Impact of preoperative left ventricular diastolic dysfunction on primary graft dysfunction and mortality following lung transplantation

Introduction

Lung transplantation (LTx) is a recognized treatment for patients with end-stage respiratory disease. Following LTx, primary graft dysfunction (PGD) is a dangerous complication characterized by increasing hypoxemia and pulmonary oedema (1). According to recent studies, the incidence of PGD after LTx can reach 8.6–44.7% (2). The in-hospital mortality rate for patients who develop PGD after LTx is 13.6%, nearly three times higher than that of patients without PGD. Their 1-, 5-, and 10-year survival rates fall to 72.8%, 43.9% and 18.7%, respectively. PGD is the main cause of short-term death and long-term poor prognosis of LTx patients (3). Therefore, it is very important to prevent PGD effectively.

Left ventricular diastolic dysfunction (LVDD) refers to the inability of the left ventricle to relax and fill effectively during diastole, which can be manifested as an increase in left ventricular end diastolic pressure (LVEDP), left atrial pressure (LAP) and pulmonary vein congestion. Due to chronic inflammation of long-term respiratory diseases and pulmonary arterial hypertension (PAH), LVDD is common in LTx patients, and its incidence can reach 20–90% (4). The role of LVDD in the prognosis of LTx has been largely ignored for a long time, and only in recent years has there been relevant clinical research. Despite clinical studies suggesting that pre-LTx LVDD may be linked to postoperative PGD and mortality, its mechanism is not completely clear, which may be related to the increase of pulmonary vein pressure caused by LVDD. It is still controversial whether LVDD affects the prognosis because of the heterogeneity of diagnostic criteria and the differences in study results (5-9).

Therefore, we conducted a retrospective analysis, which sought to determine the risk factors for the preoperative presence of LVDD in LTx patients, evaluate the influence of LVDD on the incidence of PGD and mortality, and investigate the predictive effectiveness of cardiac function indices for PGD. We present this article in accordance with the STROBE reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1447/rc).

Methods

Study design

This study used a retrospective cohort study design and included clinical data of 447 patients who underwent LTx between January 1, 2018, and June 22, 2021 at Wuxi People’s Hospital. According to the following inclusion and exclusion criteria, 439 adult LTx patients were included and 95 LTx patients were excluded.

Inclusion criteria:

• Recipients were ≥18 years of age;
• Patients underwent a complete LTx evaluation and underwent LTx;
• Relatively complete clinical information and follow-up data are available.

Exclusion criteria:

• Secondary LTx, combined organ transplantation;
• Preoperative transthoracic echocardiography (TTE) data were missing;
• Left ventricular ejection fraction (LVEF) <50%;
• Atrial septal defect;
• Moderate or severe mitral or aortic regurgitation or stenosis;
• Pericardial disease;
• Cardiomyopathy.

We excluded 82 individuals without TTE data, 8 patients of second LTx, 3 patients with atrial septal defect and 2 patients with LVEF <50%. Finally, a total of 344 patients were included in the final analysis (Figure 1). This retrospective study involved no interventions for patients. All data were anonymized to rigorously protect patient privacy. The Wuxi People’s Hospital Research Ethics Committee approved this study and waived the informed consent due to the retrospective nature of the study (approval No. KY24155; September 27, 2024). All donation procedures were approved by the Institutional Ethics Committees of the relevant Organ Procurement Organizations (http://links.lww.com/TP/B933). Donor lungs were allocated through the China Organ Transplant Response System (https://www.cot.org.cn/). This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

Figure 1 Flow chart of the study. LT, lung transplantation; LVEF, left ventricular ejection fraction; TTE, transthoracic echocardiogram.

Definition and collection

Definition of LVDD

According to the 2016 American Echocardiographic Society (ASE) and European Association for Cardiovascular Imaging (EACVI) guidelines for assessment (10), LVDD is defined by four echocardiographic parameters in individuals with normal LVEF:

• Maximum velocity of mitral annulus sidewall in early diastolic stage (e’) <10 cm/s;
• Peak E velocity of mitral inflow/average of early diastolic velocity of the lateral wall and interventricular septum at the mitral annulus e’ (E/e’) >14;
• Left atrial volume index (LAVI) >34 mL/m²;
• Maximum tricuspid regurgitant velocity (TRV_max) >2.8 m/s.

