MCL-mCL) < 24 ms significantly differentiated re-entrant ATs from focal-ATs with a sensitivity = 96.9%, specificity = 100%, positive predictive value (PPV) = 100%, and negative predictive value (NPV) = 66.7%. The beat-by-beat CL-alternation was observed in 10/138 (7.2%), all of which showed the re-entrant mechanism, meaning that beat-by-beat CL-alternation was the strong sign of re-entrant mechanism (PPV = 100%). Although the CL-respiration correlation was observed in 28/138 (20.3%) of ATs, this was predominantly in right-atrium (RA)-ATs (24/41, 85.7%), rather than left atrium (LA)-ATs (4/97, 4.1%). A positive CL-respiration correlation highly predicted RA-ATs (PPV = 85.7%), and negative CL-respiration correlation probably suggested LA-ATs (NPV = 84.5%).

Conclusion

Detailed analysis of the tachycardia CL helps predict the AT-mechanism and the active AT chamber before an initial mapping.

Keywords: Cycle length, Atrial tachycardia, Catheter ablation, High-resolution, Mapping, Activation

Graphical Abstract

Graphical abstract.

Graphical abstract


What’s new?

We studied 138 high-resolution activation maps of atrial tachycardias (ATs) made by the RhytmiaTM mapping system, including eight focal ATs, 94 macroreentrant ATs, and 36 localized ATs in 95 patients, in order to elucidate the importance of cycle length (CL) assessment in predicting the AT mechanism and AT chambers before starting activation mapping.

We demonstrated that:

  1. Both Maximum CL and minimum CL were significantly shorter in macroreentrant AT.

  2. CL-variation was significantly larger in focal-AT, and a cut-off value for CL-variation of <24 ms accurately discriminates re-entrant ATs from focal ATs.

  3. CL-respiration correlation is a strong predictor of ATs from the right atrium.

  4. Beat-by-beat CL-alternation is a strong predictor of the re-entrant mechanism.

Introduction

Atrial tachycardia (AT) is frequently observed in the context of atrial fibrillation (AF) ablation, due to both substrate and ablation scar,1–4 and it may be challenging to demonstrate the entire AT circuit using entrainment mapping alone.5 Improvements in mapping systems and catheters now allow mapping with sufficient resolution to demonstrate the precise activation sequence of these complex ATs.6–11 ATs after AF ablation can be classified as anatomical macroreentrant-AT (MAT), localized-AT, or focal-AT based on the mechanism, or as right atrial (RA) or left atrial (LA) AT based on the anatomical location of the circuit. Although the AT mechanism and circuit can usually be elucidated using a high-resolution mapping system, it would be helpful if this information were available before mapping the entire chamber. Although several studies have reported that the 12-lead electrocardiogram (ECG) is an efficient tool for predicting the type of AT and the focus of ATs,12,13 this is still challenging in scar-related ATs.14 Tachycardia cycle length (TCL) and TCL variability may instead be useful tools to predict the AT mechanism. A previous paper from our lead institution has reported that larger CL variability is more likely to suggest a focal-AT than re-entrant-AT.2

In this study, we reassess how the CL can help predict the mechanism and the circuit of patients with scar-related ATs.

Methods

Study population

We retrospectively examined 99 consecutive AT patients undergoing ablation guided by a high-resolution mapping system (RhythmiaTM) in two centres between January 2018 and December 2019. Of these patients, 95 patients who had at least one complete activation map during the procedure were included in the study. All patients gave written informed consent according to institutional guidelines with ethical approval for the study.

Electrophysiological study and mapping with Rhythmia

Antiarrhythmic medications were discontinued >5 half-lives before ablation. All patients were anticoagulated for at least 1-month before ablation. Transoesophageal echocardiography or contrast CT was performed before the procedure to exclude atrial thrombus. An activated clotting time of >300 s was maintained through the procedure. A steerable decapolar catheter was placed in the coronary sinus (CS). ATs were mapped with the OrionTM multipolar basket catheter and RhythmiaTM system (Boston Scientific, Marlborough, MA), and an activation map was created with automatic standard beat acceptance criteria based on: (i) CL variation, (ii) activation time difference variations between the CS electrograms (EGMs), (iii) catheter motion, (iv) EGM stability, (v) catheter tracking quality, and (vi) respiration gating. The confidence mask parameter was tuned for each map to be just above the noise level to allow visualization of low-voltage signals. In addition to high-resolution activation mapping, entrainment mapping was also performed. A site was considered part of the circuit if the post-pacing interval measured from the stimulation artefact to the return atrial EGM was within 20 ms of the tachycardia CL.

