Prognostic significance of left atrial volume index in patients with severe aortic stenosis after transcatheter aortic valve replacement

Introduction

Aortic stenosis (AS), as one of the most common valvular heart diseases, affects over 5% of individuals older than 65 years (1). In patients with asymptomatic AS, the mortality is low. However, the mortality in untreated patients can be nearly 50% after the onset of clinical symptoms as a 4-year outcome (2). In patients with severe AS at intermediate surgical risk, transcatheter aortic valve replacement (TAVR) is noninferior to surgical aortic valve replacement (SAVR) in terms of all-cause mortality at 2 years (3). For patients with severe symptomatic AS, TAVR, and not SAVR, appears to be the only treatment for ensuring improvement in long-term outcomes (4). Nevertheless, the mortality of patients with severe AS at high surgical risk after TAVR at 5 years is 67.8% (5). However, the prognostic indicators in patients treated with TAVR have not been identified, and further research in this area is warranted.

As AS progresses, the increasing afterload of the left ventricle (LV) results in LV hypertrophy, an increase in left atrial size, diastolic dysfunction, mitral regurgitation (MR) and tricuspid regurgitation, an elevation of pulmonary artery pressure, or even right ventricular dysfunction (6). It has been shown that the extent of extravalvular (extra-aortic valve) cardiac damage associated with AS prior to aortic valve replacement is associated with poor clinical outcomes after aortic valve replacement. According to the staging classification of AS, stage 2 is characterized by left atrial damage, with the left atrial volume index (LAVi) further increasing in stage 3 or 4 (7). Studies have suggested that LAVi which is a significant indicator of diastolic function, has considerable prognostic value for acute coronary syndrome, heart failure, and hypertrophic cardiomyopathy (8-10). For valvular heart disease, a high LAVi can be observed in patients with progressive mitral stenosis and AS and is associated with adverse clinical outcomes in these patients (11,12). However, the prognostic value of LAVi for post-TAVR patients has not been fully clarified.

We thus conducted a retrospective cohort of patients with severe AS who received TAVR at a single center to determine the associations of LAVi with mortality at 4 years in patients with severe AS after TAVR and to assess the prognostic value of LAVi for patients treated with TAVR. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-24-1304/rc).

Methods

Participants and study procedures

Patients with severe AS (13) who successfully underwent TAVR at West China Hospital were consecutively enrolled between April 2012 and October 2019. This study excluded those patients who had biological valve decay after surgical valve replacement, those complicated with moderate-to-severe mitral stenosis, those lost to follow-up, or those with inadequate echocardiographic images. Ultimately, 500 patients were included for further analysis (Figure S1). This study was approved by the institutional ethics committee of the West China Hospital of Sichuan University (No. 2023-1621) and complied with the Declaration of Helsinki (as revised in 2013), and informed consent was obtained from all the patients.

Blood measurement

Preoperative blood samples were measured 1 day before TAVR after overnight fasting. Serum levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), albumin, globulin, albumin/globulin ratio (A/G ratio), lipid panel [triglycerides, total cholesterol, high-density lipoprotein cholesterol (HDL-c), and low-density lipoprotein cholesterol (LDL-c)], creatine kinase (CK), and hemoglobin were measured using standard laboratory techniques. In this study, the cutoff value for the level of serum albumin was 40 g/L (14).

Transthoracic echocardiography

Standard transthoracic echocardiography was performed before TAVR with a iE33 or EPIQ 7C device (Philips, Amsterdam, the Netherlands) equipped with a S5-1 (1.0–5.0 MHz) transducer by an experienced echocardiographer (X.W., with more than 10 years of working experience) according to a standardized protocol (15), with all data being analyzed offline with Tomtec Image Arena 4.0 (Tomtec Imaging Systems, Unterschleissheim, Germany). All images were acquired for at least three cardiac cycles for further analysis.

