Relationship Between Circulatory Stasis in the Left Atrial Appendage Detected by Cardiac Computed Tomography Angiography With Atrial Fibrillation Recurrence After Initial Catheter Ablation

Shu Yang; Jun Wang; Ning Chen; Jincheng Jiao; Yi Xu; Minglong Chen; Mingfang Li

doi:10.1161/JAHA.125.045263

. 2026 Jan 14;15(2):e045263. doi: 10.1161/JAHA.125.045263

Relationship Between Circulatory Stasis in the Left Atrial Appendage Detected by Cardiac Computed Tomography Angiography With Atrial Fibrillation Recurrence After Initial Catheter Ablation

Shu Yang ^1,^2,^#, Jun Wang ^3,^#, Ning Chen ², Jincheng Jiao ⁴, Yi Xu ^3,^✉, Minglong Chen ^1,^2,^✉, Mingfang Li ^2,^5,^✉

PMCID: PMC12919476 PMID: 41532555

Abstract

Background

To investigate the relationship between circulatory stasis in the left atrial appendage (LAA), as detected by cardiac computed tomography angiography, and atrial fibrillation (AF) recurrence after the initial catheter ablation.

Methods

In this single‐center prospective observational study, consecutive patients with nonvalvular AF scheduled for the initial catheter ablation were enrolled from August 2018 to June 2022. The primary end point was AF recurrence (any documented atrial tachyarrhythmia lasting for ≥30 seconds after a 3‐month blanking period) during 1 year after catheter ablation.

Results

Among the enrolled 548 patients (mean age 65.3±8.8 years and 64.2% men), 131 (23.9%) were with LAA circulatory stasis. Totally, 525 patients completed the 1‐year follow‐up. AF recurrence was observed in 39.1% (50/128) of patients with circulatory stasis and 19.4% (77/397) of patients without circulatory stasis. The presence of LAA circulatory stasis was significantly associated with AF recurrence (adjusted hazard ratio [HR], 2.41 [95% CI, 1.57–3.72]). The incorporation of circulatory stasis in the LAA significantly improved the predictive accuracy of conventional scoring systems for AF recurrence, with the areas under the curve increasing from 0.524 to 0.616 (P=0.037) for the APPLE score, from 0.516 to 0.617 (P=0.035) for the CAAP‐AF score, and from 0.532 to 0.619 (P=0.001) for the CHA₂DS₂‐VASc score.

Conclusions

In patients with nonvalvular AF, circulatory stasis in the LAA could serve as a predictor for AF recurrence following the initial ablation procedure.

Keywords: atrial fibrillation, cardiac computed tomography angiography, catheter ablation, circulatory stasis, recurrence

Subject Categories: Atrial Fibrillation, Electrophysiology

graphic file with name JAH3-15-e045263-g007.jpg

Nonstandard Abbreviations and Acronyms

DCA: decision curve analysis

Clinical Perspective.

What Is New?

The presence of circulatory stasis in the left atrial appendage on cardiac computed tomography angiography was significantly associated with an increased risk of atrial fibrillation recurrence over a 1‐year follow‐up period (adjusted hazard ratio, 2.41 [95% CI, 1.57–3.72], P<0.001).
Atrial fibrillation ablation could still be safely performed in patients with circulatory stasis in the left atrial appendage on cardiac computed tomography angiography.

What Are the Clinical Implications?

In patients with nonvalvular atrial fibrillation, the presence of circulatory stasis in the left atrial appendage on cardiac computed tomography angiography could serve as a predictor for atrial fibrillation recurrence following the initial catheter ablation procedure.

Atrial fibrillation (AF) promotes the formation of atrial thrombus via various mechanisms, involving abnormal blood flow, changes in blood constituents, and alterations in vessel wall, thereby increasing the risk of thromboembolism. ¹ , ² Patients with AF are particularly prone to developing blood clots in the left atrial appendage (LAA). ³

Currently, transesophageal echocardiography (TEE) remains the predominant imaging modality for periprocedural cardiac evaluation, owing to its lack of radiation exposure, low cost, broad availability, and rapid acquisition time. Notably, TEE is considered the gold standard modality for identifying atrial thrombus before AF cardioversion or ablation. In contrast to atrial thrombus, which has a solid echo density, spontaneous echo contrast (SEC) represents abnormal blood flow in the left atrium, manifesting as dynamic, swirling, smoke‐like echoes during the cardiac cycle at the standard gain setting in TEE. ⁴ Previous studies have reported that LA SEC on TEE is associated with an increased risk of atrial thrombus formation and subsequent thromboembolic events. ⁵ , ⁶ , ⁷

CHADS₂ and CHA₂DS₂‐VASc scores, ⁸ , ⁹ which are commonly used for stroke risk stratification in patients with nonvalvular AF, have been reported to be associated with the presence of SEC. ¹⁰ , ¹¹ In addition, LA enlargement, renal dysfunction, and specific morphological characteristics of the LAA, such as more LAA lobes and nonchicken wing morphology, have also been linked to the presence of SEC. ¹² , ¹³ , ¹⁴ A recent study also highlighted elevated BNP (brain natriuretic peptide) levels and erythrocyte sedimentation rate as independent predictors of severe LA SEC. ¹⁵ Furthermore, LA SEC has been identified as an independent predictor for AF recurrence following AF ablation, ¹⁶ with a higher degree of SEC indicating an increased risk of AF recurrence. ¹⁷

However, TEE has limitations, as it is semiinvasive, time consuming, and may be challenging for patients who have difficulty swallowing the probe under conscious sedation. ¹⁸ , ¹⁹ Furthermore, TEE carries inherent risks of potentially life‐threatening complications. ²⁰ , ²¹

In contrast, cardiac computed tomography angiography (CTA) offers a noninvasive and cost‐effective alternative imaging modality. Although limited by radiation exposure, contrast use, susceptibility to elevated heart rates, and the inability to provide real‐time imaging, cardiac CTA remains clinically valuable due to its exceptional ability to delineate complex cardiac anatomy. It facilitates the evaluation of the anatomy of left atrium and pulmonary veins (PVs) before AF ablation, with remarkable sensitivity and specificity in detecting atrial thrombus. ²² , ²³ , ²⁴ Therefore, cardiac CTA is now widely used to rule out the presence of atrial thrombus before AF ablation. Circulatory stasis in the LAA on cardiac CTA, characterized by filling defects observed exclusively in the early scan phase rather than the delayed scan phase, represents another type of abnormal blood flow, distinct from atrial thrombus. ²⁵ However, the clinical significance of circulatory stasis in the LAA detected using cardiac CTA remains to be fully explored.

The aim of this study was to investigate the relationship between circulatory stasis in the LAA, as detected using cardiac CTA and the recurrence of AF following the initial catheter ablation procedure.

Methods

Data Availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Patients and Study Design

This prospective observational study was approved by the Ethics Committee of the First Affiliated Hospital with Nanjing Medical University (Approval No. 2014‐SR‐113). All patients provided their informed consent before participation in this study. The study adhered to the Strengthening the Reporting of Observational Studies in Epidemiology reporting guidelines. ²⁶

From August 2018 to June 2022, consecutive patients with nonvalvular AF who were candidates for AF ablation, had been hospitalized at our center, and had undergone preprocedure cardiac CTA were considered for inclusion in this study. In our center, all patients scheduled for AF ablation underwent preprocedural thrombus evaluation using either TEE or cardiac CTA, as determined by clinical judgment and patient preference. This individualized, patient‐centered approach was intended to ensure safety and comfort while adhering to standard clinical practices. All enrolled patients in our study had received anticoagulation therapy for at least 3 weeks before hospitalization. Patients with identified atrial thrombus, those who had undergone cardioversion or LAA intervention during hospitalization, and those with prior history of AF ablation were excluded.

Demographic, clinical, imaging and laboratory data were collected. The creatinine clearance rate (CCR) was calculated using the Cockcroft‐Gault formula. ²⁷ Elevated levels of BNP were defined following the 2021 European Society of Cardiology Heart Failure guidelines, ²⁸ with a BNP level >35 pg/mL in sinus rhythm or 105 pg/mL in AF, or an NT‐proBNP (N‐terminal prohormone of BNP) level >125 pg/mL in sinus rhythm or 365 pg/mL in AF. The only echocardiographic LA parameter collected in the present study was LA diameter (LAD). Other LA metrics, such as LA volume index or LA strain, were not routinely assessed. This practice is shaped based on several pragmatic considerations: (1) acquisition and interpretation of LA volume and strain involve time‐consuming imaging and analysis procedures, which can substantially reduce workflow efficiency in a high‐volume clinical environment; and (2) current evidence supports LAD as an accepted surrogate for LA size in routine clinical decision‐making. ²⁹ , ³⁰

Cardiac Computed Tomography Angiography

All patients underwent cardiac CTA using a dual‐source 256‐section multidetector computed tomography system (Somatom Force; Siemens) with an ECG‐gated dual‐source single‐energy protocol covering the entire heart. A 2‐phase scanning protocol was used to improve the specificity of cardiac CTA, ³¹ involving the acquisition of a second set of images after a 60‐second delay following the initial scan. Contrast‐enhanced images were obtained using a contrast agent (370 mg iodine/ml, Ultravist, Bayer Schering Pharma, Berlin, Germany) administered via a 20‐G intravenous needle, which was inserted into either the left or right antecubital vein, with an injection rate of 4 to 5 mL/s (Imeron 350, Bracco Imaging GmbH, Germany). All injections were followed by a saline flush of 40 mL. The injection duration was calculated based on the scan time plus an additional 8 seconds. The flow rate, ranging from 3.0 to 6.0 mL/s, was customized according to factors such as body weight, heart rate, and tube voltage. Ventricular rate control was ensured to be <100 beats per minute before cardiac CTA examination to optimize image quality and accuracy. Furthermore, image reconstruction was implemented to avoid the impact of motion artifacts.

In this study, filling defects on cardiac CTA were defined as low attenuation areas within the LAA, not caused by motion artifacts or other anatomical structures, such as trabeculae. Quantitative Houndsfield units (HU) analysis was systematically performed across all low attenuation areas. In cardiac CTA, regions of blood stasis exhibited reduced density due to impaired contrast opacification, displaying significantly lower HU values compared with regions with normal flow. Atrial thrombus was characterized by consistently the lowest HU values across all acquisition phases. We then classified blood flow status in the LAA into 3 categories: (1) LAA thrombus—fixed filling defects observed in early and delayed phases, with CT attenuation values ≤50 HU during the 60‐second delayed phase; (2) circulatory stasis—triangular filling defects in the LAA (CT attenuation values ≤200 HU) that exhibited attenuation similar to the left atrium during the 60‐second delayed phase; and (3) circulatory normal—normal flow (no filling defects in either early phase or delayed phase) and low blood flow (irregular filling defects with intermediate density, with CT attenuation values >200 HU during the 60‐second delayed phase). Figure 1 displayed representative images of blood flow status on cardiac CTA and TEE.

A–C, Representative images of blood flow status in the LAA on cardiac CTA during the early phase; D–F, Representative images of blood flow status in the LAA on cardiac CTA during the delayed phase (60‐sec delay); G–I. Representative images of blood flow status in the LAA on TEE. CTA indicates computed tomography angiography; LAA, left atrial appendage; SEC, spontaneous echo contrast; and TEE, transesophageal echocardiography.

All cardiac CTA images were independently interpreted by 2 experienced radiologists who were blinded to patients’ clinical data, ensuring an objective assessment of circulatory stasis in the LAA. Moreover, before the study, both radiologists underwent standardized training in the assessment of LAA circulatory status to minimize interpretative variability. Discrepancies in assessments were resolved through consensus with a third senior radiologist. Given that the presence of atrial thrombus was an exclusion criterion for this study, circulatory status in the LAA was assessed using a binary classification (0=circulatory normal, 1=circulatory stasis). Interobserver agreement was evaluated across the full study population. Following the methodology described in 2 previous publications, ³² , ³³ intraobserver variability was assessed by having the first radiologist reevaluate a randomly selected subset of 100 cases (50 with circulatory normal and 50 with circulatory stasis) 4 weeks after the initial assessment, with continued blinding to the original evaluations and clinical information.

