Abstract
Background
The importance of right atrial (RA) function assessment in arrhythmogenic right ventricular cardiomyopathy (ARVC) is increasingly being recognized. MR-feature tracking (MR-FT) has emerged as a novel approach for quantifying atrial function. Therefore, we aimed to evaluate whether early RA dysfunction, even without RA dilation, can be identified in patients with ARVC using MR-FT.
Methods
Sixty-four patients with ARVC, of whom 47 were non-RA dilated and 17 were RA dilated patients, along with 41 healthy controls were included. RA reservoir, conduit, and booster strain (εs, εe, and εa) and peak positive, early negative, and late negative strain rate (SRs, SRe, and SRa) were measured using MR-FT. Right ventricular (RV) remodeling index was calculated as the ratio of RV to left ventricular end-diastolic volumes.
Results
Patients with ARVC (both RA Dilated and non-RA Dilated group) exhibited significantly lower RA εs, εe, εa, SRs, SRe, and SRa compared to healthy controls. RA dilation patients further reduced these parameters (all P < 0.001). Among RA strain parameters, SRe showed the highest diagnostic value for RV remodeling in patients with ARVC (AUC = 0.799, 95% CI: 0.683–0.915). A strong correlation was observed between RA strain, strain rate, and RA emptying fractions in ARVC patients (P < 0.001). Intra- and inter-observer reproducibility was excellent for RA strain measurements.
Conclusion
Patients with ARVC exhibit impaired RA reservoir, conduit, and booster function even with normal RA volumes. MR-FT may serve as a promising approach for detecting early RA dysfunction in this population.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12880-026-02172-y.
Keywords: Arrhythmogenic right ventricular cardiomyopathy, MR-feature tracking, Right atrial function, Strain, Strain rate
Introduction
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare inherited cardiomyopathy, which has long been the leading cause of arrhythmic cardiac arrest among athletes and young adults [1, 2]. The pathological hallmark of this disease is the progressive fibro-fatty infiltration of the right ventricular (RV) myocardium, leading to cardiac remodeling and impaired systolic function [3], ultimately resulting in life-threatening ventricular arrhythmias, sudden cardiac death, and heart failure. Previous studies regarding the cardiac damage caused by ARVC have mainly focused on the RV or biventricular structure and function [4–6]. However, insights into right atrial (RA) involvement in patients with ARVC remain limited.
The right atrium plays a crucial role in regulating ventricular filling and sustaining normal cardiac hemodynamics through its reservoir, conduit, and booster pump function [7]. There is growing evidence that RA strain parameters, including strain and strain rate (SR), could offer a quantitative evaluation of RA myocardial deformation performance, which may be more sensitive in detecting early impairment of RA function compared to the traditional RA emptying fraction (RAEF) [8]. The importance of evaluating RA strain has been established in a spectrum of cardiovascular pathologies, such as heart failure, pulmonary hypertension, hypertrophic cardiomyopathy, etc [9–11]. Recently, a study by Gao et al. [12] found that RA strain was an independent predictor for adverse outcomes in patients with dilated cardiomyopathy. More importantly, although RA size has been shown to have considerable diagnostic and prognostic value across various cardiovascular diseases [13–15], there is a paucity of information regarding the prevalence and clinical implications of RA dilation in patients with ARVC.
Cardiac MR imaging has emerged as the reference standard for the noninvasive assessment of cardiac structure and function [16]. Based on the conventionally balanced steady-state free precession cine sequence, due to its higher spatial resolution, better reproducibility, and sharper endocardial boundaries, MR-feature tracking (MR-FT) has been introduced for semiautomatic myocardial deformation quantification, which makes it possible to objectively identify RA dysfunction [7]. However, studies focusing on RA myocardial deformation applying MR-FT in ARVC patients have rarely been reported. In addition, as the definitive indicators of cardiac adverse remodeling in the clinical scenario such as pulmonary hypertension [17], information regarding the relationship between RV remodeling and RA strain parameters in patients with ARVC has not been well established.
This study aimed to investigate the potential of RA strain and SR in detecting early RA dysfunction in both ARVC patients with or without RA dilation using MR-FT, and to explore their associations with RV remodeling in this population.
Materials and methods
Study population
This retrospective study was approved by the local institutional review board and was exempted from informed consent. Consecutive adult patients with ARVC who had undergone cardiac MR examinations at the First Affiliated Hospital of Zhejiang Chinese Medical University and the Second Affiliated Hospital, Zhejiang University School of Medicine between October 2012 and July 2024 were considered for inclusion. The diagnosis of ARVC adhered to the 2010 Task Force Criteria (TFC) [18], and patients with unqualified images affecting the assessment of RA strain and those who had congenital heart diseases or other cardiomyopathies were excluded. Finally, 64 patients with ARVC were included and further divided into 2 groups: the ARVC RA Dilated group (n = 17) and the non-RA Dilated group (n = 47) (Fig. 1). RA dilation was defined as the RA volume indexed to body surface area (BSA) > 53.1 mL/m2 for men or 48.8 > mL/m2 for women [7]. A control group of 41 age- and gender-matched healthy subjects without any cardiovascular diseases was also recruited.