According to the relevant guidelines (13,15-16), LV structure and function, MR, aortic regurgitation (AR), mean transaortic pressure gradient (PGmean), maximum aortic velocity, and effective orifice area (EOA) were analyzed. The thickness of the interventricular septum (IVS) and left ventricular posterior wall (LVPW) and the diameter of left ventricular end-diastolic (LVDd) were measured. Left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), and left ventricular ejection fraction [LVEF; LVEF = (LVEDV − LVESV)/LVEDV × 100] were calculated. Left ventricular global longitudinal strain (LVGLS) was obtained as the average peak systolic strain based on 17 segments as measured on apical 2-, 3-, and 4-chamber views. The early diastolic (E) wave peak velocity was measured from mitral pulse-Doppler inflow, the early diastolic (e') tissue velocity was measured from the septal mitral annulus, and the E/e' ratio was calculated to evaluate the LV filling pressure (17). The velocity-time integral across the aortic valve (VTI_AV) and the left ventricular outflow tract (VTI_LVOT) were measured to calculate the EOA as follows: EOA × VTI_AV = π × (LVOTd/2)² × VTI_LVOT (13).

LAVi analysis

Images were analyzed offline using Tomtec Image Arena 4.0 analysis software. Left atrial volume (LAV) was measured with the biplane Simpson method in the apical 2- and 4-chamber views, and then indexed for body surface area (BSA). The LAVi values were categorized as normal (<34 mL/m²), mildly-to-moderately abnormal (34–48 mL/m²), and severely abnormal (>48 mL/m²) (18).

Reproducibility

Forty randomly selected patients were used to assess the inter- and intra-observer reliability of LAVi. The assessment of inter-observer reproducibility involved another experienced sonographer who did not participate in the study, and the assessment of intra-observer reproducibility involved the same observer after 1 week. The intra- and intra-observer intraclass correlation coefficients (ICCs) were 0.91 (0.89–0.92) and 0.90 (0.88–0.92) respectively, indicating good intra- and inter-observer reproducibility.

Covariates

The demographic and clinical characteristics of each patient were recorded, including age, height, weight, sex, comorbidities, and New York Heart Association (NYHA) functional class. Body mass index [BMI; BMI = weight (kg)/height² (m²)], and BSA [BSA (m²) = 0.0061 × height (cm) + 0.0128 × weight (kg) − 0.1529] were also recorded. The Society of Thoracic Surgeons (STS) score was measured retrospectively (19,20).

Follow-up

The primary outcome of this study was all-cause mortality, including cardiovascular mortality (e.g., myocardial infarction, heart failure, and malignant arrhythmia) and non-cardiovascular mortality (e.g., tumor, trauma, suicide, and infection) within 4 years after TAVR. The date of the TAVR procedure was defined as the start of follow-up. Patient survival status was obtained from electronic medical records and/or telephone contact, and each patient was encouraged to return to our outpatient clinic for follow-up at least every 3 months.

Statistical analysis

SPSS 26.0 (IBM Corp., Armonk, NY, USA) was used for all statistical analyses, and GraphPad Prism 8 (GraphPad Software, La Jolla, CA, USA) was used for drawing Kaplan-Meier curves. Continuous values are expressed as the median and interquartile range (IQR), and categorical variables are expressed as counts and percentages. The normality of distributions was tested with the Kolmogorov-Smirnov test. Differences between subgroups were examined via the independent t-test or the Mann-Whitney test. The chi-square or Fisher exact test was used for categorical variables. Univariate Cox proportional hazard regression analysis was performed to evaluate the hazard ratio (HR) and 95% confidence interval (CI) of the factors associated with 4-year mortality after TAVR. Subsequently, the potential predictors associated with mortality in the univariate analysis (P<0.1) were included in the multivariate Cox regression, and backward variable elimination was performed to assess the independent risk factors of mortality. The log-rank test was used in the Kaplan-Meier analysis. Furthermore, we used Cox regression models, adjusting for baseline characteristics, laboratory data, and echocardiographic data, to estimate the relative risk of mortality according to LAVi (expressed as the HR and 95% CI). All P values were two-sided, and a P value less than 0.05 was used as the significance threshold.