Transesophageal Echocardiography

TEE was performed using a Philips EPIQ 7C ultrasound system equipped with the X7‐1 probe. Comprehensive multiplanar imaging (0°–180°) was acquired to evaluate the blood flow status in the LAA. On TEE, LAA blood flow patterns were categorized as normal, SEC, and thrombus. SEC, which was characterized by dynamic, swirling, smoke‐like echoes that change throughout the cardiac cycle, was further graded using Fatkin’s four‐point scale. ³⁴ Grades 3 and 4 were classified as severe SEC (Figure 1). Images were analyzed by 2 experienced echocardiographers who were blinded to the clinical data and the interpretations from cardiac CTA. The concordance between severe SEC on TEE and circulatory stasis detected by cardiac CTA were also assessed. Only paired studies, in which both cardiac CTA and TEE were performed within 3 days, were included in the comparative analysis.

AF Ablation and Periprocedure Management

In the present study, patients received standard periprocedural anticoagulation treatments according to guideline recommendations. ³⁵ The ablation strategies implemented at our center have been previously described. ³⁶ , ³⁷ , ³⁸ Briefly, all patients underwent the circumferential PV isolation using radiofrequency catheter ablation. If sinus rhythm was not restored after circumferential PV isolation, direct current cardioversion was administered. At our center, LA voltage mapping was selectively performed at the discretion of the operator and was not mandated for all cases. When performed, high‐density voltage mapping was conducted during sinus rhythm using a multipolar mapping catheter, with a minimum of 300 points collected per patient. Low‐voltage areas were defined as regions where a bipolar voltage was <0.5 mV in at least 3 adjacent points. Additional procedures, such as line ablation, substrate modification, ablation targeting non‐PV triggers were performed at the discretion of the operating electrophysiologist. Ablation was deemed complete upon achieving entrance and exit block for each PV, confirmed through the injection of intravenous adenosine or isoproterenol and burst pacing from the distal site of the coronary sinus electrode. Final PV isolation was confirmed after a minimum waiting period of 30 minutes following the initial isolation. Following the ablation procedure, antiarrhythmic drugs were prescribed for at least 3 months to prevent early arrhythmia recurrence, unless contraindicated.

Follow‐Up and End Points

In this study, patients were followed up routinely at 3, 6, and 12 months post ablation with a 12‐lead ECG and 24‐hour Holter ECG monitoring. Moreover, additional ECG or 24‐hour Holter ECG was performed whenever they experienced symptoms indicative of tachyarrhythmia recurrence after the ablation procedure. AF recurrence was defined as any documented atrial tachyarrhythmia (including atrial tachycardia, atrial flutter, and AF) lasting for ≥30 seconds that occurred after the 3‐month postprocedural blanking period. ³⁵

The primary end point was AF recurrence that occurred within 1 year after catheter ablation, and the secondary end point was the occurrence of severe adverse events during the periprocedural period, including acute ischemic stroke, major bleeding and cardiac tamponade. Major bleeding was defined as fatal bleeding or bleeding occurring in critical areas or organs, as well as instances resulting in a hemoglobin decrease (≥ 20g/L) or requiring a transfusion of at least 2 units of whole blood or red cells. ³⁹

Statistical Analysis

Continuous variables were expressed as means ± SDs and compared using Student’s t test or the Mann–Whitney U test, depending on the distribution of values. Categorical variables were presented as absolute and relative frequencies (percentages) and compared using chi‐square test or Fisher’s exact test, as appropriate.

To evaluate potential subgroup differences in anticoagulation, we conducted subgroup analyses stratified by key clinical variables, including age, sex, AF type, CHA₂DS₂‐VASc score, HAS‐BLED score, CCR, LAA morphology, and LAD.

Interobserver and intraobserver agreement in cardiac CTA interpretation was assessed using Cohen’s kappa statistic. Furthermore, using TEE as the reference standard, we assessed the diagnostic performance of cardiac CTA. Its sensitivity, specificity, positive predictive value, and negative predictive value were reported with 95% CIs.

The full data set was randomly divided into a training cohort and an independent validation cohort in a 7:3 ratio. Variable selection was restricted to the training cohort. Instead of using P value thresholds to perform variable selection, we implemented a 2‐stage variable selection process. Initially, least absolute shrinkage and selection operator regression (L1‐penalized) coupled with 10‐fold cross‐validation was performed to minimize overfitting. The optimal penalty parameter (λ) was selected based on minimum cross‐validated binomial deviance, identifying variables with nonzero coefficients. Subsequently, multivariable logistic regression analysis was used to confirm the statistical significance of all candidate variables. Based on these independent variables, a nomogram was developed, and its performance was evaluated through discrimination, calibration, and decision curve analysis (DCA). Discrimination was assessed by plotting the receiver operating characteristic curve and calculating the area under the curve (AUC), and calibration was evaluated using the calibration curve and the Hosmer–Lemeshow test. DCA was employed to evaluate the clinical net benefit of the nomogram model.

The correlation with the CT findings and LA voltage mapping findings was compared using chi‐square test. Moreover, to address potential confounding factors, the 1:1 propensity score matching (PSM) was used to balance baseline characteristics between patients with circulatory normal and those with circulatory stasis. The variables included in the PSM were age, sex, type of AF, CHA₂DS₂‐VASc score, hemoglobin, elevated levels of BNP, left ventricular ejection fraction, LAD, moderate or severe mitral insufficiency, and moderate or severe tricuspid insufficiency.

AF‐free survival after the 3‐month blanking period was estimated using the Kaplan–Meier method. The survival distribution between the circulatory stasis group and the circulatory normal group was compared using the log‐rank test. The 1:1 PSM was also employed to mitigate potential confounding between the 2 groups. The Cox proportional hazard models were adjusted for demographic characteristics, clinical characteristics, results of laboratory and imaging tests, and ablation strategy additional to PVI to assess the relationship between circulatory stasis in the LAA and the recurrence of AF. Hazard ratios (HR) and 95% CIs were reported. We also conducted a subgroup analysis stratified by AF type to evaluate the association between circulatory stasis and AF recurrence. In addition, to investigate whether incorporating circulatory stasis in the LAA could improve the prediction of AF recurrence, we integrated it into 3 well‐established scoring systems (the APPLE score, ⁴⁰ the CAAP‐AF score, ⁴¹ and the CHA₂DS₂‐VASc score ⁴² , ⁴³ ). The predictive performance of these models was assessed using receiver operating characteristic analysis, and the significance of AUC differences was tested with the DeLong test. ⁴⁴ To correct for optimism, internal validation was performed using 10‐fold cross‐validation. The calibration curve, Hosmer–Lemeshow test, and DCA were also employed to evaluate model calibration and clinical utility. A P value of <0.05 was regarded as statistically significant. Statistical analyses were performed using SPSS (version 26.0) and R (version 4.4.2).

The detailed criteria of all scoring systems used in this study are provided in Table S1.

Results

Baseline Characteristics

In total, 694 consecutive patients with nonvalvular AF who were candidates for AF ablation were hospitalized and undergone the preprocedure cardiac CTA at our center during the study period. We excluded 102 patients with prior history of AF ablation, 15 with identified atrial thrombus, 4 who received cardioversion, and 25 who received LAA intervention. The remaining 548 patients receiving initial AF ablation were finally analyzed (Figure 2).

AF indicates atrial fibrillation; CTA, computed tomography angiography; LA, left atrial; LAA, left atrial appendage; and NVAF, nonvalvular atrial fibrillation.

The baseline characteristics are summarized in Table 1. Among the enrolled patients, the mean age was 65.3±8.8 years and 352 (64.2%) were men. The prevalence of nonparoxysmal AF, hypertension, diabetes, prior stroke or transient ischemic attack, heart failure, and vascular disease was 41.2% (226/548), 60.9% (334/548), 17.5% (96/548), 9.1% (50/548), 5.3% (29/548), and 3.5% (19/548), respectively. The mean CHA₂DS₂‐VASc score was 2.1±1.3 and the mean CCR was 84.3±25.1 mL/min. In addition, 274 (50.0%) patients had an elevated BNP level. Among the 548 patients, the distribution of LAA morphology was as follows: chicken wing 29.7% (163/548), cactus 35.0% (192/548), windsock 30.8% (169/548), and cauliflower 4.4% (24/548). The mean left ventricular ejection fraction was 61.8±5.6% and the mean LAD was 40.7±5.0 mm.

Table 1.

Baseline Characteristics of the Study Population

Variable	Total (n=548)	Circulatory normal (n=417)	Circulatory stasis (n=131)	P value
Age, y, mean±SD	65.3±8.8	65.3±8.9	65.2±8.7	0.895
Men, n (%)	352 (64.2)	258 (61.9)	94 (71.8)	0.039
Body weight, kg, mean±SD	70.4±11.2	69.8±11.4	72.1±10.5	0.040
Type of atrial fibrillation
Nonparoxysmal, n (%)	226 (41.2)	128 (30.7)	98 (74.8)	<0.001
Medical history
Hypertension, n (%)	334 (60.9)	259 (62.1)	75 (57.3)	0.320
Diabetes, n (%)	96 (17.5)	70 (16.8)	26 (19.8)	0.421
Prior stroke/transient ischemic attack, n (%)	50 (9.1)	35 (8.4)	15 (11.5)	0.289
Heart failure, n (%)	29 (5.3)	13 (3.1)	16 (12.2)	<0.001
Vascular disease, n (%)	19 (3.5)	16 (3.8)	3 (2.3)	0.568
Oral anticoagulants				0.169
Warfarin, n (%)	54 (9.9)	37 (8.9)	17 (13.0)
Nonvitamin K antagonist oral anticoagulants, n (%)	494 (90.1)	380 (91.1)	114 (87.0)
CHA₂DS₂‐VASc score, mean±SD	2.1±1.3	2.2±1.4	2.1±1.2	0.609
HAS‐BLED score, mean±SD	1.6±1.0	1.6±1.0	1.6±0.9	0.837
Laboratory tests
White blood cells, 10^9 /L, mean±SD	5.7±1.4	5.7±1.4	5.9±1.4	0.122
Hemoglobin, g/L, mean±SD	137.0±15.3	135.2±15.4	142.6±13.5	<0.001
Platelet, 10^9 /L, mean±SD	170.4±50.1	172.6±51.4	163.5±45.2	0.068
Creatinine clearance rate, mL/min, mean±SD	84.3±25.1	84.2±25.6	84.4±23.5	0.929
Elevated levels of brain natriuretic peptide, n (%)	274 (50.0)	163 (39.1)	111 (84.7)	<0.001
Left atrial appendage morphology				0.506
Chicken wing, n (%)	163 (29.7)	121 (29.0)	42 (32.1)
Nonchicken wing, n (%)	385 (70.3)	296 (71.0)	89 (67.9)
Cactus, n (%)	192 (35.0)	143 (34.3)	49 (37.4)
Windsock, n (%)	169 (30.8)	132 (31.7)	37 (28.2)
Cauliflower, n (%)	24 (4.4)	21 (5.0)	3 (2.3)
Echocardiographic data
Left ventricular ejection fraction, %, mean±SD	61.8±5.6	62.4±4.4	59.9±7.9	<0.001
Left atrium diameter, mm, mean±SD	40.7±5.0	39.6±4.7	44.3±4.3	<0.001
Moderate or severe mitral insufficiency, n (%)	61 (11.1)	32 (7.7)	29 (22.1)	<0.001
Moderate or severe tricuspid insufficiency, n (%)	126 (23.0)	62 (14.9)	64 (48.9)	<0.001
Moderate or severe aortic insufficiency, n (%)	25 (4.6)	17 (4.1)	8 (6.1)	0.331

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According to the circulatory status in the LAA on cardiac CTA, patients were divided into 2 groups: the circulatory stasis group (n=131, 23.9%) and the circulatory normal group (n=417, 76.1%). Compared with the circulatory normal group, the circulatory stasis group exhibited significantly higher proportions of male (71.8% versus 61.9%, P=0.039), nonparoxysmal AF (74.8% versus 30.7%, P<0.001), heart failure (12.2% versus 3.1%, P<0.001), elevated BNP level (84.7% versus 39.1%, P<0.001), moderate or severe mitral regurgitation (22.1% versus 7.7%, P<0.001), and moderate or severe tricuspid regurgitation (48.9% versus 14.9%, P<0.001). Additionally, the circulatory stasis group presented with higher body weight (72.1±10.5 kg versus 69.8±11.4 kg, P=0.040), hemoglobin levels (142.6±13.5 g/L versus 135.2±15.4 g/L, P<0.001), a lower left ventricular ejection fraction (59.9±7.9% versus 62.4±4.4%, P<0.001), and an increased LAD (44.3±4.3 mm versus 39.6±4.7 mm, P<0.001).

