The value of the left atrium as detected by cardiovascular magnetic resonance in predicting reverse left ventricular remodeling in patients with ST-segment elevation myocardial infarction
Original Article

The value of the left atrium as detected by cardiovascular magnetic resonance in predicting reverse left ventricular remodeling in patients with ST-segment elevation myocardial infarction

Jianing Cui1,2#, Fei Yan1#, Wenjia Liu1, Yanan Zhao1, Chuncai Luo1, Xiuzheng Yue3, Tao Li1

1Department of Radiology, The First Medical Center of Chinese People’s Liberation Army General Hospital, Beijing, China; 2Department of Radiology, Beijing Jishuitan Hospital, Capital Medical University, Beijing, China; 3Medical Big Data Research Center, Medical Innovation Research Division of PLA General Hospital, Beijing, China

Contributions: (I) Conception and design: J Cui, F Yan, T Li; (II) Administrative support: T Li; (III) Provision of study materials or patients: J Cui, F Yan, T Li; (IV) Collection and assembly of data: W Liu, Y Zhao, C Luo; (V) Data analysis and interpretation: J Cui, X Yue; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

#These authors contributed equally to this work as co-first authors.

Correspondence to: Tao Li, MD. Department of Radiology, The First Medical Center of Chinese People’s Liberation Army General Hospital, No. 28, Fuxing Road, Haidian District, Beijing 100853, China. Email: litaofeivip@163.com.

Background: The importance of the left ventricle after ST-segment elevation myocardial infarction (STEMI) has been well established; however, the role of left atrial (LA) dynamics in reverse left ventricular remodeling (R-LVR) remains unclear. This study aimed to assess structural and functional changes in the left heart by serial cardiovascular magnetic resonance (CMR) imaging, exploring the predictive value of the left atrium and left ventricle for R-LVR.

Methods: A total of 105 patients with STEMI were retrospectively enrolled in the study, and data on their baseline clinical characteristics and CMR features at 4 days and 5 months after percutaneous coronary intervention (PCI) were collected. The CMR evaluation included the LA and left ventricular (LV) volumes, myocardial function, and infarct characteristics. The patients were categorized into two groups according to the presence of R-LVR, which was assessed by comparing the two CMR examinations; 47 patients were assigned to the R-LVR group, and 58 to the non-R-LVR group. Subsequently, the baseline clinical and CMR characteristics of these two groups were compared. The R-LVR predictors were identified by logistic regression. Three predictive models were built to explore the incremental value of the left heart function parameters for R-LVR prediction, using the Net Reclassification Index (NRI).

Results: At first CMR, the R-LVR group had higher LV and LA volumes, and LV longitudinal displacement, as well as a lower myocardial injury value and LA reservoir strain rate (all P<0.05). At the second CMR, the R-LVR group had a lower LV volume, a smaller infarct mass, and greater left ventricular ejection fraction (LVEF) (all P<0.05). Notably, the left ventricular end-diastolic volume (LVEDV) [odds ratio (OR): 1.022, 95% confidence interval (CI): 1.007–1.037, P=0.005], infarct mass (OR: 0.946, 95% CI: 0.918–0.975, P<0.001), and LA reservoir strain rate (OR: 0.224, 95% CI: 0.055–0.905, P=0.036) were independent predictors of R-LVR. When LV longitudinal displacement and the LA reservoir strain rate were introduced into the model, the NRI was 44.10%.

Conclusions: This study assessed the predictive value of the LVEDV, infarct mass, and LA reservoir strain rate by CMR, and found that the combination of the LA reservoir strain rate and LV longitudinal displacement improved model prediction of R-LVR.

Keywords: Ventricular remodeling; magnetic resonance imaging; ST-segment elevation myocardial infarction; left atrial reservoir strain rate


Submitted Nov 09, 2024. Accepted for publication Sep 04, 2025. Published online Oct 24, 2025.

doi: 10.21037/qims-2024-2497


Introduction

Over the past four decades, mortality among patients with acute ST-segment elevation myocardial infarction (STEMI) has declined steadily, partly due to effective and timely reperfusion therapy through direct percutaneous coronary intervention (PCI) (1). However, the major effect of STEMI has shifted from acute mortality to chronic progressive changes (2), mainly defined as changes in left ventricular (LV) structure, size and function modulated by hemodynamic load, neurohormonal activation and genetic factors (3). Reverse left ventricular remodeling (R-LVR) refers to chronic and favorable changes in the LV volume after STEMI through clinical interventions, and the restoration of a more normal elliptical shape, with improved or restored structure of the damaged myocardium (4). R-LVR is associated with restored left heart function, a reduced incidence of cardiovascular events, and prolonged survival (5,6). A thorough understanding of the pathogenesis and pathophysiology of R-LVR can enable effective risk stratification in patients with STEMI, help to refine therapeutic strategies, and ultimately improve patient prognosis (7).