Results

Study population and baseline characteristics

A total of 500 patients with severe AS who underwent TAVR were included in our study. All patients in this study received self-expandable valves (7.6%), balloon-expandable valves (86.4%), or mechanically expandable valves (6.0%), with 99.4% being implanted via a femoral access (21). The baseline characteristics are presented in Table 1. Of these patients, 64 (12.8%) died during the follow-up period. In this cohort, the non-survivors group was older than the survivors group (P<0.001) and had a lower proportion of females (31.3% vs. 46.3%, P=0.031). There were no significant differences in the proportion of hypertension, diabetes, chronic obstructive pulmonary disease, coronary artery disease, atrial fibrillation, or the need of a pacemaker after TAVI between the two subgroups, but the incidence of chronic kidney disease was higher in the non-survivors group than in the survivors group (20.3% vs. 7.3%, P=0.002). Furthermore, the STS scores in the non-survivors group (median 7.70, IQR, 5.47–11.22) were higher than those in the survivors group (median 6.09, IQR, 3.73–8.69) (P=0.004).

The echocardiographic parameters and laboratory data before TAVR are presented in Table 1 and Figure 1. In patients with severe AS, the median LAVi was 52.6 mL/m² (IQR, 38.3–67.6 mL/m²), 96 of 500 were categorized as normal (LAVi <34 mL/m², 19.2%), 108 of 500 were categorized as mildly-to-moderately abnormal (34–48 mL/m², 21.6%), and 296 of 500 were categorized as severely abnormal (>48 mL/m², 59.2%) (Figure 1A). Compared to the survivors group, the non-survivors group had a higher LAVi (non-survivors: median 66.5 mL/m², IQR, 48.6–85.4 mL/m²; survivors: median 51.3 mL/m², IQR, 36.9–65.1 mL/m²; P<0.001; Figure 1B) and larger E/e' ratio (non-survivors: median 20.1, IQR, 16.3–28.0; survivors: median 19.9, IQR, 14.9–26.8; P=0.039). The distribution of LAVi in the survivors group differed from that observed in the non-survivors group (Figure 1C). Moreover, the incidence of moderate-to-severe AR was higher in the non-survivors group than in the survivors group (35.9% vs. 23.2%, P=0.031). However, there were no significant differences in LV structure (e.g., IVS, LVPW, LVDd, LVEDV and LVESV) or systolic function (e.g., LVEF and LVGLS) between the two subgroups. Notably, the non-survivors group, compared to the survivors group, had a significantly lower level of serum albumin (non-survivors: median 38.8 g/L, IQR, 36.3–42.4 g/L; survivors: median 41.7 g/L, IQR, 39.1–44.0 g/L; P<0.001), A/G ratio (non-survivors: median 1.41, IQR, 1.21–1.67; survivors: median 1.57, IQR, 1.38–1.77; P=0.001), and hemoglobin level (non-survivors: median 122.0 g/L, IQR, 101.0–139.0 g/L; survivors: median 129.0 g/L, IQR, 117.0–140.0 g/L; P=0.028).

Figure 1 Distribution of LAVi in patients with severe aortic stenosis. (A) Green, LAVi <34 mL/m²; gray, LAVi =34–48 mL/m²; and red, LAVi >48 mL/m². (B) Different values of LAVi in patients with different outcomes after transcatheter aortic valve replacement. (C) The distribution of LAVi in the survivors and non-survivors. LAVi, left atrial volume index.

