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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Heart Rhythm. 2015 Sep 28;13(2):391–398. doi: 10.1016/j.hrthm.2015.09.028

Association of Left Atrial Function with Incident Atypical Atrial Flutter Following Atrial Fibrillation Ablation

Esra GUCUK IPEK *, Joseph E MARINE *, Mohammadali HABIBI *, Jonathan CHRISPIN *, Joao LIMA *, Jack RICKARD *, David SPRAGG *, Stefan L ZIMMERMAN ξ, Vadim ZIPUNNIKOV ‡, Ronald Berger, Hugh CALKINS *, Saman NAZARIAN *,†
PMCID: PMC4724482  NIHMSID: NIHMS743381  PMID: 26416618

Abstract

Background

Symptomatic left atrial (LA) flutter (LAFL) is common following atrial fibrillation (AF) ablation.

Objective

To examine the association of baseline LA function with incident LAFL following AF ablation.

Methods

The source cohort included 216 patients with cardiac magnetic resonance (CMR) prior to initial AF ablation between 2010 and 2013. Patients who underwent cryoballoon or laser ablation, patients with AF during CMR, and those with suboptimal CMR, or missing follow-up data were excluded. Baseline LA volume and function were assessed by feature-tracking CMR analysis.

Results

The final cohort included 119 patients (age 58.9±11 years, 76.5% male, 70.6% paroxysmal AF). During a median follow-up of 421 (interquartile range 235–751) days, 22 (18.5%) patients developed LAFL. Baseline LA volume was similar between the two groups. In contrast, baseline reservoir, conduit and contractile function of the LA were significantly impaired in patients with incident LAFL. Baseline global peak longitudinal atrial strain (PLAS) < 22.65% predicted incident LAFL with 86% sensitivity and 68% specificity (C-statistic 0.76). In a multivariable model adjusting for age, heart failure, and LA volume, PLAS (HR 0.9 per % increase in PLAS, p=0.003) and LA linear lesions (HR 2.94, p=0.020) were independently associated with incident LAFL. Coexistence of PLAS<22.65% and linear lesions was associated with 9-fold increased hazard of incident LAFL.

Conclusion

Baseline LA function and linear lesions were independently associated with incident LAFL after AF ablation. Linear lesions should be limited to selected cases, especially in patients with impaired LA function.

Keywords: Atrial fibrillation, atrial flutter, cardiac magnetic resonance, left atrium, pulmonary vein isolation

Introduction

Atrial fibrillation (AF) is the most common arrhythmia and is associated with significant symptoms, and mortality (1). Catheter-based AF ablation has become a well-established management strategy for symptomatic AF (2). Despite technological advances in AF ablation, evolving strategies and experience, arrhythmia recurrences remain relatively high (3, 4). Left sided atrial flutter (LAFL) accounts for a substantial proportion of symptomatic sustained recurrences after AF ablation (2, 5–8). Previous studies have reported clinical and procedure-related risk factors of post-ablation LAFL, including linear lesions, incomplete pulmonary vein isolation (PVI), persistent AF, and structural heart disease (2, 7–10).

In recent years, feature-tracking cardiac magnetic resonance (CMR) has emerged as a sophisticated tool for detailed chamber specific functional analysis (11). It has been shown that left atrial (LA) function predicts recurrences after AF ablation (12). In this study, we aimed to define feature tracking CMR-derived LA functional characteristics of patients who developed LAFL after AF catheter ablation.

Methods

Study Population

The source cohort included 216 consecutive AF patients who underwent CMR prior to initial AF ablation between 2010 and 2013. Of these, 37 patients were excluded due to cryoballoon or laser ablation. Patients with AF at the time of CMR (n=46), suboptimal/missing cine images (n=8), and missing follow-up data (n=6) were also excluded. Clinical characteristics of the final cohort, which included 119 patients, were extracted by review of electronic medical records. The Johns Hopkins Institutional Review Board approved the study and all subjects provided written informed consent.

