The value of CMR-derived left atrial strain parameters in differential diagnosis of cardiac amyloidosis and hypertrophic cardiomyopathy

Introduction

Myocardial hypertrophy represents a common compensatory and adaptive response to a variety of physiological and pathological stimuli. Myocardial remodeling associated with cardiac hypertrophy is a major contributor to the progression of heart failure. Pathological myocardial hypertrophy increases the risk of arrhythmias and sudden cardiac death. Therefore, identifying the underlying causes of myocardial hypertrophy is essential to facilitating early intervention and disease management (1).

Cardiac amyloidosis (CA) represents an infiltrative restrictive cardiomyopathy characterized by the interstitial accumulation of misfolded proteins. This proteotoxicity and structural infiltration can simultaneously involve both the atria and ventricles, leading to a spectrum of clinical complications (2). Patients with heart failure with preserved ejection fraction (HFpEF) and a moderate to severe increase in wall thickness are often mislabeled as having hypertensive cardiomyopathy, hypertrophic cardiomyopathy (HCM), aortic stenosis, and rarer genetic disorders such as Fabry disease (3). HCM is an inherited cardiac disorder with an autosomal dominant transmission, pathologically defined by disordered myocardial architecture, cellular hypertrophy, and the progressive accumulation of interstitial fibrosis (4). The structure and function of the left atrium are closely linked to left ventricular (LV) performance, with alterations in left atrial (LA) morphology and function reflecting underlying LV diastolic dysfunction (5). LA strain (LAS) has emerged as an early and sensitive noninvasive marker to quantify the extent of diastolic dysfunction (6,7). It comprises three distinct components corresponding to specific phases of the cardiac cycle: reservoir strain (εs) during systole, conduit strain (εe) during early diastole, and booster strain (εa) during late diastole (8). Karakurt et al. (9) showed that LAS can detect hypertension-related myocardial dysfunction, even if the LV function of these subjects is preserved. Therefore, comprehensive evaluation of LA mechanics using cardiac magnetic resonance (CMR) may serve as a noninvasive imaging biomarker for disease characterization and risk stratification (10). The aim of this study was to evaluate LA deformation parameters derived from CMR feature tracking and to determine their diagnostic value in differentiating CA from HCM. We present this article in accordance with the STARD reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0350/rc).

Methods

Clinical data

Consecutive hospitalized patients who met the inclusion criteria were retrospectively enrolled between January 2023 and December 2024.

The inclusion criteria were as follows: (I) HCM is defined by an LV wall thickness ≥15 mm in any myocardial segment that is not explained solely by loading conditions. Lesser degrees of wall thickening (13–14 mm) require evaluation of other features including family history, genetic findings, and ECG abnormalities (11). (II) CA: the inclusion criteria were based on the position statement of the European Society of Cardiology (ESC) working group (12): (i) CA was confirmed by cardiac biopsy positive for amyloid. (ii) CA also can be confirmed according with echocardiographic criteria for non-invasive (extracardiac biopsy-proven amyloidosis) diagnosis of CA: unexplained LV thickness (≥12 mm) plus characteristic echocardiography findings or multiparametric echocardiographic score ≥8 points or characteristic CMR findings. (iii) normal control group: Gender, age, height and weight-matched healthy individuals without known cardiovascular abnormalities or other systemic diseases affecting heart function served as controls. Electrocardiography, echocardiography, and CMR revealed no significant abnormalities. All participants were excluded if they had hypertension, diabetes mellitus, isolated valvular heart disease, or congenital heart disease.

A total of 107 participants were included in the study, comprising 29 individuals in the normal control group, 41 patients with CA, and 37 patients with HCM. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The First Affiliated Hospital of Zhengzhou University (approval number: 2024-KY-2314-001) and individual consent for this retrospective analysis was waived.