Since TRV_max data were not available, we used pulmonary artery systolic pressure (PASP) and central venous pressure (CVP) to calculate TRV_max using the following formula: PASP (mmHg) =4 × TRV_max² + CVP.

Patients were categorised as “definite LVDD”, “probable LVDD” and “non-LVDD (NLVDD)”. A definite LVDD diagnosis was confirmed if more than half of the four parameters met the defined thresholds, whereas meeting exactly half of the criteria was classified as probable LVDD, though probable cases could be upgraded to definite LVDD if comorbid with chronic hypertension and left ventricular hypertrophy; normal diastolic function was designated when fewer than half of the criteria were satisfied. We collected the latest TTE data before LTx. Two team members diagnosed LVDD based on TTE, PASP and CVP, a third team member will be consulted if the diagnosis is unclear. The diagnostic flow chart is illustrated in Figure S1.

Outcome measures

PGD grade 3 (PGD-3) was chosen as the primary outcome. Based on the 2016 International Society for Heart and Lung Transplantation (ISHLT) guidelines (1), PGD is defined by diffuse alveolar infiltrates on chest radiographs and a PaO₂/FiO₂ <300 within 72 hours after reperfusion of the second transplanted lung during LTx. PGD-3, the most severe form, is characterized by a PaO₂/FiO₂ <200 or the use of extracorporeal membrane oxygenation (ECMO) in the presence of pulmonary edema on chest radiographs. However, PGD classification excludes cases where ECMO was used for indications unrelated to hypoxemia (11). PGD-3 is associated with significantly higher mortality than PGD grade 1 or 2 (12). This binary classification (PGD-3 vs. non-PGD) provides clearer diagnostic criteria, with PaO₂/FiO₂ <200 offering minimal ambiguity (13,14). PGD diagnoses were obtained from intensive care unit (ICU) and inpatient medical records within 72 hours post-LTx. ICU doctors observed the pulmonary alveolar edema fluid through fiberoptic bronchoscopy and bedside echocardiography to rule out obvious cardiogenic pulmonary edema to ensure the reliability of PGD diagnosis.

The secondary outcome was 1-year mortality. The 1-year mortality was chosen because 1-year mortality was chosen as the outcome indicator in previous studies and to reduce the influence of confounding factors such as postoperative psychosocial factors.

Data sources and variables

Data were collected from the electronic medical record system, examination report system, outpatient system, and anesthesia system. Key preoperative and intraoperative variables included:

• Demographics: age, sex, body mass index (BMI), primary lung disease, history of hypertension, diabetes, kidney disease, smoking status, and New York Heart Association (NYHA) classification.
• Hemodynamics: preoperative support, blood pressure, PAH and PASP. PAH was defined by the British Society of Echocardiography’s guidelines as a diagnostic criterion for a PASP >35 mmHg (15).
• TTE parameters: E/e’, e’, LAVI, LVEF, and cardiac output (CO).
• Laboratory tests: preoperative levels of C-reactive protein (CRP), dimer, N-terminal pro-brain natriuretic peptide (N-BNP), creatine kinase (CK), creatine kinase isoenzyme-MB (CK-MB), lactate dehydrogenase (LDH).
• Surgical data: operation type, duration, cold ischemia time and ECMO usage.

LTx management platform recorded the follow-up and post-visit information. The follow-up period lasted until June 23, 2024, based on data derived from the LTx follow-up management platform. The fixed follow-up times were 30-, 90-, 180-days, and 1-, and 3-year following LTx. In-hospital deaths were considered by “automatic discharge” or “death” during hospitalization according to the electronic medical record system.

Statistical analysis

According to their preoperative left ventricular function, the 344 LTx patients who were ultimately included in the analysis of this study were split into two groups: the LVDD group and NLVDD group. Continuous variables with normal distribution were expressed as mean ± standard deviation (SD), and comparisons between groups were made using an independent samples t-test. Continuous variables that were not normally distributed were expressed as median (interquartile range, P25–P75), and comparisons between groups were analyzed using the Mann-Whitney U test. Categorical variables were expressed as counts (percentages), and comparisons between groups were made by Chi-squared test or Fisher’s exact test.