CMR Protocol

Pre-procedural (average 4 days before ablation) CMR was performed using a 1.5-Tesla MR scanner (Avanto and Aera, Siemens, Erlangen, Germany) equipped with a phased array cardiac coil. Vertical and horizontal long-axis cine CMR was performed using a steady-state free precession sequence (minimal TR/TE, 8 mm slice thickness, 2 mm spacing, 78° flip angle, 36–40 cm field of view) with 1.5 x 1.5 mm in-plane resolution.

Feature Tracking CMR

The Multimodality Tissue Tracking software (MTT; version 6.0, Toshiba, Japan) was used to measure phasic LA volumes, strain and strain rate on vertical and horizontal long-axis cine images. After manual contouring of end systolic endocardial and epicardial LA borders, the software automatically tracked pixel features within the tissue throughout the cardiac cycle as previously described (13). In all cases, pulmonary veins and LA appendage were excluded from the contours. Manual adjustments were performed when tracking was suboptimal. The software generated a volume curve for each phase by using the biplane area-length method (Figure 1). Maximum, pre-contraction, and minimum LA volumes were obtained from the phasic volume curve to calculate the following functional parameters:

Figure 1.

Figure 1

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Quantitative CMR-derived functional analysis of the LA in a healthy volunteer. Panel A: Tissue tracking at end systolic 4-chamber cine image, pulmonary veins are excluded. Panel B: Tissue tracking at end systolic 2-chamber cine image, the appendage and pulmonary veins are excluded. C: Volume curve of the LA, blue dotted line represents 4-chamber view; green dotted line represents 2-chamber view and pink dotted line represents bi-plane LA volume. The peak volumes during ventricular systole and pre-atrial contraction represent LAV-max and pre-contraction volumes, respectively. B: Global LA longitudinal strain curve, the peak of the curve during ventricular systole corresponds to PLAS. C: Global LA longitudinal strain rate curve, peaks at ventricular systole, early diastole and late diastole correspond to SR-s, SR-ed and SR-ld, respectively.

  • Total LA emptying fraction: 100 × (Maximum LA volume – minimum LA volume) / Maximum LA volume

  • Passive LA emptying fraction: 100 × (Maximum LA volume – pre-contraction LA volume) / Maximum LA volume

  • Active LA emptying fraction: 100 × (Pre-contraction LA volume – minimum LA volume) / Pre-contraction LA volume

Global LA longitudinal strain and strain rate curves were calculated as the mean longitudinal strain and strain rate of all segments (Figure 1). Peak longitudinal LA strain (PLAS), peak systolic LA strain rate (SR-s), peak early diastolic LA strain rate (SR-ed) and peak late diastolic LA strain rate (SR-ld) were measured. The SR-ed and SR-ld were presented as absolute values. Reservoir function was represented by PLAS, SR-s and total LA emptying fraction; conduit function was represented by passive LA emptying fraction and SR-ed; and contractile function was represented by SR-ld and active LA emptying fraction. We previously reported on the reproducibility of CMR derived LA functional parameters using MTT software (14).

Catheter Ablation

All patients underwent radiofrequency ablation as previously described (15). After obtaining double atrial transseptal puncture, electroanatomic mapping (CARTO, Biosense-Webster, Diamond Bar, CA) of the LA endocardium was performed with registeration onto a previously acquired CMR image. An irrigated 3.5 mm tip catheter (Thermocool, Biosense-Webster, Diamond Bar, CA) was used for mapping and ablation. A circular multipolar electrode-mapping catheter (Lasso, Biosense, Diamond Bar, CA) was used to confirm PVI by presence of entrance and exit block. Additional linear lesion sets, connecting the right and left pulmonary venous antra across the LA roof, floor or posterior wall, and complex fractionated atrial electrogram (CFAÉ) ablations were performed per operator discretion. High-frequency stimulation for identification of ganglionated plexi was not performed. However, transient >50% prolongation of the RR interval and sudden >20 mmHg transient decreases in systolic radial artery pressure were noted as vagal responses consistent with ganglionated plexus ablation. Repeat PVI was performed during follow-up depending on symptoms and clinician’s preference. During the repeat procedure the diagnosis and characteristics of LAFL were confirmed based on activation and entrainment mapping. Sites with fractionated potentials that participated in the LAFL circuit were targeted for ablation.

