Application of cardiac magnetic resonance feature tracking (CMR-FT) for quantitative assessment of left atrial function in nonobstructive hypertrophic cardiomyopathy

Introduction

Hypertrophic cardiomyopathy (HCM) is a common hereditary cardiomyopathy with a prevalence of about 1/200 to 1/500, and it is estimated that over 1 million adults in China have HCM (1). The clinical phenotypes of HCM vary and can be classified based on the location of hypertrophy into interventricular septal hypertrophy, apical hypertrophy, left ventricular (LV) homogeneous hypertrophy, and other forms. HCM can also be categorized by hemodynamic characteristics into non-obstructive, latent obstructive, and obstructive types, with the non-obstructive form being the most common (2). Patients with non-obstructive HCM often lack noticeable clinical symptoms, leading to it being overlooked by both patients and clinicians. The clinical outcomes of HCM are diverse, ranging from atrial fibrillation (AF) and heart failure to sudden cardiac death (1).

Several studies have shown that the prognosis of HCM patients is closely linked to left atrial (LA) size and function (3-5). The primary functional impairment in HCM is LV diastolic dysfunction, which raises LV filling pressure, obstructs LA blood return, and consequently affects LA function and size (6). This can lead to AF and other adverse outcomes, making early detection of LA changes crucial for the prognosis of HCM patients (7). Some researchers have developed a risk stratification model for sudden cardiac death in 500 HCM patients, incorporating LA diameter as one of the risk factors (8), whereas others (5) have found that LA volume (LAV) is significantly associated with poor clinical outcomes in HCM patients. However, LA diameter and LAV alone do not fully capture the complexity of LA function, and further investigation is needed. Additionally, myocardial functional impairment often precedes structural changes, as seen in early stages of hypertension and paroxysmal AF (9). Therefore, studying changes in LA function can provide an earlier insight into the onset and progression of HCM, thereby guiding timely clinical interventions (10).

Currently, LA function is assessed using common parameters such as myocardial strain and LA ejection fraction (LAEF). Magnetic resonance imaging (MRI) techniques that reflect myocardial strain include feature tracking (FT), tissue tagging, cardiac deformation stress analysis, velocity vector imaging, and strain coding techniques (11). The cardiac magnetic resonance FT (CMR-FT) technique used in this study employs a cardiac phased array receiver coil and a steady-state free precession (SSFP) sequence to manually outline the surface contours of the atrial endocardium based on CMR cine images obtained through retrospective electrocardiographic gating. An automated tracking algorithm is then applied to capture myocardial motion throughout the cardiac cycle, analyzing myocardial strain (12,13). This technique has garnered increasing attention from cardiologists and radiologists due to its ease of use, lack of need for specialized acquisition sequences and complex post-processing, and ability to address issues faced by other techniques, such as low signal-to-noise ratios, lengthy scan times, and missed strain data (14). It can be directly applied to standard CMR SSFP sequences (15). Although the technique allows for both global and segmental strain analysis, this study only conducted global strain analysis of the left atrium, as segmental tracking can yield unreliable values when smoothing is applied (16), and segmental strain values may vary significantly across different vendors (17).

In this study, LA strain analysis using the CMR-FT technique was conducted to evaluate LA function in patients with nonobstructive hypertrophic cardiomyopathy (NOHCM). The analysis aimed to further investigate the effects of NOHCM on the left atrium and left ventricle, exploring the relationship between their structure and function. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-24-2259/rc).

Methods

Patients

This study included 58 patients with a confirmed diagnosis of NOHCM at Shanxi Cardiovascular Hospital between January 2020 and December 2022, along with 30 healthy controls (HC) who underwent CMR.

The inclusion criteria for the NOHCM group (2) were as follows: (I) CMR or echocardiographic findings of a maximal end-diastolic ventricular wall thickness of ≥15 mm in one or more LV segments; (II) for family members in familial HCM, excluding the proband, or individuals with a positive genetic test, a maximal end-diastolic ventricular wall thickness of ≥13 mm; (III) a diagnosis of NOHCM on echocardiography, defined as a peak pressure gradient between the LV outflow tract and the aorta <30 mmHg at rest and during exertion; and (IV) exclusion of other physiological factors, cardiac diseases, systemic diseases, or metabolic disorders that could cause ventricular wall thickening.