Independent risk factors for preoperative LVDD in LTx patients were tested using multifactorial logistic regression. Cumulative probabilities of endpoint occurrence were estimated using the Kaplan-Meier method, and log-rank tested whether survival curves were statistically different between different preoperative left ventricular diastolic function states. Correlations between LVDD, E/e’, e’, LAVI and PGD-3 or 1-year mortality were assessed using univariate and multivariate logistic regression or Cox regression models. Schoenfeld residuals were assessed to evaluate the assumption of equal proportionality of risk for the correlation between covariates and survival time. In the case of covariate covariance, the most significant variables were selected for inclusion in the multifactorial analysis. Odds ratios (OR), hazard ratios (HR), and 95% confidence intervals (CI) were calculated. Further subgroup analyses were performed considering confounding factors, and interaction tests were used to assess potential interactions between these factors. The predictive ability of cardiac function indices for PGD was assessed using receiver operating characteristic (ROC) curves, and the area under the ROC curve (AUC), specificity, sensitivity, and cut-off values were calculated. In this study, the missing data of all variables were <30%, and 3 cases (0.8%) of follow-up data were missing; the complete data method was used to delete all missing data and keep only complete data.

Statistical software was used IBM SPSS version 26.0, R version 4.4.3 and GraphPad Prism version 9.5.1, and all statistical tests were two-tailed, and statistical significance was set at P≤0.05.

Results

Patient characteristics

Males made up 268 (80.5%) of the donors, with a median age of 39 years. A total of 330 cases of donor brain death (DBD) (95.9%), 5 cases of donor cardiac death (DCD) (1.5%) and 5 cases of donor brain and cardiac death (DBCD) (1.5%) were all related to the donors’ cause of death. Based on left ventricular diastolic functional status, LTx patients were split into two groups. The NLVDD group had more male donors than the LVDD group (84.4% vs. 70.8%, P=0.005), and duration of mechanical ventilation in NLVDD group was marginally longer than in the LVDD group [5.0 (3.0–9.8) vs. 5.0 (3.0–7.0), P=0.04] (Table S1).

A total of 344 cases of LTx recipients were 82.6% male, with a median age of 57 years and a median BMI of 20 kg/m². Chronic obstructive pulmonary disease (COPD) (13.4%) and PAH (1.5%) were the next most common pre-LTx diagnoses, after interstitial lung disease (ILD) (78.8%) (Table 1). LVDD patients frequently needed intraoperative ECMO assistance (88.7% vs. 78.6%, P=0.03) and had a greater prevalence of preoperative PAH (94.9% vs. 42.3%, P<0.001) than NLVDD patients (Table 1).

PGD-3 was found in 30.2% of patients after LTx, and the incidence of PGD-3 after LTx was higher in patients with LVDD than in those with NLVDD (43.9% vs. 24.7%, P<0.001). The 1-year and postoperative in-hospital mortality rates for LTx patients were 34.9% and 27.9%, respectively. LVDD patients had significantly greater postoperative in-hospital (41.2% vs. 22.5%, P=0.001) and 1-year mortality (44.9% vs. 30.9%, P=0.01) following LTx than NLVDD patients. Furthermore, although statistically significant, the observed increases in mechanical ventilation duration [median 2 (IQR: 2–4) days vs. 2 (IQR: 1–3) days, P=0.003] and ICU length of stay (Los) [median 6 (IQR: 4–10) days vs. 4 (IQR: 3–8) days, P=0.01] in the LVDD group were numerically small. However, LVDD did not significantly affect extubation difficulties, acute kidney injury (AKI) incidence, and total Los (Table 2).

Prevalence and predictors of preoperative LVDD in LTx

LVDD was present in 28.5% (n=98) of patients prior to LTx, including 13 confirmed LVDD and 85 probable LVDD. Advanced age and preoperative PAH were independent risk factors for the preoperative LVDD in LTx patients (age—OR 1.029, 95% CI: 1.002–1.057, P=0.04; preoperative PAH—OR 35.064, 95% CI: 11.790–104.286, P<0.001) (Table S2).