Follow-up

After the procedure, patients were observed for 24 hours. In the absence of AF recurrence, pre-procedurally ineffective antiarrhythmic medications were discontinued after 3 months. Symptom prompted 24-hour Holter monitoring and scheduled electrocardiography at 3, 6, and 12 months were performed. Incident LAFL was defined as symptomatic or asymptomatic documented LAFL > 30 seconds in duration. In the absence of electrophysiology study, an LAFL diagnosis was made on the basis of agreement between two expert reviewers, masked to clinical and imaging information. The readers diagnosed LAFL if a) high frequency (180–260 ms) F waves with continuous oscillation without a flat baseline were noted, and b) the F wave morphology was not suggestive of typical cavotricuspid isthmus dependent AFL (sawtooth pattern in inferior leads, positive F-waves in lead V1, isoelectric or negative in leads V5–V6). Patients without LAFL were censored at the time of last available follow-up.

Statistical Analysis

The distribution of continuous variables was evaluated using the Shapiro-Wilk test. Continuous variables were expressed as mean ± standard deviation or median (interquartile range [IQR]) and compared using the Student’s t-test or Mann Whitney U test as appropriate. Categorical variables were expressed as number (percentages) and compared using the χ2 or Fisher exact tests. The association between LA volume and LA functional parameters was evaluated using Spearman correlation and graphically assessed using a scatter matrix plot. The optimal threshold for PLAS to estimate LAFL free survival was selected by maximizing the area under the receiver-operating characteristic (ROC) curve. Kaplan-Meier survival curves were used to assess LAFL free survival in patient subgroups based upon the optimal PLAS threshold. Univariable and multivariable Cox proportional hazards models were used to examine the association of clinical and functional independent variables with time to incident LAFL. Model proportionality assumptions were verified using Schoenfeld residuals. Statistical analyses were performed using SPSS software version 22.0 (IBM Corp., Armonk, NY).

Results

The final cohort included 119 patients. Mean age was 58.9±11 years, 76.5% were male, and 70.6% had paroxysmal AF. The detailed baseline characteristics are shown in Table 1. During a median follow-up of 421 days, 22 (18.5%) patients developed incident LAFL. Median time to LAFL incidence was 198 (IQR 42 – 409) days. History of heart failure was more common in patients with LAFL. Among the entire cohort of 119 patients included in this report, 28 patients (23.5%) received linear ablation lines at the initial AF ablation. The most common linear lesion was a roof line, followed by a posterior line, both of which connected the left to right sided PVI lesion sets. Of the 28 patients with linear lesion sets, 11 (39%) developed LAFL during follow-up. LAFL was less commonly observed among patients who did not have linear lesions created during the initial ablation (11/91, 12%, p=0.001). Overall, 2 patients had CFAÉ ablation, and both patients were LAFL free during follow-up. Significant vagal pause consistent with ganglionated plexus ablation was noted in 13 patients. There was no difference in occurrence of LAFL in these patients (Table 1).

Table 1.

Baseline characteristics of patients with (LAFL) and without (No LAFL) left atrial flutter at follow-up.