Cardiovascular magnetic resonance (CMR) can be used to detect R-LVR and explore the course of chronic changes in the left ventricle after STEMI, as it accurately measures changes in LV volume and function (8,9). In addition, CMR is the gold standard for assessing the extent of myocardial infarction (MI) and microvascular obstruction (MVO) (10). To date, few studies have examined the predictive power of LV CMR characteristics for R-LVR. Bodi et al. (3) found that infarct size and MVO after infarction were valuable in predicting R-LVR. In a previous study, we found that MVO mass and LV infarct zone peak longitudinal displacement were independent predictors of R-LVR (11). These results indicate that the CMR characteristics of LV infarction and function can serve as useful predictors of R-LVR.

In recent years, the importance of left atrial (LA) function and structure has been increasingly recognized in cardiovascular risk stratification, particularly in predicting adverse outcomes such as heart failure and mortality following acute MI (12). LA dysfunction and enlargement are strongly associated with cardiovascular diseases, including ischemic heart disease, valvular heart disease, and heart failure (13). An increased LA volume has been shown to predict mortality beyond left ventricular ejection fraction (LVEF) in STEMI (14,15). There is an emerging evidence that LA strain is a more sensitive marker of atrial dysfunction than LA volume, enabling the real-time assessment of filling pressures (16). For instance, Leng et al. (12) showed that LA strain provided incremental prognostic information beyond established predictors (e.g., LVEF) in STEMI. Similarly, Schuster et al. (17) reported that LA peak reservoir strain derived from cardiovascular magnetic resonance feature tracking (CMR-FT) improved the prediction of major adverse cardiovascular events (MACEs) compared to conventional risk factors (e.g., LV strain).

These studies established LA parameters as prognostic markers in STEMI; however, a number of critical gaps remain. First, current evidence focuses primarily on hard endpoints such as mortality, and data on R-LVR outcomes are limited. Second, the value of LA measures in predicting R-LVR has not been systematically evaluated. Therefore, this study aimed to evaluate the changes in LA and LV structure and function between the first week and 5 months following STEMI by performing two CMR scans in STEMI patients and to assess the predictive power of baseline CMR characteristics for R-LVR. We present this article in accordance with the TRIPOD reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2497/rc).


Methods

Study population

This study retrospectively enrolled 105 consecutive STEMI patients from The First Medical Center of Chinese People’s Liberation Army General Hospital between January 2014 and January 2023 (Figure 1). Patients were included in the study if they met the following inclusion criteria: (I) had an initial diagnosis of STEMI based on the European Society of Cardiology/American College of Cardiology committee guidelines (18); (II) had undergone successful PCI within 12 hours of symptom onset; and (III) had undergone two CMR examinations (one during the hospital stay and another after discharge). Patients were excluded from the study if they met any of the following exclusion criteria: (I) had a history of MI; (II) had undergone prior revascularization surgery (either coronary artery bypass grafting or PCI); (III) had not undergone the follow-up CMR; and/or (IV) had poor-quality CMR.

Figure 1 Flow chart of grouped method. CMR, cardiovascular magnetic resonance; LV, left ventricular; MI, myocardial infarction; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction.

The patients were categorized into groups based on the presence or absence of R-LVR on the second CMR scan. Based on serial cardiac MRI measurements, the patients were divided into the following two groups based on the LV remodeling status: (I) the R-LVR group, demonstrating ≥10% reduction in left ventricular end-systolic volume (LVESV) at the second CMR compared with the baseline CMR; and (II) the non-R-LVR group, demonstrating <10% change in LVESV between examinations (19).

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the local ethics committee of the Chinese People’s Liberation Army General Hospital (No. S2022-567-01), and the requirement of individual consent for this retrospective analysis was waived.

CMR scanning protocol

CMR was performed using either a 1.5- or 3.0 T-scanner (Multiva, INGENIA CX, Philips Medical Systems, The Netherlands) with the application of 8-channel surface-phased array coils. Cine imaging was performed using the balanced turbo field echo sequence in the two-, three-, and four-chamber long-axis slices, along with continuous 10–12 short-axis slices covering the left ventricle. Approximately 10–15 minutes after the intravenous administration of 0.1 mmol/kg of a gadolinium-based contrast agent (Gadopentetate Dimeglumine, BeiLu, Beijing, China), late gadolinium enhancement imaging was performed using a two-dimensional phase-sensitive inversion-recovery sequence at identical slice locations. A detailed description of the imaging parameters used in the 1.5- and 3.0 T-scanners is provided in Table S1.