The exclusion criteria for the NOHCM group were as follows: (I) history of coronary artery disease, myocardial infarction, or myocarditis; (II) history of interventricular septal myocardial ablation or resection; (III) history of AF; and (IV) contraindications to CMR, such as the presence of pacemakers, prosthetic metal heart valves, ferromagnetic foreign bodies, early third-trimester pregnancy, or claustrophobia.

Included cases in the HC group had no history of cardiovascular disease, normal physical examinations, and no significant abnormalities on electrocardiogram, echocardiogram, or CMR.

This study was conducted in accordance with the Declaration of Helsinki (as revised in 2013). This retrospective study was approved by the Ethics Committee of Shanxi Cardiovascular Hospital (No. 2023wz035), with an exemption of informed consent.

CMR protocol

Using a GE HD-XT 1.5T (GE Medical Systems, Chicago, IL, USA) and a UMR 588 1.5T magnetic resonance scanner (Shanghai United Imaging Healthcare Co., Ltd., Shanghai, China), with dedicated cardiac phased array coils and electrocardiographic and respiratory gating technologies, participants were placed in the supine position. A single excitation fast spin-echo sequence was used for localization, and CMR images were acquired using a fast balanced SSFP sequence. Scanning parameters (LV short-axis, two-chamber, and four-chamber views) were as follows: slice thickness, 8 mm; slice gap, 2 mm; repetition time (TR), 3.7 ms; echo time (TE), 1.5 ms; field of view (FOV), 350 × 280 mm; and matrix, 224×224.

CMR image analysis

Images were imported into the commercial post-processing software CVI 42 (Circle Cardiovascular Imaging 42 version 5.14, Circle Cardiovascular Imaging, Calgary, Canada). LV structure and function were first analyzed using the short-axis module: the software automatically outlined the LV endocardium at each short-axis level, with manual corrections, to obtain the LV ejection fraction (LVEF), LV end-diastolic volume index (LVEDVi), LV end-systolic volume index (LVESVi), LV cardiac output (LVCO), LV cardiac index (LVCI), LV maximum wall thickness (LVWT_max), LV mass (LVM), and LV mass index (LVMI).

Next, routine structural and functional parameters of the left atrium were obtained in the biplane module, including LAV and LAEF. The LA endocardium was automatically outlined at the two-chamber and four-chamber cine image (excluding structures such as pulmonary veins and the LA appendage) and manually corrected to obtain the LA maximum volume (LAV_max), LA minimum volume (LAV_min), and LAV before LV systole (LAV_pre-a). Based on these values, LAEF-related variables were calculated, including LA total ejection fraction (LATEF), LA passive ejection fraction (LAPEF), LA active ejection fraction (LAAEF), and LA volume index (LAVI), using the following formula:

LATEF=LAVmax−LAVminLAVmax×100%[1]

LAPEF=LAVmax−LAVpre-aLAVmax×100%[2]

LAAEF=LAVpre-a−LAVminLAVpre-a×100%[3]

LAVI=LAVmaxBSA[4]

Where BSA is the body surface area, calculated using Mosteller’s formula.

Finally, the FT technique was applied in the strain module for LA strain analysis (Figure 1): the LA endocardium and epicardium were manually outlined at the end-diastolic stage in both the two-chamber and four-chamber cine image (excluding structures such as the pulmonary veins and LA appendage). The outline was automatically tracked throughout the entire cardiac cycle (25 frames per cycle). Manual corrections were performed when tracking was insufficiently accurate. The software then automatically analyzed the global strain and strain rate (SR) of the left atrium, averaging each strain parameter over the two-chamber and four-chamber cine image measurements. In this study, LA strain parameters were primarily obtained in three temporal phases: total strain (εs, reflecting LA reservoir function), active strain (εa, reflecting LA pump function), and passive strain (εe, reflecting LA conduit function). The corresponding strain rate parameters included peak positive strain rate (SRs, indicating reservoir function), peak early negative strain rate (SRe, indicating conduit function), and peak late negative strain rate (SRa, indicating booster pump function). The authors independently repeated the cardiac outlining three times and averaged the three measurements.