LAFL (n=22) No LAFL (n=97) P
Clinical characteristics
 Age (years) 59.46±7.9 58.9±11.6 0.8
 Male gender 86.4% (19) 74.2% (72) 0.23
 BMI (kg/m2) 29.5 (26.4–32.9) 27.7 (24–31.1) 0.13
 Hypertension 59.1% (13) 46.4% (45) 0.28
 Diabetes mellitus 18.2% (4) 7.2% (7) 0.12
 Coronary artery disease 9.1% (2) 11.3% (11) 0.99
 Heart failure 22.7% (5) 7.2% (7) 0.045
 Cerebrovascular event 18.2% (4) 8.2% (8) 0.23
 Sleep apnea 31.8% (7) 17.5% (17) 0.15
 CHA2DS2VASC≥2 50% (11) 40.2% (39) 0.4
 Persistent AF 27.3% (6) 29.9% (29) 0.81
Procedural characteristics
 Total RF time (minutes) 48.2±15.2 45.2±15.6 0.43
 CFAÉ ablation 0% (0) 2.1% (2) 0.66
 Vagal Response consistent with GP ablation 13.6% (3) 10.3% (10) 0.71
 Linear lesions 50% (11) 17.5% (17) 0.001
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AF: Atrial fibrillation, AFL: Atrial flutter, BMI: Body mass index, CFAÉ: Complex fractionated atrial electrograms, RF: Radiofrequency

Baseline LA volume and functional parameters are shown in Table 2. LA volume was similar in patients with and without incident LAFL. In contrast, all baseline LA functional parameters were lower in patients with LAFL, indicating impaired LA function in all phases (reservoir, conduit and contractile functions). The association of LA volume and LA functional parameters is displayed in Figure 2. Due to significant co-linearity among all phasic LA functional parameters, PLAS was used as a surrogate of LA function. In the multivariable model adjusted for age, heart failure, and LA volume; PLAS (HR 0.9 per % increase in PLAS, CI 0.84–0.96) and linear ablation lesions (HR 2.94, CI 1.23–7) were the only predictors of LAFL.

Table 2.

Baseline LA volume and LA functional characteristics

LAFL (n=22) No LAFL (n=97) P
LVEF (%) 55.4±7.8 57.7±5.5 0.21
LAV max (ml) 98.6 (81.7–125.6) 95.5 (76.2–116.4) 0.46
Indexed LAV max (ml/m2) 48.7±13.9 47.9±13.7 0.81
PLAS (%) 18.2 (13.3–22) 25.5 (20.4–32.4) <0.001
LA SR-s sn−1 0.74 (0.5–1.1) 0.99 (0.8–1.31) 0.004
LA SR-ed sn−1 0.71 (0.52–0.98) 0.95 (0.65–1.34) 0.01
LA SR-ld sn−1 0.81 (0.4–1.14) 1.22 (0.88–1.63) <0.001
LATEF (%) 37.2±12.8 46±9.6 <0.001
LAPEF (%) 16.7±6 19.3±6 0.08
LAAEF (%) 25.1±12.2 33.3±9.2 <0.001
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AF: Atrial fibrillation, EF: Emptying fraction, LA: Left atrium, LVEF: Left ventricular ejection fraction, LAAEF: Active left atrial emptying fraction, LAPEF: Passive left atrial emptying fraction, LATEF: Total left atrial emptying fraction LAV max: Maximum left atrial volume, PLAS: Peak left atrial longitudinal strain, SR-s: Systolic strain rate, SR-ed: Early diastolic strain rate, SR-ld: Late diastolic strain rate

Figure 2.

Figure 2

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Scatter matrix plots illustrate associations between LA volume and LA functional parameters and results of the spearman correlation analysis.

Management of the patients with incident LAFL is summarized in Table 3. Of the 22 patients with LAFL, 14 had repeat ablation. Of the 14 that underwent repeat ablation, 4 only underwent repeat PVI, whereas 10 underwent activation and/or entrainment mapping with demonstration of macro-reentry. The most common circuit was peri-mitral macro-reentry (60%). The remaining 8 patients underwent cardioversion and have been maintained on antiarrhythmic drug therapy.

Table 3.