CMR image analysis

All the patients underwent CMR scans over 4 days [interquartile range (IQR), 3–6 days] and 5 months (IQR, 3–6 months) after successful PCI treatment. All the CMR analyses were conducted offline using dedicated software (cvi42 v5.13, Circle Cardiovascular Imaging, Calgary, Canada) by an experienced radiologist blinded to all clinical and imaging information.

LV volume, function, and infarct characteristics

The LV structure and function parameters were performed by delineating the LV endocardial and epicardial borders on all LV short-axis cine slices at the end of the LV diastolic and systolic phases, excluding the trabeculae and papillary muscles. If the movement of the outline differed from the actual myocardial movement, the contours were manually modified. The left ventricular end-diastolic volume (LVEDV), LVESV, LVEF, and LV myocardial mass were obtained.

LV strain and displacement were analyzed using the CMR-FT method in continuous short-axis and long-axis two-, three- and four-chamber cine sequences. The end-systolic and end-diastolic epicardial and endocardial contours of the LV were delineated, and the right ventricular insertion point was determined. The software automatically propagated profiles across all phases of the entire cardiac cycle, and the derived global LV displacement and strain were assessed in the radial, circumferential, and longitudinal orientations. The propagation of the myocardial tissue was verified by the operator, and in case of insufficient border tracking, manual adjustments were made, followed by the subsequent reapplication of the algorithm. The LV radial and circumferential strain and displacement were obtained using short-axis cine views. The LV longitudinal strain and displacement were obtained from three long-axis views, which included the two-, three- and four-chamber orientations respectively. Peak values for LV displacement and strain were identified as the peak absolute measurements recorded throughout the full cardiac cycle (Figure 2).

Figure 2 An example of left ventricular strain and displacement curves in radial, circumferential, and longitudinal directions from a patient with R-LVR at 1 week and 5 months after PCI. LV, left ventricular; PCI, percutaneous coronary intervention; R-LVR, reverse left ventricular remodeling.

The late gadolinium enhancement images showed that the signal intensity in the infarcted region was elevated by five standard deviations (SDs) compared to that of the remote, non-infarcted myocardial tissue (20). MVO was characterized as a zone of reduced enhancement within the hyper-enhanced infarct area.

LA volume and function

By tracing the LA endocardial border on long-axis two- and four-chamber cine views, LA maximal, diastasis, and minimal volumes were calculated at left atrial end-diastole volume (LAVmax), left atrial early-end systole volume (LAVpre-a), and left atrial late-end systole volume (LAVmin) phases according to the biplane area-length method (21), excluding the pulmonary veins and LA appendages. The left atrial emptying fractions (LAEFs) were defined as the fractional volume changes using the following equations: Total LAEF = (LAVmax – LAVmin) / LAVmax × 100%; Passive LAEF = (LAVmax – LAVpre-a) / LAVmax × 100%; and Active LAEF = (LAVpre-a – LAVmin) / LAVpre-a × 100%. An automatic tracking algorithm was used, and manual adjustment was needed to achieve adequate tracking. The curves of LA strain and strain rate change during the cardiac cycle were then generated automatically using the feature-tracking post-processing method (Figure 3). The LA reservoir strain and LA booster strain were recorded. LA conduit strain was defined as follows: LA conduit strain = LA reservoir strain – LA booster strain. Three LA strain rates were evaluated, including LA reservoir strain rate, LA conduit strain rate, and LA booster strain rate.

Figure 3 An example of LA strain and the strain rate parameters in a patient with R-LVR at 1 week and 5 months after PCI, which were obtained by delineating the LA endocardial and epicardial contours. (A,E) The LV end-diastolic phase in the four-chamber view. (B,F) The LV end-systolic phase in the two-chamber view. (C,G) The LA strain curve. (D,H) The LA strain rate curve. The red line represents the LA endocardial contour. The green line represents the LA epicardial contour. The blue lines represent the atrioventricular junction line, and the line between the posterior wall of the LA and the midpoint of the mitral valve. εs and SRs reflect LA reservoir function; εe and SRe reflect LA conduit function; and εa and SRa reflect LA booster function. LA, left atrial; LV, left ventricular; PCI, percutaneous coronary intervention; R-LVR, reverse left ventricular remodeling; SRa, booster strain rate; SRe, conduit strain rate; SRs, reservoir strain rate; εa, booster strain; εe, conduit strain; εs, reservoir strain.

