The correlation between left atrial appendage morphology and thromboembolic risk in atrial fibrillation

The correlation between left atrial appendage morphology and thromboembolic risk in atrial fibrillation | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed. Data may be preliminary. 24 February 2025 V1 Latest version Share on The correlation between left atrial appendage morphology and thromboembolic risk in atrial fibrillation Authors : Chengyi Li 0009-0006-0912-3586 , Yaoji wang , and Buyun Xu 0000-0001-7261-7876 [email protected] Authors Info & Affiliations https://doi.org/10.22541/au.174040926.66196506/v1 Published Frontiers in Stroke Version of record Peer review timeline 254 views 117 downloads Contents Abstract Article Type: Review Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Atrial fibrillation (AF) is the most common cardiac arrhythmia and a major cause of ischemic stroke. Between 91% and 100% of cardiogenic thrombi are in the left atrial appendage (LAA), and the morphology of the LAA might be associated with the formation of LAA thrombus (LAAT). This review provides a detailed discussion of the LAA’s anatomy and the LAAT’s diagnosis. It focuses on analyzing the role of LAA morphology in blood stasis, morphological abnormality, and hypercoagulable states. Accurate evaluation of the morphology of the LAA can assist with risk stratification in patients with AF. The commonly used LAA morphological evaluation indicators must be more comprehensive and objective. Recently, new imaging protocols allow for LA morphological remodeling and fibrosis assessment, which has been demonstrated to correlate with assessing the individual’s risks of thromboembolic events and practical imaging of patients with LAAT. Article Type: Review The correlation between left atrial appendage morphology and thromboembolic risk in atrial fibrillation Chengyi Li (MD) a , Yaoji wang (MD) b , Buyun Xu (MD, PhD) b, * a Department of Cardiology, Shaoxing University School of Medicine, 312000 Shaoxing, Zhejiang, People’s Republic of China b Department of Cardiology, Shaoxing People’s Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), 568 # Zhongxing North Road, Shaoxing, Zhejiang Province 312000, People’s Republic of China Chengyi Li and Yaoji wang are contributed equally. Declarations of interest: none Acknowledgements None. Author Contributions Buyun Xu: Conceptualization, Methodology, Software; Chengyi Li: Data curation, Writing- Original draft preparation; Yaoji Wang: Writing- Reviewing and Editing. Funding This work was supported by the Medical Science and Technology Projects of Health Commission of Zhejiang Province, China (grant no. 2024KY481), and the Medical Science and Technology Projects of Health Commission of Shaoxing, China (grant no. 2022KY031). Disclosure statement The Authors declare that there is no conflict of interest. * Corresponding author: Buyun Xu, Department of Cardiology, The First Affiliated Hospital of Shaoxing University, 568 # Zhongxing North Road, Shaoxing, Zhejiang Province 312000, People’s Republic of China E-mail: [email protected] Tel: +8615088681639 Keywords: Atrial fibrillation; Left atrial appendage; Left atrial appendage thrombus; Left atrial appendage morphology Abstract : Atrial fibrillation (AF) is the most common cardiac arrhythmia and a major cause of ischemic stroke. Between 91% and 100% of cardiogenic thrombi are in the left atrial appendage (LAA), and the morphology of the LAA might be associated with the formation of LAA thrombus (LAAT). This review provides a detailed discussion of the LAA’s anatomy and the LAAT’s diagnosis. It focuses on analyzing the role of LAA morphology in blood stasis, morphological abnormality, and hypercoagulable states. Accurate evaluation of the morphology of the LAA can assist with risk stratification in patients with AF. The commonly used LAA morphological evaluation indicators must be more comprehensive and objective. Recently, new imaging protocols allow for LA morphological remodeling and fibrosis assessment, which has been demonstrated to correlate with assessing the individual’s risks of thromboembolic events and practical imaging of patients with LAAT. Introduction Atrial fibrillation (AF) is one of the most common arrhythmias encountered in practice. According to the Global Burden of Disease Study 2019, the estimated prevalence of AF in adults is between 2% and 4%. Fifty million people worldwide are estimated to be affected [1]. Thromboembolic events are a primary complication of AF, with