Baseline characteristics and management of each case with LAFL

Cases Clinical Characteristics PLAS (%) iLAV (ml/m2) Linear Lesion Time to LAFL (Days) Management
1 61 y/o F, Parox AF 20.9 41.9 Roof 64 Cardioversion
2 55 y/o M, HTN, Parox AF 21.6 37.9 None 582 Medical management
3 58 y/o F, h/o CVA, OSA Parox AF 9.8 71.3 Roof 44 Cardioversion, repeat PVI
4 56 y/o M, HTN, DM, OSA, Parox AF 18.6 34.1 None 966 Repeat PVI, posterior mitral anulus ablation
5 69 y/o M, HTN, CVA, Parox AF 17.7 37.1 Roof 671 Repeat PVI, mitral isthmus flutter ablation
6 55 y/o M, HTN, CHF, Parox AF 15.9 58.7 Posterior 258 Cardioversion
7 62 y/o M, HTN, DM, Parox AF 17.8 59.9 None 37 Repeat PVI, perimitral flutter ablation
8 58 y/o M, HTN, Parox AF 21.7 36.2 Roof 338 Repeat PVI, perimitral ablation
9 46 y/o M, OSA, Pers AF 19.3 63.7 None 1044 Cardioversion
10 69 y/o M, DM, CHF, Pers AF 21.9 54.3 Roof 36 Cardioversion
11 64 y/o M, Pers AF 11.9 60.2 None 103 Cardioversion
12 55 y/o M, HTN, CVA, Parox AF 22.4 44.9 None 351 Repeat PVI, roof line terminated flutter
13 77 y/o M, HTN, CAD, CHF, OSA, Pers AF 10.7 48.8 None 264 Repeat PVI, peri LPV and mitral isthmus flutter
14 52 y/o M, HTN, Parox AF 16.3 49.7 None 611 Repeat PVI, LSPV ablation terminated flutter
15 52 y/o M, DM, CAD, CHF, OSA, Parox AF 16 32.9 None 20 Cardioversion, repeat PVI
16 65 y/o M, OSA, Parox AF, MVr, AVR 34.2 44.8 None 21 Repeat PVI, roof line terminated flutter
17 68 y/o M, HTN, Parox AF 12.8 81.3 None 85 Repeat PVI, roof and perimitral ablation
18 48 y/o F, HTN, Parox AF 28.1 60.8 Posterior 97 Repeat PVI, cardioverted before mapping, hypotensive
19 53 y/o M, HTN, CHF, CVA, OSA, Pers AF 13.5 23.3 Roof 207 Cardioversion
20 57 y/o M, HTN, Parox AF 9.4 40.1 Roof 190 Cardioversion, repeat PVI
21 61 y/o M, Pers AF 41 46.3 Posterior 206 Cardioversion
22 69 y/o M, Parox AF 22.6 43.2 Roof 31 Repeat PVI, reentry originating from RSPV
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AF: Atrial fibrillation, AVR: Aortic valve replacement, CAD: Coronary artery disease, CHF: Congestive heart failure, DM: Diabetes mellitus, F: Female, HTN: Hypertension, iLAV: Indexed left atrial volume, LPV: Left sided pulmonary veins, LSPV: Left superior pulmonary vein, M: Male, MVr: Mitral valve repair, OSA: Sleep apnea, Parox: Paroxysmal, Pers: Persistent, PLAS: Peak longitudinal strain, PVI: Pulmonary vein isolation, RSPV: Right superior pulmonary vein, y/o: year old

Baseline PLAS < 22.65% predicted LAFL with 86% sensitivity and 68% specificity (C-statistic 0.76; Figure 3). Patients were divided into 2 groups based on this threshold. Median time to LAFL was: 152 (IQR 97–206) days in patients with PLAS ≥ 22.65% and linear lesions, 190 (IQR 40–298) days in patients with PLAS < 22.65% and linear lesions; and 308 (IQR 73–700) days in patients with PLAS < 22.65% and without linear lesions. Figure 4 demonstrates Kaplan Meier curves of LAFL free survival among PLAS < 22.65% and PLAS ≥ 22.65% patient subgroups further stratified by the presence or absence of linear lesion sets. Coexistence of PLAS <22.65% and linear lesions was associated with 9-fold increased hazard of LAFL incidence.