However, no significant difference was observed in anticoagulation between the circulatory normal and circulatory stasis groups. As shown in Figure S1, across all subgroups–including age, sex, AF type, CHA₂DS₂‐VASc score, HAS‐BLED score, CCR, LAA morphology, and LAD–nonvitamin K antagonist oral anticoagulants showed a consistent protective trend against the presence of circulatory stasis, with odds ratios (ORs) <1 in all comparisons (all P for interaction >0.05). Nevertheless, none of these associations reached statistical significance. There were also no significant differences in CHA₂DS₂‐VASc score, HAS‐BLED score, CCR, and LAA morphology between these 2 groups (Table 1).

Observer Agreement in Cardiac CTA

The results showed excellent reproducibility, with a kappa value of 0.882 (95% CI, 0.836–0.928) for interobserver consistency (Table S2) and 0.900 (95% CI, 0.815–0.985) for intraobserver consistency (Table S3). Discrepancies (24 cases, 4.4%) were resolved through consensus with a third senior radiologist.

Comparison of Cardiac CTA and TEE

As part of our center’s cost‐containment strategy, we routinely use either TEE or cardiac CTA for preprocedural thrombus evaluation in patients undergoing AF ablation. Between August 2018 and June 2022, 88 patients who underwent both TEE and cardiac CTA within 3 days were included in the comparative analysis. The analysis demonstrated a high level of agreement between the 2 modalities, with a sensitivity of 96.2% (95% CI, 78.4%–99.8%) and specificity of 87.1% (95% CI, 75.6%–93.9%). The positive predictive value was 75.8% (95% CI, 57.4%–88.3%), and the negative predictive value reached 98.2% (95% CI, 89.0%–99.9%) (Table S4).

Development and Validation of the Nomogram for Estimating the Risk of Circulatory Stasis in the LAA

The full data set (n=548) was randomly (in a 7:3 ratio) divided into a training cohort (n=384) and an independent validation cohort (n=164). As shown in Table S5, baseline characteristics between the training and validation cohorts were well balanced, with no significant difference observed (all P>0.05), ensuring data set comparability. The least absolute shrinkage and selection operator regression analysis identified nonparoxysmal AF, hemoglobin level (g/L), elevated levels of BNP, LAD (mm), and moderate or severe tricuspid regurgitation as predictors of circulatory stasis in the LAA (Figure 3). Subsequently, multivariable logistic regression analysis confirmed the statistical significance of all 5 candidate variables: nonparoxysmal AF (OR, 2.58 [95% CI, 1.33–5.10], P=0.006), elevated hemoglobin level (OR, 1.37 per 10 g/L increase [95% CI, 1.12–1.68], P=0.003), elevated BNP level (OR, 2.16 [95% CI, 1.06–4.51], P=0.036), increased LAD (OR, 1.90 per 5 mm increase [95% CI, 1.32–2.81], P<0.001), and the presence of moderate or severe tricuspid regurgitation (OR, 2.71 [95% CI, 1.46–5.05], P=0.002) were independently associated with circulatory stasis in the LAA (Table 2).

A, Coefficient profiles of the 23 variables; B, Optimal λ selection based on minimum binomial deviance via 10‐fold cross‐validation method. LASSO indicates least absolute shrinkage and selection operator.

Table 2.

Multivariable Logistic Regression Analysis for Circulatory Stasis in the Left Atrial Appendage based on Least Absolute Shrinkage and Selection Operator Regression

Variable	β	z	OR (95% CI)	P value
Nonparoxysmal atrial fibrillation	0.948	2.773	2.58 (1.33–5.10)	0.006
Hemoglobin, per 10 g/L increase	0.311	2.982	1.37 (1.12–1.68)	0.003
Elevated levels of brain natriuretic peptide	0.772	2.096	2.16 (1.06–4.51)	0.036
Left atrium diameter, per 5 mm increase	0.642	3.329	1.90 (1.32–2.81)	<0.001
Moderate or severe tricuspid insufficiency	0.996	3.154	2.71 (1.46–5.05)	0.002

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OR indicates odds ratio.

Based on the least absolute shrinkage and selection operator regression and multivariable logistic regression analysis, a nomogram was developed to estimate the risk of circulatory stasis in the LAA. In the nomogram, each of the 5 factors were assigned a point value according to its relative contribution, and the total score was calculated by summing the individual scores derived from the nomogram. Figure 4 illustrates the clinical application of the nomogram in predicting the individualized risk of circulatory stasis. For example, a patient with nonparoxysmal AF (76 points), a hemoglobin level of 120 g/L (43 points), elevated levels of BNP (72 points), a LAD of 45 mm (68 points), and moderate to severe tricuspid insufficiency (78 points) achieves a total score of 337 points, corresponding to a risk score of 0.503. This indicates that the patient has a 50.3% probability of circulatory stasis formation in the LAA.

AF indicates atrial fibrillation; BNP, brain natriuretic peptide; LAD, left atrium diameter; and Pr, probability.

Internal and External Validation of the Nomogram for Estimating the Risk of Circulatory Stasis in the LAA

After the construction of the nomogram, the discriminatory ability of the nomogram model was assessed using the receiver operating characteristic curve analysis. As shown in Figure S2, the nomogram model demonstrated good discriminative performance, with an AUC of 0.853 (95% CI, 0.809–0.892, P<0.001) in the internal validation (1000 bootstraps). Consistent results were observed in both training cohort (0.848 [95% CI, 0.807–0.890], P<0.001) and validation cohort (0.826 [95% CI, 0.759–0.893], P<0.001), all of which significantly outperformed conventional scores, including CHADS₂, CHA₂DS₂‐VASc, and ATRIA ⁴⁵ scores (Figure S3). Calibration curves (Figure S4) and the Hosmer–Lemeshow goodness‐of‐fit test (training cohort: χ²=3.506, P=0.899; validation cohort: χ²=3.788, P=0.876) showed good agreement between the predicted and observed risk. The DCA showed that the nomogram consistently provided higher net benefit across a wide range of threshold probabilities (4.1%–89.1% in training and 4.8%–58.0% in validation cohorts), outperforming conventional scores (Figure S5).

The Relationship Between Circulatory Stasis in the LAA and Low‐Voltage Areas

Among the 548 consecutive patients included in this study, 393 (71.7%) underwent voltage mapping‐guided ablation, ands the remaining 155 (28.3%) received conventional ablation without voltage mapping. Of those with LA voltage mapping, 273 were in the circulatory normal group and 120 in the circulatory stasis group. Compared with patients with circulatory normal in the LAA, those with circulatory stasis in the LAA exhibited distinct baseline characteristics (Table S6). To account for baseline differences between groups, we performed a 1:1 PSM (Figure S6). After PSM, 102 matched pairs with well‐balanced characteristics (all P>0.05) were analyzed (Table S6). The results demonstrated that patients with circulatory stasis had significantly higher proportions of low‐voltage areas compared with those without circulatory stasis, both before (56.7% versus 30.4%, P<0.001) and after (55.9% versus 33.3%, P=0.001) PSM (Figure S7).

The Relationship Between Circulatory Stasis in the LAA and AF Recurrence

In this study, 23 patients (4.2%) were lost to follow‐up. After a 3‐month blanking period, AF recurrence was observed in 39.1% (50/128) of patients with circulatory stasis in the LAA, compared with 19.4% (77/397) of those without circulatory stasis in the LAA. To address potential confounding factors, the 1:1 PSM was performed. After PSM, 114 patients remained in each group (Figure S8), with balanced baseline characteristics (all P>0.05, Table S7). Kaplan–Meier analysis showed a significantly higher recurrence rate in patients with circulatory stasis, both before (log‐rank 22.30, P<0.001, Figure 5) and after PSM (log‐rank 10.60, P=0.001, Figure S9).

In the Cox regression analysis, the presence of circulatory stasis in the LAA was associated with an increased risk of postablation AF recurrence (unadjusted HR, 2.29 [95% CI, 1.61–3.27]; P<0.001). After full adjustment, the presence of circulatory stasis in the LAA remained independently associated with AF recurrence (adjusted HR, 2.41 [95% CI, 1.57–3.72]; P<0.001), as shown in Table 3.

Table 3.

Cox Regression Analysis to Show the Association Between Circulatory Stasis on Cardiac CTA and Atrial Fibrillation Recurrence

	Circulatory normal	Circulatory stasis	P value
No.	397	128
AF recurrence	77	50
Annual incidence rate of AF recurrence, % (95% CI)	19.4 (13.9–24.9)	39.1 (32.3–45.8)
HR (95% CI), model 0	1	2.29 (1.61–3.27)	<0.001
HR (95% CI), model 1	1	2.29 (1.60–3.28)	<0.001
HR (95% CI), model 2	1	2.31 (1.55–3.45)	<0.001
HR (95% CI), model 3	1	2.43 (1.58–3.74)	<0.001
HR (95% CI), model 4	1	2.41 (1.57–3.72)	<0.001

Open in a new tab

Model 0: unadjusted. Model 1: adjusted for demographic characteristics, including age and sex. Model 2: Model 1 + adjustment for medical history, including hypertension, diabetes, prior stroke/transient ischemic attack, heart failure, vascular disease, and nonparoxysmal atrial fibrillation. Model 3: Model 2 + elevated levels of natriuretic peptides, left ventricular ejection fraction, and left atrium diameter. Model 4: Model 3 + ablation strategy other than pulmonary vein isolation, including additional linear ablation and substrate modification.

AF indicates atrial fibrillation; CTA, computed tomography angiography; and HR, hazard ratio.

Moreover, in the subgroup analysis stratified by AF type, we found that in patients with nonparoxysmal AF, circulatory stasis was significantly associated with AF recurrence (HR, 2.72 [95% CI, 1.61–4.57], P<0.001). For patients with paroxysmal AF, although the association did not reach statistical significance (HR, 1.65 [95% CI, 0.84–3.24], P=0.145), its direction and magnitude suggest a clinically relevant trend. No statistically significant interaction was found between AF type and the association of circulatory stasis on recurrence (Interaction P=0.243).