Instruments and methods

All CMR examinations were performed using a Siemens Skyra 3.0T MR scanner equipped with a 32-channel phased-array cardiac coil. Retrospective electrocardiogram gating was applied for scan triggering. Cine images of the four-chamber, two-chamber, and three-chamber long-axis views, including the left atrium, as well as short-axis views of the left ventricle were obtained using balanced steady-state free precession sequences. Scans were performed during end-expiratory breath-hold, and 25 cine frames were reconstructed per cardiac cycle. The scan parameters were as follows: repetition time (TR) 35.5 to 42.4 ms, echo time (TE) 1.1 to 1.4 ms, flip angle (FA) 45° to 55°, field of view (FOV) 290 mm × 290 mm to 350 mm × 350 mm, slice thickness 6–8 mm, and pixel size 1.8 mm × 1.8 mm. The temporal resolution of used images was ≤45 ms.

CMR image post-processing

Image quality assessment

All CMR cine images were reviewed for image quality prior to post-processing by two experienced observers who were blinded to clinical information and the tissue characterization results of CMR, including late gadolinium enhancement and T1 mapping outcomes. Image quality was assessed based on the presence of motion artifacts, signal-to-noise ratio, accurate anatomical positioning and the clarity of LA endocardial border delineation throughout the cardiac cycle. Images with excellent or good quality were included for quantitative LA strain analysis. Cases with fair image quality were re-evaluated by consensus; if accurate LA contouring and feature tracking were considered feasible after careful manual adjustment, these cases were included, whereas images with inaccurate positioning, low signal-to-noise ratio or unresolvable artifacts were excluded. The main reasons for exclusion were severe motion artifacts, inadequate visualization of the LA endocardium, or incomplete atrial coverage. For examinations with localized artifacts, a slice-by-slice quality control approach was applied, excluding only the affected portions rather than the entire dataset. All disagreements were resolved by consensus.

In total, 16 examinations were excluded due to insufficient image quality. Baseline characteristics did not differ significantly between included and excluded subjects.

LV volume and function analysis

Images in DICOM format were analyzed using CVI42 software (version 5.14.2; Circle Cardiovascular Imaging, Canada). In the Short-3D module, the endocardial and epicardial contours of the short-axis cine sequences were manually delineated from the apex to the base of the heart at end-diastole and end-systole. Papillary muscles and trabeculae were excluded from volumetric calculations. The following parameters were derived: left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular stroke volume (LVSV), left ventricular cardiac output (LVCO), and left ventricular ejection fraction (LVEF). Body surface area (BSA) was calculated using the Mosteller formula [BSA(m2)=height(cm)×weight(kg)3600] (13), and LV functional parameters were indexed to BSA.

LA volume and function analysis

During the image post-processing process, the observer observes the automatically tracked LA wall on 25 phase images. If any deviation is detected, manual correction is carried out. The LV outflow tract was included in the scanning sequence, but was not enrolled into analysis of LAS. Left atrial volumes (LAVs) were quantified using the Biplanar Function module. The endocardial borders of the left atrium were automatically traced on the two-chamber and four-chamber views, excluding the LA appendage and pulmonary vein confluences. The following volume parameters were obtained: maximal left atrial volume (LAV_max): volume at end-systole before mitral valve opening; minimal left atrial volume (LAV_min): volume at end-diastole after mitral valve closure; pre-atrial contraction volume (LAV_pac): volume before atrial contraction, the biplane area-length method was used for calculation: LAV=0.848×Area2ch×Area4ch(Length2ch+Length4ch)/2 (14). Left atrial total emptying fraction (LATEF), left atrial passive emptying fraction (LAPEF), and left atrial active emptying fraction (LAAEF) were calculated using the following formulas: LATEF = (V_max − V_min)/V_max, LAPEF = (V_max − V_pac)/V_max, and LAAEF = (V_pac − V_min)/V_pac. All LA functional parameters were corrected with BSA.