nearly one-quarter of ischemic strokes potentially attributable to AF [2]. Thromboembolic complications in AF patients arise because AF is associated with multiple thromboembolic risk factors, such as advanced age, hypertension, diabetes, coronary artery disease, and heart failure [1,3-5]. More importantly, AF itself can lead to cardiogenic thrombus formation [6], with 91%–100% of these thrombi located in the left atrial appendage (LAA) [7]. LAA thrombus (LAAT) significantly increases the risk of thromboembolism and is strongly correlated with outcomes of thromboembolic events and overall mortality [8-10]. Current practice guidelines place significant emphasis on assessing the risk of thromboembolic events in AF patients, particularly the risk of stroke, often overlooking the evaluation of the risk factors of LAAT [1]. As previously mentioned, not all thromboembolic events in AF patients are caused by cardiogenic thrombi; there may be differences in the prevention and treatment of thromboembolic events depending on the underlying mechanisms [4]. Conversely, assessing LAAT risk aids in more precise risk stratification, enhancing individualized treatment and research for AF patients. As a primary source of thrombi in AF patients, the morphology of the LAA might be associated with the formation of LAAT. On the one hand, the morphology of the LAA can serve as a biomarker for atrial myopathy and various complications associated with AF, and it is thus related to LAAT. On the other hand, the morphology of the LAA itself may directly or indirectly contribute to thrombus formation. To better understand the relationship between LAA morphology and LAAT formation in AF patients, this paper will first provide a brief introduction to LAA anatomy and LAAT diagnosis; then, a detailed discussion will be presented on the role of LAA morphology in the formation of LAAT and its ability to predict the risk of LAAT. LAA anatomy The LAA exhibits considerable variability in size, shape, and anatomical relationships with surrounding structures [11]. It is located laterally to the LA and anterior to the left pulmonary veins, separated by Warthin’s ridge. It is positioned superiorly and anteriorly adjacent to the pulmonary artery and inferiorly adjacent to the left atrioventricular groove and the left circumflex branch. The left phrenic nerve may traverse it laterally. The definitions of the LAA orifice opening vary, including the anatomical definition, the narrowest part of the LAA body, and Warthin’s ridge-circumflex branch plane [12]. Using the ridge-circumflex plane to define the LAA orifice may aid in standardizing the morphological research on the LAA [13]. The shape of the LAA orifice can be classified as oval (68.9%), tubular (10%), triangular (7.7%), teardrop (7.7%), and round (5.7%) [14]. The shape and size of the LAA orifice are influenced by various factors such as LA filling status and heart rhythm [13,15]. Typically, the body of the LAA extends anteriorly and superiorly, with some patients exhibiting lateral or posterior extension and a few extending to the pericardial sinus. The average length of the LAA body is 45 mm [14]. The endocardial thickness is uneven, and the atrial wall between the pectinate muscles is relatively thin (less than 1 mm). Thicker pectinate muscles seen on imaging might be misdiagnosed as LAAT. [11,14]. The morphology of the LAA body is diverse, with multiple lobes possible. In an autopsy study of nearly 500 cases, 54% of patients had two lobes, 23% had three lobes, 20% had one lobe, and 3% had four or more lobes [14]. Various classification methods have been proposed for LAA morphology based on lobes and characteristics. Due to its ability to predict stroke risk effectively and its guiding significance for LAA closure therapy, the classification method proposed by Wang et al. is currently commonly used, including chicken wing, windbag, cactus, and cauliflower types [16]. In summary, the LAA is one of the most variable parts of cardiac anatomy, and it is highly diverse and irregular. Therefore, a unified, comprehensive, and objective description of LAA morphology is currently needed. LAAT diagnosis Transesophageal echocardiography (TEE) is currently the primary method for diagnosing LAAT. With the intraoperative confirmation of LAAT as the gold standard, TEE has a sensitivity of 93%–100% and specificity of 99%–100% for detecting LAAT [17]. TEE can directly assess the presence of thrombus in the LAA and evaluate LAA morphology, blood flow