Figure 1 Measurement of left atrial strain in HC and NOHCM patients using CMR-FT, along with strain and strain rate curves of the left atrium. (A-D) HC: (A) four-chamber view, displaying the left atrial myocardial region, color-coded with red indicating positive strain values (more reddish indicates larger strain values) and blue indicating negative strain values (more bluish indicates smaller strain values); (B) two-chamber view, showing the left atrial myocardial region; (C) overall time-strain curve of the left atrium, illustrating the three temporal variability values (εs, εa, and εe); (D) overall left atrial time-strain rate curve, presenting the three corresponding variability values (SRs, SRe, SRa). (E-H) NOHCM patients: (E) four-chamber view; (F) two-chamber view; (G) overall left atrial time-strain curves, indicating the corresponding variability at three times (εs, εa, εe), with each strain value decreased compared to HC; (H) overall left atrial time-strain rate curves, presenting the corresponding variability at three times (SRs, SRe, SRa), with each strain rate decreased compared to HC. εa, active strain; εe, passive strain; εs, total strain; HC, healthy controls; NOHCM, nonobstructive hypertrophic cardiomyopathy; SRa, peak late negative strain rate; SRe, peak early negative strain rate; SRs, peak positive strain rate.

Additionally, the NOHCM group was divided into six subgroups based on the site of hypertrophy: Group 1 (localized basal septal hypertrophy), Group 2 (reverse curvature septal hypertrophy), Group 3 (apical hypertrophy), Group 4 (concentric hypertrophy), Group 5 (mid-cavity obstruction with apical aneurysm), and Group 6 (hypertrophy in other locations). In this study, the LAVI was used to assess LA size, with LAVI >34 mL/m² indicating an enlarged left atrium (2). The NOHCM group was further categorized into a group with an enlarged left atrium (28 individuals) and a group with normal LA size (30 individuals).

Reproducibility analysis

A total of 20 cases (10 HC and 10 NOHCM patients) were randomly selected for reproducibility analysis. For intra-observer reproducibility, the CMR images of these 20 cases were re-analyzed by the same investigator after one month using a blinding method, with quantitative parameters measured again. For inter-observer reproducibility, another investigator with the same qualifications, unaware of the results of the first analysis, independently analyzed the images of these 20 cases and measured the LA strain parameter values. Repeated measurements were assessed for consistency using the intraclass correlation coefficient (ICC).

Statistical analysis

SPSS 26.0 statistical software (IBM Corp., Armonk, NY, USA) was utilized for the analysis. The data for each group were tested for normality. Measurements conforming to a normal distribution were expressed as mean ± standard deviation; a two-sample t-test was applied for comparisons between two groups, and one-way analysis of variance (ANOVA) was used for comparisons among multiple groups, with Bonferroni’s test for pairwise comparisons. Measurements not conforming to a normal distribution were expressed as median with interquartile range, with the Mann-Whitney U test for comparisons between two groups and the Kruskal-Wallis H test for differences among multiple groups. The χ² test was employed to compare differences between groups for count data. The diagnostic efficacy of LA parameters was assessed using receiver operating characteristic (ROC) curves. Pearson or Spearman correlation coefficients (r) were used to analyze correlations between structural and functional parameters of the left atrium and ventricle. Statistical significance was defined as P<0.05.

Results

Baseline characteristics

The results comparing the baseline characteristics between the NOHCM and HC groups are presented in Table 1. No statistically significant differences were observed between the two groups in terms of age, gender composition, body mass index (BMI), heart rate, or BSA (P>0.05).

In the NOHCM group, there were 24 asymptomatic cases and 34 symptomatic cases. According to the New York Heart Association (NYHA) grading criteria for cardiac function, there were 52 cases classified as class I, four cases as class II, and two cases as class III. Additionally, 41 cases (70.7%) presented with mitral regurgitation, 19 cases (32.8%) experienced chest tightness, and 15 cases (25.9%) reported chest pain. There were two cases (3.4%) with a family history of HCM.

Comparison of structural and functional parameters of the left ventricle

The results comparing the quantitative parameters of LV structure and function between the two groups are presented in Table 2. There were no statistically significant differences in LVEDVi and LVESVi between the NOHCM group and the HC group (P>0.05). However, the differences in LVEF, LVWT_max, LVCO, LVCI, LVM, and LVMI were all statistically significant (P<0.05).

Comparison of structural and functional parameters of the left atrium

The results comparing the structural and functional parameters of the left atrium between the NOHCM group and the HC group are presented in Table 3. The differences in these parameters between the two groups were statistically significant (P<0.05).