Measurement of LAS parameters

LAS was measured according to previously described methods (15). The end-diastolic phase of the left ventricle served as the reference frame. The endocardial border of the left atrium was manually traced on both the two-chamber and four-chamber views, excluding the LA appendage and pulmonary vein junctions. The software automatically generated strain-time and strain rate-time curves for LA longitudinal strain. On the strain-time curve, the peak value represented LA εs, the second lower peak value following the peak corresponded to εa, and εe was calculated as εs − εa. On the strain rate-time curve, the first positive peak represented the reservoir strain rate (SRs), the first negative peak represented the conduit strain rate (SRe), and the second negative peak represented the booster strain rate (SRa), as presented in Figure 1.

Figure 1 Representative examples of LAS values. LA strain-time curves and strain rate-time curves in normal controls (A₁, A₂), hypertrophic cardiomyopathy (B₁, B₂), and cardiac amyloidosis (C₁, C₂). εa, booster strain; εs, reservoir strain; LA, left atrial; LAS, left atrial strain; SRa, booster strain rate; SRe, conduit strain rate; SRs, reservoir strain rate.

Statistical methods

Statistical analyses were performed using SPSS software (version 21.0, IBM), MedCalc (version 15.2.2, Ostend Belgium) and GraphPad Prism software (version 10.3.1, San Diego, California USA). Normally distributed data are expressed as means ± standard deviations, non-normally distributed data were presented as medians (IQRs). For data that did not follow a normal distribution or lacked homogeneity of variance, the Kruskal-Wallis test was used for comparisons among multiple groups, and the Bonferroni test was applied for pairwise comparisons. P value of less than 0.05 was considered statistically significant. Categorical variables were presented as frequencies or percentages and analyzed using the chi-squared (χ²) test or Fisher’s exact test as appropriate. P value <0.05 was considered statistically significant.

Receiver operating characteristic (ROC) curves were plotted using MedCalc software to assess the diagnostic performance of LAS parameters in differentiating CA from HCM. The pairwise ROC curves were compared using the DeLong test. The best cut-off values were estimated according to the Youden index.

Intra- and interobserver reproducibility for LAS and strain rate measurements were evaluated using the intraclass correlation coefficient (ICC). Fifteen participants were randomly selected for reproducibility testing each group. Intraobserver reproducibility was assessed by repeating the measurements after a 14-day interval by the same observer, while interobserver reproducibility was evaluated by two independent observers. ICC values were interpreted as follows: less than 0.50 indicated poor reliability, between 0.50 and 0.75 moderate reliability, between 0.75 and 0.90 good reliability, and greater than 0.90 indicated excellent reliability. To account for the precision of the estimates, the 95% confidence intervals (CIs) of the ICCs were also evaluated (16).

Results

Comparison of clinical characteristics and LV function parameters

A total of 107 participants were included in the analysis, comprising 29 individuals in the normal control group (16 males, 55.2%; median age, 51 years), 41 patients with CA (29 males, 70.7%; median age, 56 years), and 37 patients with HCM (24 males, 64.9%; median age, 53 years). There were 32 patients with AL-type CA and 9 patients with ATTR-type CA, including 2 cases of hereditary variant ATTR (ATTRv) and 7 cases of wild-type ATTR (ATTRwt). Nine patients with CA had paroxysmal atrial fibrillation, compared with 5 patients with HCM. Among the 37 patients with HCM, 17 had obstructive HCM and 20 had non-obstructive HCM. Of the 37 patients, 31 had asymmetric HCM (including 4 with apical hypertrophy), and 6 had symmetric HCM.

No statistically significant differences were observed among the three groups in age, sex, height, weight, BSA, or body mass index (BMI).

The LVEF in the HCM group was significantly higher than that in both the normal control and CA groups, whereas the LVEF in the CA group was significantly lower than that in the normal control group. The LVEDV and LVEDV index (LVEDVI) were significantly higher in the HCM group compared with the CA group. Conversely, the LVESV and LVESV index (LVESVI) were significantly lower in HCM compared with CA.

Furthermore, stroke volume (SV), cardiac output (CO), stroke volume index (SVI), and cardiac index (CI) were all significantly higher in the HCM group compared with the CA group (Table 1).