Risk factors associated with 4-year mortality after TAVR

In the univariate Cox proportional hazard regression analysis, older age (HR =1.076; P<0.001), higher STS score (HR =1.082; P<0.001), chronic kidney disease (HR =2.831; P=0.001), moderate-to-severe AR (HR =1.770; P=0.028), higher LAVi (HR =1.021; P<0.001), higher maximum aortic velocity (HR =1.078; P=0.028), and higher serum globulin level (HR =1.058; P=0.031) were associated with an increased risk of 4-year mortality. Conversely, female sex and higher levels of serum albumin (HR =0.886; P<0.001) and hemoglobin (HR =0.982; P=0.005) were associated with decreased mortality. After inclusion of those baseline characteristics with a P value <0.1 into the multivariate Cox regression analysis, age (HR =1.072; 95% CI: 1.023–1.124; P=0.004), LAVi level (HR =1.023; 95% CI: 1.013–1.033; P<0.001), and serum albumin level (HR =0.862; 95% CI: 0.796–0.934; P<0.001) were found to be the independent risk factors for the estimation of 4-year mortality after TAVR (Table 2).

Association of long-term survival with age, LAVi and serum albumin level

The 4-year outcomes after TAVR were stratified by the selected cutoff values of LAVi, age, and serum albumin level (Figure 2). The Kaplan-Meier curve showed a strong graded association between the extent of LAVi before TAVR and all-cause mortality (Figure 2A) and cardiovascular mortality (Figure 2B) after TAVR but no significant difference in non-cardiovascular mortality (Figure 2C). The log-rank test demonstrated that all-cause mortality (P=0.003) and cardiovascular mortality (P=0.008) increased significantly in each successive subgroup of worsening LV diastolic dysfunction. Moreover, patients with serum albumin levels ≤40 g/L had higher all-cause mortality (Figure 2G), cardiovascular mortality (Figure 2H), and non-cardiovascular mortality (Figure 2I).

Figure 2 Association of 4-year outcomes after transcatheter aortic valve replacement with LAVi, age, and serum albumin level. Association of LAVi with (A) all-cause mortality; (B) cardiovascular mortality and (C) non-cardiovascular mortality. Association of age with (D) all-cause mortality; (E) cardiovascular mortality; and (F) non-cardiovascular mortality. Association of serum albumin level with (G) all-cause mortality; (H) cardiovascular mortality; and (I) non-cardiovascular mortality. LAVi, left atrial volume index.

The association of baseline characteristics, physiological parameters, echocardiographic parameters, and laboratory data with LAVi

According to the LAVi, all patients were divided into three groups: LAVi <34 mL/m², LAVi =34–48 mL/m², and LAVi >48 mL/m². With the increase of LAVi, there were significant increases in the proportion of patients chronic kidney disease, atrial fibrillation, STS scores, LVDd, LVEDV, LVESV, E/e', moderate-to-severe MR and AR, maximum aortic velocity, PGmean, and NT-proBNP level, and significant decreases in LVEF, LVGLS, and HDL-c level (Table S1).

LAVi-dependent mortality risk factors after TAVR

We performed Cox regression analysis to assess the prognostic value of LAVi in patients with severe AS after TAVR (Table S2). Patients with higher LAVi level had a significantly higher incidence of all-cause mortality. After conditioning was completed on matching factors (model 1: matched for age, sex and BMI), the HR for the comparison of the highest and the lowest category of LAVi was 2.900 (95% CI: 1.240–6.781). A similar association between LAVi and mortality was observed when LAVi was as a continuous variable (HR =1.022; 95% CI: 1.014–1.030). After comorbidities, NYHA functional class, STS score, laboratory and other echocardiographic data, IVS, LVPW, LVEF, LVGLS, septal E/e', EOA, maximum aortic velocity, and PGmean were controlled for, the HR for the comparison of the highest and lowest category of LAVi was 4.796 (95% CI: 1.137–20.238). The fully adjusted HR per unit increase in LAVi was 1.023 (95% CI: 1.013–1.033).

Discussion

In our study, age, LAVi, and serum albumin level were the independent risk factors for the estimation of 4-year mortality after TAVR. Moreover, the mortality rate in patients with LAVi >48 mL/m² was significantly higher than that in those with a normal or mild-to-moderate increase in LAVi, and the multivariable HR of the highest category of LAVi was 4.796. These results suggest that LAVi is a valuable prognostic factor for the long-term clinical outcome of patients treated with TAVR.