Definition of re-entrant-AT

ATs were classified into three types: focal-AT, localized-AT, and MAT. In this study, we defined localized-AT as an AT with an entire circuit on a single atrial wall. When the circuit included more than two atrial walls (e.g. anatomical macroreentrant-ATs),6,7,15 the AT was classified as MAT. MAT also included all typical anatomical MAT such as peri-tricuspid, peri-mitral, and roof-dependent ATs. Multiple-loop ATs were defined as those composed of more than one independent active circuit sharing one common isthmus, including dual-loop ATs and triple-loop ATs, with the TCL entirely corresponding to each of the circuits. After the activation map was completed, entrainment pacing was performed to confirm the diagnosis and define the circuit unless there were unstable ATs or ATs with short CL (<200 ms), where entrainment pacing might result in the conversion or termination of the index AT.

Assessment of AT cycle length

The regularity of the tachycardia was assessed using recordings from the CS. Maximum and minimum CL over 1 min and the variation between them were measured. CL-correlation to respiration was analysed using the RhythmiaTM system as shown in Figure 1. Alternating CL was defined as beat-by-beat alternation between longer and shorter CL.

Figure 1.

Figure 1

CL-respiration correlation.

Catheter ablation

After diagnosis of the AT mechanism and identification of the origin or circuit, ablation was performed. Earliest activation with a QS pattern in the local unipolar EGMs was targeted in focal-ATs. In re-entrant-ATs, the appropriate ablation site was determined based on anatomical length, catheter stability, tissue thickness, nearby vulnerable structures, and physiological conduction. In most cases, this represented the narrowest bridge of conducting tissue between scars or anatomical obstacles. When the ablation site was related to the vein of Marshall or mitral isthmus, ethanol infusion was considered.16The end-point for ablation, irrespective of the type of isthmus selected in the re-entrant circuit, was the achievement of bidirectional conduction block.11–14 Pulmonary veins (PVs) were re-isolated when needed.

Radiofrequency energy was delivered using an irrigated 3.5-mm-tip ablation catheter (Thermocool® SF catheter, Biosense Webster, Diamond Bar, CA), with a power of 30–40 W and a cut-off temperature of 45°C. Sites with AT termination during ablation were tagged.

Statistical analysis

Data are expressed as median (25%ile–75%ile) for continuous variables, and as numbers and percentages for categorical variables. Chi-square analysis or Fisher’s exact test was used for categorical variables, and an ANOVA analysis or Kruskal–Wallis test was used for continuous variables. P-values < 0.05 were considered statistically significant.

Results

Patient and AT characteristics and outcomes

The baseline characteristics of the 95 patients are shown in Table 1 and the features of the 138 ATs in those patients are shown in Table 2. Sixty-nine (72.6%) patients had ATs after AF ablation and 26 (27.4%) had ATs after cardiac surgery. A median of 2 (1–3) procedures were performed before the present procedure. One hundred and thirty-eight ATs were composed of focal-AT (n = 8), localized re-entry (n = 36), and MAT (n = 94). Eight focal-ATs originated from the peri-nodal region (n = 2), tricuspid annulus (n = 2), CS (n = 1), right atrial (RA) appendage (n = 1), PV (n = 1), and left atrial (LA) appendage (n = 1). All localized-ATs were associated with spontaneous scars, previous ablation lesions, or previous surgical incisions. Those circuits were localized at the lateral RA (n = 4), septal RA (n = 2), anterior LA (n = 13), septal LA (n = 7), posterior LA (n = 1), inferior LA (n = 1), and lateral LA (n = 8). Localized ATs at the lateral LA were all associated with the CS-Marshall ligament system.

Table 1.