velocity, emptying fraction, contraction ability, and spontaneous echo contrast, all closely related to LAAT risk. Spontaneous echo contrast is mainly considered a ”pre-thrombotic state” for LAAT and, in some studies, has even been used as a surrogate marker for LAAT [18]. Despite its numerous advantages, TEE is semi-invasive, which can lead to poor patient experience and potential complications such as esophageal perforation. Additionally, TEE has some relative contraindications, such as a history of swallowing difficulties, restricted neck mobility, esophageal varices, and coagulation disorders [19]. A meta-analysis of patients not on anticoagulation therapy showed that the prevalence of LAAT in non-valvular AF patients ranges from 5% to 27% [17]. Due to the asymptomatic nature of LAAT and the invasiveness of TEE, current epidemiological studies on LAAT can only provide approximate prevalence rates, making it challenging to determine incidence and other related metrics. Due to the limitations of TEE, guidelines recommend cardiac-enhanced computed tomography (CT) with biphasic scanning as an alternative to TEE for ruling out LAAT before AF cardioversion or catheter treatment [1]. Using TEE results as the gold standard, cardiac-enhanced CT has a specificity and sensitivity of 89% and 95%, respectively, with single-phase scanning. In the biphasic CT, specificity and sensitivity improve to 100% and 99% [20]. However, the significant radiation exposure associated with biphasic CT has led to studies suggesting that radiomics analysis based on single-phase CT images significantly improves the diagnostic accuracy for LAAT [21-22]. Nonetheless, current radiomics research has limited sample sizes and numerous influencing factors, such as scanning parameters, equipment, and parameter extraction algorithms, requiring validation [23]. Compared to TEE, cardiac-enhanced CT offers lower invasiveness, higher patient acceptance, and more comprehensive anatomical information but lacks assessment of LAA function and carries higher radiation risks and potential contrast-related complications. Additionally, when the scanning time for biphasic CT is short, there may be an increased risk of false-positive results. Intracardiac echocardiography (ICE) provides a close-range and multi-angle examination of the LAA, achieves a 97% concordance with TEE in diagnosing LAAT, and can detect LAATs that TEE might miss [26]. It is an alternative for patients unsuitable for TEE or cardiac CT [27]. Recent ICE-TEE studies indicate that ICE can directly replace TEE as the preferred strategy to rule out LAAT before AF catheter ablation procedures. However, due to its highly invasive nature and high cost, ICEis primarily used as an adjunct tool during catheter-based treatments [28]. Current research indicates that the sensitivity and specificity of cardiac MRI in diagnosing LAAT are comparable to those of enhanced CT. Additionally, MRI effectively avoids the radiation exposure associated with cardiac-enhanced CT and the invasiveness of TEE. Additionally, advancements in new technologies are expected to improve diagnostic accuracy while reducing patient impact [24-25]. Notably, with advancements in cardiac MRI technology, new MRI sequences are expected to improve diagnostic accuracy for LAAT further and may even eliminate the need for contrast agents, minimizing the impact on patients [25]. Pathogenesis of LAAT in patients with AF Although the association between AF and thrombus formation has long been recognized, the mechanisms underlying the formation of LAAT are not fully understood. According to Virchow’s triad for thrombus formation—blood stasis, morphological abnormality, and hypercoagulable states—this section will elucidate the mechanisms of LAAT formation and analyze the roles of LAA and LA morphology in this process. 4.1 Blood stasis Blood stasis is one of the primary mechanisms for thrombus formation in patients with AF [29]. The LAA, with its morphology characterized by a ”narrow opening,” ”deep body,” and ”abundant pectinate muscles,” exhibits particularly pronounced blood stasis. TEE assessing the blood flow velocity within the LAA of patients with paroxysmal AF shows that the flow velocity during AF is only half that during sinus rhythm [30]. When the local blood flow velocity within the LAA decreases, especially when the mean flow velocity falls below 20 cm/s, the risk of thrombus formation within the LAA and subsequent stroke increases significantly [31-32]. It is noteworthy that, even in sinus