Left atrial dysfunction in different morphologic phenotypes of hypertrophic cardiomyopathy: a cardiac magnetic resonance feature tracking study

Introduction

Hypertrophic cardiomyopathy (HCM) is an inherited myocardial disorder characterized by unexplained left ventricular (LV) hypertrophy without concomitant chamber dilation (1). With an estimated prevalence of 1:500 in the general population, HCM represents the most common genetic cardiovascular disease and a leading cause of sudden cardiac death in young adults and athletes (2,3). The condition demonstrates substantial phenotypic heterogeneity and has been typically classified into several morphological subtypes based on the pattern of hypertrophy, including septal, apical, and concentric variants (4). In recent years, left atrial (LA) function has garnered considerable attention as a robust prognostic marker across the spectrum of HCM (5,6). However, whether LA functional impairment differs among the distinct morphologic phenotypes remains incompletely understood, limiting insight into phenotype-specific atrial impairment and disease heterogeneity in HCM.

Cardiac magnetic resonance (CMR) is widely regarded as the reference standard for noninvasive myocardial tissue characterization and functional assessment, offering superior spatial resolution, enhanced tissue characterization capabilities, and accurate volumetric quantification compared to echocardiography (7,8). Leveraging these foundations, CMR feature tracking (CMR-FT) has further expanded the capacity for sophisticated quantification of LA deformation parameters, including reservoir, conduit, and booster pump functions (9). This technique could provide valuable insights into atrial mechanics and demonstrate greater sensitivity in detecting early LA dysfunction than traditional metrics such as LA emptying fraction (LAEF) (9,10). However, despite these technical advances, studies applying CMR-FT to evaluate LA mechanics across different HCM phenotypes remain limited. As distinct hypertrophic patterns may involve different loading conditions and remodeling processes (11,12), investigating phenotype-specific LA mechanics may provide valuable insights into disease heterogeneity in HCM.

Therefore, this study aimed to investigate the potential differences in LA function among HCM phenotypic subtypes using CMR-FT and to evaluate the associations of LA strain parameters with LV systolic function within each subgroup. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1-2699/rc).

Methods

Study population

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Institutional Review Board of The First Affiliated Hospital of Zhejiang Chinese Medical University (No. 2022-KLS-207-01), with approval acknowledged by The First Affiliated Hospital, Zhejiang University School of Medicine and The First Affiliated Hospital of Wenzhou Medical University, and the requirement for written informed consent was waived owing to its retrospective design. From March 2023 to October 2024, 276 consecutive patients with HCM who underwent CMR at The First Affiliated Hospital of Zhejiang Chinese Medical University, The First Affiliated Hospital of Zhejiang University School of Medicine, and The First Affiliated Hospital of Wenzhou Medical University were initially included. The diagnosis of HCM was based on an LV wall thickness ≥15 mm on CMR, or ≥13 mm in individuals with a family history of HCM (3). The exclusion criteria were as follows: (I) history of coronary artery disease, myocardial infarction, or myocarditis; (II) prior septal myectomy or alcohol septal ablation; (III) myocardial hypertrophy secondary to other conditions, including cardiac amyloidosis, valvular heart disease, or Fabry disease; (IV) history of atrial fibrillation (AF); and (V) inadequate image quality for LA deformation analysis. After exclusions, 225 patients with HCM were finally included. Based on the predominant location of maximal myocardial hypertrophy on CMR, patients were classified into three phenotypic subgroups: apical HCM, septal HCM, and concentric HCM (13). Apical HCM was defined as hypertrophy predominantly involving the LV apex, septal HCM as asymmetric hypertrophy mainly affecting the interventricular septum, and concentric HCM as relatively uniform thickening of the LV myocardium involving multiple segments without a predominant septal or apical distribution. Phenotype classification was performed independently by two experienced observers blinded to clinical information, with a third senior cardiovascular radiologist providing adjudication in cases with discrepancies. Moreover, 68 age- and sex-matched healthy volunteers without hypertension, diabetes, or cardiovascular disease were recruited as the healthy control (HC) group (Figure 1).

Figure 1 Study flowchart of patient inclusion. HCM, hypertrophic cardiomyopathy.