Patient characteristics

Patient characteristics N=95
Age, y 60.3 [54.5–69.7]
Female 23 (24.2%)
SHD 51 (53.7%)
CHF 28 (29.5%)
HT 40 (42.1%)
DM 15 (16.3%)
Stroke 7 (7.4%)
CHA2DS2-VASc score 1 [0–3]
LVEF, % 59.7 [51.6–65.0]
No of prior procedure 2 [1–3]
Post-procedure 84 (88.4%)
 post-cardiovascular surgery 26 (27.4%)
 post-AF ablation 70 (73.7%)
 PVI 70 (73.7%)
 Focal ablation 10 (10.5%)
 Linear ablation 62 (65.3%)
 CFAE ablation 45 (47.4%)
 EI-VOM 11 (11.6%)
Number of mappable ATs per patient 2 [1–3]

Data are presented as n (%) or mean (standard deviation).

AF, atrial fibrillation; AT, atrial tachycardia; CFAE, complex fractionated atrial electrogram; CHF, congestive heart failure; DM, diabetes mellitus; EI-VOM, ethanol-infusion to the vein of Marshall; HT, hypertension; LVEF, left ventricular ejection fraction; PVI, pulmonary vein isolation; SHD, structural heart disease.

Table 2.

Atrial tachycardia characteristics

  N = 138
Focal AT 8 (5.8%)
Macroreentrant-AT 94 (68.1%)
 Anatomical MAT 82 (61.2%)
 Peri-tricuspid AT 25 (18.7%)
 Peri-mitral AT 27 (20.1%)
 Roof-dependent AT 28 (20.9%)
 Other MATs (e.g. PV-gap related AT) 14 (10.1%)
Localized re-entry (only one wall) 36 (26.1%)
Multiple loops AT 10 (7.2%)

Data are presented as n (%) or mean (standard deviation).

AT, atrial tachycardia; MAT, macroreentrant-AT.

137/138 (99.3%) ATs were terminated or changed to another AT with RF applications or ethanol infusion to the vein of Marshall. At 1 year, 82/95 (86.3%) patients had been followed up; 20/95 (21.1%) had developed AT recurrence and 3/95 (3.2%) had developed AF.

AT mechanism and tachycardia cycle length

As shown in Table 3, both maximum cycle length (MCL) and minimum cycle length (mCL) were significantly shorter in MAT [MCL = 288 (253–348) ms, P = 0.0001; mCL = 283 (243–341) ms, P = 0.0012], and also shorter in localized-AT [MCL = 314 (261–349) ms, P = 0.0016; mCL = 295 (248–340) ms, P = 0.0047] compared to focal-AT [MCL = 506 (421–555) ms, mCL = 427 (347–508) ms]. Absolute CL-variation was significantly smaller in MAT [6 (4–10) ms] compared to localized-AT [12 (6–17) ms, P = 0.0002], and focal-AT [46 (38–82) ms, P < 0.0001]. This tendency was also observed for the CL-variation ratio.

Table 3.

CL variation and AT-mechanism

  Total Focal AT
(N = 8)
Localized AT
(N = 36)
Macroreentrant-AT
(N = 94)
P-value
Mapping points 17 872 [11 893–27 440] 6359 [5225–9423] 16 511 [13 439–31 562] 19 183 [13 560–27 920] 0.0002ab
Atrial volume with Rhythmia 163 [129–189] 92.5 [57–152] 166 [146–188] 163 [129–191] 0.03ab
MCL, ms 297 [255–357] 506 [421–555] 314 [261–349] 288 [253–348] 0.0002ab
mCL, ms 290 [247–348] 427 [347–508] 295 [248–340] 283 [243–341] 0.0018ab
Absolute CL-variation (MCL-mCL), ms 8 [5–13] 46 [38–82] 12 [6–17] 6 [4–10] <0.0001abc
%CL-variation (MCL-mCL)/MCL*100, % 2.4 [1.7–4.4] 9.7 [7.3–18.8] 3.8 [2.1–5.9] 2.1 [1.5–3.2] <0.0001abc
Spontaneous AT at the beginning of the procedure 99 (71.7%) 5 (62.5%) 19 (52.8%) 75 (79.8%) 0.008ac
CL-respiration correlation 28 (20.3%) 1 (12.5%) 7 (19.4%) 20 (21.3%) 0.83
CL-Alternation 10 (7.3%) 0 (0%) 2 (5.6%) 8 (8.5%) 0.61
AT termination or change during ablation 137 (99.3%) 8 (100%) 36 (5.6%) 93 (98.9%) 0.79

AT, atrial tachycardia; CL, cycle length; MCL, maximum cycle length; mCL, minimum cycle length.

a

P < 0.05 between focal-ATs and macroreentrant-ATs.

b

P < 0.05 between focal-ATs and localized-ATs.

c

P < 0.05 between localized-ATs and macroreentrant-ATs.