rhythm, there are significant differences in blood flow velocity and other indicators of blood stasis between AF and non-AF patients[34-35]. Therefore, in addition to the AF rhythm, various systemic factors (such as age, obesity, diabetes, heart failure, CHA2DS2-VASc score) and local factors (such as LAA function and morphology) may also contribute to blood stasis. Even in non-AF patients, LAA function and morphology are related to the state of blood stasis within the LAA [35]. Different studies use various metrics to assess LAA function and morphology. Table 1 summarizes research on the correlation between LAA morphology and blood stasis in AF patients. Table 1 shows that current evaluations of LAA morphology focus on size and traditional LAA morphology classifications. Larger LAA volumes are associated with more severe blood stasis in the LAA. Traditional LAA morphology classifications suggest that chicken wing-type LAA is associated with less severe blood stasis, while cauliflower-type LAA is associated with more severe stasis. Table 1 Study on the Correlation Between LA and LAA Morphology and Blood Stasis in the LAA Kishima H et al. [37] 2015 102 Compared to non-wings-type LAA, patients with wings-type LAA have an 8.6-fold increased risk of LAA flow velocity (LAAFV) < 35 cm/s. Lee JM et al. [38] 2015 360 The blood flow velocity in wings-type LAA is higher compared to non-wings-type LAA (55 ± 19 cm/s vs. 41 ± 20 cm/s). Petersen M et al. [39] 2015 131 Compared to wings-type LAA, patients with non-wings-type LAA have a 2.2-fold increased risk of SEC and a lower LAAFV (39.7 ± 18.8 cm/s vs. 51.4 ± 25.1 cm/s). Fukushima K et al. [40] 2016 96 Compared to cauliflower-type (52.7 cm/s) and cactus-type LAA (55.3 cm/s), wings-type (73.7 cm/s) and windbag-type LAA (61.9 cm/s) have higher blood flow velocities. Matsumoto Y et al. [41] 2017 194 LAAFV is negatively correlated with the area of the LAA orifice and the depth of the LAA. Korhonen M et al. [42] 2018 808 Compared to non-cauliflower-type LAA, cauliflower-type LAA shows poorer contrast agent filling. Zhu MR et al. [43] 2018 130 For each 1 ml/m² increase in LAA volume index, the risk of SEC increases by 5%. Yaghi S et al. [44] 2020 408 When the LAA angle is acute, the risk of LAAFV < 20 cm/s increases by 53%. Chen L et al. [45] 2021 81 Compared to non-wings-type LAA, wings-type LAA patients have higher LAAFV (49.1 ± 22.0 cm/s vs. 36.2 ± 15.0 cm/s) and a negative correlation with the LAA orifice area. Ouchi K et al. [46] 2022 440 For each 1 ml/m² increase in LAA volume index, the risk of LAAFV < 40 cm/s increases by 9%. Ouchi K et al. [47] 2023 641 For each 1 ml/m² increase in LAA volume index, the risk of SEC increases by 31%. LA: Left Atrium; LAA: Left Atrial Appendage; LAAFV: Left Atrial Appendage Flow Velocity; SEC: Spontaneous Echo Contrast In summary, blood stasis is one of the critical mechanisms of LA thrombus formation in AF patients. AF rhythm is not the sole cause of blood stasis within the LAA. Systemic factors, as well as the morphology and function of the LA and LAA, are significantly related to the blood stasis state within the LAA. Furthermore, relative blood flow velocity concerning the LAA wall may be more crucial in LA thrombus formation than the ”absolute” blood flow velocity within the LAA. Therefore, in some patients, LAA strain and contraction function may be critical assessment indicators. 4.2 Morphological abnormality 4.2.1 Endothelial injury The endothelium consists of a layer of flattened cells lining the inner surfaces of the heart and blood vessels. It plays roles in anti-inflammatory responses, coagulation balance, and regulation of vascular tone. While the association between AF and endothelial dysfunction is recognized, the causal relationship is more complex. In catheter ablation procedures for paroxysmal AF, comparing intracardiac endothelial function markers before and after AF episodes suggests that AF is a crucial contributor to endothelial damage [48]. Regardless of the causal relationship between AF and endothelial function, endothelial dysfunction is crucial in AF-related thrombus formation. To exclude systemic factors that could increase circulating endothelial damage markers, such as hypertension, diabetes, and renal dysfunction, researchers compared blood samples from the atrial chamber and peripheral blood, finding significant differences in endothelial function indicators like von Willebrand factor and nitric oxide between different sample sources. Even between LAA and