As shown in Figure 6, the incorporation of circulatory stasis in the LAA into three conventional scoring systems significantly improved their discriminative ability. Specifically, the AUC increased from 0.524 to 0.616 (P=0.037) for the APPLE score, from 0.516 to 0.617 (P=0.035) for the CAAP‐AF score, and from 0.532 to 0.619 (P=0.001) for the CHA₂DS₂‐VASc score. The 10‐fold cross‐validation AUCs also demonstrated consistent improvement after incorporating circulatory stasis in the LAA, rising from 0.522±0.034 to 0.621±0.119 for the APPLE score, from 0.547±0.051 to 0.636±0.113 for the CAAP‐AF score, and from 0.570±0.111 to 0.623±0.111 for the CHA₂DS₂‐VASc score. The calibration curves (Figure S10) and the Hosmer–Lemeshow goodness‐of‐fit test for the new composite models (APPLE + circulatory stasis: χ²=0.846, P=0.932; CAAP‐AF + circulatory stasis: χ²=8.462, P=0.206; CHA₂DS₂‐VASc + circulatory stasis: χ²=10.187, P=0.117) demonstrated good agreement between the predicted and observed risk. Moreover, DCA showed a greater net clinical benefit of the new composite models (19.0%–39.4% for APPLE + circulatory stasis, 19.1%–49.0% for CAAP‐AF + circulatory stasis, and 18.9%–37.2% for CHA₂DS₂‐VASc + circulatory stasis) compared with the original scores across clinically relevant threshold probability ranges (22.8%–24.8% for APPLE, 23.5%–25.7% for CAAP‐AF, and 23.1%–26.4% for CHA₂DS₂‐VASc), as shown in Figure S11.

The Safety of AF Ablation in Patients with Circulatory Stasis in the LAA

Among the 548 patients who underwent the initial AF ablation, no periprocedural severe adverse events—including acute ischemic stroke, major bleeding, and cardiac tamponade—were observed in either the circulatory normal group or the circulatory stasis group.

Discussion

In this prospective observational study, our main findings were as follows: (1) nonparoxysmal AF, elevated levels of hemoglobin and BNP, increased LAD, and moderate or severe tricuspid regurgitation were identified as independent risk factors associated with the presence of circulatory stasis in the LAA; (2) the presence of circulatory stasis was determined to be an independent risk factor for AF recurrence after the initial AF ablation; (3) the incorporation of circulatory stasis in the LAA significantly enhanced the predictive accuracy of conventional scoring systems for AF recurrence; and (4) in patients with circulatory stasis in the LAA, AF ablation could be safely performed.

Due to the limitation of TEE, intracardiac echocardiography has been increasingly used as an alternative in clinical practice. However, intracardiac echocardiography also has its drawbacks, including the need for additional vascular access, higher procedural costs, and limited availability in some centers. ⁴⁶ In contrast, cardiac CTA is a completely noninvasive modality. Moreover, the limitations of CTA are being progressively mitigated. Advances in scanner technology, including delayed imaging, ECG gating, and high‐pitch protocols, allow for improved image acquisition even in patients with higher heart rates, whereas new contrast agents and dose‐optimization techniques help reduce both nephrotoxicity and radiation burden. ⁴⁷ , ⁴⁸ , ⁴⁹ Given these advantages, cardiac CTA is increasingly being adopted in clinical practice, especially in patients who are poor candidates for TEE or in centers where intracardiac echocardiography is not routinely available.

The LAA, a finger‐like structure protruding from the LA cavity, is both structurally complex and functionally important. It plays a crucial role in intravascular volume regulation through its contractile properties and the release of natriuretic peptides in response to hemodynamic changes. ⁵⁰ In the presence of AF, the LAA loses its ability to constrict, resulting in reduced flow velocity, ultimately leading to the formation of abnormal blood flow. ⁵¹ Previous studies have demonstrated an association between certain LAA morphology (eg, nonchicken‐wing type and complex LAA) and thrombus formation. ⁵² , ⁵³ However, our study did not find a significant correlation between LAA morphology and circulatory stasis. Several factors may account for this discrepancy: (1) differences in morphology distribution—in our cohort, the distribution of LAA morphologies was chicken‐wing (29.7%, 163/548), cactus (35.0%, 192/548), windsock (30.8%, 169/548), and cauliflower (4.4%, 24/548). These proportions differ notably from those reported by Di Biase et al., ⁵⁴ where the chicken‐wing type was more prevalent (48.4%, 451/932). This variation may be attributed to differences in patient characteristics and relatively smaller sample size of our study. (2) Differences in pathophysiological mechanisms between circulatory stasis and thrombus formation: Although prior studies have demonstrated that LAA morphology is associated with thrombus formation, it may exert a less pronounced influence on circulatory stasis alone. Thrombus formation is a multifactorial process that involves not only blood flow stasis, but also endothelial dysfunction and hypercoagulability. ⁵⁵ In contrast, circulatory stasis—as assessed in our study—is primarily a hemodynamic phenomenon. Therefore, the contribution of LAA morphology might be more significant when considering the full thrombotic pathway than when evaluating stasis in isolation. This mechanistic distinction may partially explain the lack of association between LAA morphology and circulatory stasis observed in our analysis.

Our study revealed that nonparoxysmal AF, elevated hemoglobin and BNP levels, increased LAD, and moderate or severe tricuspid regurgitation were independently associated with circulatory stasis in the LAA. Nonparoxysmal AF, elevated hemoglobin and BNP levels, along with increased LAD, might increase blood viscosity and prolong blood retention in the LAA, creating a prothrombotic environment favorable for the development of circulatory stasis in the LAA. ⁵⁶ , ⁵⁷ In addition, moderate or severe tricuspid regurgitation may lead to right heart volume overload, triggering the release of systemic inflammatory mediators that contribute to endothelial damage, ultimately fostering circulatory stasis in the LAA. ⁵⁸ Interestingly, although previous studies have highlighted an association between LA SEC and the CHA₂DS₂‐VASc score, ¹⁰ our study did not demonstrate significant differences in CHA₂DS₂‐VASc score between the circulatory stasis group and the circulatory normal group. This suggests that the CHA₂DS₂‐VASc score may not be a reliable indicator for assessing circulatory stasis in the LAA in all clinical settings. Furthermore, our findings underscore the importance of preprocedural cardiac CTA in assessing circulatory status in the LAA in patients with nonparoxysmal AF, elevated levels of hemoglobin and BNP, an increased LAD, and moderate or severe tricuspid regurgitation. Further studies are warranted to comprehensively identify all factors contributing to circulatory stasis in the LAA.

Kim et al. ⁵⁹ reported that in patients with successful cardioversion, those who experienced AF recurrences had a higher incidence of SEC on TEE (68.1% versus 40.0%, P=0.0106). A recent study has also demonstrated that SEC could serve as a predictor for AF recurrence after catheter ablation, particularly in AF patients with LA dilation, with a higher degree of SEC associated with an increased risk of recurrence. ¹⁷ A meta‐analysis by Raval et al. ⁶⁰ further highlighted the prognostic value of LAA velocity in predicting postablation AF recurrence, providing important evidence for impaired LAA function as a surrogate marker of adverse atrial remodeling. Unlike Doppler‐derived velocities used in echocardiographic studies, our study sought to expand on this concept by investigating the association between circulatory stasis in the LAA assessed via cardiac CTA and AF recurrence after initial catheter ablation. In line with these findings, our study observed that AF recurrence was significantly higher in patients with circulatory stasis in the LAA on cardiac CTA. Moreover, after adjusting for demographic and clinical characteristics, examination results, and additional ablation strategies, we found that the presence of circulatory stasis in the LAA on cardiac CTA remained significantly associated with AF recurrence following the initial AF ablation. Our findings further support the concept that impaired LAA function, regardless of the imaging modality used, may serve as a predictor of AF recurrence after catheter ablation. In addition, our study found a strong correlation between LAA circulatory stasis detected on CTA and electroanatomic markers of atrial fibrosis, as represented by low‐voltage areas. This supports the hypothesis that stasis reflects more advanced atrial remodeling and may serve as a noninvasive surrogate for adverse atrial substrate. The more unfavorable atrial substrate could probably explain the poorer sinus rhythm maintenance after catheter ablation in patients with circulatory stasis in the LAA. These findings may facilitate timely interventions to modify the arrhythmogenic substrate, potentially eliminating the risk of AF recurrence following the initial ablation procedure.

It was well established that the presence of LA thrombus is a contradiction for cardioversion and AF ablation. However, whether AF ablation can be safely performed in patients with circulatory stasis in the LAA remained controversial. Kavlak et al. ⁶¹ reported that SEC on TEE could predispose embolization. Lowe et al. ⁵⁷ also noticed that sludge within the LAA on TEE was an independent predictor for subsequent thromboembolic events and all‐cause mortality. Furthermore, both Takigawa et al. ⁶² and Kim et al. ⁶³ demonstrated that in patients with AF, SEC was associated with an elevated risk of late‐phase thromboembolic events following successful catheter ablation. In contrast, Patel et al. ⁶⁴ concluded that the risk of cardioembolic stroke after cardioversion in patients with SEC was low. Similarly, Chilukuri et al. ⁶⁵ found that the presence of SEC did not increase the risk of periprocedural cerebrovascular accidents after AF ablation, suggesting that SEC on TEE should not be considered as a contradiction of cardioversion. In our current study, none of the patients with circulatory stasis in the LAA on cardiac CTA experienced severe adverse events during the periprocedural period. This suggested that, despite the presence of circulatory stasis in the LAA on cardiac CTA, AF ablation can still be safely performed.

Our study has some limitations. First, as a single‐center cohort study with a modest sample size, our findings and the associated predictive model require external validation in multicenter studies with larger cohorts to confirm generalizability and mitigate potential biases. Second, in the present study, the choice of imaging modality for preprocedural thrombus evaluation (TEE or cardiac CTA) was guided by clinical judgment and patient preference, which might affect the generalizability of our findings. Third, we did not conduct a quantitative assessment of the LA function. We fully agree that more comprehensive assessment of LA function may provide valuable insights. Future studies incorporating detailed echocardiographic LA functional parameters are needed. Forth, some asymptomatic recurrence may have been undetected, and the follow‐up period was not long enough (12 months). In addition, patients were followed up with 24‐hour Holter ECG monitoring instead of long‐term continuous ECG monitoring, which limited our ability to assess AF burden. Moreover, although the presence of circulatory stasis in the LAA was significantly associated with an increased risk of AF recurrence following ablation, additional data might be necessary for more reliable prediction analysis. Future studies with larger cohorts and extended follow‐up durations are needed to better evaluate AF recurrence following the initial AF ablation.

Conclusions

In patients with nonvalvular AF, the presence of circulatory stasis within the LAA on cardiac CTA could serve as a predictor for AF recurrence following the initial catheter ablation procedure. AF ablation could be safely performed in patients with circulatory stasis in the LAA.

Sources of Funding

The study was funded by the National Natural Science Foundation of China (grant number 82270329) and Postgraduate Research & Practice Innovation Program of Jiangsu Province (JX54814307).

Disclosures

None.

Supporting information

Tables S1–S7

Figures S1–S11

JAH3-15-e045263-s001.pdf^{(1,004.5KB, pdf)}

Supplemental Material is available at https://www.ahajournals.org/doi/suppl/10.1161/JAHA.125.045263

For Sources of Funding and Disclosures, see page 13 and 14.

Prior Presentations: Oral presentation titled “Association of Circulatory Stasis in Left Atrial Appendage Detected by Cardiac Computed Tomography Angiography with Atrial Fibrillation Recurrence after Initial Catheter Ablation.” 16th Asia Pacific Heart Rhythm Society Scientific Session in Conjunction with CardioRhythm 2023, August 31–September 3, 2023, Hong Kong.

This article was sent to Shaan Khurshid, MD, MPH, Associate Editor, for review by expert referees, editorial decision, and final disposition.

Contributor Information

Yi Xu, Email: yixu@njmu.edu.cn.

Minglong Chen, Email: chenminglong@njmu.edu.cn.

Mingfang Li, Email: mingflee@hotmail.com.