TAVR, which is noninferior to SAVR, is recommended for older patients with severe AS (22,23). In our study, the all-cause mortality in patients with severe AS after TAVR was 12.8% at 4-year follow-up, which was consistent with previously published data (24). Compared to the mortality reported in the PARTNER (Placement of Aortic Transcatheter Valves) 2 study, the all-cause mortality in our study was markedly lower, which may be attributed to the lower STS scores and preserved LVEF (25,26). Therefore, TAVR, which is a key approach for patients with severe AS, is associated with high mortality, and its risk factors are complex but unclear. In a study with long-term follow-up, younger patients or female patients with severe AS who underwent TAVR had lower all-cause mortality than did older adults or males (27), which is consistent with our findings. Meanwhile, our findings were also similar to other studies reporting that chronic kidney disease was independently associated with long-term outcomes in patients who underwent TAVR (28,29). In addition to the above factors, several other prognostic factors have been suggested to contribute to the high mortality after TAVR, including oxygen intake at home (30), low habitual physical activity (31), MR (32), AR (33), low LVEF (34), and low serum albumin level (35).

Additionally, several studies, including the PARTNER trials, found that the staging system according to the extent of cardiac damage is a strong independent predictor of mortality after TAVR after adjustments for STS score, presence of frailty, coronary artery disease, and renal dysfunction (7,36-38). This staging system involves the following: stage 1 is characterized by LV changes, such as increased left ventricular mass index, mitral E/e' >14, and LVEF <50%; stage 2 is characterized by left atrial or mitral changes, including LAVi >34 mL/m², moderate-to-severe MR, and atrial fibrillation; stage 3 is characterized by pulmonary artery or tricuspid changes, including pulmonary artery systolic pressure >60 mmHg and moderate-to-severe tricuspid regurgitation; and stage 4 is characterized by right ventricle changes. Importantly, it has been demonstrated that advanced LV diastolic dysfunction at baseline is associated with increased mortality and adverse events after TAVR (39).

LAVi, both a primary characteristic in stage 2 of the staging system and a non-invasive estimation of LV diastolic dysfunction, is a predictor of worse outcomes in several cardiac diseases (40-44). For patients with severe AS who have undergone TAVR, previous studies have only described the relationship between LAVi level and B-type natriuretic peptide level (45) or MR improvement (46) after TAVR or the relationship between baseline diastolic dysfunction grade and adverse 1-year outcomes (47). In our study, after 4-year follow-up, we further found that the level of LAVi was significantly higher in non-survivors than in survivors, and LAVi was an independent predictor of all-cause mortality in patients with severe AS after TAVR. Moreover, we demonstrated that the severely abnormal LAVi was associated with the worse mortality in patients. Finally, LAVi is a reliable echocardiographic measure, which is easily obtainable and independent of cardiac rhythm (47). Hence, LAVi should be considered as a marker with considerable prognostic implications due to its convenience and reliability.

Limitations

Our study had several limitations which should be mentioned. First, we employed a retrospective, single-center design. Second, the number of participants was relatively small in our study. Third, although we adjusted the measured the variates in the multivariate model, unmeasured variates might have confounded the results. Further prospective investigations are needed to confirm our findings.

Conclusions

Given the high mortality in patients with severe AS after TAVR, it is crucial to identify the easy-to-obtain routine risk factors for mortality in this group of patients. Our study demonstrated that higher preoperative LAVi was an independent predictor of mortality in patients with severe AS after TAVR, and LAVi could be used as a risk stratification tool for long-term prognosis. Further studies are needed to confirm our results.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-24-1304/rc

Funding: This work was supported by the National Natural Science Foundation of China (Nos. 82170375 and U23A20395); Key Research and Development Project of Science & Technology Department of Sichuan Province (No. 2022ZDZX0020); and Sichuan Science and Technology Program (No. 2024NSFSC1715).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-24-1304/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013). The study was approved by the institutional ethics committee of the West China Hospital of Sichuan University (No. 2023-1621). And informed consent was obtained from all the patients.

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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