Correlation of LVDD and related parameters with PGD-3

Multivariate logistic regression models incorporated clinical variables with P<0.20 affecting PGD-3 and LVDD (Table 1, Tables S1,S3), including donor sex, days of mechanical ventilation in the donor, age of recipients, BMI, primary lung disease, preoperative PAH, preoperative LVDD, type of surgery, and intraoperative ECMO assistance. Model 1 was not adjusted, Model 2 was adjusted for recipients age and BMI, Model 3 was adjusted by adding donor gender and donor mechanical ventilation days to Model 2, and Model 4 (fully adjusted) was adjusted by adding primary lung disease, PAH, type of surgery, and intraoperative ECMO assistance to Model 3.

As shown in Table 3, Models 1, 2, 3, and 4 all found that LVDD, lower e’, and e’<10 were associated with an increased risk of PGD-3 (Model 1: LVDD, OR 2.385, 95% CI: 1.455–3.909, P=0.001; e’, OR 0.913, 95% CI: 0.839–0.994, P=0.04; e’<10, OR 1.772, 95% CI: 1.082–2.903, P=0.02. Model 2: LVDD, OR 2.562, 95% CI: 1.479–4.438, P=0.001; e’, OR 0.905, 95% CI: 0.825–0.993, P=0.04; e’<10, OR 2.077, 95% CI: 1.194–3.613, P=0.01. Model 3: LVDD, OR 2.473, 95% CI: 1.409–4.343, P=0.002; e’, OR 0.906, 95% CI: 0.824–0.996, P=0.04; e’<10, OR 2.056, 95% CI: 1.163–3.636, P=0.01; Model 4: LVDD, OR 2.099, 95% CI: 1.071–4.116, P=0.03; e’, OR 0.904, 95% CI: 0.820–0.996, P=0.04; e’<10, OR 2.139, 95% CI: 1.177–3.889, P=0.01). In Models 1, 2, 3 and 4, E/e’, E/e’>8, LAVI, and LAVI>34 had no significant effect on the risk of PGD-3 (Table 3).

Postoperative mortality in both groups

The 30-, 90-, 180-day, and 1-, 3-year survival rates after LTx for LVDD patients were 70.1%, 62.4%, 58.8%, 52.4%, and 32.8%, respectively. The 30-, 90-, 180-day, and 1-, 3-year survival rates for NLVDD patients were 80.7%, 75.5%, 72.6%, 67.3%, and 56.9%, respectively. The median survival time after LTx for patients in the LVDD group was 436 days. The cumulative mortality for LVDD patients was significantly higher than that for NLVDD patients (log-rank P<0.001) (Figure 2).

Figure 2 K-M survival curves in the LVDD group and NLVDD group. K-M, Kaplan-Meier; LVDD, left ventricular diastolic dysfunction; NLVDD, non-LVDD.

Correlation of LVDD and related parameters with 1-year mortality

According to the Schoenfeld residual test, the risk of 1-year mortality and overall mortality in LVDD patients varied equiproportionally with time (P=0.70; P=0.25). As shown in Table 4, in Model 1 (unadjusted), LVDD was associated with 1-year mortality (HR 1.638, 95% CI: 1.129–2.375, P=0.009); however, in Model 2, LVDD was no longer statistically significant to 1-year mortality (HR 1.476, 95% CI: 0.994–2.192, P=0.05). In Models 3 and 4, the association of LVDD with 1-year mortality remained statistically insignificant. In Models 1, 2, 3 and 4, E/e’, E/e’ >8, e’, e’ <10, LAVI, and LAVI >34 did not have a significant effect on 1-year mortality after LTx (Table 4).

Subgroup analysis and interaction test

Although subgroup analyses demonstrated statistically significant differences in some subgroups, interaction tests revealed that age, sex, BMI, operation type, and preoperative PAH did not significantly modify the association between LVDD and 1-year mortality (P interaction >0.05) (Figure 3).

Figure 3 Subgroup analysis of LVDD on PGD-3 risk (A) and 1-year mortality risk (B). BMI, body mass index; CI, confidence interval; LVDD, left ventricular diastolic dysfunction; OR, odds ratio; PAH, pulmonary arterial hypertension; PGD, primary graft dysfunction.

Predictive value of LVDD and cardiac function indices for PGD-3

The clinical threshold for PGD-3 prediction by e’ was 9.85, with a sensitivity of 0.677 and a specificity of 0.480. E/e’, e’ and LAVI combined (AUC, 0.830; 95% CI: 0.737–0.923, P<0.001) improved the prediction of PGD-3 compared to e’ alone (AUC, 0.792; 95% CI: 0.690–0.894; P<0.001). Preoperative N-BNP had the strongest predictive ability for PGD-3 (AUC, 0.944; 95% CI, 0.870–1.000; P<0.001) (Figure 4).