Fig. 1.
Flowchart of patient inclusion. ARVC = arrhythmogenic right ventricular cardiomyopathy; RA = right atrial
Cardiac MR acquisition
Cardiac MR examinations were performed using 1.5T (Signa HD excite, General Electric Healthcare, Chicago, USA; Magnetom Avanto, Siemens Healthineers, Erlangen, Germany) and 3.0T (Discovery MR750 and Signa Premier, General Electric Healthcare, Chicago, USA) MR scanners. Briefly, we conducted ECG-gated breath-hold and retrospective ECG-gated SSFP cine images, capturing the entire left ventricle in continuous short-axis slices from base to apex, as well as in long-axis views (2-, 3-, and 4-chamber) encompassing the entire heart. Detailed cardiac MR image acquisition parameters were as follows: the First Affiliated Hospital of Zhejiang Chinese Medical University: repetition time = 3.2 ms, echo time = 1.4 ms, field of view = 340 × 340 mm2, slice thickness = 8 mm, slice gap = 2 mm, and 25–30 phases per cardiac cycle (Discovery MR750); repetition time = 2.9 ms, echo time = 1.1 ms, field of view = 340 × 340 mm2, slice thickness = 8 mm, slice gap = 2 mm, and 30 phases per cardiac cycle (Signa Premier); the Second Affiliated Hospital, Zhejiang University School of Medicine: repetition time = 3.5 ms, echo time = 1.5 ms, field of view = 360 × 360 mm2, slice thickness = 8 mm, slice gap = 2 mm, and 20–25 phases per cardiac cycle (Signa HD excite); repetition time = 2.6 ms, echo time = 1.1 ms, field of view = 340 × 276 mm2, slice thickness = 8 mm, slice gap = 2 mm, and 25 phases per cardiac cycle (Magnetom Avanto).
Cardiac MR image analysis
All cardiac MR images were analyzed offline using the cvi42® software (Circle Cardiovascular Imaging, version 5.14.2, Canada) by an experienced observer (J.S. > 3 years’ experience in cardiac MR analysis), blinded to clinical data. As previously described [12], LV and RV endocardial and epicardial borders were manually traced using a point-and-click approach in end-systole and end-diastole on the stacks of short-axis cine images, respectively. Biventricular end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), and ejection fraction (EF) were derived from the short-axis cine images. LV mass was obtained from the end-diastolic frames. Heart rate (HR) was recorded during the cardiac MR scan. Cardiac output (CO) was determined by multiplying SV and HR. RV remodeling index was calculated as the ratio of RVEDV to LVEDV. Cut-off values of RVEDV/LVEDV ratio for moderate-to-severe RV remodeling were 1.41 [19].
RA endocardial borders were manually drawn in the 4-chamber view [7]. RA maximal volume (RAVmax, at the ventricular end-systole), pre-atrial contractile volume (RAVpac, at the ventricular diastole before RA contraction), and minimal volume (RAVmin, at the late ventricular end-diastole after RA contraction) were automatically derived by the software. Total RA emptying fraction (RAEF total, corresponding to atrial reservoir function), passive RA emptying fraction (RAEF passive, corresponding to atrial conduit function), and active RA emptying fraction (RAEF booster, corresponding to atrial contractile booster pump function) were calculated as follows [7]:
RAEF total = (RAVmax - RAVmin) × 100 / RAVmax;
RAEF passive = (RAVmax - RAVpac) × 100 / RAVmax;
RAEF booster = (RAVpac - RAVmin) × 100 / RAVpac.
Biventricular and RA volumes were indexed by body surface area (BSA). BSA was calculated using the Mosteller formula: BSA (m2) = [height (cm) × weight (kg)/3,600]1/2.
Cardiac MR-FT analysis for RA strain
RA strain parameters were obtained using cvi42® software (Circle Cardiovascular Imaging, version 5.14.2, Canada) by J.S. with more than 3 years of experience in cardiac MR analysis, blinded to the clinical data. The endocardial and epicardial contours of RA were manually traced in the 4-chamber views by a point-and-click approach at the minimum RA volume after atrial contraction [9]. As previously described [8], the superior vena cava and RA appendix were excluded from RA endocardial contours followed by the automated tracking algorithm. The accuracy of automatic tracking was visually checked, and manual adjustments were performed if necessary.