Comparison of LA and LV structural and functional parameters among subgroups with different hypertrophic sites in the NOHCM group

The results comparing the structural and functional parameters of the left atrium and left ventricle among subgroups with different hypertrophic sites in the NOHCM group are detailed in Table 4. Of all the quantitative parameters, only LVWT_max demonstrated a statistically significant difference between the subgroups (P<0.05). The results of the post hoc analysis for this parameter across different subgroups are illustrated in Figure 2. The analysis revealed significant differences in LVWT_max between the apical hypertrophy group and the groups with reverse curvature septal hypertrophy, concentric hypertrophy, mid-cavity obstruction with apical aneurysm, and hypertrophy in other locations. Additionally, there was a significant difference in LVWT_max between the localized basal septal hypertrophy group and the concentric hypertrophy group (P<0.05). For the remaining subgroups, the differences in LVWT_max were not statistically significant in pairwise comparisons (P>0.05).

Figure 2 Bonferroni analysis of maximum ventricular wall thickness among subgroups with different hypertrophic sites in the NOHCM group. Statistically significant differences were found between Group 3 and Groups 2, 4, 5, and 6, as well as between Group 1 and Group 4 (P<0.05). The subgroups are designated as follows: (I) localized basal septal hypertrophy; (II) reverse curvature septal hypertrophy; (III) apical hypertrophy; (IV) concentric hypertrophy; (V) mid-cavity obstruction with apical aneurysm; (VI) hypertrophy in other locations. LVWT_max, left ventricular maximum wall thickness; NOHCM, nonobstructive hypertrophic cardiomyopathy.

Comparison of LA function in patients with normal LAVI in the NOHCM group and in the HC group

The total number of patients with normal LAVI in the NOHCM group was 28. Figure 3 illustrates the comparison of LA functional parameters between these patients and the HC group (30 patients). The differences in LAAEF, εa, and SRa were not statistically significant (P>0.05). However, LATEF (53.57%±8.56% vs. 61.20%±7.59%, P=0.001), LAPEF (22.36%±6.26% vs. 30.80%±6.71%, P<0.001), εs (29.97%±9.57% vs. 42.60%±10.88%, P<0.001), εe (15.48%±6.44% vs. 25.30%±7.95%, P<0.001), SRs (1.57±0.52 vs. 2.02±0.53 s⁻¹, P=0.001), and SRe [−1.48 (−1.88, −0.79) vs. −2.08 (−2.96, −1.70) s⁻¹, P<0.001] exhibited statistically significant differences between the two groups. Additionally, ROC curve analysis of these six indicators, along with their combined tests for diagnosing patients with normal LAVI in the NOHCM group, was conducted (Table 5 and Figure 4). The combined indicator test demonstrated the highest diagnostic efficacy for detecting LA damage in this cohort [area under the curve (AUC) =0.838].

Figure 3 A jittered scatter plot with boxplot for each left atrial function index in patients with normal LAVI in the NOHCM group compared to the HC group. (A) εa, εe, and εs; (B) SRa, SRe, and SRs; (C) LAAEF, LAPEF, and LATEF. Statistically significant differences were observed between the two groups for LATEF, LAPEF, εs, SRs, εe, and SRe (P<0.05). εa, active strain; εe, passive strain; εs, total strain; HC, healthy controls; LAAEF, left atrial active ejection fraction; LAPEF, left atrial passive ejection fraction; LATEF, left atrial total ejection fraction; LAVI, left atrial volume index; NOHCM, nonobstructive hypertrophic cardiomyopathy; SRe, peak early negative strain rate; SRa, peak late negative strain rate; SRs, peak positive strain rate.

Figure 4 ROC curves of patients with normal LAVI in the NOHCM group diagnosed by each index and combined indicators. εe, passive strain; εs, total strain; AUC, area under the curve; LAPEF, left atrial passive ejection fraction; LATEF, left atrial total ejection fraction; LAVI, left atrial volume index; NOHCM, nonobstructive hypertrophic cardiomyopathy; pred-AUC, AUC for combined prediction using six indicators; ROC, receiver operating characteristic; SRe, peak early negative strain rate; SRs, peak positive strain rate.

Correlation analysis

The scatter plots depicting the correlation analysis between the LA strain parameters at each time phase and LAEF are presented in Figures 5-7. Additionally, the results of the correlation analysis between the structural and functional parameters of the left atrium and ventricle in the NOHCM group are detailed in Table 6. The strongest correlations were observed between LATEF and εs, LAPEF and εe, and LAAEF and εa (r>0.70). In contrast, the correlations between all functional parameters of the left atrium and the structural and functional parameters of the left ventricle (LVEF, LVCO, LVCI, LVEDVi, LVESVi) were weaker (r<0.50).