Statistical analysis

All the statistical analyses were conducted using SPSS (SPSS Statistics 26.0; IBM, Armonk, New York, USA). The continuous variables are presented as the mean ± standard deviation (SD), or the median with the IQR, while the categorical variables are reported as the number or percentage. The normality of the continuous data was assessed using the Shapiro-Wilk test. Group comparisons (the R-LVR vs. non-R-LVR) for the continuous variables were performed using the independent samples t-test for the normally distributed data and the Mann-Whitney U test for the non-normally distributed data. The categorical variables were compared using the Chi-squared test.

To identify the independent predictors of R-LVR, all the baseline clinical and CMR variables were initially entered into a univariate model. Variables showing a significant association (P<0.05) in the univariate analysis were subsequently included in a backward stepwise multivariate logistic regression model. Finally, the predictive ability of three different models was compared. Model 1 included traditional clinical indicators such as age and heart rate (HR). These two variables are important components of cardiovascular disease risk assessment because they are strongly associated with the development of many heart diseases (22,23). Model 2 comprised Model 1 plus conventional CMR variables (i.e., LVEDV and infarct mass, which were found to be significant in the multivariate logistic regression analysis). Model 3 comprised Model 2 plus the left heart function variables (i.e., LV longitudinal displacement and the LA reservoir strain rate, which were found to be significant in the logistic regression analysis). To assess the differences in the predictive ability of the three models for R-LVR, the area under the curve (AUC) values were comparatively analyzed using the log-rank test. In addition, the degree of improvement in the R-LVR prediction ability after the introduction of new biomarkers into an existing predictive model was assessed using the Net Reclassification Index (NRI). A two-sided P value of less than 0.05 was considered statistically significant.


Results

Patient characteristics

A cohort of 212 STEMI patients received CMR scans within 7 days of PCI. Of these, 107 patients were excluded for the following reasons: a history of MI (n=22), prior revascularization surgery (n=16), poor-quality CMR images (n=15), and missing follow-up CMR data (n=54). Thus, 105 patients were included in the final analysis. These patients were classified into the following two groups based on the presence or absence of R-LVR: the R-LVR group (n=47) and the non-R-LVR group (n=58).

The baseline clinical features of the patients are detailed in Table 1. Overall, the patients had a median age of 56 years (IQR, 49–64 years), and 88% of the sample were male. Compared to the patients without R-LVR, those with R-LVR had significantly lower HRs (P=0.015).

Table 1

Baseline clinical characteristics of patient groups

Characteristics R-LVR group (n=47) Non-R-LVR group (n=58) P value
Demographics
   Age (years) 57 [51, 64] 55 [46, 64] 0.407
   Sex (male) 41 [87] 51 [88] 0.914
   BSA (m2) 1.9 [1.8, 2.0] 1.9 [1.7, 2.0] 0.960
   Risk factors
    Smoking 29 [61] 39 [67] 0.388
    Family history of CAD 12 [25] 14 [24] 0.869
    Hypertension 27 [57] 27 [47] 0.906
    Diabetes mellitus 14 [30] 11 [19] 0.195
    Hypercholesterolemia 9 [19] 16 [28] 0.313
HR (/min) 67 [61, 77] 73 [67, 81] 0.015*
Day CMR after PCI 4 [3, 6] 4 [3, 6] 0.772
Angiographic characteristics
   Number of affected vessels 0.600
    1 13 [28] 17 [29]
    2 16 [34] 24 [41]
    3 18 [38] 17 [29]
   Coronary artery 0.920
    LAD 14 [30] 27 [47]
    LCX 5 [11] 10 [17]
    RCA 21 [45] 19 [33]
    Multi-vessel 7 [15] 2 [3]
Concomitant medications at discharge
   Aspirin 47 [100] 58 [100] NA
   Beta-blocker 34 [72] 45 [76] 0.536
   RAAS-blocker 18 [38] 21 [36] 0.645
   Statin 42 [89] 54 [93] 0.728

Values are presented as the median [interquartile range], or n [%]. *, statistically significant difference. BSA, body surface area; CAD, coronary artery disease; CMR, cardiovascular magnetic resonance; HR, heart rate; LAD, left anterior descending artery; LCX, left circumflex artery; NA, not available; PCI, percutaneous coronary intervention; RAAS, renin-angiotensin-aldosterone system; RCA, right coronary artery; R-LVR, reverse left ventricular remodeling.

Comparative CMR features: R-LVR and non-R-LVR groups

Table 2 sets out the differences between the patients with and without R-LVR. At first CMR, the patients with R-LVR had significantly higher LVEDV, LAVpre-a, and LV longitudinal displacement values than those without R-LVR (all P<0.05). In addition, the R-LVR group had lower infarct mass, MVO mass, and LA reservoir strain rate values than the non-R-LVR group (all P<0.05) (Figure 4). At the second CMR, compared to the non-R-LVR group, the R-LVR group had significantly reduced LVEDV, LVESV, and infarct mass values, along with higher LVEF values (all P<0.05) (Figure 4).