The longitudinal RA strain and SR values were measured in the 4-chamber views [20]. Representative cases of RA strain parameters measured with cardiac MR-FT in healthy controls, the ARVC non-RA Dilated group, and the ARVC RA Dilated group were presented in Fig. 2.
Fig. 2.
Representative cases of RA strain parameters derived from cardiac MR-feature tracking in healthy controls (A-C), the ARVC non-RA Dilated group (D-F), and the ARVC RA Dilated group (H-G), respectively. ARVC = arrhythmogenic right ventricular cardiomyopathy; εa = booster strain; εe = conduit strain; εs = reservoir strain; RA = right atrial; SRa = peak late negative strain rate; SRe = peak early negative strain rate; SRs = peak positive strain rate
Reproducibility of RA strain measurements
Reproducibility was assessed on 20 randomly selected cardiac MR images in ARVC patients. Inter-observer agreement was assessed by two independent investigators (J.S. with more than 3 years of experience and Y.G. with more than 7 years of experience in cardiac MR analysis), and intra-observer agreement (J.S.) was determined by repeating measurements one month apart.
Statistical analysis
All statistical analyses were conducted utilizing SPSS (version 26.0, IBM SPSS Inc, Chicago, IL, USA) and GraphPad Prism (version 10.2.3, La Jolla, CA, USA). Continuous variables following normal distribution were given as mean ± standard deviation. Categorical variables were presented as frequencies with percentages. Continuous data comparison of 2 groups was performed using student’s t-test for normally distributed data, one-way analysis of variance (ANOVA) with post hoc LSD tests was applied for comparisons of 3 groups, the Mann-Whitney U test for non-normally distributed data, and the chi-square test for categorical variables. Receiver operating characteristic (ROC) curves were applied to determine the diagnostic value of RA parameters for identifying RV remodeling. The De-Long test was used to compare the diagnostic performance of RA parameters. Simple linear regression analysis was applied to investigate the correlation between RAEF and RA strain parameters [21]. The reproducibility was assessed using intraclass correlation coefficients (ICCs) based on the two-way random effects model and Bland-Altman scatter plots. A P-value of 0.05 was considered to indicate a significant difference.
Results
Baseline characteristics of the study population
A total of 70 patients with ARVC met the initial inclusion criteria. Of these, 2 patients had congenital heart disease and 4 had inadequate cardiac MR image quality, leaving 64 patients with ARVC. The baseline characteristics of the ARVC RA Dilated group, the ARVC non-RA Dilated group, and healthy control group are summarized in Table 1. In a total of 64 patients with ARVC, 17 (26.56%) of patients exhibited RA enlargement. There was no significant difference in gender, age, body height, and BSA among the three groups (all P > 0.05). Compared with healthy controls, the ARVC RA Dilated group exhibited significantly higher systolic and diastolic blood pressure. There were 2 patients with a family history of sudden cardiac death in the ARVC non-RA Dilated group.
Table 1.
Baseline characteristics of the ARVC RA dilated group, the ARVC non-RA dilated group, and the healthy controls
| Variable | ARVC RA Dilated (n = 17) | ARVC non-RA Dilated (n = 47) | Healthy Controls (n = 41) | P-Value |
|---|---|---|---|---|
| Age (years) | 39.88 ± 17.08 | 35.53 ± 14.65 | 36.49 ± 11.76 | 0.549 |
| Male gender, n (%) | 13 (76.47) | 29 (61.70) | 21 (65.85) | 0.554 |
| Body height (cm) | 170.82 ± 9.43 | 168.38 ± 8.14 | 168.57 ± 8.48 | 0.577 |
| BMI (kg/m2) | 23.52 ± 2.31 | 22.53 ± 4.19 | 22.56 ± 3.28 | 0.598 |
| BSA (m2) | 1.80 ± 0.17 | 1.73 ± 0.22 | 1.73 ± 0.21 | 0.394 |
| SBP (mmHg) | 123.29 ± 17.67* | 121.53 ± 17.96* | 111.15 ± 12.92 | 0.004 |
| DBP (mmHg) | 78.76 ± 14.96* | 74.96 ± 12.87 | 70.39 ± 10.31 | 0.046 |
| Heart rate (bpm) | 71.59 ± 15.02 | 67.57 ± 10.34 | 69.73 ± 9.32 | 0.189 |
| FBG (mmol/L) | 4.99 ± 1.13 | 4.74 ± 0.65 | 4.99 ± 0.52 | 0.377 |
| Hypertension, n (%) | 6 (35.29) | 8 (17.02) | - | - |
| Diabetes, n (%) | 6 (35.29) | 2 (4.26) | - | - |
| ECG, n (%) | ||||