Figure 5 Scatter plot of the correlation between εs and LATEF. εs is strongly positively correlated with LATEF. εs, total strain; LATEF, left atrial total ejection fraction.

Figure 6 Scatter plot of correlation between εe and LAPEF. εe is strongly positively correlated with LAPEF. εe, passive strain; LAPEF, left atrial passive ejection fraction.

Figure 7 Scatter plot of correlation between εa and LAAEF. εa is strongly positively correlated with LAAEF. εa, active strain; LAAEF, left atrial active ejection fraction.

Intra- and inter-observer reproducibility

The intra- and inter-observer reproducibility of LA strain parameter measurements across all time phases was high, as detailed in Table 7. In both intra- and inter-observer agreement analyses, SRe exhibited the highest reproducibility, with ICC values of 0.957 and 0.945, respectively.

Discussion

The data from this study indicated that all temporal phases of LA function were significantly reduced in the NOHCM group compared to the HC group. Patients with normal LAVI exhibited diminished LA reservoir function and conduit function, yet normal booster pump function. Among the LA parameters, the combined index test demonstrated the highest diagnostic efficacy for detecting LA impairment in patients with normal LAVI in the NOHCM group (AUC =0.838). The reduction in LA function across all time phases was independent of the site of LV hypertrophy, and LAEF at all temporal phases correlated strongly with strain parameters.

Effects of NOHCM on LA function

As established, the overall function of the left atrium during a complete cardiac cycle consists of three phases: (I) the reservoir phase occurs during LV systole and isovolumic diastole, where the left atrium serves as a “reservoir” to receive blood from the pulmonary veins, primarily related to its compliance; (II) the conduit phase happens early in LV diastole, involving the passive emptying of the left atrium; and (III) the booster pump phase occurs in late LV diastole, reflecting the active emptying of the left atrium, linked to intrinsic myocardial properties (18). Total LA strain (during LV systole) equals the sum of εe (during early LV diastole) and εa (during late LV diastole), thus representing LV diastolic function. Our data demonstrate that all three temporal parameters of LA strain are reduced in patients with NOHCM compared to HC, aligning with previous findings by Kowallick et al. (19). The primary characteristic of HCM is LV diastolic dysfunction (6), which explains the decrease in total LA strain reflecting reservoir function. In addition, decreased LA reservoir function is associated with its compliance. In HCM patients, when the LA myocardium becomes fibrotic, wall stiffness increases and compliance decreases, leading to a reduction in LA reservoir function (7). The decline in conduit function of the left atrium is primarily related to LV compliance. In HCM patients, fibrosis often occurs within the hypertrophied LV myocardium, resulting in decreased compliance and impairing the pressure gradient between the left atrium and left ventricle. This reduction in the pressure gradient decreases the conduit function of the left atrium, consequently diminishing its εe. LA booster pump function is influenced by pulmonary venous return (preload), LV end-diastolic pressure (afterload), and LA systolic reserve (an intrinsic characteristic of myocardial contraction strength and velocity). When LV end-diastolic pressure is elevated and LA systolic reserve is reduced due to myocardial fibrosis, LA booster pump function declines, leading to decreased εa (20). Yang et al. (21) found no statistically significant difference in LA booster pump function between NOHCM patients and normal controls, likely because their study screened patients according to inclusion criteria such as LVEF >50% and normal LA size. The lack of such requirements in our study, along with differences in disease progression among participants, accounts for the discrepancies in results. Moreover, previous studies on HCM patients reported inconsistent findings regarding LA booster pump function, with outcomes varying from normal to increased or decreased (19,22,23).