Figure 3.

Figure 3

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The receiver operating characteristic curve of baseline PLAS for prediction of post-ablation LAFL.

Figure 4.

Figure 4

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The Kaplan Meier survival curves demonstrate the association of LA function and linear lesions with LAFL incidence.

Discussion

Major Findings

To the best of our knowledge, this is the first study to examine the association of baseline LA functional properties with incident LAFL after AF ablation. We showed that 1) baseline LA functional parameters were lower in patients with LAFL, indicating impaired function in all phases; 2) LA function was an independent predictor of LAFL along with linear lesions; and 3) the co-existence of linear lesions and impaired LA function was associated with the highest risk of LAFL.

LAFL following AF ablation

LAFL may comprise up to 50% of all recurrences after ablation (2). The risk has been reported to be low after cryoballoon ablation; however, the incidence may rise to 25% after radiofrequency ablation (7, 8). Patients with LAFL often present with more severe symptoms, including the development of a rate-related cardiomyopathy, reflecting the challenges of effective rate control in these patients (5, 6).

Post-ablation LAFL has been mainly attributed to sequelae of LA linear lesions; but may also results from ablation-induced conduction slowing, gaps in the ablation lines or organization of AF into a reentry circuit (5, 8, 16). According to our results, LA function is associated with incident post-ablation LAFL independent of additional lesion sets. Fibrosis and LA remodeling clearly play a role in the pathogenesis of AF recurrences (17). Our data highlight the association of LA remodeling and LAFL. Fibrosis likely serves as a substrate for slow conduction and creates anatomical obstacles that enable the development of a critical isthmus. In a previous study, a significant association was found between lower PLAS and the presence of low voltage regions (18). Similarly, LA contractile function is associated with the extent of low voltage (< 0.5 mV) (19). Therefore, non-invasive assessment of LA function prior to AF ablation procedure may be used as an indicator of the extent of fibrosis.

Previous studies reported early presentation of LAFL after AF ablation (8). Due to the relatively long follow-up in our study, a subset of patients with very late recurrences after AF ablation, defined as >12 months, were noted. In this subset, the prevalence of pulmonary vein reconnection was significantly lower, and impaired baseline left ventricular systolic and diastolic function was more common, suggesting that patient-related rather than procedure-related factors may primarily account for late LAFL (20).

The 2012 HRS/EHRA/ECAS Consensus Document on AF ablation states that for patients with persistent AF, additional substrate ablation either targeting of CFAE or additional linear lesion sets may be appropriate (2). These recommendations are likely to evolve following the recent STAR AF II trial, which revealed fewer recurrences in the PVI versus the PVI plus substrate modification group (21). In this trial, the investigators concluded that extensive ablation may cause arrhythmogenic areas and that persistent AF patients do not derive benefit from linear lesions. Our findings are consistent with the results of the STAR AF II trial and suggest that linear lesion sets are particularly arrhythmogenic in patients with pre-existing LA dysfunction.

Association of LA fibrosis with LA function

Reservoir function represents distensibility and is closely associated with the extent of interstitial fibrosis. A previous study evaluated patients prior to mitral valve surgery with speckle-tracking echocardiography and examined LA tissue samples obtained at cardiac surgery (22). Histopathogical analysis of tissue fibrosis was compared with pre-surgical PLAS. In patients with moderate (PLAS<20%) and severe (PLAS<10%) LA dysfunction, the extent of the fibrosis was more than 50% and 70%, respectively. Likewise, there was an inverse relationship between LA fibrosis as estimated on late gadolinium enhancement (LGE) CMR with LA strain and strain rate (23). Our group has shown similar associations between the extent of LA LGE and LA function, suggesting that both of the CMR-derived assessments can be used as non-invasive surrogates of LA fibrosis (14). The association of LGE extent with LAFL incidence post ablation warrants future study. However, in contrast to LGE-CMR, which is not available in many centers and requires extensive technical expertise for image acquisition and analysis, LA functional analysis is easy to perform and widely available via echocardiography, MRI, and phasic computed tomography.