| Atrial arrhythmias | 3 (17.65) | 3 (6.38) | - | - |
| Ventricular tachycardia | 6 (35.29) | 19 (40.43) | - | - |
| Family history of sudden cardiac deaths, n (%) | 0 | 2 (4.26) | - | - |
| Previous viral myocarditis, n (%) | 0 | 1 (2.13) | - | - |
| ICD, n (%) | 6 (35.29) | 8 (17.02) | - | - |
| Medication, n (%) | ||||
| Beta-blocker | 8 (47.05) | 24 (51.06) | - | - |
| ACEI/ARB | 5 (29.41) | 12 (36.17) | - | - |
| Calcium blocker | 2 (12.76) | 3 (6.38) | - | - |
| Diuretics | 7 (41.18) | 4 (8.51) | - | - |
Normally distributed values are mean ± standard deviation; categorical variables are number (percentage); *Indicates P < 0.05 when compared with healthy controls
ACEI = angiotensin converting enzyme inhibitor; ARB = angiotensin receptor blockers; ARVC = arrhythmogenic right ventricular cardiomyopathy; BMI = body mass index; BSA = body surface area; DBP = diastolic blood pressure; ECG = electrocardiogram; FBG = fasting blood glucose; ICD = implantable cardioverter defibrillator; RA = right atrial; SBP = systolic blood pressure
Conventional biventricular parameters among three groups
The comparisons of conventional biventricular parameters among the three groups are presented in Table 2. There was no significant difference in the indexed LVSV, LVCO, and LV mass among the groups (all P > 0.05). However, patients with ARVC (both RA Dilated and non-Dilated group) exhibited significantly lower LVEF and RVEF, as well as higher indexed LVEDV, LVESV, RVEDV, and RVESV compared with healthy controls, with the RA Dilated group demonstrating greater values than the non-RA Dilated group (all P < 0.05).
Table 2.
Biventricular conventional parameters of the ARVC RA dilated Group, the ARVC non-RA dilated Group, and the healthy controls
| Variable | P-Value | ||||||
|---|---|---|---|---|---|---|---|
| ARVC RA Dilated (n = 17) | ARVC non-RA Dilated (n = 47) | Healthy Controls (n = 41) | ANOVA Test | Post Hoc | |||
| RA Dilated vs. Controls | Non-RA Dilated vs. Controls | RA Dilated vs. Non-RA Dilated | |||||
| Left ventricle | |||||||
| LVEDVi (mL/m2) | 96.45 ± 23.84 | 79.15 ± 16.53 | 65.36 ± 9.19 | < 0.001 | < 0.001 | < 0.001 | < 0.001 |
| LVESVi (mL/m2) | 53.21 ± 30.94 | 35.51 ± 11.65 | 21.04 ± 4.90 | < 0.001 | < 0.001 | < 0.001 | < 0.001 |
| LVSVi (mL/m2) | 43.24 ± 17.71 | 43.62 ± 11.18 | 44.33 ± 6.60 | 0.928 | - | - | - |
| LVEF (%) | 47.06 ± 18.17 | 55.47 ± 9.54 | 68.02 ± 5.19 | < 0.001 | < 0.001 | < 0.001 | 0.004 |
| LVCO (L/min) | 5.43 ± 2.49 | 5.01 ± 1.31 | 5.44 ± 1.39 | 0.388 | - | - | - |
| LV mass (g) | 113.35 ± 29.38 | 94.24 ± 23.40 | 99.30 ± 36.96 | 0.089 | - | - | - |
| Right ventricle | |||||||
| RVEDVi (mL/m2) | 133.94 ± 46.17 | 94.86 ± 32.27 | 71.50 ± 11.31 | < 0.001 | < 0.001 | < 0.001 | < 0.001 |
| RVESVi (mL/m2) | 98.40 ± 51.22 | 58.79 ± 33.17 | 29.70 ± 6.85 | < 0.001 | < 0.001 | < 0.001 | < 0.001 |
| RVSVi (mL/m2) | 35.54 ± 16.77 | 35.66 ± 10.53 | 41.67 ± 7.64 | 0.023 | 0.052 | 0.011 | 0.969 |
| RVEF (%) | 30.05 ± 15.11 | 40.52 ± 12.02 | 59.53 ± 6.06 | < 0.001 | < 0.001 | < 0.001 | 0.001 |
| RVCO (L/min) | 4.66 ± 2.63 | 4.16 ± 1.31 | 5.22 ± 1.34 | 0.010 | 0.224 | 0.002 | 0.271 |
Data are presented as means ± standard deviation
ARVC = arrhythmogenic right ventricular cardiomyopathy; LV = left ventricular; LVCO = LV cardiac output; LVEDVi = LV end-diastolic volume index; LVEF = LV ejection fraction; LVESVi = LV end-systolic volume index; LVSVi = LV stroke volume index; RA = right atrial; RV = right ventricular; RVCO = RV cardiac output; RVEDVi = RV end-diastolic volume index; RVEF = RV ejection fraction; RVESVi = RV end-systolic volume index; RVSVi = RV stroke volume index
RA volumetric and strain parameters among three groups
The ARVC RA Dilated group exhibited significantly higher indexed RAVmax, RAVmin, and RAVpac than healthy controls, while the ARVC non-RA Dilated group demonstrated values comparable to the controls. Except for RAEF passive in the ARVC non-RA Dilated group, both ARVC groups demonstrated significantly lower RAEF total, RAEF passive, and RAEF booster compared to controls. Compared with the ARVC non-RA Dilated group, the ARVC RA Dilated group showed significantly lower RAEF total, RAEF passive, and RAEF booster (Table 3).