Figure 4 ROC curve. CK, creatine kinase; CK-MB, creatine kinase isoenzyme-MB; LAVI, left atrial volume index; LDH, lactate dehydrogenase; LVDD, left ventricular diastolic dysfunction; N-BNP, N-terminal pro brain natriuretic peptide; ROC, receiver operating characteristic.

Discussion

Our study found that 28.5% of LTx patients had preoperative LVDD, consistent with previous studies reporting a prevalence of 26–31.8% (4). LVDD patients generally have comorbid PAH and tend to be more in need of intraoperative ECMO support. Intraoperative ECMO assistance in patients with LVDD, specifically veno-arterial (VA)-ECMO, can reduce the left ventricular load and serve a supportive role. According to the 2024 ISHLT consensus on extracorporeal life support (ECLS) utilization in LTx (16,17), integrating structured echocardiographic protocols into perioperative management is recommended. Previous studies have demonstrated that severe right ventricular dysfunction prolongs postoperative ECMO duration. In our investigation focusing on left ventricular function, we found that LVDD in PAH patients did not extend ECMO duration (Table 1). Furthermore, Kim et al. (18) reported that TTE parameters e′ (any amount of increase) and tricuspid S′ (>10% increase) appear to reliably predict successful VA-ECMO weaning. However, our study failed to demonstrate significant associations between ECMO duration and echocardiographic parameters, including e’ <10 cm/s, E/e’ >8, LAVI >34 mL/m² (Table S4).

Age, female gender, BMI, hypertension, and diabetes mellitus are all known risk factors for LVDD (19). However, only the preoperative PAH and advanced age were independent predictors of LVDD in our study. Age-related progressive deterioration in left ventricular function is an irreversible physiological process (20). Clinically significant, PAH patients have a 35-fold increased risk of preoperative LVDD. This interventional hemodynamic index can be effectively regulated by medications like prostacyclin, phosphodiesterase-5 inhibitors, and endothelin receptor antagonists (21,22). Accordingly, it is highly beneficial from a therapeutic standpoint to identify and improve PAH patients perioperative cardiac performance early on during LTx (23).

According to this study, LVDD was linked to a worse prognosis for LTx, manifested primarily as a higher death rate and a greater incidence of PGD-3 (24). Additionally, although statistically significant increases in mechanical ventilation duration and ICU Los were observed, the absolute differences were modest, and their clinical relevance should be interpreted with caution. Previous studies on the impact of LVDD on PGD or 1-year mortality following LTx have shown contradictory findings (5-9). Although the 2016 ISHLT consensus report on PGD (25) states that a number of factors influence PGD, such as PAH in recipients, abnormal BMI in recipients, preoperative infections and inflammation, intraoperative use of extracorporeal circulation, operative time, and ischemic duration, LVDD has not been identified as an independent risk factor for PGD. In this study, LVDD, e’ and e’ <10 cm/s were all found to be independently linked to PGD. In fully adjusted models, LVDD increased PGD-3 risk 2.099-fold, e’ increased PGD-3 risk 0.904-fold, and e’ <10 cm/s increased PGD-3 risk 2.139-fold. The clinical threshold for e’ 9.85 cm/s is near the diastolic parameter e’ <10 cm/s for diagnosing LVDD, which further supports our conclusion. Combining multiple indicators improved predictive accuracy compared to using single parameter. There may be a connection between LVDD and PGD; however, the mechanism of this interaction is yet completely unclear. According to the current perspective, the pathophysiology of LVDD is similar to that of PGD and is based on endothelial dysfunction and chronic inflammation. According to certain research, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-8, and IL-10 are among the inflammatory factors that LVDD and PGD have in common (26,27). In addition to harming cardiovascular endothelial cells, the same inflammatory agents also harm pulmonary vascular endothelial cells, which raises pulmonary vascular permeability. The second primary pathological characteristic of LVDD is the increase in left ventricular filling pressure, which raises LAP and, in turn, raises pulmonary vascular pressure. This increases ischemia-reperfusion injury in the pulmonary vasculature, which leads to PGD (4,28). In our statistical analysis, PAH was included as a covariate in multivariate models to eliminate its confounding effect on the independent variable. Moreover, interaction tests demonstrated that PAH did not compromise the robustness of our findings. After eliminating the interference of PAH on PGD by statistical method, we cautiously believe that LVDD is an independent risk factor for PGD.