Table 2

CMR characteristics between the R-LVR and non-R-LVR groups

Characteristics Baseline Follow-up
R-LVR group (n=47) Non-R-LVR group (n=58) P value R-LVR group (n=47) Non-R-LVR group (n=58) P value
LVEDV (mL) 156.73 (140.39, 216.65) 147.17 (120.67, 176.35) 0.038* 141.57 (127.67, 156.69) 161.07 (141.27, 190.52) 0.002*
LVESV (mL) 79.35 (63.65, 98.92) 73.18 (58.79, 94.62) 0.226 62.33 (46.87, 75.37) 84.19 (63.61, 105.25) <0.001*
LVEF (%) 48.61±11.64 49.88±8.80 0.916 56.92±9.55 49.54±10.82 <0.001*
Myocardial mass (g) 108.79 (94.14, 136.31) 115.74 (91.62, 135.22) 0.784 93.84 (79.02, 123.37) 105.61 (85.28, 122.17) 0.633
Infarct size (%) 18.81 (10.14, 26.32) 31.08 (18.59, 35.70) <0.001* 14.36 (9.81, 14.36) 21.54 (13.68, 29.22) 0.001*
Infarct mass (g) 21.4 (10.91, 32.14) 31.76 (21.86, 47.74) 0.001* 13.83 (8.89, 21.56) 23.10 (13.49, 33) 0.002*
MVO mass (g) 0 (0, 0) 1.12 (0, 3.31) <0.001* 0 (0, 0) 0 (0, 0) 0.373
LV strain
   Radial (%) 20.73 (14.83, 25.92) 18.80 (15.36, 25.01) 0.689 24.22 (16.21, 28.6) 20.36 (16.58, 24.78) 0.109
   Circumferential (%) –13.07±3.76 –13.02±3.23 0.884 –14.87±3.94 –13.75±2.90 0.099
   Longitudinal (%) –11.67 (–13.15, –9.44) –11.14 (–13.08, –8.62) 0.319 –13.01 (–14.86, –10.47) –11.77 (–13.34, –10.43) 0.156
LV displacement
   Radial (mm) 4.01±1.13 3.96±0.94 0.714 4.42±1.15 4.28±1.79 0.450
   Circumferential (deg) 1.6 (1.03, 2.02) 1.7 (0.83, 2.37) 0.638 1.32 (1, 1.83) 1.47 (0.73, 2.32) 0.914
   Longitudinal (mm) 2.63±0.94 2.27±1.03 0.042* 2.99±0.79 2.82±0.87 0.295
LA volume (mL)
   LAVmax 68.23 (51.44, 82.98) 61.98 (47.03, 75.72) 0.160 63.16 (53.97, 76.85) 70.10 (55.12, 84.96) 0.408
   LAVpre-a 56.27±22.08 48.03±17.86 0.026* 51.93±18.48 53.84±19.51 0.792
   LAVmin 31.08 (21.58, 45.18) 26.30 (19.58, 33.38) 0.136 27.61 (20.12, 36.74) 28.55 (19.97, 37.90) 0.771
LA emptying fraction (%)
   Total 43.24 (47.24, 59.67) 55.96 (48.57, 63.81) 0.152 57.40 (50.11, 64.50) 57.42 (50.18, 64.16) 0.923
   Passive 21.34 (15.81, 24.93) 21.44 (17.34, 28.13) 0.214 24.03 (19.35, 27.80) 23.89 (19.46, 29.97) 0.633
   Active 41.58 (36.04, 47.56) 43.24 (34.11, 48.70) 0.451 44.74 (38.74, 51.74) 43.13 (36.53, 49.91) 0.614
LA strain (%)
   Reservoir 20.70±6.62 21.63±7.86 0.449 23.19±8.54 24.38±9.20 0.551
   Conduit 10.03 (7.00, 13.41) 10.21 (7.46, 14.02) 0.645 11.77 (8.50, 13.69) 11.64 (9.88, 16.25) 0.700
   Booster 10.70 (7.39, 12.7) 10.24 (7.35, 12.49) 0.635 10.50 (8.65, 13.90) 10.67 (8.19, 13.76) 0.965
LA strain rate (s–1)
   Reservoir 0.96±0.30 1.11±0.40 0.038* 1±0.36 1.06±0.38 0.447
   Conduit –0.8 (–1.34, –0.60) –1.07 (–1.32, –0.63) 0.400 –0.94 (–1.24, –0.70) –1.15 (–1.40, –0.72) 0.271
   Booster –1.3 (–1.60, –0.97) –1.415 (–1.71, –1.03) 0.449 –1.23 (–1.80, –0.82) –1.22 (–1.67, –0.94) 0.915