Table 3.
Comparisons of RA parameters among the ARVC RA dilated Group, the ARVC non-RA dilated Group, and the healthy controls
| Variable | P-Value | ||||||
|---|---|---|---|---|---|---|---|
| ARVC RA Dilated (n = 17) | ARVC non-RA Dilated (n = 47) | Healthy Controls (n = 41) | ANOVA Test | Post Hoc | |||
| RA Dilated vs. Controls | Non-RA Dilated vs. Controls | RA Dilated vs. Non-RA Dilated | |||||
| RA volume indexes (mL/m 2 ) | |||||||
| RAVmaxi | 70.08 ± 23.36 | 29.92 ± 8.77 | 32.21 ± 6.63 | < 0.001 | < 0.001 | 0.362 | < 0.001 |
| RAVpaci | 49.04 ± 25.13 | 16.85 ± 5.95 | 15.21 ± 4.62 | < 0.001 | < 0.001 | 0.491 | < 0.001 |
| RAVmini | 25.47 ± 6.79 | 22.10 ± 7.05 | 24.31 ± 5.95 | < 0.001 | < 0.001 | 0.381 | < 0.001 |
| RA function volumetric (%) | |||||||
| RAEF total | 32.52 ± 14.47 | 43.72 ± 9.24 | 53.10 ± 9.08 | < 0.001 | < 0.001 | < 0.001 | < 0.001 |
| RAEF passive | 19.31 ± 10.55 | 26.21 ± 8.20 | 24.75 ± 9.91 | 0.035 | 0.045 | 0.465 | 0.010 |
| RAEF booster | 17.02 ± 9.43 | 23.74 ± 9.54 | 37.60 ± 9.32 | < 0.001 | < 0.001 | < 0.001 | 0.014 |
| RA Strain (%) | |||||||
| εs | 22.34 ± 13.15 | 36.02 ± 12.91 | 53.01 ± 15.29 | < 0.001 | < 0.001 | < 0.001 | 0.010 |
| εe | 12.21 ± 7.80 | 21.05 ± 9.30 | 35.29 ± 13.72 | < 0.001 | < 0.001 | < 0.001 | 0.016 |
| εa | 10.13 ± 6.80 | 14.97 ± 7.29 | 17.72 ± 4.85 | 0.004 | 0.002 | 0.023 | 0.131 |
| RA strain rate (s − 1 ) | |||||||
| SRs | 1.21 ± 0.72 | 1.97 ± 0.83 | 2.52 ± 0.83 | < 0.001 | < 0.001 | 0.001 | 0.028 |
| SRe | -0.99 ± 0.85 | -1.85 ± 1.02 | -2.97 ± 1.38 | < 0.001 | < 0.001 | < 0.001 | 0.030 |
| SRa | -1.03 ± 0.81 | -1.76 ± 0.95 | -2.17 ± 0.58 | < 0.001 | < 0.001 | 0.010 | 0.029 |
Data are presented as means ± standard deviation
ARVC = arrhythmogenic right ventricular cardiomyopathy; εa = booster strain; εe = conduit strain; εs = reservoir strain; RA = right atrial; RAEF = RA emptying fraction; RAVmaxi = RA maximum volume index; RAVmini = RA minimum volume index; RAVpaci = RA pre-atrial contraction volume index; SR = strain rate; SRa = peak late negative SR; SRe = peak early negative SR; SRs = peak positive SR
With respect to RA strain parameters, patients with ARVC (both RA Dilated and non-RA Dilated groups) had lower RA εs, εe, εa, SRs, SRe, and SRa than healthy controls (all P < 0.05), with the RA Dilated group showing significantly lower values compared to the non-RA Dilated group (Table 3; Fig. 3).
Fig. 3.