Image acquisition

CMR examinations were performed at three centers using 1.5 tesla (T) or 3.0 T scanners equipped with phased-array surface coils. Short-axis cine images encompassing both ventricles from base to apex were acquired using a retrospective electrocardiogram-gated balanced steady-state free precession sequence. Additionally, three long-axis views (two-, three-, and four-chamber) were obtained. Late gadolinium enhancement (LGE) imaging was performed 10–15 minutes after intravenous injection of a gadolinium-based contrast agent [0.15–0.20 mmol/kg of gadopentetate dimeglumine (Beilu Pharmaceutical, Beijing, China) or gadobutrol (Bayer Healthcare, Leverkusen, Germany)] using a phase-sensitive inversion recovery gradient-echo sequence. Detailed CMR acquisition parameters are summarized in Table S1.

Image analysis

All image analyses were performed using dedicated software (cvi42, Version 6.3.1; Circle Cardiovascular Imaging, Calgary, AB, Canada) by a researcher (Wenqi Liu, with 3 years of experience in CMR analysis) who was blinded to all clinical information. LV volumetric and functional parameters, including end-diastolic volume index (LVEDVi), end-systolic volume index (LVESVi), stroke volume index (LVSVi), ejection fraction (LVEF), cardiac index (LVCI), and LV mass (LVMass), were evaluated from short-axis cine images. Additionally, LV strain parameters, including global radial strain (LVGRS), global circumferential strain (LVGCS), and global longitudinal strain (LVGLS), were measured using CMR-FT according to previously described methods (14). LA maximum volume index (LAVmaxi), minimum volume index (LAVmini), and LAEF were obtained in the two- and four-chamber views using the bi-plane area-length method (15).

LA feature tracking

LA feature tracking strain analysis was performed using the same post-processing software by a researcher (Wenqi Liu). All analyses were conducted under rigorously blinded conditions, with no access to patient demographic or clinical data. The LA endocardial and epicardial borders were manually delineated in both the two- and four-chamber views at the phase of minimal LA volume following atrial contraction, using a point-and-click method (16). Pulmonary veins and LA appendage were excluded from the LA endocardial borders, and the automated tracking algorithm was subsequently applied. The tracking quality was meticulously verified through visual inspection, and manual adjustments to the initial contours were made when necessary. From the resultant strain-time and strain rate-time curves, key LA deformation parameters were derived, including: reservoir strain (εs), conduit strain (εe), booster strain (εa), and their corresponding strain rates: peak positive strain rate (SRs), peak early negative strain rate (SRe), and peak late negative strain rate (SRa).

Reproducibility

To assess inter-observer reproducibility of LA deformation parameters, 20 patients with HCM were randomly selected and independently analyzed by two observers (Wenqi Liu and Wanzhen Li, with 3 and 5 years of respective experience in CMR analysis). For intra-observer reproducibility, the same set of cases were reanalyzed by the first observer (Wenqi Liu) after an interval of more than 1 month.

Statistical analysis

Continuous variables were presented as mean ± standard deviation (SD) if normally distributed, or as median and interquartile range if nonnormally distributed, as assessed by the Shapiro-Wilk test. Categorical variables were summarized as frequencies and percentages. Comparisons among three or more groups were performed using one-way analysis of variance (ANOVA) with least significant difference (LSD) post hoc tests or Kruskal-Wallis test with post hoc Dunn’s test as appropriate for continuous variables, and a Chi-squared test with Bonferroni correction post hoc pairwise comparisons for categorical variables. The associations of LVEF and LV strain with LA strain parameters were assessed using Pearson correlation analysis, and were considered strong, moderate, and weak when |r|≥0.7, 0.4≤|r|<0.7, and |r|<0.4, respectively. Intra- and inter-observer reproducibility were evaluated using intraclass correlation coefficients (ICCs) and Bland-Altman plots. ICC values greater than 0.75 were considered indicative of excellent reproducibility, values between 0.40 and 0.75 represented good reproducibility, and values below 0.40 indicated poor reproducibility (17). All statistical analyses were conducted using the software SPSS 29.0.1.0 (IBM Corp., Armonk, NY, USA) and GraphPad Prism 10.2.3 (GraphPad Software, San Diego, CA, USA). A two-sided P value <0.05 was considered statistically significant.