As shown in Table 4, absolute CL-variation of <24 ms differentiated re-entrant-ATs from focal-ATs with an area under the curve (AUC) = 0.992, sensitivity = 96.9%, specificity = 100%, positive predictive value (PPV) = 100%, and negative predictive value (NPV) = 66.7%, meaning that AT with stable CL (CL-variation < 24 ms) strongly suggested a re-entrant mechanism. %CL-variation (absolute CL-variation/MCL*100) of <6.2% also strongly discriminated re-entrant-ATs from focal-ATs (AUC = 0.976).

Table 4.

Accuracy of CL-parameters to differentiate re-entrant-ATs from focal-ATs

  AUC Cut-off Specificity Sensitivity PPV NPV
MCL, ms 0.926 <414 87.5 92.3 99.2 41.2
mCL, ms 0.874 <402 75.0 90.8 98.3 33.3
Absolute CL-variation
(MCL-mCL), ms
0.992 <24 100.0 96.9 100.0 66.7
%CL-variation
(MCL-mCL)/MCL*100, %
0.976 <6.2 100.0 91.5 100.0 42.1
CL-respiration correlation (+) 87.5 20.8 96.4 6.4
CL-Alternation (+) 100.0 77.0 100.0 6.3

AT, atrial tachycardia; AUC, area under the curve; CL; cycle length; MCL, maximum cycle length; mCL, minimum cycle length; NPV, negative predictive value; PPV, positive predictive value.

CL-alternation was observed in 10 (7.3%) ATs in 10 patients, all of which had a re-entrant mechanism including two peri-mitral-ATs, two roof-dependent ATs, two scar-related RA-ATs, one PV-related AT, one cavo-tricuspid isthmus (CTI)-dependent AT, one bi-atrial AT, and one scar-related AT around the LA anterior scar. All of them had large scar areas based on prior catheter ablation (n = 5), both prior cardiovascular surgeries and catheter ablation (n = 3), and spontaneous scars probably based on the underlying heart disease (n = 2). Both CL-alternation and CL-respiration correlation significantly raise the possibility of re-entrant-ATs.

AT chamber and tachycardia cycle length

Although MCL and mCL did not differ between LA-ATs and RA-ATs, absolute CL variation was significantly larger in RA-ATs [13 (8–18) ms] than in LA-ATs [6 (4–10) ms, P < 0.0001], and %CL-variation ratio was also larger in RA-ATs as demonstrated in Table 5. Although CL-respiration correlation was observed in 28/138 (20.3%) of ATs, they were mostly observed in RA-ATs (24/41, 58.5%), and not in LA-ATs (4/97, 4.1%). CL-respiration correlation predicted RA-ATs with a sensitivity of 58.5%, specificity of 95.9%, PPV of 85.7%, and NPV of 84.5% as shown in Table 6.

Table 5.

CL variation and active chamber

  Total LA (N = 97) RA (N = 41) P-values
Mapping points 17 872 [11 893–27 440] 19 210 [14 919–32 069] 11 932 [8246–21 178] 0.0003
Atrial volume with Rhythmia 163 [129–189] 166 [140–191] 154 [107–186] 0.11
MCL, ms 297 [255–357] 297 [249–350] 308 [274–401] 0.06
mCL, ms 290 [247–348] 289 [240–341] 290 [267–393] 0.15
Absolute CL-variation (MCL-mCL), ms 8 [5–13] 6 [4–10] 13 [8–18] <0.0001
%CL-variation (MCL-mCL)/MCL*100, % 2.4 [1.7–4.4] 2.1 [1.5–3.7] 4.0 [2.5–6.2] <0.0001
Spontaneous AT at the beginning of the procedure 99 (71.7%) 73 (75.3%) 26 (63.4%) 0.21
CL-respiration correlation 28 (20.3%) 4 (4.1%) 24 (58.5%) <0.0001
CL-Alternation 10 (7.3%) 7 (7.2%%) 3 (7.3%) 0.98
AT termination or change during ablation 137 (99.3) 96 (100%) 40 (97.6%) 0.12

AT, atrial tachycardia; CL, cycle length; LA, left atrium; MCL, maximum cycle length; mCL, minimum cycle length; RA, right atrium

Table 6.