RA strain (A) and strain rate (B) in healthy controls, the ARVC non-RA Dilated group and the ARVC RA Dilated group. ARVC = arrhythmogenic right ventricular cardiomyopathy; εa = booster strain; εe = conduit strain; εs = reservoir strain; RA = right atrial; SRa = peak late negative strain rate; SRe = peak early negative strain rate; SRs = peak positive strain rate
Diagnostic value of RA strain parameters for RV remodeling in all patients with ARVC
ROC analysis demonstrated that RA εe and SRe were significant for identifying moderate-to-severe RV remodeling in ARVC patients (Fig. 4). The optimal threshold of εe was 19.4%, with a sensitivity of 51.0% and a specificity of 63.3% (AUC = 0.703; 95% CI: 0.564–0.841), and the optimal threshold of SRe was 1.29 s− 1, with a sensitivity of 73.5% and a specificity of 80.0% (AUC = 0.799; 95% CI: 0.683–0.915). In contrast, there was no diagnostic value in RAEF total, RAEF passive, and RAEF active for identifying RV remodeling in ARVC patients (all P > 0.05, Table 4). The De-Long test showed RA SRe had a higher AUC value than RA εe and RAEF passive (both P < 0.001; Table S1).
Fig. 4.
ROC curves for diagnostic value of RA strain parameters for RV remodeling in patients with ARVC. ARVC = arrhythmogenic right ventricular cardiomyopathy; εa = booster strain; εe = conduit strain; εs = reservoir strain; RA = right atrial; RAEF = right atrial emptying fraction; ROC = receiver operator characteristic; RV = right ventricular; SRa = peak late negative strain rate; SRe = peak early negative strain rate; SRs = peak positive strain rate
Table 4.
Diagnostic value of RA strain parameters for RV remodeling in all patients with ARVC (n = 64)
| Variable | AUC | 95% CI | Sensitivity (%) | Specificity (%) | Cut-off | P-Value |
|---|---|---|---|---|---|---|
| εs (%) | 0.617 | 0.465 to 0.770 | 36.73 | 93.33 | 37.25 | 0.173 |
| εe (%) | 0.703 | 0.564 to 0.841 | 51.02 | 63.33 | 19.4 | 0.018 |
| εa (%) | 0.501 | 0.325 to 0.677 | 46.67 | 65.31 | 10.35 | 0.994 |
| SRs (s− 1) | 0.629 | 0.473 to 0.785 | 83.67 | 40.00 | 1.11 | 0.134 |
| SRe (s− 1) | 0.799 | 0.683 to 0.915 | 73.47 | 80.00 | 1.29 | < 0.001 |
| SRa (s− 1) | 0.564 | 0.408 to 0.719 | 28.89 | 93.33 | 0.89 | 0.463 |
| RAEF total (%) | 0.525 | 0.352 to 0.698 | 91.84 | 26.67 | 29.66 | 0.769 |
| RAEF passive (%) | 0.630 | 0.462 to 0.798 | 67.35 | 60.00 | 21.48 | 0.130 |
| RAEF booster (%) | 0.512 | 0.337 to 0.687 | 83.67 | 33.33 | 12.98 | 0.887 |
AUC = Area under ROC curve; CI = confidence interval; Other abbreviations as in Table 3
Association of RA strain and SR with RAEF in all patients with ARVC
The correlations between RA strain parameters and RAEF are shown in Fig. 5. Simple linear regression analysis showed a strong correlation between RA strain/SR and RAEF components, including RA reservoir, conduit, and booster pump function, in all ARVC patients:
Fig. 5.
Associations of RA strain (A-C) and strain rate (D-F) with RAEF in patients with ARVC. ARVC = arrhythmogenic right ventricular cardiomyopathy; εa = booster strain; εe = conduit strain; εs = reservoir strain; RA = right atrial; RAEF = right atrial emptying fraction; SRa = peak late negative strain rate; SRe = peak early negative strain rate; SRs = peak positive strain rate
RA strain: εs and RAEF total: r = 0.670, P < 0.001; εe and RAEF passive: r = 0.732, P = 0.001; εa and RAEF booster: r = 0.634, P < 0.001;
RA SR: SRs and RAEF total: r = 0.527, P < 0.001; SRe and RAEF passive: r = -0.663, P = 0.001; and SRa and RAEF booster: r = -0.513, P < 0.001) (Table S2).
Reproducibility
Intra- and inter-observer reproducibility for RA deformation measurements are shown in Table 5 and Fig. S1-2. These results demonstrated excellent reproducibility for RA strain and SR measured by MR-FT with all ICCs > 0.80 and narrow limits of agreement in Bland–Altman plots.
Table 5.