Results

Baseline characteristics

The study cohort consisted of 40 patients with apical HCM, 153 with septal HCM, 32 with concentric HCM, and 68 HC. Baseline demographic and clinical characteristics are summarized in Table 1. No significant differences were observed in age (P=0.565) or male proportion (P=0.760) among the four groups. Compared with HC, all three HCM subgroups exhibited significantly higher body mass index (BMI), systolic blood pressure (SBP), and maximum wall thickness (all P<0.001), whereas no significant differences were observed among the HCM subgroups for these parameters (all P>0.05). Among HCM subgroups, no significant differences were observed in the prevalence of family history of HCM or sudden cardiac death, unexplained syncope, hypertension, or diabetes (all P>0.05). However, the frequency of LV outflow tract (LVOT) obstruction was more common in the septal and concentric HCM subgroups than in apical HCM subgroup (both P<0.05). Moreover, no significant differences were found among HCM subgroups in LGE presence, LGE mass, or LGE extent (all P>0.05). Regarding medication use, no significant differences were observed among HCM subgroups for β-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, diuretics, antiplatelet, or calcium antagonists (all P>0.05).

LV conventional and strain parameters

As shown in Table 2, all HCM subgroups demonstrated significantly greater LVEDVi, LVESVi, and LVMass, along with significantly lower LVEF, compared with HC (all P<0.05). Among the three HCM subgroups, the concentric HCM subgroup exhibited the greatest LVMass (both P<0.05). Myocardial deformation was significantly impaired in all HCM subgroups compared to HC, as evidenced by reduced LVGRS, LVGCS, and LVGLS (all P<0.05). The apical HCM subgroup showed the most pronounced impairment, with significantly lower GRS, GCS, and GLS values compared to the septal HCM subgroup (all P<0.05). The corresponding effect sizes and 95% confidence intervals (CIs) are provided in Table S2.

LA conventional and strain parameters

Compared with HC, all HCM subgroups exhibited significantly greater LAVmaxi and LAVmini, and lower LAEF (all P<0.001) (Figure 2, Table 3). However, no significant differences in these LA parameters were observed among the apical, septal, and concentric HCM subgroups (all P>0.05). Regarding LA myocardial deformation, significant impairment was also detected across all HCM variants compared with HC (all P<0.05). Notably, the concentric HCM subgroup demonstrated a more pronounced reduction in LA εs and εa compared with the septal HCM subgroup (both P<0.05). The corresponding effect sizes and 95% CIs are provided in Table S3. Representative LA strain and strain rate curves derived from CMR-FT for each subgroup and HC are presented in Figure 3.

Figure 2 Comparison of left atrial strain parameters among HC and HCM patients with septal, apical, and concentric subtypes. ***, P<0.001; ns, not significant. HC, healthy controls; HCM, hypertrophic cardiomyopathy; LA, left atrial.

Figure 3 Representative cases of left atrial strain analysis in HC (A), septal HCM (B), apical HCM (C), and concentric HCM (D). εa, booster strain; εe, conduit strain; εs, reservoir strain; HC, healthy control; HCM, hypertrophic cardiomyopathy; LA, left atrial.

Association of LV parameters with LA strain in HCM patients

Table 4 summarizes the associations of LA εs, εe, and εa with LV functional parameters, including LVEF, LVGCS, LVGRS, LVGLS, and LGE extent across the different HCM subgroups. In the septal HCM subgroup, LA εs, εe, and εa showed weak to moderate correlations with LVEF, LVGCS, LVGRS, and LVGLS, with |r| ranging from 0.322 to 0.503 (all P<0.001), whereas no significant correlations were observed between LGE extent and any LA strain parameters (all P>0.05). In apical HCM, both LA εs and εe exhibited weak positive correlations with LVEF and LVGRS but inverse correlations with LVGCS and LVGLS (|r|≥0.317, all P<0.05), whereas LA εa only correlated with LVGCS and LVGRS (|r|≥0.325, both P<0.05). No significant associations were found between LGE extent and LA strain parameters in this subgroup (all P>0.05). By contrast, in the concentric HCM subgroup, significant correlations were primarily observed between LA εa and LVEF, LVGCS, LVGRS, and LVGLS (|r|≥0.389, all P<0.05) (Figure 4). Although LA εs showed a weak correlation with LVGRS (r=0.369, P=0.038), neither LA εs nor LA εe was significantly associated with remaining LV functional parameters in this subgroup. In addition, LGE extent showed a moderate inverse correlation with LA εs (r=−0.459, P=0.008), whereas its associations with LA εe and εa were not statistically significant (both P>0.05).