LA samples, concentration gradients were observed, indicating localized endothelial dysfunction in AF patients and an increased risk of local thrombus formation [49]. Recent human specimen studies show that LAA endothelial function in AF patients is the best predictor of stroke and LAAT risk. At the same time, blood stasis is not an independent risk factor for LAAT and stroke [50]. Hemodynamics at the endothelial cell surface is crucial in regulating endothelial function. Recently, Lai et al. demonstrated that fluid shear stress characteristics, including magnitude, direction, and change frequency, influence endothelial function through fluid dynamics [51]. Since LAA morphology is a decisive factor in hemodynamics [52], it can significantly impact LAA endothelial function. However, directly studying the relationship between LAA endothelial function and LAA morphology presents challenges. On the one hand, evaluating local endothelial function in vivo requires invasive methods, posing ethical issues. On the other hand, numerous confounding factors affecting endothelial function make it difficult to provide direct causal evidence in vivo. To address these challenges, computational fluid dynamics (CFD) research offers a practical approach to exploring the relationship between morphology and endothelial dysfunction. CFD studies simulate blood flow conditions, calculate shear stress applied to the endothelial cell surface, and assess the impact of hemodynamics on endothelial cell function. CFD-calculated LAA wall shear stress magnitude and shear stress oscillation coefficient are related to stroke risk [53]. Parameters derived from CFD-calculated shear stress correlate highly with myocardial fibrosis regions shown by cardiac MRI [54]. Compared to general clinical studies, the advantage of CFD research is that it can isolate the LAA morphology as a single variable while keeping other parameters constant. Using CFD models, researchers have found that AF significantly reduces blood flow velocity within the LAA and decreases the rate of change of LAA wall shear stress, with the extent of reduction independent of LAA overall morphology classification (cauliflower-type, chicken wing-type, windbag-type, and cactus-type). Instead, local angles and lobar features of the LAA are decisive factors for the rate of change in wall shear stress [55-56]. Additionally, different fusion methods of LAA models with simulated atria have shown that the relative position of the LAA to the LA significantly affects the blood flow state within the LAA, including LAA wall shear stress [36]. Although CFD research builds a bridge to explore the relationship between morphology and endothelial function, it still has limitations. Current CFD models are based on multiple assumptions, such as blood viscosity, initial flow field conditions, and the rigid morphology of the LA and LAA. Variations in assumptions can lead to significant deviations in CFD results, so careful interpretation of CFD findings is necessary before developing biomimetic CFD models [54,57]. In addition to CFD research, our previous studies have found that in AF patients, compared to non-cauliflower-type LAA, cauliflower-type LAA has higher local von Willebrand factor, interleukin-6, and plasminogen activator inhibitor-1, and lower nitric oxide content, supporting the correlation between LAA morphology and local endothelial function [49]. In summary, AF is associated with localized endothelial dysfunction in the LAA. The LAA’s morphology may affect local endothelial function through changes in hemodynamics. 4.2.2 Atrial cardiomyopathy Atrial cardiomyopathy refers to a myocardial disorder characterized by morphological changes, mechanical dysfunction, and electrophysiological alterations of the atria, leading to clinically relevant manifestations. Based on the primary pathological features, it can be classified into cardiomyocyte type, fibroblast type, mixed cardiomyocyte and fibroblast type, and non-collagen deposits type [58]. On the one hand, atrial cardiomyopathy can increase the risk of thromboembolism due to AF; on the other hand, atrial cardiomyopathy may itself be a risk factor for thromboembolic events. Atrial fibrosis is one of the most significant features of atrial cardiomyopathy. Compared to other types of stroke, patients with cryptogenic embolic stroke have significantly increased LA fibrosis [59]. Pathological results from surgically removed LAA show a close correlation between LAA fibrosis and thrombus formation [50]. When specific stimuli are present, inflammatory cells become activated, which can directly or indirectly exacerbate the fibrosis in the LAA, potentially increasing the risk of thrombosis. A critical cell type found in the atrial appendages of patients with AF is the macrophage, which contributes to inflammation and fibrosis [60]. In addition to atrial fibrosis and inflammatory cell activation, atrial cardiomyopathy is associated with mechanisms such as atrial amyloidosis, fat deposition, and endothelial dysfunction, which promote thrombosis [30,58]. Although the clinical importance of atrial cardiomyopathy is evident, its diagnosis remains challenging and largely relies on imaging studies, especially cardiac MRI. However, due to the time-consuming nature of cardiac MRI, its widespread use is limited. Therefore, echocardiography and CT for evaluating atrial morphology and function present more clinically applicable diagnostic indicators. The size of the LA and LAA, the LA sphericity index, the degree of LA asymmetry, and the shape of the LA roof are morphological parameters associated with atrial fibrosis and AF outcomes, potentially representing manifestations of atrial cardiomyopathy. Recently, comprehensive analysis of LA and LAA shapes using statistical shape modeling (SSM) has led researchers to develop new, more extensive, and objective methods for LA and LAA shape assessment. These methods may predict outcomes following AF catheter ablation better than traditional shape parameters and potentially become new diagnostic indicators for atrial cardiomyopathy [61-62]. 4.3 Hypercoagulable states A substantial body of evidence confirms that patients with AF exhibit abnormalities in various anticoagulant and procoagulant factors. These factors include fibrinogen, activated factor VIII, thrombin-antithrombin complex, tissue factor, D-dimer, soluble P-selectin, von Willebrand factor, and thrombomodulin. Recent reviews have summarized the correlations between these coagulation system markers and AF so that this topic will be elaborated on here [63-64]. It is essential to note that most studies have only assessed the relationship between systemic blood markers and AF. To determine whether a hypercoagulable state exists locally in the LAA of AF patients, our team’s previous research found significant differences in levels of plasminogen activator inhibitor-1, von Willebrand factor, interleukin-6, and platelet activation ratio in blood samples from the LA or LAA of AF patients compared to peripheral blood samples, but no ”centripetal” distribution pattern for fibrinogen, D-dimer, and thrombin-antithrombin complex levels [49]. This might be because most patients in our study were on long-term oral anticoagulant therapy, and prolonged AF episodes might lead to a gradual equilibration of blood marker levels between the intracardiac and peripheral blood. Bartus et al. found that even when there are no significant differences in blood marker concentrations, thrombus tests on samples from different sources show that thrombi formed from LAA samples are denser and require a longer time for fibrinolysis than those from peripheral blood [65]. Assessing a hypercoagulable state based solely on blood marker concentrations may not be comprehensive; thrombus characteristics and other evaluations are also necessary. Currently, there is a lack of studies on the relationship between LAA morphology and local hypercoagulable states. As mentioned, hemodynamic factors may influence the configuration and activity of coagulation factors, so theoretically, the morphology of the LAA could impact local hypercoagulability. Our previous research found that AF patients with a cauliflower-type LAA had a higher local platelet activation ratio than those with non-cauliflower LAA. At the same time, thrombin-antithrombin complexes, D-dimer, and fibrinogen levels were not associated with LAA morphology [49]. Similarly, Kosiuk et al. found that platelet activation within the LAA was primarily related to LAA size rather than its morphological classification [66]. In summary, AF patients are in a hypercoagulable state, with systemic comorbidities potentially being a significant factor. AF itself may contribute to the formation of local hypercoagulability. More evidence is needed regarding whether the morphology of the LAA or LA is related to local hypercoagulable states, and research is needed in this area. LAA morphology and risk of LAAT 5.1 Current status of research on LAA morphology Numerous studies