Values are presented as the mean ± standard deviation, or median (interquartile range). *, statistically significant difference. CMR, cardiovascular magnetic resonance; LA, left atrial; LAVmax, left atrial end-diastole volume; LAVmin, left atrial late-end systole volume; LAVpre-a, left atrial early-end systole volume; LV, left ventricular; LVEDV, left ventricular end-diastolic volume; LVEF, left ventricular ejection fraction; LVESV, left ventricular end-systolic volume; MVO, microvascular obstruction; R-LVR, reverse left ventricular remodeling.

Figure 4 CMR characteristics at two CMR scans in patients with R-LVR and non-R-LVR. CMR, cardiovascular magnetic resonance; LAVpre-a, LA early-end systole volume; LA, left atrial; LVEDV, left ventricular end-diastolic volume; R-LVR, reverse left ventricular remodeling.

Dynamic CMR changes from 1 week to 5 months post-PCI

Table S2 presents the longitudinal evolution of the CMR parameters between 1 week and 5 months post-PCI. LVEDV decreased over time in the R-LVR group, but it increased significantly in the non-R-LVR group (both P<0.05). LVEF improved significantly among the patients with R-LVR, but remained stable in those without R-LVR (P<0.001 and P=0.935, respectively). Myocardial mass, infarct mass, and MVO mass decreased in both groups (all P<0.05).

The LV strains in three directions and LV displacements in radial and longitudinal directions were significantly improved in both groups (all P<0.05). There was no significant change in the LAVmax in the R-LVR group, while the LAVmax was significantly increased in the non-R-LVR group (P=0.741 and P=0.038, respectively). There were no significant changes in LA function in the two groups.

Associations between the LA and LV CMR parameters at the baseline

Table 3 shows the associations between the LA with LV parameters at the baseline. The LAVmax, LAVpre-a, and LAVmin were moderately positively correlated with the LVEDV (r=0.52, r=0.51, and r=0.48, respectively; all P<0.001). The LA conduit strain rate was moderately correlated with LVEF (r=–0.43; P<0.001).

Table 3

Associations between the LA and LV CMR parameters at the baseline

Characteristics LAVmax LAVpre-a LAVmin LA reservoir strain rate LA conduit strain rate LA booster strain rate
r P r P r P r P r P r P
LVEDV 0.52 <0.001* 0.51 <0.001* 0.48 <0.001* 0.01 0.982 –0.15 0.141 0.09 0.376
LVEF –0.09 0.387 –0.15 0.123 –0.14 0.170 0.26 0.009* –0.43 <0.001* –0.23 0.021*
Infarct mass 0.14 0.164 0.15 0.127 0.2 0.049* –0.05 0.655 0.19 0.055 0.14 0.155
LV longitudinal displacement 0.11 0.299 0.06 0.523 0.01 0.890 0.13 0.195 –0.22 0.025* –0.07 0.461

*, statistically significant difference. CMR, cardiovascular magnetic resonance; LA, left atrial; LV, left ventricular; LVEDV, left ventricular end-diastolic volume; LVEF, left ventricular ejection fraction.

Factors predicting R-LVR

The univariate logistic regression analysis revealed that several variables were significant predictors of R-LVR, including the LVEDV, HR, infarct mass, MVO mass, LV longitudinal displacement, LAVpre-a, and LA reservoir strain rate (Table 4). After the multivariate analysis, only the LVEDV [odds ratio (OR): 1.022, 95% confidence interval (CI): 1.007–1.037, P=0.005], infarct mass (OR: 0.946, 95% CI: 0.918–0.975, P<0.001) and LA reservoir strain rate (OR: 0.224, 95% CI: 0.055–0.905, P=0.036) were independent predictors of R-LVR (Figure 5). In predicting R-LVR, the best cutoff values were identified as 128.63 mL for LVEDV, 21.45 g for infarct mass, and 1.34 s¹ for LA reservoir strain rate.