Figure 4 Associations of left atrial strain with left ventricular ejection fraction (A-C) and global longitudinal strain (D-F) across the three HCM subtypes. εa, booster strain; εe, conduit strain; εs, reservoir strain; HCM, hypertrophic cardiomyopathy; LA, left atrial; LVEF, left ventricular ejection fraction; LVGLS, left ventricular global longitudinal strain.

Inter- and intra-observer reproducibility

The inter- and intra-observer reproducibility of LA strain and SR measurements are summarized in Table 5. Both intra- and inter-observer agreements for LA deformation parameters were excellent, with all ICCs exceeding 0.75. Bland-Altman analyses, presented in Figures S1,S2, further confirmed strong reproducibility, demonstrating narrow limits of agreement.

Discussion

In this study, we employed CMR-FT to comprehensively evaluate LA phasic function across various phenotypes of HCM. The principal findings are as follows: first, all HCM subgroups exhibited impaired LA function compared to HC, with the concentric HCM demonstrating more pronounced reductions in LA εs and εa than septal HCM. Second, we observed distinct patterns of LA-LV functional impairment among the HCM subtypes. Specifically, most LA strain parameters correlated significantly with LV functional indices in both septal and apical HCM, whereas these correlations were mostly restricted to LA εa in the concentric HCM subtype. These findings underscore the presence of subtype-specific alterations in atrioventricular mechanical coupling in HCM.

LV hypertrophy (LVH) phenotypes and dysfunction in HCM

LVH, the pathological hallmark of HCM, exhibits distinct epidemiological and geometric patterns (18). The asymmetrical septal phenotype is the most common phenotypic expression, accounting for up to 70% of the HCM population, and has been strongly associated with mutations in thick-filament genes such as myosin heavy chain (MYH7) and myosin binding protein C (MYBPC3) (19). In contrast, apical and concentric subtypes are relatively less prevalent in HCM (19,20). Notably, specific geometric patterns of LVH have been confirmed to be associated with adverse cardiovascular outcomes in both general and hypertensive populations, with concentric hypertrophy conferring a particularly elevated risk of major cardiovascular events and all-cause mortality (21,22). This adverse prognosis may be intrinsically linked to the more severe impact of concentric remodeling on LV diastolic function and filling pressures (23). Moreover, a prior study by Urbano-Moral et al. (24) demonstrated that hypertrophied myocardial segments are associated with regional functional impairment in HCM. This may provide a mechanistic explanation for the more impaired global LV longitudinal strain observed in concentric HCM compared with septal HCM in the present study, possibly related to its more diffusely distributed hypertrophy (25). Regarding apical HCM, which is characterized by unique mechanical inefficiency (26), the underlying pathophysiology may be attributed to the disrupted LV torsion due to apical rotation reduction, contributing to a loss of early diastolic suction, and compounded by systolic cavity obliteration leading to myocardial ischemia and apical fibrosis (20).

LA dysfunction in HCM phenotypes

In this study, the concentric HCM subgroup demonstrated relatively lower LA εs and εa compared to the septal subgroup. This observation may be attributed to the complex multifactorial regulation of LA function, which involves LA compliance, pre-load, intrinsic contractile function, LV end-diastolic pressure, and LV systolic reserve (27). In patients with HCM, LVH promotes elevated LV filling pressures, which are directly transmitted to the left atrium, thereby impairing its reservoir function (28). In this context, an animal study from Røe et al. (23) provided evidence of further deterioration in LV compliance in concentric LVH, which may additionally compromise LA deformation. Consistent with findings reported by Baxi et al. (29), the prevalence of LVOT obstruction was relatively common in our concentric HCM cohort, which may potentially contribute to altered hemodynamic conditions (30). Furthermore, a previous study reported that concentric hypertrophy was more frequently associated with specific sarcomere mutations, which may lead to more severe LV diastolic dysfunction and potentially concurrent primary LA myopathy (31). Collectively, these pathophysiological mechanisms may contribute to the more pronounced impairment in LA mechanics observed in concentric HCM than in the septal HCM subtype. Notably, although LA strain parameters showed significant differences among subgroups, the LA emptying fraction did not differ significantly, suggesting that strain analysis may provide more sensitive detection of subtle LA dysfunction than conventional volumetric indices. Given the established prognostic value of LA strain in patients with HCM (5,32), these subtype-specific alterations of LA function may deserve particular attention in clinical management. In addition, this study observed a moderate inverse correlation between LGE extent and LA εs only in the concentric HCM group. This finding suggests that myocardial fibrosis may partly contribute to impaired LA function in HCM (33), although this association was not consistently observed across phenotypes.