have confirmed the association between the morphology of the LAA and stroke, as detailed in other reviews [12,67]. However, studies examining the relationship between LAA morphology and LAAT are relatively limited, as summarized in Table 2. Unlike stroke and systemic embolic events, LAAT is asymptomatic and commonly diagnosed through invasive techniques such as TEE and CT scans, which involve X-ray radiation, making prospective studies challenging. All the studies listed in Table 2 are single-center, retrospective analyses. These studies predominantly include patients who underwent AF cardioversion or catheter ablation, leading to significant selection bias. Therefore, caution is required when interpreting these study results. The findings from Table 2 indicate that indicators reflecting LAA size, including volume, LAA orifice diameter, LAA orifice area, and LAA depth, are the most common morphological parameters associated with LAAT. Notably, the correlation between LAA orifice size and LAAT remains contentious [18,68-70]. This may be because LAA orifice size results from LA and LAA remodeling, which is positively correlated with the severity of remodeling and, consequently, with the risk of LAAT. Conversely, an enlarged LAA orifice may facilitate blood exchange between the LAA and LA, potentially alleviating blood stasis and acting as a protective factor against LAAT formation. 5.2 Limitations and prospects In addition to LAA size parameters, another category of LAAT-related parameters can be summarized as the complexity of the LAA, including LAA morphological classification, the number of LAA lobes, and the angle of the pectinate muscles (Table 2). As mentioned, the anatomical morphology of the LAA is highly variable, and these parameters are defined based on specific LAA characteristics, making it challenging to evaluate LAA comprehensively. Moreover, these parameters can be highly subjective; for instance, definitions of LAA morphological classification vary across studies [70-72]. Even with standardized definitions, there are significant inter- and intra-researcher variations in LAA morphological classification and lobe count [73]. Despite these limitations, research summarized in Table 2 generally suggests that more complex LAA morphology correlates with a higher risk of LAAT, such as cauliflower-shaped LAA, increased lobation, and larger pectinate muscle angles relative to the main lobe of the LAA. To address the limitations in evaluating the morphological characteristics of the LAA, recent studies have employed auxiliary techniques such as fractal dimension analysis, SSM, and CFD to enhance the assessment. Recently, Lei and colleagues employed fractal analysis to quantitatively assess the complexity of LAA morphology based on surface curvature and roughness—referred to as fractal dimension—and found it to be significantly correlated with LAAT and stroke, patients with LAAT have significantly higher fractal dimensions. Receiver operating characteristic (ROC) analysis indicates that in patients with low to moderate risk of AF, the diagnostic accuracy of combining fractal dimension with the CHA2DS2-VASc score is significantly greater than that of using the CHA2DS2-VASc score alone (area under the curve 0.8479 vs. 0.6958, p = 0.009) [74]. Although the fractal dimension provides a more objective and comprehensive assessment of LAA morphology compared to previous parameters, it only evaluates the complexity of LAA morphology, not its overall shape. Additionally, this study only assessed the fractal dimension, overlooking the role of the LA, while the interaction between the LA and LAA is an essential factor in LAAT formation [36]. Recently, SSM has gained wide application and achieved significant results in the medical field [75-76]. SSM constructs shape space vectors through a series of landmark points, mathematically describing shapes, thereby converting shape data into statistical models. This method offers a comprehensive, objective, and quantitative description of shape. Bieging and colleagues utilized cardiac MRI data to create an SSM for the LA and LAA. When combined with the CHA2DS2-VASc score, the area under the ROC curve increased from 0.640 to 0.778 (p = 0.003), significantly outperforming the use of the CHA2DS2-VASc score alone and further enhancing the predictive capability for stroke [62]. As previously mentioned, CFD research not only bridges the gap between structure and endothelial function. Recently, Zingaro et al. evaluated stroke risk