Tsang et al. (24) evaluated LA size—including diameter, area, and volume—in 432 patients with cardiovascular events, finding that LAV was a more significant marker of these events compared to diameter and area. The latest guidelines indicate that an LAVI >34 mL/m² is the criterion for LA enlargement (2). In this study, we also utilized LAVI to assess LA size, categorizing the NOHCM group into those with LA enlargement and those with normal LA size. We analyzed differences in LA function between the normal LAVI group and HC, discovering that parameters such as LATEF, LAPEF, εs, SRs, εe, and SRe were significantly lower in the normal LAVI group, whereas LAAEF, εa, and SRa showed no significant differences. This suggests that reservoir and conduit functions were reduced in NOHCM patients before any enlargement of the left atrium, whereas booster pump function remained normal. This finding aligns with Yang et al. (21), indicating that patients with normal LA size may still be experiencing declining LV compliance, with LA pump function still capable of compensation. Prior research has established LA size as a predictor for the development of AF (25). Some studies have noted a correlation between increased LAV and reduced function (11), and our study showed that decreases in LA strain parameters occurred before any enlargement, suggesting that these strain parameters can identify LA dysfunction earlier than volume measurements, enhancing the predictive ability for AF risk. Previous studies, including one by Raman et al. (26), also indicated that total and active LA strain could improve the prediction of new-onset AF risk in HCM patients. ROC curve analysis revealed that LAEF combined with strain parameters offered the highest differential diagnostic value for patients with normal LAVI in NOHCM compared to HC, emphasizing the incremental diagnostic value of strain parameters in assessing impaired LA function.

Comparison of LV structure and function between subgroups with different hypertrophic sites in the NOHCM group

To our knowledge, this is one of the first studies examining the correlation between the site of LV hypertrophy and LA function in patients with NOHCM. A key pathophysiological feature of HCM is myocardial ischemia (27). At the cellular level, cardiomyocytes at hypertrophic sites exhibit hypertrophy and disordered arrangement, leading to structural malformations that impair the physiological function of intramyocardial blood vessels. This results in wall thickening, lumen narrowing, and decreased elasticity of intramyocardial arteries, ultimately causing compromised microcirculation and affecting local myocardial blood flow, potentially leading to small focal myocardial infarctions and local myocardial functional decline. Krams et al. (28) corroborated this perspective, indicating that changes in the coronary microcirculatory system correlate with the degree of myocardial hypertrophy. In HCM patients, myocardial hypertrophy can manifest in various regions, and due to the differing distribution of coronary blood vessels, its impact on local microcirculation varies, subsequently affecting myocardial function. Our results revealed that only the maximum thickness of the LV wall was associated with the site of hypertrophy. This may relate to the distribution of coronary vessels. Other structural and functional parameters of the left atrium and ventricle did not show statistical significance, likely explaining why the site of hypertrophy is rarely used for patient categorization and management in clinical practice, where grouping is primarily based on hemodynamic characteristics. It is also possible that the small sample size in this study limited the ability to detect differences between subgroups, and further research with a larger cohort may reveal statistical differences.

Correlation of structural and functional parameters of the left atrium and ventricle in patients with NOHCM

Finally, we also found that in NOHCM patients, LAEF across all phases of LA function correlated most strongly with strain parameters. LAEF is derived from LAV measurements, whereas strain parameters come from LA myocardial strain analysis, suggesting a potential link between LA size and myocardial strain. Additionally, the weak correlation between LA function parameters and LV function parameters may stem from the fact that LA function is primarily associated with the diastolic function of the left ventricle, whereas conventional LV parameters mainly reflect systolic function (21).

Limitations

This study has the following limitations: first, it is a retrospective analysis with a moderate sample size conducted at a single center, and future prospective studies involving multiple centers and various manufacturers are anticipated. Second, due to the invasive nature of the examinations, this study did not measure physiological cardiac parameters such as LA and LV pressures. Lastly, accurately tracing the endocardium and epicardium of the left atrium remains challenging due to its thin walls and complex structure, including surrounding attachments such as the pulmonary veins and left auricle (29).

Conclusions

LA strain measured by CMR-FT is a feasible and reliable method for assessing LA function. These strain parameters facilitate early detection of LA dysfunction in NOHCM patients, where reservoir and conduit functions decline before any enlargement occurs. Furthermore, combining LA strain parameters with ejection fraction enhances the diagnostic accuracy for LA dysfunction. Notably, LAEF across all time phases exhibits a strong correlation with strain parameters.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-24-2259/rc

Funding: This study was supported by the Scientific Research Project of Shanxi Provincial Health Commission (grant No. 2020038) and Research Incentive Program of Shanxi Provincial Cardiovascular Hospital (grant No. XYS20190203).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-24-2259/coif). The authors report that this study was supported by the Scientific Research Project of Shanxi Provincial Health Commission (grant No. 2020038) and Research Incentive Program of Shanxi Provincial Cardiovascular Hospital (grant No. XYS20190203). The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki (as revised in 2013). This retrospective study was approved by the Ethics Committee of Shanxi Cardiovascular Hospital (No. 2023wz035), with an exemption of informed consent.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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