References

1. Lip GY. Does atrial fibrillation confer a hypercoagulable state? Lancet. 1995;346:1313–1314. doi: 10.1016/s0140-6736(95)92339-x [DOI] [PubMed] [Google Scholar]
2. Watson T, Shantsila E, Lip GY. Mechanisms of thrombogenesis in atrial fibrillation: Virchow’s triad revisited. Lancet. 2009;373:155–166. doi: 10.1016/S0140-6736(09)60040-4 [DOI] [PubMed] [Google Scholar]
3. Cresti A, García‐Fernández MA, Sievert H, Mazzone P, Baratta P, Solari M, Geyer A, De Sensi F, Limbruno U. Prevalence of extra‐appendage thrombosis in non‐valvular atrial fibrillation and atrial flutter in patients undergoing cardioversion: a large transoesophageal echo study. EuroIntervention. 2019;15:e225–e230. doi: 10.4244/eij-d-19-00128 [DOI] [PubMed] [Google Scholar]
4. Beppu S, Nimura Y, Sakakibara H, Nagata S, Park YD, Izumi S. Smoke‐like echo in the left atrial cavity in mitral valve disease: its features and significance. J Am Coll Cardiol. 1985;6:744–749. doi: 10.1016/s0735-1097(85)80476-9 [DOI] [PubMed] [Google Scholar]
5. Leung DY, Black IW, Cranney GB, Hopkins AP, Walsh WF. Prognostic implications of left atrial spontaneous echo contrast in nonvalvular atrial fibrillation. J Am Coll Cardiol. 1994;24:755–762. doi: 10.1016/0735-1097(94)90025-6 [DOI] [PubMed] [Google Scholar]
6. Jones EF, Calafiore P, McNeil JJ, Tonkin AM, Donnan GA. Atrial fibrillation with left atrial spontaneous contrast detected by transesophageal echocardiography is a potent risk factor for stroke. Am J Cardiol. 1996;78:425–429. doi: 10.1016/s0002-9149(96)00331-1 [DOI] [PubMed] [Google Scholar]
7. Bernhardt P, Schmidt H, Hammerstingl C, Luderitz B, Omran H. Patients with atrial fibrillation and dense spontaneous echo contrast at high risk a prospective and serial follow‐up over 12 months with transesophageal echocardiography and cerebral magnetic resonance imaging. J Am Coll Cardiol. 2005;45:1807–1812. doi: 10.1016/j.jacc.2004.11.071 [DOI] [PubMed] [Google Scholar]
8. Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of atrial fibrillation. JAMA. 2001;285:2864–2870. doi: 10.1001/jama.285.22.2864 [DOI] [PubMed] [Google Scholar]
9. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor‐based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137:263–272. doi: 10.1378/chest.09-1584 [DOI] [PubMed] [Google Scholar]
10. Puwanant S, Varr BC, Shrestha K, Hussain SK, Tang WH, Gabriel RS, Wazni OM, Bhargava M, Saliba WI, Thomas JD, et al. Role of the CHADS2 score in the evaluation of thromboembolic risk in patients with atrial fibrillation undergoing transesophageal echocardiography before pulmonary vein isolation. J Am Coll Cardiol. 2009;54:2032–2039. doi: 10.1016/j.jacc.2009.07.037 [DOI] [PubMed] [Google Scholar]
11. Zhang E, Liu T, Li Z, Zhao J, Li G. High CHA2DS2‐VASc score predicts left atrial thrombus or spontaneous echo contrast detected by transesophageal echocardiography. Int J Cardiol. 2015;184:540–542. doi: 10.1016/j.ijcard.2015.02.109 [DOI] [PubMed] [Google Scholar]
12. Han D, Chu Y, Wu Y, Wang X. Determinants of left atrial thrombus or spontaneous echo contrast in nonvalvular atrial fibrillation. Thromb Res. 2020;195:233–237. doi: 10.1016/j.thromres.2020.07.055 [DOI] [PubMed] [Google Scholar]
13. Wang F, Zhu M, Wang X, Zhang W, Su Y, Lu Y, Pan X, Gao D, Zhang X, Chen W, et al. Predictive value of left atrial appendage lobes on left atrial thrombus or spontaneous echo contrast in patients with non‐valvular atrial fibrillation. BMC Cardiovasc Disord. 2018;18:153. doi: 10.1186/s12872-018-0889-y [DOI] [PMC free article] [PubMed] [Google Scholar]
14. Petersen M, Roehrich A, Balzer J, Shin DI, Meyer C, Kelm M, Kehmeier ES. Left atrial appendage morphology is closely associated with specific echocardiographic flow pattern in patients with atrial fibrillation. Europace. 2015;17:539–545. doi: 10.1093/europace/euu347 [DOI] [PubMed] [Google Scholar]
15. Wang H, Xi S, Chen J, Zhao L, Gan T, He B. Severe left atrial spontaneous Echo contrast in Nonvalvular atrial fibrillation: clinical characteristics and impact on ischemic risk Postablation. Thromb Haemost. 2023;123:522–534. doi: 10.1055/a-1983-0516 [DOI] [PubMed] [Google Scholar]
16. Gerede DM, Candemir B, Vurgun VK, Aghdam SM, Acibuca A, Ozcan OU, Goksuluk H, Kervancioglu C, Erol C. Prediction of recurrence after cryoballoon ablation therapy in patients with paroxysmal atrial fibrillation. Anatol J Cardiol. 2015;16:482–488. doi: 10.5152/AnatolJCardiol.2015.6309 [DOI] [PMC free article] [PubMed] [Google Scholar]
17. Lin C, Bao Y, Xie Y, Wei Y, Luo Q, Ling T, Jin Q, Pan W, Xie Y, Wu L, et al. Prognostic implications of left atrial spontaneous Echo contrast with catheter ablation of Nonvalvular atrial fibrillation patients with left atrial dilation. J Cardiovasc Dev Dis. 2022;9:9. doi: 10.3390/jcdd9090306 [DOI] [PMC free article] [PubMed] [Google Scholar]
18. Daniel WG, Erbel R, Kasper W, Visser CA, Engberding R, Sutherland GR, Grube E, Hanrath P, Maisch B, Dennig K. Safety of transesophageal echocardiography. A multicenter survey of 10,419 examinations. Circulation. 1991;83:817–821. doi: 10.1161/01.cir.83.3.817 [DOI] [PubMed] [Google Scholar]
19. Khandheria BK, Seward JB, Tajik AJ. Transesophageal echocardiography. Mayo Clin Proc. 1994;69:856–863. doi: 10.1016/s0025-6196(12)61788-1 [DOI] [PubMed] [Google Scholar]
20. Hilberath JN, Oakes DA, Shernan SK, Bulwer BE, D’Ambra MN, Eltzschig HK. Safety of transesophageal echocardiography. J Am Soc Echocardiogr. 2010;23:1115–1127. doi: 10.1016/j.echo.2010.08.013 [DOI] [PubMed] [Google Scholar]
21. Cote G, Denault A. Transesophageal echocardiography‐related complications. Can J Anaesth. 2008;55:622–647. doi: 10.1007/BF03021437 [DOI] [PubMed] [Google Scholar]
22. Hur J, Kim YJ, Lee HJ, Ha JW, Heo JH, Choi EY, Shim CY, Kim TH, Nam JE, Choe KO, et al. Left atrial appendage thrombi in stroke patients: detection with two‐phase cardiac CT angiography versus transesophageal echocardiography. Radiology. 2009;251:683–690. doi: 10.1148/radiol.2513090794 [DOI] [PubMed] [Google Scholar]
23. Romero J, Cao JJ, Garcia MJ, Taub CC. Cardiac imaging for assessment of left atrial appendage stasis and thrombosis. Nat Rev Cardiol. 2014;11:470–480. doi: 10.1038/nrcardio.2014.77 [DOI] [PubMed] [Google Scholar]
24. Bilchick KC, Mealor A, Gonzalez J, Norton P, Zhuo D, Mason P, Ferguson JD, Malhotra R, Michael Mangrum J, Darby AE, et al. Effectiveness of integrating delayed computed tomography angiography imaging for left atrial appendage thrombus exclusion into the care of patients undergoing ablation of atrial fibrillation. Heart Rhythm. 2016;13:12–19. doi: 10.1016/j.hrthm.2015.09.002 [DOI] [PMC free article] [PubMed] [Google Scholar]
25. Hur J, Kim YJ, Lee HJ, Nam JE, Hong YJ, Kim HY, Lee JW, Choi BW. Cardioembolic stroke: dual‐energy cardiac CT for differentiation of left atrial appendage thrombus and circulatory stasis. Radiology. 2012;263:688–695. doi: 10.1148/radiol.12111691 [DOI] [PubMed] [Google Scholar]
26. von Elm E, Altman DG, Egger M, Pocock SJ, Gotzsche PC, Vandenbroucke JP, Initiative S. The strengthening the reporting of observational studies in epidemiology (STROBE) statement: guidelines for reporting observational studies. J Clin Epidemiol. 2008;61:344–349. doi: 10.1016/j.jclinepi.2007.11.008 [DOI] [PubMed] [Google Scholar]
27. Michels WM, Grootendorst DC, Verduijn M, Elliott EG, Dekker FW, Krediet RT. Performance of the Cockcroft‐gault, MDRD, and new CKD‐EPI formulas in relation to GFR, age, and body size. Clin J Am Soc Nephrol. 2010;5:1003–1009. doi: 10.2215/CJN.06870909 [DOI] [PMC free article] [PubMed] [Google Scholar]
28. Authors/Task Force M , McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Bohm M, Burri H, Butler J, Celutkiene J, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: developed by the task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). With the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2021;24:4–131. doi: 10.1002/ejhf.2333 [DOI] [PubMed] [Google Scholar]
29. Vaziri SM, Larson MG, Benjamin EJ, Levy D. Echocardiographic predictors of nonrheumatic atrial fibrillation. The Framingham Heart Study. Circulation. 1994;89:724–730. doi: 10.1161/01.cir.89.2.724 [DOI] [PubMed] [Google Scholar]
30. Kizer JR, Bella JN, Palmieri V, Liu JE, Best LG, Lee ET, Roman MJ, Devereux RB. Left atrial diameter as an independent predictor of first clinical cardiovascular events in middle‐aged and elderly adults: the Strong Heart Study (SHS). Am Heart J. 2006;151:412–418. doi: 10.1016/j.ahj.2005.04.031 [DOI] [PubMed] [Google Scholar]
31. Nakanishi T, Hamada S, Takamiya M, Naito H, Imakita S, Yamada N, Kimura K, Hirose Y, Nagata S. A pitfall in ultrafast CT scanning for the detection of left atrial thrombi. J Comput Assist Tomogr. 1993;17:42–45. doi: 10.1097/00004728-199301000-00006 [DOI] [PubMed] [Google Scholar]
32. Hajduczok ZD, Weiss RM, Stanford W, Marcus ML. Determination of right ventricular mass in humans and dogs with ultrafast cardiac computed tomography. Circulation. 1990;82:202–212. doi: 10.1161/01.cir.82.1.202 [DOI] [PubMed] [Google Scholar]
33. Liu X, Zhang Q, Yang ZG, Shi K, Xu HY, Xie LJ, Jiang L, Diao KY, Guo YK. Assessment of left ventricular deformation in patients with Ebstein’s anomaly by cardiac magnetic resonance tissue tracking. Eur J Radiol. 2017;89:20–26. doi: 10.1016/j.ejrad.2017.01.013 [DOI] [PubMed] [Google Scholar]
34. Fatkin D, Kelly RP, Feneley MP. Relations between left atrial appendage blood flow velocity, spontaneous echocardiographic contrast and thromboembolic risk in vivo. J Am Coll Cardiol. 1994;23:961–969. doi: 10.1016/0735-1097(94)90644-0 [DOI] [PubMed] [Google Scholar]