Inter-observer and intra-observer reproducibility for RA strain and strain rate in patients with ARVC (n = 20)
| Inter-observer | Intra-observer | |||||
|---|---|---|---|---|---|---|
| ICC | 95% CI | Mean difference ± SD | ICC | 95% CI | Mean difference ± SD | |
| εs (%) | 0.940 | 0.857–0.976 | -1.56 ± 6.01 | 0.952 | 0.885–0.981 | -0.87 ± 5.22 |
| εe (%) | 0.915 | 0.798–0.965 | -0.48 ± 5.45 | 0.926 | 0.823–0.970 | -0.35 ± 4.73 |
| εa (%) | 0.887 | 0.740–0.953 | -1.08 ± 3.60 | 0.882 | 0.727–0.951 | -0.52 ± 4.01 |
| SRs (s− 1) | 0.828 | 0.620–0.928 | -0.10 ± 0.51 | 0.895 | 0.730–0.959 | -0.22 ± 0.44 |
| SRe (s− 1) | 0.852 | 0.670–0.938 | 0.22 ± 0.87 | 0.930 | 0.834–0.971 | 0.15 ± 0.56 |
| SRa (s− 1) | 0.917 | 0.806–0.966 | -0.10 ± 0.35 | 0.922 | 0.818–0.968 | 0.08 ± 0.34 |
ICC = intraclass correlation coefficient; CI = confidence interval; Other abbreviations as in Table 3
Discussion
The importance of RA function assessment is increasingly acknowledged for its role in the diagnosis and prognosis of various cardiovascular diseases [22–25]. The current study utilized the MR-FT technique to comprehensively evaluate RA function in patients with ARVC, both with or without RA dilation. The main findings were as follows: (1) MR-FT is a promising tool for detecting early RA dysfunction in ARVC patients with good reproducibility; (2) Both ARVC groups (RA Dilation and non-RA Dilation) exhibited impaired RA strain parameters in comparison to healthy controls, suggesting RA dysfunction prior to RA enlargement in this population; (3) RA conduit strain and SR derived from MR-FT may contribute to identifying moderate-to-severe RV remodeling in patients with ARVC.
RA dilation in patients with ARVC
RA enlargement has been reported to be a crucial indicator in clinical assessment and risk stratification [13–15]. For instance, Ricardo et al. [26] noted that RA enlargement could contribute to identifying patients at higher risk of atrial arrhythmias, while Tarek et al. [27] further demonstrated that RA dilation may predict the incidence of atrial arrhythmias, emphasizing the involvement of atrial changes in the progression of ARVC. Additionally, Bourfiss et al. [28] identified genotype-specific patterns of volumetric changes among ARVC patients, revealing that those without identified mutations exhibited significantly larger atrial dimensions, in contrast to PKP2 mutation carriers, who presented with notably smaller atrial sizes compared to controls with idiopathic right ventricular outflow tract tachycardia. Despite these insights, data regarding the prevalence of RA enlargement in ARVC patients remain limited. In this study, we observed that 26.56% of ARVC patients exhibited RA dilation, which was consistent with several echocardiography studies [29, 30].
RA dysfunction in patients with ARVC
Previous studies on RA dysfunction in patients with ARVC remained controversial. Specifically, Zghaib et al. [27] found that ARVC patients exhibited lower RA reservoir, conduit, and booster function than controls on cardiac magnetic resonance examination. In comparison, a prior speckle tracking echocardiography study by Anwer et al. [31] reported a reduction in RA reservoir and booster strain in patients with ARVC compared to healthy controls, while RA conduit strain was comparable. We speculate that these discrepancies may be attributed to variations in sample size and disease progression. In the current study, we stratified ARVC patients based on the presence of RA dilation. Our findings revealed that both groups of ARVC patients, regardless of RA dilation status, showed significant impairment in RA reservoir, conduit, and booster pump function, as evidenced by decreased magnitudes of RA εs, εe, εa, SRs, SRe, and SRa derived from MR-FT. Collectively, our results indicated that RA dysfunction was already present even when RA volumes appeared normal.
The underlying mechanisms of RA dysfunction in ARVC patients remain elusive. Previous study shows altered hemodynamics, including advanced diastolic dysfunction and secondary tricuspid regurgitation, may play a pivotal role in exacerbating RA dysfunction [31]. Notably, in the early stages of ARVC, structural changes may be subtle or nonexistent [18]. Alternatively, it is hypothesized that fibro-fatty replacement of the atrial myocardium contributed significantly to the decline in RA function [32–34]. These observations suggest that RA involvement in ARVC may not be solely attributable to hemodynamic consequences secondary to RV pathology, yet may also reflect the presence of a primary atrial cardiomyopathic process. In this study, we observed no difference in RAEF passive between the ARVC non-RA Dilated Group and healthy controls, while both RA εe and SRe derived from MR-FT in the non-dilated group were significantly reduced. Therefore, MR-FT may emerge as a valuable tool for the early detection of RA functional impairment in ARVC patients, even prior to the onset of RA dilation.