Table 4

Logistic regression analysis for the prediction of R-LVR

Characteristics Univariate analysis Multivariate analysis
OR 95% CI P value OR 95% CI P value
Age 0.993 0.963–1.025 0.682
Sex (male) 1.060 0.329–3.420 0.922
HR 0.954 0.917–0.992 0.017*
LVEDV 1.013 1.001–1.024 0.031* 1.022 1.007–1.037 0.005*
LVESV 0.990 0.977–1.003 0.122
LVEF 1.224 0.030–49.264 0.915
Infarct mass 0.962 0.938–0.987 0.003* 0.946 0.918–0.975 <0.001*
MVO mass 0.755 0.593–0.960 0.022*
LV displacement
   Radial 0.930 0.635–1.362 0.711
   Circumferential 0.972 0.753–1.255 0.830
   Longitudinal 1.515 1.009–2.276 0.045*
LA volume
   LAVmax 0.985 0.968–1.002 0.085
   LAVpre-a 1.023 1.002–1.045 0.031*
   LAVmin 0.979 0.956–1.003 0.087
LA strain rate
   Reservoir 0.291 0.089–0.959 0.042* 0.224 0.055–0.905 0.036*
   Conduit 0.639 0.302–1.355 0.243
   Booster 0.701 0.359–1.371 0.300

*, statistically significant difference. HR, heart rate; LA, left atrial; LAVmax, left atrial end-diastole volume; LAVmin, left atrial late-end systole volume; LAVpre-a, left atrial early-end systole volume; LV, left ventricular; LVEDV, left ventricular end-diastolic volume; LVEF, left ventricular ejection fraction; LVESV, left ventricular end-systolic volume; MVO, microvascular obstruction; OR, odds ratio; R-LVR, reverse left ventricular remodeling.

Figure 5 Parameters for predicting reverse left ventricular remodeling in the univariate and multivariate logistic regression analyses. CI, confidence interval; HR, heart rate; LA, left atrial; LAVpre-a, left atrial early-end systolic volume; LV, left ventricular; LVEDV, left ventricular end-diastolic volume; MVO, microvascular obstruction; OR, odds ratio.

To investigate the incremental predictive value of the LV and LA CMR parameters for R-LVR, three different models were built (Table 5). The AUC values of models 1, 2, and 3 were 0.646 (95% CI: 0.547–0.737), 0.779 (95% CI: 0.688–0.854), and 0.797(95% CI: 0.708–0.869). The NRI values of models 2 and 3 were 88.70% (95% CI: 32.90–132.24%) and 44.10% (95% CI: 4.76–94.97%).

Table 5

Additional benefits of different models in predicting R-LVR based on the AUC and NRI

Model AUC (95% CI) NRI (95% CI) (%)
Model 1 0.646 (0.547–0.737)
Model 2 0.779 (0.688–0.854) 88.70 (32.90–132.24)
Model 3 0.797 (0.708–0.869) 44.10 (4.76–94.97)

Model 1: traditional clinical variables (age and heart rate); Model 2: Model 1 + conventional CMR variables (LVEDV and infarct mass); Model 3: Model 2 + left heart function variables (LV longitudinal displacement and LA reservoir strain rate). AUC, area under the curve; CI, confidence interval; NRI, Net Reclassification Index; R-LVR, reverse left ventricular remodeling.

Reproducibility analysis of CMR parameters

A randomly chosen subset of 20 patients was included for assessing inter-observer reliability by two independent readers, as well as for evaluating intra-observer consistency. As summarized in Table S3, all the CMR parameters showed favorable reproducibility.


Discussion

The value of the LA CMR parameters in predicting R-LVR in patients with STEMI remains unclear. This study aimed to investigate the alterations in left heart function and structure occurring between 1 week and 5 months post-PCI, to explore the best predictors of R-LVR, and to assess whether functional parameters of LA and LV could improve the predictive value of traditional models. The study found the following results: (I) initially, the patients in the R-LVR group had larger LV and LA volumes than those in the non-R-LVR group; however, by the second CMR examination, these volumes were lower in the R-LVR group relative to the non-R-LVR group; (II) infarct mass values decreased in both groups over time, but were consistently smaller in the R-LVR group than the non-R-LVR group; (III) the LVEDV, infarct mass, and LA reservoir strain rate were identified as significant independent predictors of R-LVR; and (IV) the left heart function variables (i.e., LV longitudinal displacement and LA reservoir strain rate) had additional value in predicting R-LVR than the conventional CMR markers in the patients with STEMI.

Left heart features of patients with and without R-LVR

According to our findings, a significant percentage (45%) of the patients who received successful PCI had R-LVR. The high incidence of R-LVR in our study, which was roughly the same as that reported in another study (4), was mainly due to the fact that the STEMI patients who received timely PCI treatment had rapid restoration of coronary blood flow and reduced myocardial damage.