35. Calkins H, Hindricks G, Cappato R, Kim YH, Saad EB, Aguinaga L, Akar JG, Badhwar V, Brugada J, Camm J, et al. 2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation. Europace. 2018;20:e1–e160. doi: 10.1093/europace/eux274 [DOI] [PMC free article] [PubMed] [Google Scholar]
36. Yang B, Jiang C, Lin Y, Yang G, Chu H, Cai H, Lu F, Zhan X, Xu J, Wang X, et al. STABLE‐SR (electrophysiological substrate ablation in the left atrium during sinus rhythm) for the treatment of nonparoxysmal atrial fibrillation: a prospective, multicenter randomized clinical trial. Circ Arrhythm Electrophysiol. 2017;10:10. doi: 10.1161/CIRCEP.117.005405 [DOI] [PubMed] [Google Scholar]
37. Yang G, Zheng L, Jiang C, Fan J, Liu X, Zhan X, Li J, Wang L, Yang H, Zhu W, et al. Circumferential pulmonary vein isolation plus low‐voltage area modification in persistent atrial fibrillation: the STABLE‐SR‐II trial. JACC Clin Electrophysiol. 2022;8:882–891. doi: 10.1016/j.jacep.2022.03.012 [DOI] [PubMed] [Google Scholar]
38. Chen H, Li C, Han B, Xiao F, Yi F, Wei Y, Jiang C, Zou C, Shi L, Ma W, et al. Circumferential pulmonary vein isolation with vs without additional low‐voltage‐area ablation in older patients with paroxysmal atrial fibrillation: a randomized clinical trial. JAMA Cardiol. 2023;8:765–772. doi: 10.1001/jamacardio.2023.1749 [DOI] [PMC free article] [PubMed] [Google Scholar]
39. Schulman S, Kearon C; Subcommittee on Control of Anticoagulation of the S, Standardization Committee of the International Society on T, Haemostasis . Definition of major bleeding in clinical investigations of antihemostatic medicinal products in non‐surgical patients. J Thromb Haemost. 2005;3:692–694. doi: 10.1111/j.1538-7836.2005.01204.x [DOI] [PubMed] [Google Scholar]
40. Kornej J, Hindricks G, Shoemaker MB, Husser D, Arya A, Sommer P, Rolf S, Saavedra P, Kanagasundram A, Patrick Whalen S, et al. The APPLE score: a novel and simple score for the prediction of rhythm outcomes after catheter ablation of atrial fibrillation. Clin Res Cardiol. 2015;104:871–876. doi: 10.1007/s00392-015-0856-x [DOI] [PMC free article] [PubMed] [Google Scholar]
41. Winkle RA, Jarman JW, Mead RH, Engel G, Kong MH, Fleming W, Patrawala RA. Predicting atrial fibrillation ablation outcome: the CAAP‐AF score. Heart Rhythm. 2016;13:2119–2125. doi: 10.1016/j.hrthm.2016.07.018 [DOI] [PubMed] [Google Scholar]
42. Letsas KP, Efremidis M, Giannopoulos G, Deftereos S, Lioni L, Korantzopoulos P, Vlachos K, Xydonas S, Kossyvakis C, Sideris A. CHADS2 and CHA2DS2‐VASc scores as predictors of left atrial ablation outcomes for paroxysmal atrial fibrillation. Europace. 2014;16:202–207. doi: 10.1093/europace/eut210 [DOI] [PubMed] [Google Scholar]
43. Jacobs V, May HT, Bair TL, Crandall BG, Cutler M, Day JD, Weiss JP, Osborn JS, Muhlestein JB, Anderson JL, et al. The impact of risk score (CHADS2 versus CHA2DS2‐VASc) on long‐term outcomes after atrial fibrillation ablation. Heart Rhythm. 2015;12:681–686. doi: 10.1016/j.hrthm.2014.12.034 [DOI] [PubMed] [Google Scholar]
44. DeLong ER, DeLong DM, Clarke‐Pearson DL. Comparing the areas under two or more correlated receiver operating characteristic curves: a nonparametric approach. Biometrics. 1988;44:837–845. doi: 10.2307/2531595 [DOI] [PubMed] [Google Scholar]
45. Singer DE, Chang Y, Borowsky LH, Fang MC, Pomernacki NK, Udaltsova N, Reynolds K, Go AS. A new risk scheme to predict ischemic stroke and other thromboembolism in atrial fibrillation: the ATRIA study stroke risk score. J Am Heart Assoc. 2013;2:e000250. doi: 10.1161/JAHA.113.000250 [DOI] [PMC free article] [PubMed] [Google Scholar]
46. Alkhouli M, Chaker Z, Alqahtani F, Raslan S, Raybuck B. Outcomes of routine Intracardiac echocardiography to guide left atrial appendage occlusion. JACC Clin Electrophysiol. 2020;6:393–400. doi: 10.1016/j.jacep.2019.11.014 [DOI] [PubMed] [Google Scholar]
47. Romero J, Husain SA, Kelesidis I, Sanz J, Medina HM, Garcia MJ. Detection of left atrial appendage thrombus by cardiac computed tomography in patients with atrial fibrillation: a meta‐analysis. Circ Cardiovasc Imaging. 2013;6:185–194. doi: 10.1161/CIRCIMAGING.112.000153 [DOI] [PubMed] [Google Scholar]
48. Zou H, Zhang Y, Tong J, Liu Z. Multidetector computed tomography for detecting left atrial/left atrial appendage thrombus: a meta‐analysis. Intern Med J. 2015;45:1044–1053. doi: 10.1111/imj.12862 [DOI] [PubMed] [Google Scholar]
49. Thai WE, Wai B, Lin K, Cheng T, Heist EK, Hoffmann U, Singh JP, Truong QA. Pulmonary venous anatomy imaging with low‐dose, prospectively ECG‐triggered, high‐pitch 128‐slice dual‐source computed tomography. Circ Arrhythm Electrophysiol. 2012;5:521–530. doi: 10.1161/CIRCEP.111.968313 [DOI] [PMC free article] [PubMed] [Google Scholar]
50. Karim N, Ho SY, Nicol E, Li W, Zemrak F, Markides V, Reddy V, Wong T. The left atrial appendage in humans: structure, physiology, and pathogenesis. Europace. 2020;22:5–18. doi: 10.1093/europace/euz212 [DOI] [PubMed] [Google Scholar]
51. Beigel R, Wunderlich NC, Ho SY, Arsanjani R, Siegel RJ. The left atrial appendage: anatomy, function, and noninvasive evaluation. JACC Cardiovasc Imaging. 2014;7:1251–1265. doi: 10.1016/j.jcmg.2014.08.009 [DOI] [PubMed] [Google Scholar]
52. Negrotto SM, Lugo RM, Metawee M, Kanagasundram AN, Chidsey G, Baker MT, Michaud GF, Piana RN, Benjamin Shoemaker M, Ellis CR. Left atrial appendage morphology predicts the formation of left atrial appendage thrombus. J Cardiovasc Electrophysiol. 2021;32:1044–1052. doi: 10.1111/jce.14922 [DOI] [PubMed] [Google Scholar]
53. Yamamoto M, Seo Y, Kawamatsu N, Sato K, Sugano A, Machino‐Ohtsuka T, Kawamura R, Nakajima H, Igarashi M, Sekiguchi Y, et al. Complex left atrial appendage morphology and left atrial appendage thrombus formation in patients with atrial fibrillation. Circ Cardiovasc Imaging. 2014;7:337–343. doi: 10.1161/CIRCIMAGING.113.001317 [DOI] [PubMed] [Google Scholar]
54. Di Biase L, Santangeli P, Anselmino M, Mohanty P, Salvetti I, Gili S, Horton R, Sanchez JE, Bai R, Mohanty S, et al. Does the left atrial appendage morphology correlate with the risk of stroke in patients with atrial fibrillation? Results from a multicenter study. J Am Coll Cardiol. 2012;60:531–538. doi: 10.1016/j.jacc.2012.04.032 [DOI] [PubMed] [Google Scholar]
55. Lip GY, Gibbs CR. Does heart failure confer a hypercoagulable state? Virchow’s triad revisited. J Am Coll Cardiol. 1999;33:1424–1426. doi: 10.1016/s0735-1097(99)00033-9 [DOI] [PubMed] [Google Scholar]
56. Rekosz J, Karwowski J, Kowalik I, Wiktorska A, Wrzosek K, Solecki M, Szmarowska K, Szymanska A, Mierzejewska B, Syska‐Suminska J, et al. Risk factors for thrombosis and spontaneous echocardiographic contrast with sludge in atrial fibrillation patients treated with oral anticoagulants before electrical cardioversion. Kardiol Pol. 2024;82:516–526. doi: 10.33963/v.phj.100078 [DOI] [PubMed] [Google Scholar]
57. Lowe BS, Kusunose K, Motoki H, Varr B, Shrestha K, Whitman C, Tang WH, Thomas JD, Klein AL. Prognostic significance of left atrial appendage “sludge” in patients with atrial fibrillation: a new transesophageal echocardiographic thromboembolic risk factor. J Am Soc Echocardiogr. 2014;27:1176–1183. doi: 10.1016/j.echo.2014.08.016 [DOI] [PubMed] [Google Scholar]
58. Sanders‐van Wijk S, Tromp J, Beussink‐Nelson L, Hage C, Svedlund S, Saraste A, Swat SA, Sanchez C, Njoroge J, Tan RS, et al. Proteomic evaluation of the comorbidity‐inflammation paradigm in heart failure with preserved ejection fraction: results from the PROMIS‐HFpEF study. Circulation. 2020;142:2029–2044. doi: 10.1161/CIRCULATIONAHA.120.045810 [DOI] [PMC free article] [PubMed] [Google Scholar]
59. Kim SK, Pak HN, Park JH, Ko KJ, Lee JS, Choi JI, Choi DH, Kim YH. Clinical and serological predictors for the recurrence of atrial fibrillation after electrical cardioversion. Europace. 2009;11:1632–1638. doi: 10.1093/europace/eup321 [DOI] [PubMed] [Google Scholar]
60. Raval M, Katukuri N, Venugopalan S, Jain A, Majmundar V, Siddiq S, Desai R. Abstract 16517: Association of low Left Atrial Appendage Velocity with Increased Risk of atrial fibrillation recurrence after catheter ablation: a meta‐analysis. Circulation. 2023;148:A16517. doi: 10.1161/circ.148.suppl_1.16517 [DOI] [Google Scholar]
61. Kavlak ES, Kucukoglu H, Yigit Z, Okcun B, Baran T, Ozkan AA, Kucukoglu S. Clinical and echocardiographic risk factors for embolization in the presence of left atrial thrombus. Echocardiography. 2007;24:515–521. doi: 10.1111/j.1540-8175.2007.00420.x [DOI] [PubMed] [Google Scholar]
62. Takigawa M, Takahashi A, Kuwahara T, Takahashi Y, Okubo K, Nakashima E, Watari Y, Nakajima J, Takagi K, Yamao K, et al. Late‐phase thromboembolism after catheter ablation for paroxysmal atrial fibrillation. Circ J. 2014;78:2394–2401. doi: 10.1253/circj.cj-14-0525 [DOI] [PubMed] [Google Scholar]
63. Kim YG, Shim J, Oh SK, Lee KN, Choi JI, Kim YH. Risk factors for ischemic stroke in atrial fibrillation patients undergoing radiofrequency catheter ablation. Sci Rep. 2019;9:7051. doi: 10.1038/s41598-019-43566-z [DOI] [PMC free article] [PubMed] [Google Scholar]
64. Patel SV, Flaker G. Is early cardioversion for atrial fibrillation safe in patients with spontaneous echocardiographic contrast? Clin Cardiol. 2008;31:148–152. doi: 10.1002/clc.20172 [DOI] [PMC free article] [PubMed] [Google Scholar]
65. Chilukuri K, Mayer SA, Scherr D, Dalal D, Abraham T, Henrikson CA, Cheng A, Nazarian S, Sinha S, Spragg D, et al. Transoesophageal echocardiography predictors of periprocedural cerebrovascular accident in patients undergoing catheter ablation of atrial fibrillation. Europace. 2010;12:1543–1549. doi: 10.1093/europace/euq295 [DOI] [PubMed] [Google Scholar]