Correlation between LA and LV in HCM phenotypes

The correlations between LA and LV function parameters suggested distinct pathophysiological mechanisms across HCM subtypes. In septal HCM, robust correlations across all LA functional phases—εs, εe, and εa—may be related to the mechanical impact of septal hypertrophy on the mitral apparatus, imposing a diffuse burden on LA dynamics throughout the cardiac cycle (34). This proximity may interfere with normal LA reservoir expansion during LV systole, limit passive emptying during the early-diastolic conduit phase, and may increase reliance on LA active contractile function in late diastole (35). In apical HCM, the inverse relationship between LA strain and LVGLS may be related to characteristic alterations in LV mechanics, including potential changes in torsional dynamics and apical deformation (36), which may influence intracavitary flow dynamics and diastolic filling patterns that lead to the modulation of LA emptying (37). Notably, in concentric HCM, the predominant correlation of LA εa with LV function suggests a compensatory adaptation to elevated filling pressures, whereby the atrium may rely more on its contractile function to maintain ventricular filling. Thus, these subtype-specific LA-LV dysfunction patterns provide insight into distinct pathophysiological pathways and highlight the heterogeneity of atrioventricular interaction in HCM.

Limitations

This study has several limitations. First, the retrospective design may have introduced potential selection bias, although standardized inclusion criteria were applied to mitigate this concern. Second, the inherent differences in prevalence among HCM phenotypic subtypes resulted in an imbalanced distribution of sample sizes across groups, which may have influenced the statistical power of intergroup comparisons. Third, echocardiographic parameters including mitral regurgitation severity and LVOT obstruction indices were not comprehensively available, and their potential confounding effects warrant further investigation. In addition, the potential influence of coexisting hypertension in the concentric HCM group should be considered, although strict diagnostic criteria were applied. Finally, the exclusion of AF and limited follow-up warrant further prospective studies with broader inclusion to assess the temporal evolution and prognostic significance of LA dysfunction across HCM phenotypes.

Conclusions

LA dysfunction varies significantly across HCM phenotypic subtypes, with the concentric variant exhibiting greater impairment in reservoir and booster functions compared with the septal subtype. These findings provide insight into underlying pathophysiological mechanisms and underscore the subtype-specific alterations in atrial mechanics in HCM, as well as the potential utility of CMR-FT for comprehensive phenotypic characterization.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1-2699/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1-2699/dss

Funding: This study was supported by the “Pioneer” and “Leading Goose” R&D Program of Zhejiang (No. 2022C03046 to M.X.), the Talent Cultivation Program for Outstanding Innovative Individuals at Zhejiang Chinese Medical University (No. 2024YJSBJ002 to Y.G.), and Jinhua Public Welfare Technology Application Research Project (No. 2025-4-274 to Wanzhen Li).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1-2699/coif). Y.G. reports funding from Talent Cultivation Program for Outstanding Innovative Individuals at Zhejiang Chinese Medical University (No. 2024YJSBJ002). Wanzhen Li reports funding from Jinhua Public Welfare Technology Application Research Project (No. 2025-4-274). M.X. reports funding from “Pioneer” and “Leading Goose” R&D Program of Zhejiang (No. 2022C03046). L.T. is a current employee of Circle Cardiovascular Imaging Inc. The other 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. This study was approved by the institutional review board of The First Affiliated Hospital of Zhejiang Chinese Medical University (No. 2022-KLS-207-01), with approval acknowledged by The First Affiliated Hospital of Zhejiang University School of Medicine and The First Affiliated Hospital of Wenzhou Medical University, and the requirement for patients’ consent was waived due to its retrospective nature.

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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