LA function and outcome

In recent years, LA deformation studies have revealed strong associations between clinical outcomes and LA function in the general as well as AF populations (13, 24–27). In AF patients, AF recurrence is closely associated with baseline LA function (28, 29). In routine practice, LA volume is frequently used to predict LA dysfunction and remodeling, however, LA deformation indices are more sensitive and their impairment can be detected before dilatation occurs. According to our results, unlike LA volume, baseline LA function analysis (particularly reservoir and contractile function) provides useful adjunctive information and may help to optimize management to prevent post-ablation LAFL. In our study, we only included patients that were in sinus rhythm at the time of CMR. Recent data suggest that LA strain can be measured via speckle tracking echocardiography in patients with non-sinus rhythm, albeit with analyses limited to the reservoir phase (30). The presence of AF prior to ablation, however, may confound not only the measurement of LA strain, but also the association of that measurement with outcomes following ablation. Therefore, further studies are necessary to examine the association reservoir function during AF with outcomes following ablation.

Limitations

This is a single center study and patients with rhythm other than sinus at the time of baseline CMR were excluded; therefore, our results may not be generalizable to all patients with AF and study power was limited for multivariable analyses. In 10 patients, activation mapping and entrainment confirmed LAFL. In others, review of ECG by two experienced reviewers suggested LAFL. We cannot exclude the possibility that the surface ECG may have been misleading in a minority of cases. Finally, differences in LAFL incidence existed compared to some prior studies (5–8), and may reflect variability in patient characteristics, length of follow up, methods for LAFL detection, and procedural techniques.

Conclusions

Baseline LA function and creation of linear lesions is associated with incident LAFL after an initial AF ablation. These findings, combined with the recent results of the STAR AF II Trial, suggest that careful consideration should be given prior to creation of linear ablation lesions to treat AF.

Clinical Perspectives.

This manuscript examines the association of baseline left atrial functional properties with incident left atrial flutter following after atrial fibrillation ablation. Baseline left atrial functional was impaired in all phases in patients with incident left atrial flutter. After adjusting for potential confounders and linear lesions left atrial function remained independently associated with incident left atrial flutter. Importantly, the co-existence of linear lesions and impaired left atrial function was associated with the highest risk of incident left atrial flutter. Our findings are consistent with the results of the STAR AF II trial, which revealed fewer recurrences in the pulmonary vein isolation versus the pulmonary vein isolation plus substrate modification group, and suggest that linear lesion sets are particularly arrhythmogenic in patients with pre-existing left atrial dysfunction.

Acknowledgments

Funding: The study was funded by NIH grants K23HL089333 and R01HL116280 as well as a Biosense-Webster grant to Dr. Nazarian, The Roz and Marvin H Weiner and Family Foundation, The Dr. Francis P. Chiaramonte Foundation, Marilyn and Christian Poindexter, and The Norbert and Louise Grunwald Cardiac Arrhythmia Research Fund.

Abbreviations

AF

Atrial fibrillation

LAFL

Left sided atrial flutter

PVI

pulmonary vein isolation

CMR

cardiac magnetic resonance

LA

left atrial

PLAS

Peak longitudinal LA strain

SR-s

systolic LA strain rate

SR-ed

peak early diastolic LA strain rate

SR-ld

peak late diastolic LA strain rate

CFAÉ

complex fractionated atrial electrograms

ROC

receiver-operating characteristic

LGE

late gadolinium enhancement

Footnotes

Disclosures: Dr. Nazarian is a scientific advisor to Medtronic, CardioSolv, and Biosense Webster Inc and principal investigator for research funding to Johns Hopkins University from Biosense-Webster Inc.

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