Associated Data

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

Supplementary Materials

Tables S1–S7

Figures S1–S11

JAH3-15-e045263-s001.pdf^{(1,004.5KB, pdf)}

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

[jah370160-bib-0001] 1. Lip GY. Does atrial fibrillation confer a hypercoagulable state? Lancet. 1995;346:1313–1314. doi: 10.1016/s0140-6736(95)92339-x [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0002] 2. Watson T, Shantsila E, Lip GY. Mechanisms of thrombogenesis in atrial fibrillation: Virchow’s triad revisited. Lancet. 2009;373:155–166. doi: 10.1016/S0140-6736(09)60040-4 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0003] 3. Cresti A, García‐Fernández MA, Sievert H, Mazzone P, Baratta P, Solari M, Geyer A, De Sensi F, Limbruno U. Prevalence of extra‐appendage thrombosis in non‐valvular atrial fibrillation and atrial flutter in patients undergoing cardioversion: a large transoesophageal echo study. EuroIntervention. 2019;15:e225–e230. doi: 10.4244/eij-d-19-00128 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0004] 4. Beppu S, Nimura Y, Sakakibara H, Nagata S, Park YD, Izumi S. Smoke‐like echo in the left atrial cavity in mitral valve disease: its features and significance. J Am Coll Cardiol. 1985;6:744–749. doi: 10.1016/s0735-1097(85)80476-9 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0005] 5. Leung DY, Black IW, Cranney GB, Hopkins AP, Walsh WF. Prognostic implications of left atrial spontaneous echo contrast in nonvalvular atrial fibrillation. J Am Coll Cardiol. 1994;24:755–762. doi: 10.1016/0735-1097(94)90025-6 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0006] 6. Jones EF, Calafiore P, McNeil JJ, Tonkin AM, Donnan GA. Atrial fibrillation with left atrial spontaneous contrast detected by transesophageal echocardiography is a potent risk factor for stroke. Am J Cardiol. 1996;78:425–429. doi: 10.1016/s0002-9149(96)00331-1 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0007] 7. Bernhardt P, Schmidt H, Hammerstingl C, Luderitz B, Omran H. Patients with atrial fibrillation and dense spontaneous echo contrast at high risk a prospective and serial follow‐up over 12 months with transesophageal echocardiography and cerebral magnetic resonance imaging. J Am Coll Cardiol. 2005;45:1807–1812. doi: 10.1016/j.jacc.2004.11.071 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0008] 8. Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of atrial fibrillation. JAMA. 2001;285:2864–2870. doi: 10.1001/jama.285.22.2864 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0009] 9. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor‐based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137:263–272. doi: 10.1378/chest.09-1584 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0010] 10. Puwanant S, Varr BC, Shrestha K, Hussain SK, Tang WH, Gabriel RS, Wazni OM, Bhargava M, Saliba WI, Thomas JD, et al. Role of the CHADS2 score in the evaluation of thromboembolic risk in patients with atrial fibrillation undergoing transesophageal echocardiography before pulmonary vein isolation. J Am Coll Cardiol. 2009;54:2032–2039. doi: 10.1016/j.jacc.2009.07.037 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0011] 11. Zhang E, Liu T, Li Z, Zhao J, Li G. High CHA2DS2‐VASc score predicts left atrial thrombus or spontaneous echo contrast detected by transesophageal echocardiography. Int J Cardiol. 2015;184:540–542. doi: 10.1016/j.ijcard.2015.02.109 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0012] 12. Han D, Chu Y, Wu Y, Wang X. Determinants of left atrial thrombus or spontaneous echo contrast in nonvalvular atrial fibrillation. Thromb Res. 2020;195:233–237. doi: 10.1016/j.thromres.2020.07.055 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0013] 13. Wang F, Zhu M, Wang X, Zhang W, Su Y, Lu Y, Pan X, Gao D, Zhang X, Chen W, et al. Predictive value of left atrial appendage lobes on left atrial thrombus or spontaneous echo contrast in patients with non‐valvular atrial fibrillation. BMC Cardiovasc Disord. 2018;18:153. doi: 10.1186/s12872-018-0889-y [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0014] 14. Petersen M, Roehrich A, Balzer J, Shin DI, Meyer C, Kelm M, Kehmeier ES. Left atrial appendage morphology is closely associated with specific echocardiographic flow pattern in patients with atrial fibrillation. Europace. 2015;17:539–545. doi: 10.1093/europace/euu347 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0015] 15. Wang H, Xi S, Chen J, Zhao L, Gan T, He B. Severe left atrial spontaneous Echo contrast in Nonvalvular atrial fibrillation: clinical characteristics and impact on ischemic risk Postablation. Thromb Haemost. 2023;123:522–534. doi: 10.1055/a-1983-0516 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0016] 16. Gerede DM, Candemir B, Vurgun VK, Aghdam SM, Acibuca A, Ozcan OU, Goksuluk H, Kervancioglu C, Erol C. Prediction of recurrence after cryoballoon ablation therapy in patients with paroxysmal atrial fibrillation. Anatol J Cardiol. 2015;16:482–488. doi: 10.5152/AnatolJCardiol.2015.6309 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0017] 17. Lin C, Bao Y, Xie Y, Wei Y, Luo Q, Ling T, Jin Q, Pan W, Xie Y, Wu L, et al. Prognostic implications of left atrial spontaneous Echo contrast with catheter ablation of Nonvalvular atrial fibrillation patients with left atrial dilation. J Cardiovasc Dev Dis. 2022;9:9. doi: 10.3390/jcdd9090306 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0018] 18. Daniel WG, Erbel R, Kasper W, Visser CA, Engberding R, Sutherland GR, Grube E, Hanrath P, Maisch B, Dennig K. Safety of transesophageal echocardiography. A multicenter survey of 10,419 examinations. Circulation. 1991;83:817–821. doi: 10.1161/01.cir.83.3.817 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0019] 19. Khandheria BK, Seward JB, Tajik AJ. Transesophageal echocardiography. Mayo Clin Proc. 1994;69:856–863. doi: 10.1016/s0025-6196(12)61788-1 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0020] 20. Hilberath JN, Oakes DA, Shernan SK, Bulwer BE, D’Ambra MN, Eltzschig HK. Safety of transesophageal echocardiography. J Am Soc Echocardiogr. 2010;23:1115–1127. doi: 10.1016/j.echo.2010.08.013 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0021] 21. Cote G, Denault A. Transesophageal echocardiography‐related complications. Can J Anaesth. 2008;55:622–647. doi: 10.1007/BF03021437 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0022] 22. Hur J, Kim YJ, Lee HJ, Ha JW, Heo JH, Choi EY, Shim CY, Kim TH, Nam JE, Choe KO, et al. Left atrial appendage thrombi in stroke patients: detection with two‐phase cardiac CT angiography versus transesophageal echocardiography. Radiology. 2009;251:683–690. doi: 10.1148/radiol.2513090794 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0023] 23. Romero J, Cao JJ, Garcia MJ, Taub CC. Cardiac imaging for assessment of left atrial appendage stasis and thrombosis. Nat Rev Cardiol. 2014;11:470–480. doi: 10.1038/nrcardio.2014.77 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0024] 24. Bilchick KC, Mealor A, Gonzalez J, Norton P, Zhuo D, Mason P, Ferguson JD, Malhotra R, Michael Mangrum J, Darby AE, et al. Effectiveness of integrating delayed computed tomography angiography imaging for left atrial appendage thrombus exclusion into the care of patients undergoing ablation of atrial fibrillation. Heart Rhythm. 2016;13:12–19. doi: 10.1016/j.hrthm.2015.09.002 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0025] 25. Hur J, Kim YJ, Lee HJ, Nam JE, Hong YJ, Kim HY, Lee JW, Choi BW. Cardioembolic stroke: dual‐energy cardiac CT for differentiation of left atrial appendage thrombus and circulatory stasis. Radiology. 2012;263:688–695. doi: 10.1148/radiol.12111691 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0026] 26. von Elm E, Altman DG, Egger M, Pocock SJ, Gotzsche PC, Vandenbroucke JP, Initiative S. The strengthening the reporting of observational studies in epidemiology (STROBE) statement: guidelines for reporting observational studies. J Clin Epidemiol. 2008;61:344–349. doi: 10.1016/j.jclinepi.2007.11.008 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0027] 27. Michels WM, Grootendorst DC, Verduijn M, Elliott EG, Dekker FW, Krediet RT. Performance of the Cockcroft‐gault, MDRD, and new CKD‐EPI formulas in relation to GFR, age, and body size. Clin J Am Soc Nephrol. 2010;5:1003–1009. doi: 10.2215/CJN.06870909 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0028] 28. Authors/Task Force M , McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Bohm M, Burri H, Butler J, Celutkiene J, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: developed by the task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). With the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2021;24:4–131. doi: 10.1002/ejhf.2333 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0029] 29. Vaziri SM, Larson MG, Benjamin EJ, Levy D. Echocardiographic predictors of nonrheumatic atrial fibrillation. The Framingham Heart Study. Circulation. 1994;89:724–730. doi: 10.1161/01.cir.89.2.724 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0030] 30. Kizer JR, Bella JN, Palmieri V, Liu JE, Best LG, Lee ET, Roman MJ, Devereux RB. Left atrial diameter as an independent predictor of first clinical cardiovascular events in middle‐aged and elderly adults: the Strong Heart Study (SHS). Am Heart J. 2006;151:412–418. doi: 10.1016/j.ahj.2005.04.031 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0031] 31. Nakanishi T, Hamada S, Takamiya M, Naito H, Imakita S, Yamada N, Kimura K, Hirose Y, Nagata S. A pitfall in ultrafast CT scanning for the detection of left atrial thrombi. J Comput Assist Tomogr. 1993;17:42–45. doi: 10.1097/00004728-199301000-00006 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0032] 32. Hajduczok ZD, Weiss RM, Stanford W, Marcus ML. Determination of right ventricular mass in humans and dogs with ultrafast cardiac computed tomography. Circulation. 1990;82:202–212. doi: 10.1161/01.cir.82.1.202 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0033] 33. Liu X, Zhang Q, Yang ZG, Shi K, Xu HY, Xie LJ, Jiang L, Diao KY, Guo YK. Assessment of left ventricular deformation in patients with Ebstein’s anomaly by cardiac magnetic resonance tissue tracking. Eur J Radiol. 2017;89:20–26. doi: 10.1016/j.ejrad.2017.01.013 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0034] 34. Fatkin D, Kelly RP, Feneley MP. Relations between left atrial appendage blood flow velocity, spontaneous echocardiographic contrast and thromboembolic risk in vivo. J Am Coll Cardiol. 1994;23:961–969. doi: 10.1016/0735-1097(94)90644-0 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0035] 35. Calkins H, Hindricks G, Cappato R, Kim YH, Saad EB, Aguinaga L, Akar JG, Badhwar V, Brugada J, Camm J, et al. 2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation. Europace. 2018;20:e1–e160. doi: 10.1093/europace/eux274 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0036] 36. Yang B, Jiang C, Lin Y, Yang G, Chu H, Cai H, Lu F, Zhan X, Xu J, Wang X, et al. STABLE‐SR (electrophysiological substrate ablation in the left atrium during sinus rhythm) for the treatment of nonparoxysmal atrial fibrillation: a prospective, multicenter randomized clinical trial. Circ Arrhythm Electrophysiol. 2017;10:10. doi: 10.1161/CIRCEP.117.005405 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0037] 37. Yang G, Zheng L, Jiang C, Fan J, Liu X, Zhan X, Li J, Wang L, Yang H, Zhu W, et al. Circumferential pulmonary vein isolation plus low‐voltage area modification in persistent atrial fibrillation: the STABLE‐SR‐II trial. JACC Clin Electrophysiol. 2022;8:882–891. doi: 10.1016/j.jacep.2022.03.012 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0038] 38. Chen H, Li C, Han B, Xiao F, Yi F, Wei Y, Jiang C, Zou C, Shi L, Ma W, et al. Circumferential pulmonary vein isolation with vs without additional low‐voltage‐area ablation in older patients with paroxysmal atrial fibrillation: a randomized clinical trial. JAMA Cardiol. 2023;8:765–772. doi: 10.1001/jamacardio.2023.1749 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0039] 39. Schulman S, Kearon C; Subcommittee on Control of Anticoagulation of the S, Standardization Committee of the International Society on T, Haemostasis . Definition of major bleeding in clinical investigations of antihemostatic medicinal products in non‐surgical patients. J Thromb Haemost. 2005;3:692–694. doi: 10.1111/j.1538-7836.2005.01204.x [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0040] 40. Kornej J, Hindricks G, Shoemaker MB, Husser D, Arya A, Sommer P, Rolf S, Saavedra P, Kanagasundram A, Patrick Whalen S, et al. The APPLE score: a novel and simple score for the prediction of rhythm outcomes after catheter ablation of atrial fibrillation. Clin Res Cardiol. 2015;104:871–876. doi: 10.1007/s00392-015-0856-x [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0041] 41. Winkle RA, Jarman JW, Mead RH, Engel G, Kong MH, Fleming W, Patrawala RA. Predicting atrial fibrillation ablation outcome: the CAAP‐AF score. Heart Rhythm. 2016;13:2119–2125. doi: 10.1016/j.hrthm.2016.07.018 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0042] 42. Letsas KP, Efremidis M, Giannopoulos G, Deftereos S, Lioni L, Korantzopoulos P, Vlachos K, Xydonas S, Kossyvakis C, Sideris A. CHADS2 and CHA2DS2‐VASc scores as predictors of left atrial ablation outcomes for paroxysmal atrial fibrillation. Europace. 2014;16:202–207. doi: 10.1093/europace/eut210 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0043] 43. Jacobs V, May HT, Bair TL, Crandall BG, Cutler M, Day JD, Weiss JP, Osborn JS, Muhlestein JB, Anderson JL, et al. The impact of risk score (CHADS2 versus CHA2DS2‐VASc) on long‐term outcomes after atrial fibrillation ablation. Heart Rhythm. 2015;12:681–686. doi: 10.1016/j.hrthm.2014.12.034 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0044] 44. DeLong ER, DeLong DM, Clarke‐Pearson DL. Comparing the areas under two or more correlated receiver operating characteristic curves: a nonparametric approach. Biometrics. 1988;44:837–845. doi: 10.2307/2531595 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0045] 45. Singer DE, Chang Y, Borowsky LH, Fang MC, Pomernacki NK, Udaltsova N, Reynolds K, Go AS. A new risk scheme to predict ischemic stroke and other thromboembolism in atrial fibrillation: the ATRIA study stroke risk score. J Am Heart Assoc. 2013;2:e000250. doi: 10.1161/JAHA.113.000250 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0046] 46. Alkhouli M, Chaker Z, Alqahtani F, Raslan S, Raybuck B. Outcomes of routine Intracardiac echocardiography to guide left atrial appendage occlusion. JACC Clin Electrophysiol. 2020;6:393–400. doi: 10.1016/j.jacep.2019.11.014 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0047] 47. Romero J, Husain SA, Kelesidis I, Sanz J, Medina HM, Garcia MJ. Detection of left atrial appendage thrombus by cardiac computed tomography in patients with atrial fibrillation: a meta‐analysis. Circ Cardiovasc Imaging. 2013;6:185–194. doi: 10.1161/CIRCIMAGING.112.000153 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0048] 48. Zou H, Zhang Y, Tong J, Liu Z. Multidetector computed tomography for detecting left atrial/left atrial appendage thrombus: a meta‐analysis. Intern Med J. 2015;45:1044–1053. doi: 10.1111/imj.12862 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0049] 49. Thai WE, Wai B, Lin K, Cheng T, Heist EK, Hoffmann U, Singh JP, Truong QA. Pulmonary venous anatomy imaging with low‐dose, prospectively ECG‐triggered, high‐pitch 128‐slice dual‐source computed tomography. Circ Arrhythm Electrophysiol. 2012;5:521–530. doi: 10.1161/CIRCEP.111.968313 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0050] 50. Karim N, Ho SY, Nicol E, Li W, Zemrak F, Markides V, Reddy V, Wong T. The left atrial appendage in humans: structure, physiology, and pathogenesis. Europace. 2020;22:5–18. doi: 10.1093/europace/euz212 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0051] 51. Beigel R, Wunderlich NC, Ho SY, Arsanjani R, Siegel RJ. The left atrial appendage: anatomy, function, and noninvasive evaluation. JACC Cardiovasc Imaging. 2014;7:1251–1265. doi: 10.1016/j.jcmg.2014.08.009 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0052] 52. Negrotto SM, Lugo RM, Metawee M, Kanagasundram AN, Chidsey G, Baker MT, Michaud GF, Piana RN, Benjamin Shoemaker M, Ellis CR. Left atrial appendage morphology predicts the formation of left atrial appendage thrombus. J Cardiovasc Electrophysiol. 2021;32:1044–1052. doi: 10.1111/jce.14922 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0053] 53. Yamamoto M, Seo Y, Kawamatsu N, Sato K, Sugano A, Machino‐Ohtsuka T, Kawamura R, Nakajima H, Igarashi M, Sekiguchi Y, et al. Complex left atrial appendage morphology and left atrial appendage thrombus formation in patients with atrial fibrillation. Circ Cardiovasc Imaging. 2014;7:337–343. doi: 10.1161/CIRCIMAGING.113.001317 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0054] 54. Di Biase L, Santangeli P, Anselmino M, Mohanty P, Salvetti I, Gili S, Horton R, Sanchez JE, Bai R, Mohanty S, et al. Does the left atrial appendage morphology correlate with the risk of stroke in patients with atrial fibrillation? Results from a multicenter study. J Am Coll Cardiol. 2012;60:531–538. doi: 10.1016/j.jacc.2012.04.032 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0055] 55. Lip GY, Gibbs CR. Does heart failure confer a hypercoagulable state? Virchow’s triad revisited. J Am Coll Cardiol. 1999;33:1424–1426. doi: 10.1016/s0735-1097(99)00033-9 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0056] 56. Rekosz J, Karwowski J, Kowalik I, Wiktorska A, Wrzosek K, Solecki M, Szmarowska K, Szymanska A, Mierzejewska B, Syska‐Suminska J, et al. Risk factors for thrombosis and spontaneous echocardiographic contrast with sludge in atrial fibrillation patients treated with oral anticoagulants before electrical cardioversion. Kardiol Pol. 2024;82:516–526. doi: 10.33963/v.phj.100078 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0057] 57. Lowe BS, Kusunose K, Motoki H, Varr B, Shrestha K, Whitman C, Tang WH, Thomas JD, Klein AL. Prognostic significance of left atrial appendage “sludge” in patients with atrial fibrillation: a new transesophageal echocardiographic thromboembolic risk factor. J Am Soc Echocardiogr. 2014;27:1176–1183. doi: 10.1016/j.echo.2014.08.016 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0058] 58. Sanders‐van Wijk S, Tromp J, Beussink‐Nelson L, Hage C, Svedlund S, Saraste A, Swat SA, Sanchez C, Njoroge J, Tan RS, et al. Proteomic evaluation of the comorbidity‐inflammation paradigm in heart failure with preserved ejection fraction: results from the PROMIS‐HFpEF study. Circulation. 2020;142:2029–2044. doi: 10.1161/CIRCULATIONAHA.120.045810 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0059] 59. Kim SK, Pak HN, Park JH, Ko KJ, Lee JS, Choi JI, Choi DH, Kim YH. Clinical and serological predictors for the recurrence of atrial fibrillation after electrical cardioversion. Europace. 2009;11:1632–1638. doi: 10.1093/europace/eup321 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0060] 60. Raval M, Katukuri N, Venugopalan S, Jain A, Majmundar V, Siddiq S, Desai R. Abstract 16517: Association of low Left Atrial Appendage Velocity with Increased Risk of atrial fibrillation recurrence after catheter ablation: a meta‐analysis. Circulation. 2023;148:A16517. doi: 10.1161/circ.148.suppl_1.16517 [DOI] [Google Scholar]