Accuracy of CL-parameters to differentiate RAATs from LAATs

  AUC Cut-off Specificity Sensitivity PPV NPV
Absolute CL-variation
(MCL-mCL), ms
0.741 ≥11 77.3 65.9 55.1 84.3
%CL-variation
(MCL-mCL)/MCL*100, %
0.718 ≥2.7 71.1 73.2 51.7 86.3
CL-respiration correlation (+) 95.9 58.5 85.7 84.5

AT, atrial tachycardia; AUC, area under the curve; CL, cycle length; LA, left atrium; MCL, maximum cycle length; mCL, minimum cycle length; RA, right atrium; NPV, negative predictive value; PPV, positive predictive value.

AT mechanism and AT induction

Spontaneous ATs were observed at the beginning of the procedure without induction in 75/94 (79.8%) of macroreentrant-ATs, 19/36 (52.8%) of localized-ATs, and 5/8 (62.5%) of focal-ATs. Spontaneously stable ATs were more suggestive of macroreentrant-ATs (P = 0.004).

Discussion

Major findings

In the present study, we elucidated the importance of CL assessment in predicting the AT mechanism and AT chambers before starting activation mapping. We demonstrated that:

  1. Both MCL and mCL were significantly shorter in MAT.

  2. CL-variation was significantly larger in focal-ATs, and a cut-off value for CL-variation < 24 ms accurately differentiates re-entrant-ATs from focal-ATs.

  3. CL-respiration correlation is a strong predictor of ATs from the RA and is also suggestive for re-entrant-ATs.

  4. Beat-by-beat CL-alternation is a strong predictor of re-entrant-ATs.

  5. Sinus rhythm at the beginning of the procedure may increase the possibility of localized-AT and focal-AT, while stable persistence of the AT is more likely observed in macroreentrant-ATs

CL and At-mechanism

In this study, focal-ATs demonstrated a longer CL compared to re-entrant-ATs such as macroreentrant-ATs and localized-ATs. The median mCL of the eight focal-ATs was 427 (347–508) ms. Several reports have summarized and discussed the characteristics of focal-ATs. Morris et al. beautifully summarized 548 AT-cases over a 16-year period, in which the mean CL of the focal-ATs was 408±100 ms.17 Although the mean CLs of ATs in the CS (369±110 ms) and in the PVs (366±91 ms) were relatively shorter, most AT-CLs were distributed around 400 ms. Whitaker J et al. also summarized 293 ATs over 10-years, describing a median CL of 370 (200–670) ms in focal-ATs.18 Other studies have also demonstrated that the CL of most focal-ATs is >350 ms.19–23

In contrast, the median CL of re-entrant-ATs including both localized re-entry and macroreentry was relatively shorter in this study (e.g. < 300 ms). We previously examined 214 consecutive ATs and similarly demonstrated a shorter CL in re-entrant-ATs8; e.g. a mean CL of focal-ATs = 305±84 ms (n = 20), localized-ATs = 287±76 ms (n = 57), and macroreentrant-ATs = 277±62 ms (n = 129). Previous reports also support this finding,2,24 and the mean CL of macroreentrant-ATs has been reported to be distributed around 250–300 ms.6,25 However, it may be difficult to differentiate the AT-mechanism through the ATCL alone because the number of focal-ATs in the present study was small, and the CL range may overlap between focal-ATs and re-entrant-ATs at around 300 ms. Based on past literatures, a CL > 350 ms more likely has a focal mechanism and a CL < 250 ms more likely has a re-entrant mechanism. However, the greater extent and number of conduction delays within the circuits and the longer length of the entire circuit in re-entrant-ATs may result in a longer cycle length (CL) even in ATs with a re-entrant mechanism. For example, a type-I single-loop macroreentrant bi-AT, including the entire right and left atriums as a circuit, reported by Kitamura et al.,9 had a long AT circuit, resulting in a tachycardia CL of 334–450 ms despite a re-entrant mechanism.