using LA-CFD simulations. Although the hemodynamic parameters obtained from cardiac MRI and the independent analysis of functional and morphological data from CFD did not yield distinct characteristics to reliably differentiate stroke patients from controls, combining both datasets into a predictive model significantly improved the ability to distinguish stroke patients[77]. Therefore, auxiliary techniques such as fractal dimension analysis, SSM, and CFD hold promise as a new method for comprehensive and objective evaluation of the overall morphology of the LA and LAA, offering new insights into the role of LA and LAA morphology in LAAT formation. Table 2 Study on the Correlation Between LA and LAA Morphology and the Risk of Thrombus Formation in the LAA LAA Volume Chen Z et al. [70] （2017） 28/444 1.8 ± 1.3 TEE An LAA diastolic volume > 8.6 ml increases the risk of LAAT by 6 times. LAA Orifice Area Yusuke Miki et al. [68] （2022） 26/149 3.1 ± 1.9 TEE An LAA orifice area > 4.09 cm² increases the risk of LAAT/SEC by 1.6 times. Castellani C et al. [69] （2023） 61/122 4.3 ± 0.3 TEE LAA orifice area is inversely related to LAAT risk (OR = 0.98 per 1 mm² increase). LAA Orifice Diameter Chen Z et al. [70] （2017） 28/444 1.8 ± 1.3 TEE The maximum diameter of the LAA orifice is inversely related to LAAT risk (OR = 0.26 per 1 cm increase). Wang X et al. [18] （2023） 213/2591 ≥2 points 64.8% TEE Each 1 mm increase in LAA orifice diameter increases the risk of LAAT/SEC by 24%. LAA Depth Chen Z et al. [70] （2017） 28/444 1.8 ± 1.3 TEE Each 1 cm increase in LAA depth raises the risk of LAAT by 1.7 times. LAA Lobes Yamamoto M et al. [78] （2014） 36/564 NA TEE Each additional lobe in the LAA increases the risk of LAAT by 1.5 times. Table 3 Study on the Correlation Between LA and LAA Morphology and the Risk of Thrombus Formation in the LAA (continued) Wang F et al. [79] （2018） 80/472 2.9 ± 1.8 CTA Each additional lobe in the LAA increases the risk of LAAT/SEC by 1.4 times. He J et al. [72] （2020） 46/336 ≥2 points 51.4% CTA The risk of LAAT in patients with lobulated LAA is 3.2 times higher compared to those with non-lobulated LAA. LAA Morphology Classification Chen Z et al. [70] （2017） 28/444 1.8 ± 1.3 TEE The risk of LAAT in patients with cauliflower-type LAA is 10.2 times higher than in those with chicken-wing-type LAA. Negrotto SM et al. [71] （2020） 102/306 Median (IQR): 4 (2, 5) TEE The risk of LAAT in patients with cauliflower-type and wind-sock-type LAA is 6.6 times and 4 times higher, respectively, compared to those with chicken-wing-type LAA. Relative Position of LA and LAA Zhao Y et al. [80] （2015） 42/323 2.7 ± 1.7 CTA When the upper edge of the LAA orifice is higher than the upper edge of the left upper pulmonary vein orifice, the risk of LAAT increases by 7.6 times. not-yet-known not-yet-known not-yet-known unknown BSA: Body Surface Area; CTA: Computed Tomography Angiography; LA: Left Atrium; LAA: Left Atrial Appendage; LAAT: Left Atrial Appendage Thrombus; LAV: Left Atrium Volume; OR: Odds Ratio; SEC: Spontaneous Echogenicity Contrast; TEE: Transesophageal Echocardiography; TTE: Transthoracic Echocardiography; *: Number of cases with positive left atrial appendage thrombus/Total number of cases Summary The LAA is the primary source for thromboembolism in AF. The morphology of the LAA plays a significant role in blood stasis, morphological changes, and hypercoagulable states, which might be associated with thrombus formation. Accurate evaluation of the morphology of the LAA can assist with risk stratification in patients with AF. 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Information & Authors Information Version history V1 Version 1 24 February 2025 Peer review timeline Published Frontiers in Stroke Version of Record 9 Dec 2025 Published Copyright This work is licensed under a Non Exclusive No Reuse License. Keyword basic: atrial fibrillation/atrial arrhythmias Authors Affiliations Chengyi Li 0009-0006-0912-3586 Shaoxing University View all articles by this author Yaoji wang Shaoxing People's Hospital View all articles by this author Buyun Xu 0000-0001-7261-7876 [email protected] Shaoxing People's Hospital View all articles by this author Metrics & Citations Metrics Article Usage 254 views 117 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Chengyi Li, Yaoji wang, Buyun Xu. The correlation between left atrial appendage morphology and thromboembolic risk in atrial fibrillation. Authorea . 24 February 2025. 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