We observed a significant decrease in the LV volume over time in the R-LVR group, but a significant increase in the non-R-LVR group. Consequently, at the second CMR examination, the R-LVR group exhibited significantly lower LVESV and LVEDV values than the non-R-LVR group. Additionally, the infarct mass values remained consistently higher in the non-R-LVR group at both CMR scans, even though the myocardial injury recovered in both groups over time. In the non-R-LVR group, more extensive MI caused greater cardiomyocyte necrosis, leading to subsequent replacement by myofibroblasts. This process resulted in increased LV stiffness and impaired blood flow from the left atrium to the left ventricle (24). Previous studies have suggested that healing after MI should not be considered only at the LV level but should also be considered in terms of LA changes (25,26). During hemodynamic stress or exertion, the left atrium regulates LV diastolic filling and cardiac function through reservoir, conduit, and pump functions (27). No significant change in the LA volume was observed in the R-LVR group, suggesting that LV function did not decline further. However, there was an increase in both the LV volume and LA filling pressure in the non-R-LVR group, suggesting secondary LA volume overload, reduced LA compliance, and LV “decompensation” (28). Interestingly, the patients presenting with R-LVR initially had a lower LA strain rate, and larger LV and LA volumes. Previous studies have reported that patients with R-LVR had lower LA strain at the initial CMR, which may be related to the existence of the contractile reserve, and a better prognosis (29,30). Thus, patients with a contractile reserve may initially have lower LA strain, and larger LV and LA volumes, but will show more marked improvement after treatment. However, more studies are needed to confirm this hypothesis.

Predictors of R-LVR

Identifying patients with R-LVR after STEMI has important implications for risk stratification and prognosis prediction (31). A growing number of recent studies have shown that the left atrium plays an important role in maintaining the entire cardiac cycle and function, which has important implications for clinical research. However, few studies have evaluated the predictive value of LA for R-LVR. Our study found that the LA reservoir strain rate was an independent predictor of R-LVR. The LA strain rate was a better predictor of R-LVR than the LA volume for a number of reasons. First, LA function can predict hemodynamics more effectively than the LA volume. In a study of 329 patients with diastolic dysfunction, 23% had impaired LA strain, but their LA geometry was normal (32). LA volume alone is an insensitive biomarker of early phases of LV diastolic dysfunction, as left atrium remodeling may require time. Because the primary function of the left atrium is to modulate LV filling, functional LA changes become evident at the earliest stages of diastolic dysfunction (33). Second, Vattay et al. (34) found that improvements in LV functional remodeling were correlated with improvements in LA function. Leng et al. (12) investigated the importance of LA strain in STEMI prognosis, and found that LA reservoir strain was an independent predictor of MACEs. In addition to the LA reservoir strain rate, the LVEDV and infarct mass served as significant independent predictors of R-LVR, which is consistent with previous findings (35,36). Our study innovatively combined LA and LV functional parameters with traditional clinical and CMR markers, and found that LV longitudinal displacement and the LA reservoir strain rate enhance the prediction of R-LVR beyond conventional risk factors. This extends established knowledge of LA-LV hemodynamic coupling (37). Notably, LA and LV strain changes precede geometric remodeling, offering earlier prognostic insights (17,38,39). These findings support a novel parametric approach to guide R-LVR management in STEMI patients; however, further research is needed to define the role of the left atrium in clinical decision-making.

The study had a number of limitations. First, the follow-up period in this study was relatively short, so it may not fully capture long-term changes in the CMR characteristics of patients. Second, because the study was a single-center retrospective study with a relatively small number of patients, and excluded dynamically unstable patients who could not undergo CMR imaging and those with previous MI, the generalizability of the findings may be limited.


Conclusions

Early post-STEMI CMR assessment of the LVEDV, infarct mass, and LA reservoir strain rate provides valuable predictive insights for R-LVR. Importantly, the combination of the LA reservoir strain rate and LV longitudinal displacement enhanced the predictive accuracy of the model beyond conventional risk factors, offering a potential strategy for the early risk stratification and personalized management of STEMI patients.


Acknowledgments

None.


Footnote

Reporting Checklist: The authors have completed the TRIPOD reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2497/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2497/dss

Funding: This research was supported by the New Technology and Business of Chinese People’s Liberation Army General Hospital (No. 20230116).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2497/coif). All authors report that this research was supported by the New Technology and Business of Chinese People’s Liberation Army General Hospital (No. 20230116). 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. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the local ethics committee of the Chinese People’s Liberation Army General Hospital (No. S2022-567-01) 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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Cite this article as: Cui J, Yan F, Liu W, Zhao Y, Luo C, Yue X, Li T. The value of the left atrium as detected by cardiovascular magnetic resonance in predicting reverse left ventricular remodeling in patients with ST-segment elevation myocardial infarction. Quant Imaging Med Surg 2025;15(11):10819-10833. doi: 10.21037/qims-2024-2497

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