CL-variation and At-mechanism

CL-variation may be more helpful than absolute CL in determining the AT mechanism. Cut-off values of absolute CL-variation < 24 ms, and %CL-variation < 6.2% may differentiate re-entrant-ATs from focal-ATs. Specifically, an absolute CL-variation of < 24 ms could predict re-entrant-ATs with a sensitivity = 96.9%, specificity = 100%, PPV = 100%, and NPV = 66.7%. For a re-entrant mechanism, circuits including slow conduction areas are usually observed and the activation wavefront runs between anatomical obstacles and scars. Since the length of the circuit and the electrophysiological properties of the critical isthmus are fixed, large CL-variation may be less frequently observed in the re-entrant mechanism (Figure2A and B). Conversely, the main mechanism of focal-ATs is automaticity or triggered activity, which may be more sensitive to dynamic autonomic adjustment, resulting in more frequent CL-variation (Figure 2C). Jais P et al. previously analysed 246 sustained ATs in 128 post-AF AT patients and reported that >15% CL variability is suggestive of focal-AT.25 This cut-off value is different from our study, which possibly results from a mis-classification between focal-ATs, microreentrant-ATs, and re-entrant-ATs related to epicardial structures26 due to the use of conventional mapping and diagnosis without the use of a 3D-mapping system.

Figure 2.

Figure 2

Figure 2

CL assessment vs. AT. (A) LA roof-dependent AT around the right pulmonary vein (RPV) demonstrates a small CL-variation between 345 and 353 ms without CL-respiration correlation. (B) RA localized-AT around an incision related to cardiovascular surgery demonstrates a small CL-variation between 312 and 324 ms with CL-respiration correlation. (C) RA focal-AT demonstrates a large CL-variation between 405 and 512 ms with a clear CL-respiration correlation. (D) RA-Common flutter demonstrates a CL-variation of 218–234 ms with a clear CL-respiration correlation.

CL-respiration correlation

CL-respiration correlation was more frequently observed in ATs originated from the RA (Figure2B, C and D). In cases with CL-respiration correlation, the CL usually increased during inspiration and decreased during expiration. Although the exact mechanism of CL-respiration correlation is unknown, physiological effects on the atrial chamber during respiration may help in understanding this.

Under MRI examination, inspiration is demonstrated to result in a transient increase in right ventricle (RV) volumes and a reciprocal decrease in LV volumes, whereas expiration causes reciprocal changes.27 Thus, respiration causes a direct ventricular interaction whereby enhanced filling of one ventricle corresponds with reduced filling of the other. In addition, the volume change between inspiration and expiration is much more dramatic in the RV. The mechanisms underpinning this phenomenon may include respiratory variations in afterload,28 transient inspiratory pooling of blood in the lungs,29 and alterations in LV compliance via diastolic ventricular interdependence.30 Respiration changes in atrial volume should follow this. Based on this mechanism, a significant and immediate increase in right atrial volume during inspiration may be associated with the expansion of the tachycardia circuit, resulting in an increase in the tachycardia CL in RA ATs. In contrast, this haemodynamic change is less dynamic in the LA, leading to a less dramatic change in LA volume, resulting in a less frequent incidence of CL-respiration correlation in LA ATs.