Clinically, atrial arrhythmias, including atrial fibrillation, flutter, and tachycardia, are relatively common in ARVC and are closely related to atrial size and RV dysfunction [26, 35]. Moreover, a combined assessment of RA and RV strain has been shown to further improve risk stratification in ARVC, and isolated RA dysfunction alone is associated with a significantly higher incidence of adverse events [36]. These findings collectively highlight the clinical value of early RA dysfunction detection using advanced techniques such as MR-FT in the management of ARVC patients.
Diagnostic value of RA strain parameters for RV remodeling in ARVC
RV remodeling is generally defined as genomic expression, molecular, cellular, and interstitial changes that manifest clinically as alterations in RV size, shape, and function following cardiac injury [37]. A previous study by Tse et al. [38] reported that RV remodeling was strongly related to adverse outcomes and could be helpful for the decision-making and risk assessment strategy in patients with multiple valvular heart diseases. Moreover, another cardiac MR study has shown that RV remodeling has prognostic value in patients with pulmonary arterial hypertension [39]. In this study, we found that RA εs and SRe exhibited good diagnostic value for identifying moderate to severe RV remodeling in ARVC patients. In contrast, RAEF did not show diagnostic value, suggesting that RA strain parameters could be more sensitive to identifying RV remodeling than traditional RAEF metrics in patients with ARVC. To our knowledge, this is the first study to investigate the association of RA strain parameters with RV remodeling in patients with ARVC. Moreover, we observed a strong correlation between RA strain parameters derived from MR-FT and RAEFs for RA reservoir, conduit, and booster pump function in all ARVC patients, aligning with findings from several previous studies [8, 40].
Within the contemporary framework of arrhythmogenic cardiomyopathy (ACM), accumulating evidence indicates that fibro-fatty myocardial replacement frequently involves both ventricles. This understanding underpins the broader ACM concept and the 2020 Padua criteria, which refined the 2010 TFC by incorporating advanced CMR tissue characterization together with updated electrical and arrhythmic markers [41]. Although our cohort was defined according to the 2010 TFC criteria due to earlier inclusion, our findings highlight the right atrium as a significant contributor to the ARVC pathophysiology. Thus, interpretation of MR-FT–derived RA function may contribute to a better understanding of this broader and evolving disease concept in contemporary context of ACM.
Limitations
There are several limitations in this study. First, the rarity of ARVC results in a relatively limited sample size, potentially impacting the generalizability of our findings. Second, the lack of genotype data restricted our ability to investigate potential genotype-phenotype correlations. Third, the measurement of strain requires specialized post-processing software, which has limited availability and systematic differences among various software vendors [42, 43]. This limitation may restrict the broader application of RA strain measurement in patients with ARVC. Finally, we did not assess the prognostic value of RA strain parameters in ARVC patients, which necessitates further exploration in future research.
Conclusion
ARVC patients exhibit impaired RA reservoir, conduit, and booster pump function, even with normal RA volumes. RA conduit strain and SR could contribute to identifying RV remodeling in this population. MR-FT may serve as a promising method for detecting early RA dysfunction in patients with ARVC.
Supplementary Information
Below is the link to the electronic supplementary material.
Acknowledgements
Not applicable.
Author contributions
J. S. and Y. G. completed the statistical analyses, prepared tables & figures and wrote the main manuscript text; X. W., W. L., W. L., J. L., Q. L., W. Y., and Q. Z. collected the data; F. Z. and M. M. prepared tables & figures; P. X. was responsible for project administration；R.Y. and M.X. designed the study, reviewed and edited the manuscript.All authors read and approved the final manuscript and agree to be personally accountable for their contributions.
Funding
This study has received funding by the National Natural Science Foundation of China (No. 81971600), “Pioneer” and “Leading Goose” R&D Program of Zhejiang (No. 2022C03046), and the Talent Cultivation Program for Outstanding Innovative Individuals at Zhejiang Chinese Medical University (No. 2024YJSBJ002).
Data availability
The datasets used and analyzed in the current study are available from the corresponding author on reasonable request.
Declarations
Ethics approval and consent to participate
This retrospective study was approved by the Ethics Committee of the First Affiliated Hospital of Zhejiang Chinese Medical University (2022-KLS-207-01) and was conducted in accordance with the ethical standards of the Declaration of Helsinki. The requirement for informed consent was waived due to the retrospective nature of the study.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Jingjing Shi and Yiyuan Gao contributed equally to this work.
Contributor Information
Risheng Yu, Email: risheng-yu@zju.edu.cn.
Maosheng Xu, Email: xums166@zcmu.edu.cn.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The datasets used and analyzed in the current study are available from the corresponding author on reasonable request.