Comparison of LA function parameters among the three groups

The LAV_max, LAV_pac, LAV_min, and corresponding indices [LAV_max indexed (LAV_maxI), LAV_pac indexed (LAV_pacI), LAV_min indexed (LAV_minI)] were significantly higher in both the HCM and CA groups compared with the normal control group. No significant differences were observed between the two cardiomyopathy groups. The LATEF and LAPEF were significantly lower in both the HCM and CA groups compared with the normal control group. The LAAEF was significantly lower in the CA group than in the normal control group. Additionally, both LATEF and LAAEF were significantly lower in CA compared with HCM.

The absolute values of strain parameters (εs, εe, εa) and strain rate parameters (SRs, SRe, SRa) were significantly reduced in both HCM and CA compared with the normal control group. Moreover, these parameters were markedly lower in CA than in HCM (Table 2; Figures 1,2).

Figure 2 Comparison of left atrial strain parameters [(A) εs, (B) εe, (C) εa, (D) SRs, (E) SRe, (F) SRa] among the normal control group, HCM group, and CA group. *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001. εa, booster strain; CA, cardiac amyloidosis; εe, conduit strain; HCM, hypertrophic cardiomyopathy; NC, normal control; εs, reservoir strain; SRa, booster strain rate; SRe, conduit strain rate; SRs, reservoir strain rate.

Intraobserver and interobserver consistency analysis of LAS parameters

The LAS parameters of each group (εs, εe, εa, SRs, SRe, SRa) demonstrated moderate to excellent intraobserver and interobserver reproducibility (Table 3).

Diagnostic performance of LAS parameters in differentiating CA from HCM

LAS parameters demonstrated strong diagnostic performance in differentiating CA from HCM. The areas under the ROC curves (AUC) for εs, εe, εa, SRs, SRe, and SRa were 0.921, 0.869, 0.888, 0.816, 0.727, and 0.857, respectively. Detailed diagnostic performance data are presented in Table 4 and Figure 3.

Figure 3 ROC curves illustrating the diagnostic performance of left atrial strain parameters (εs, εe, εa, SRs, SRe, SRa) for differentiating cardiac amyloidosis from hypertrophic cardiomyopathy. εa, booster strain; εe, conduit strain; ROC, receiver operating characteristic; εs, reservoir strain; SRa, booster strain rate; SRe, conduit strain rate; SRs, reservoir strain rate.

Intergroup variability analysis of LAS parameters

Compared with the normal control group, both the CA and HCM groups showed increased variability in all parameters, with the CA group exhibiting more pronounced variation. The coefficients of variation (CVs) for LAS parameters across the three groups are summarized in Table 5.

Discussion

Myocardial remodeling associated with cardiac hypertrophy represents a key mechanism contributing to the development of heart failure. Differentiating among various forms of hypertrophic myocardial diseases arising from distinct etiologies remains clinically challenging; however, accurate etiological identification is essential for selecting appropriate therapeutic strategies and assessing prognosis. Myocardial strain reflects the deformation capacity of myocardial fibers and enables a quantitative assessment of myocardial contractile function. LAS and strain rate serve as sensitive markers of atrial functional alterations and provide an assessment that is independent of LAV (17).

From an anatomical and physiological perspective, the left atrium and left ventricle are closely interconnected. The LA reservoir phase occurs during LV systole and isovolumic relaxation, during which the left atrium acts as a reservoir for pulmonary venous return. The conduit phase occurs during early LV diastole, allowing passive blood transfer from the left atrium to the left ventricle. The booster phase occurs during late diastole, when the left atrium actively contracts to augment ventricular filling (18). The parameters εs and SRs reflect LA reservoir function, εe and SRe represent conduit function, and εa and SRa indicate booster pump function. The present study provides quantitative evidence for the etiological differentiation of hypertrophic myocardial diseases through analysis of LAS in CA and HCM, along with correlations between LAS parameters and LV functional indices.