CL alternation

Beat-by-beat CL-alternation was generally rare (N = 10, 7.3%) and all instances were observed in ATs with a re-entrant mechanism in this study. CL-alternation in AT is reported to be occasionally (1.5%) observed in patients with previous cardiac surgery or extensive ablation beyond pulmonary vein isolation (PVI) for AF,31 where the mechanism is re-entry with conduction block or delays in the AT circuit. Zhang et al. classified CL-alternation into two groups. The first type is composed of two potential re-entrant circuits with different routes and CL yet sharing certain segments of the loop. CL alternans resulted from an intermittent 2:1 conduction block through a channel within the scar. With the shorter CL, activation was capable of passing through the channel with a relatively shorter circuit. With the longer CL, a line of conduction block in the original conducting channel was observed, resulting in detouring around the line of the block with a longer route. The other group is composed of one circuit with the same route, but within the pre-existing linear lesions, there may exist two conduction gaps with different conduction velocities in the immediate vicinity of each other, which cannot be differentiated on the activation map. With the longer CL, there is slower conduction through one gap compared with the other, manifested by alteration of the duration of fractionated potentials at the gap. Based on this report and our findings, CL-alteration might be specifically observed in re-entrant mechanisms associated with iatrogenic or spontaneous scars, where two possible circuits share a substantial proportion of the circuit with different electrophysiological properties in the slow conduction area. Interestingly, as shown in Figure 3, we found one case with CL-alternation where the slowest conduction area was shared with a similar activation duration between slower and faster CLs, but activation in an outer-loop contributed to the different AT-CL. Since the number of channels and the extent of conduction is varied in scar-related ATs, detouring of the pathway may occur not only in the critical isthmus (with the slowest conduction) but anywhere in the circuit. In any case, CL-alternation may be a strong indicator of a re-entrant mechanism.

Figure 3.

Figure 3

CL-alternation and AT. A representative case of CL-alternation between 240 and 280 ms. In this case, the activation duration at the critical isthmus at the slowest conduction area was similar between the two CLs, but conduction in the outer-loop contributed to the difference in CL.

Clinical implications

Although the high-resolution contact mapping of the entire chamber may provide an accurate mechanism and a AT circuit, it is often time-consuming.32,33 The findings of this study demonstrate that basic information about the CL helps predict the AT-mechanism and the active AT chamber, which may decrease mapping and procedure times. Not only CL itself, but also CL variation, CL-respiration correlation, and CL-alternation should be assessed before mapping. Potentially with the use of machine learning that includes this information, the mechanism and localization of the AT may be more accurately and rapidly diagnosed before mapping commences.34,35

Limitations

First, since this study was retrospectively performed, a prospective randomized study should be performed to clarify whether our proposed strategy can facilitate and shorten ablation procedures and improve outcomes. Second, focal-ATs were rare in our consecutive scar-related AT cohort compared to previous reports.1–3 However, we believe that previous studies overestimated the number of focal-ATs in scar-related ATs, because of the use of lower-resolution mapping systems or the absence of 3D-mapping. Third, most scar-related ATs were mapped with the RhythmiaTM system to acquire an accurate diagnosis including a precise AT circuit, because this system provides extremely high-resolution maps. Finally, although all cases were performed under conscious sedation in this study, the relation between CL-respiration correlation and AT mechanism/AT localization may be different in active ventilation under general anaesthesia. This should be examined in further studies.

Conclusion

Basic information regarding the CL helps predict the AT-mechanism and the active AT chamber before mapping initiation.

Acknowledgement

We appreciate the support from Mr. Tomohiro Nagao from Boston Scientific Japan for image creation.

Contributor Information

Masateru Takigawa, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France; Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo; Department of Advanced Arrhythmia Research, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Tsukasa Kamakura, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Claire Martin, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; Cardiology Department, Royal Papworth Hospital, Cambridge CB2 0AY, UK; Department of Medicine, Cambridge University, Cambridge CB2 0QQ, UK.

Nicolas Derval, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Ghassen Cheniti, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Josselin Duchateau, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Thomas Pambrun, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Frederic Sacher, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Hubert Cochet, IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Meleze Hocini, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Miho Negishi, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Tasuku Yamamoto, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Takashi Ikenouchi, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Kentaro Goto, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Takatoshi Shigeta, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Takuro Nishimura, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Susumu Tao, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Shinsuke Miyazaki, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo; Department of Advanced Arrhythmia Research, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Masahiko Goya, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France.

Tetsuo Sasano, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, 113-8510, Tokyo.

Michel Haissaguierre, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Pierre Jais, Department of Cardiac Pacing and Electrophysiology, Bordeaux University Hospital (CHU), Av. Magellan, 33600 Pessac, France; IHU Liryc, Electrophysiology and Heart Modelling Institute, Univ. Bordeaux, Av. du Haut Lévêque, 33600 Pessac, France.

Funding

This research was partly funded by a grant from Investissement d’avenir: IHU LIRYC ANR-10-IAHU-04

Data availability

The data underlying this article will be shared on reasonable request to the corresponding author.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The data underlying this article will be shared on reasonable request to the corresponding author.


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