[jah370160-bib-0061] 61. Kavlak ES, Kucukoglu H, Yigit Z, Okcun B, Baran T, Ozkan AA, Kucukoglu S. Clinical and echocardiographic risk factors for embolization in the presence of left atrial thrombus. Echocardiography. 2007;24:515–521. doi: 10.1111/j.1540-8175.2007.00420.x [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0062] 62. Takigawa M, Takahashi A, Kuwahara T, Takahashi Y, Okubo K, Nakashima E, Watari Y, Nakajima J, Takagi K, Yamao K, et al. Late‐phase thromboembolism after catheter ablation for paroxysmal atrial fibrillation. Circ J. 2014;78:2394–2401. doi: 10.1253/circj.cj-14-0525 [DOI] [PubMed] [Google Scholar]

[jah370160-bib-0063] 63. Kim YG, Shim J, Oh SK, Lee KN, Choi JI, Kim YH. Risk factors for ischemic stroke in atrial fibrillation patients undergoing radiofrequency catheter ablation. Sci Rep. 2019;9:7051. doi: 10.1038/s41598-019-43566-z [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0064] 64. Patel SV, Flaker G. Is early cardioversion for atrial fibrillation safe in patients with spontaneous echocardiographic contrast? Clin Cardiol. 2008;31:148–152. doi: 10.1002/clc.20172 [DOI] [PMC free article] [PubMed] [Google Scholar]

[jah370160-bib-0065] 65. Chilukuri K, Mayer SA, Scherr D, Dalal D, Abraham T, Henrikson CA, Cheng A, Nazarian S, Sinha S, Spragg D, et al. Transoesophageal echocardiography predictors of periprocedural cerebrovascular accident in patients undergoing catheter ablation of atrial fibrillation. Europace. 2010;12:1543–1549. doi: 10.1093/europace/euq295 [DOI] [PubMed] [Google Scholar]

PERMALINK

Relationship Between Circulatory Stasis in the Left Atrial Appendage Detected by Cardiac Computed Tomography Angiography With Atrial Fibrillation Recurrence After Initial Catheter Ablation

Shu Yang, MD

Jun Wang, MD

Ning Chen, MD

Jincheng Jiao, MD

Yi Xu, MD

Minglong Chen, MD

Mingfang Li, MD

Abstract

Background

Methods

Results

Conclusions

Nonstandard Abbreviations and Acronyms

Clinical Perspective.

What Is New?

What Are the Clinical Implications?

Methods

Data Availability

Patients and Study Design

Cardiac Computed Tomography Angiography

Figure 1. Representative images of blood flow status on cardiac CTA and TEE.

Transesophageal Echocardiography

AF Ablation and Periprocedure Management

Follow‐Up and End Points

Statistical Analysis

Results

Baseline Characteristics

Figure 2. Patient flow chart.

Table 1.

Observer Agreement in Cardiac CTA

Comparison of Cardiac CTA and TEE

Development and Validation of the Nomogram for Estimating the Risk of Circulatory Stasis in the LAA

Figure 3. Screening of variables based on LASSO regression in the training cohort.

Table 2.

Figure 4. Nomogram for estimating the risk of circulatory stasis in the left atrial appendage.

Internal and External Validation of the Nomogram for Estimating the Risk of Circulatory Stasis in the LAA

The Relationship Between Circulatory Stasis in the LAA and Low‐Voltage Areas

The Relationship Between Circulatory Stasis in the LAA and AF Recurrence

Figure 5. Kaplan–Meier curves comparing the AF‐free survival after the initial ablation treatment between the circulatory stasis and circulatory normal groups.

Table 3.

Figure 6. Receiver operating characteristic curves for estimating the risk of recurrence after atrial fibrillation ablation.

The Safety of AF Ablation in Patients with Circulatory Stasis in the LAA

Discussion

Conclusions

Sources of Funding

Disclosures

Supporting information

Contributor Information

References

Associated Data

Supplementary Materials

Data Availability Statement

ACTIONS

PERMALINK

RESOURCES

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