In terms of clinical characteristics, no significant differences were observed in age, sex, height, weight, BSA, or BMI among the CA, HCM, and normal control groups. However, significant variations were observed in LV functional parameters across the three groups. Pairwise comparisons demonstrated that LVEF, SV, SVI, and CI were significantly lower in CA than in the normal control group, whereas LVEF, SV, CO, and SVI were significantly higher in HCM than in the normal control group. Compared with CA, HCM exhibited higher values of LVEF, LVEDV, LVEDVI, SV, CO, SVI, and CI, while LVESV and LVESVI were lower.

The differences in LV parameters can be explained by the distinct pathophysiological features of HCM and CA. HCM progresses through four clinical stages (19): stage I (subclinical stage with no phenotypic expression), stage II (classic HCM with LVEF >65%), stage III (reverse remodeling stage with LVEF between 50–65%), and stage IV (end-stage disease with LVEF <50%). Most patients in the present cohort were in stage II (classic HCM), accounting for the significantly elevated LVEF compared with the participants in the normal control group. In contrast, CA, an infiltrative cardiomyopathy characterized by extracellular deposition of amyloid protein, leads to progressive myocardial stiffness and impaired contractility, thereby reducing overall cardiac function. Consequently, the LV functional parameters in CA differed markedly from participants in both the HCM and normal control groups.

Analysis of LA function revealed significant differences in LAV and functional parameters among the three groups. Pairwise comparisons indicated that LAV_min, LAV_pac, LAV_max, and their respective indices (LAV_minI, LAV_pacI, LAV_maxI) were significantly higher in participants in both the CA and HCM group than in the normal control group, consistent with previous findings (20). LATEF, LAPEF, and LAAEF were lower in both cardiomyopathy groups compared with the normal control group; however, the reduction in LAAEF between participants in the HCM and normal control groups was not statistically significant. In contrast, both LATEF and LAAEF were significantly lower in CA than in HCM.

Although most HCM cases in this study were classified as stage II, characterized by increased LVEF, this parameter alone was insufficient to capture subtle cardiac functional impairment. LA functional assessment provided more detailed insight, revealing increased LAV_min, conduit-phase volume, and LAV_max, accompanied by decreased ejection fractions across different functional phases. LA dysfunction was more pronounced in CA. Both HCM and CA exhibit early diastolic dysfunction, which is often subclinical. Elevated LV filling pressure secondary to diastolic dysfunction transmits to the left atrium, resulting in atrial dilation and subsequent dysfunction, ultimately leading to progressive atrial remodeling (21).

CA involves two pathophysiological mechanisms that exacerbate LA dysfunction: increased afterload due to impaired ventricular diastolic relaxation and direct amyloid deposition within the atrial wall. The latter contributes to structural rigidity and mechanical dysfunction. In addition, inflammatory reactions and oxidative stress triggered by amyloid-associated protein toxicity promote cardiomyocyte apoptosis and autophagic activity (22). Consequently, the combined effects of hemodynamic burden and amyloid infiltration lead to more severe LA dysfunction in CA than in HCM (23).

In the present study, no significant differences were observed in the LAV parameters between CA and HCM, indicating that structural assessment of the left atrium alone is insufficient for distinguishing between these two forms of hypertrophic myocardial disease. However, when comparing LA ejection fractions across different functional phases, both LATEF and LAAEF were significantly lower in CA compared with HCM. This finding indicates that both overall and active ejection functions of the left atrium are more severely impaired in CA. Consequently, even in the absence of significant structural differences, functional indices provide a more sensitive reflection of LA dysfunction.

LA ejection fraction, particularly during the reservoir and booster phases, demonstrated greater discriminative value for differentiating CA from HCM than volume-based parameters. This finding aligns with previous reports indicating that LA functional indices provide more comprehensive pathophysiological information than structural parameters such as the LAVI (24).

LA function is closely interrelated with LV performance, quantifying atrial myocardial deformation facilitates the detection of subclinical myocardial dysfunction. Importantly, myocardial strain analysis based on CMR can be derived from standard cardiac cine sequences without the need for additional image acquisition, thereby enhancing its practicality and clinical applicability (25).

LAS and strain rate reflect the comprehensive deformation process of the atrial myocardium throughout the cardiac cycle. During the reservoir phase, the atrial volume increases progressively, and the myocardial fibers elongate to their maximum extent. The peak strain at this point represents the LA εs, while the corresponding positive strain rate peak reflects the LA reservoir SRs. As blood flows from the left atrium into the left ventricle during the conduit phase, the strain curve reaches a plateau, the height of which corresponds to the εa. The εe is calculated as the difference between the reservoir and booster strain (εs − εa). On the strain rate curve, the first negative peak represents the conduit SRe, whereas the second negative peak—occurring during active atrial contraction in late diastole—corresponds to the booster SRa.

In this study, LAS measurements demonstrated excellent intraobserver and interobserver reproducibility. Comparison among the three groups revealed that LAS (εs, εe, εa) and strain rate (SRs, SRe, SRa) values were significantly lower in CA and HCM than in the normal control group. Furthermore, these parameters were markedly lower in CA than in HCM. It is important to note that the negative values of SRe and SRa represent myocardial fiber shortening from a lengthened state; thus, a reduction in their absolute values indicates diminished myocardial deformation capacity. These findings confirm that LAS analysis can sensitively identify abnormalities in reservoir, conduit, and booster functions. The present findings are consistent with those of previous studies (10,26). Nochioka et al. reported, based on echocardiographic assessment, that LAS was significantly reduced in patients with light-chain amyloidosis, hereditary transthyretin amyloidosis, and non-hereditary transthyretin amyloidosis compared to normal controls. This finding supports the consistency between echocardiographic and CMR-based assessments of LAS in CA (23). Other studies have demonstrated that reduced LAS in HCM is associated with an increased risk of adverse clinical outcomes (20).

Further analysis of LAS parameters for differentiating CA from HCM demonstrated strong diagnostic performance, with the highest AUC observed for εs (AUC =0.921). The εe and εa parameters also exhibited high diagnostic accuracy, with AUCs of 0.869 and 0.888, respectively. Although most previous research has focused primarily on HCM prognosis, accurate etiological differentiation of hypertrophic myocardial diseases remains clinically challenging. The present findings suggest that quantitative analysis of LAS serves as a sensitive biomarker for distinguishing these disease entities and may facilitate earlier identification of cardiac diastolic dysfunction.

This study has several limitations. First, the sample size was relatively small. HCM includes various morphologic subtypes—such as symmetric, asymmetric, and apical forms—while CA encompasses both immunoglobulin light-chain and transthyretin types. Although subtype classification was performed, further research is required to clarify inter-subtype differences. Second, the analysis was limited to CA and HCM. Clinically, myocardial hypertrophy may occur in a range of conditions, including less common disorders not addressed in this study. Amyloid subtype (AL vs. ATTR) has substantial implications for cardiac morphology and function, including characteristic differences in LV remodeling, LA mechanics, and clinical prognosis. Third, dynamic intraventricular gradients were not systematically assessed in all patients. Further studies could include systematic assessment of intraventricular gradients to further explore their relationship with LA function. In addition, the results of the study lacked external validation, which limited the generalizability. Future prospective study incorporating a broader spectrum of hypertrophic myocardial disorders and larger patient cohorts, and conducting classification of CA and external validation will improve diagnostic precision and generalizability. Last, whether LAS provides additional diagnostic value beyond conventional CMR parameters was not investigated, which need further prospective multi-center study to explore.

Conclusions

LAS parameters effectively detect early LV diastolic dysfunction and provide high diagnostic efficacy in distinguishing CA from HCM, which need further prospective study including patients with all HCM types and conducting internal and external validation to confirm credibility and expand generalizability.

Acknowledgments

We would like to acknowledge the hard and dedicated work of all the staff that implemented the intervention and evaluation components of the study.

Footnote

Reporting Checklist: The authors have completed the STARD reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0350/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0350/dss

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0350/coif). The authors have no 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. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The First Affiliated Hospital of Zhengzhou University (approval number: 2024-KY-2314-001) and individual consent for this retrospective analysis was waived.

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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