In previous studies, only Porteous (9) and Li (6) et al. have reached positive conclusions, which are in line with ours. Porteous et al. found that LVDD and E/e’ were associated with PGD risk. We attempted to reproduce the results according to their same experimental design and only found that LVDD, e’, and e’ <10 were associated with the PGD risk, and did not find that E/e’ and E/e’ >8 were associated with the PGD risk. E/e’ is a more accurate predictor of LVDD filling pressures than e’ and is theoretically independent of volume loading. However, due to the low positive rate of E/e’ in our study, there was not a large enough sample size to achieve a statistically significant difference. Li et al. observed that LVEDP >15 mmHg increased the risk of PGD-3. The gold standard for detecting LVDD is the direct measurement of LVEDP using a left ventricular floating catheter. According to Li, who noted that there is no consistency between LVEDP, PCWP, and E/e′ because LTx patients receive mechanical ventilation or ECMO, which affects the accuracy of floating catheter measurements. To ascertain LVDD, Li underlined that a mix of diastolic function indexes is required, and that it is better to combine TTE with floating catheter measures to enhance the Li underlined. To identify LVDD, it is necessary to combine several diastolic function markers.

Yadlapati et al. (8) used the 2009 ASE guidelines for the diagnosis of LVDD and found that E/a, E’/a’, PCWP, and mortality were not related. The 2009 ASE guidelines were missing the TRV_max parameter compared to the 2016 ASE guidelines, which may have underestimated the predictive value of LVDD for prognosis. Until the study of Aggarwal et al. (5-7,9), they used the 2016 ASE guidelines. Aggarwal et al. concluded that LVDD was not associated with PGD because LTx patients in their cohort had worse preoperative cardiac function than that of conventional LTx patients. In our study, the pre-LTx patients had fair cardiac function, with the median preoperative N-BNP in the LVDD patients being 111 pg/mL and the median CO being 4.3 L/min (Table S5). And because Aggarwal et al. included a single-LTx cohort of 180 PAH patients, whereas our study included 344 LTx recipients covering the full range of diseases, this is more appropriate for actual clinical outcomes.

When we adjusted the age and BMI, LVDD is not an independent risk factor for death after LTx. Because LVDD is the precursor and pathophysiological basis of heart failure preserved ejection fraction (HFpEF), it was once a relative contraindication for LTx. If LVDD has no obvious effect on mortality, it will improve the selection of LTx candidates. In the future, we will further study the mediating effect between LVDD and post-LTx mortality.

Moreover, we were surprised to find that N-BNP was also quite good at predicting PGD-3. BNP significantly improved the prediction of tricuspid annulus planar systolic excursion, the presence of PAH, and TRV for PGD-3, according to a study that examined the relationship between parameters related to right heart function and PGD-3 in pediatric TTE. The study also found that maximal BNP values during the year before LTx were a good discriminator for the development of PGD-3 (29). Thus, from a left ventricular perspective, it may be further explored in the future if N-BNP could improve the prognostic power of diastolic function indices in TTE (30).

In summary, our study has strengthened the following key points and innovations: Firstly, this study represents the largest cohort to date examining the relationship between preoperative LVDD and PGD. Secondly, the use of multiple indicators for LVDD diagnosis, combined with clinic condition, enhances result reliability. Thirdly, novel predictors such as N-BNP were analyzed for PGD prediction, highlighting the clinical utility of routine pre-LTx TTE. However, there are still some limitations: Firstly, the inherent limitations of retrospective investigations made it impossible to acquire data on right ventricular function. Secondly, this study reduced selection bias while introducing confounding factors by including patients from all illness categories and surgery kinds. Thirdly, due to variations in the scheduling of postoperative TTE, we were unable to record and contrast the dynamic changes in left ventricular diastolic function before and after LTx.

Conclusions

Preoperative LVDD increases the risk of PGD following LTx, and several diastolic function indices are able to better predict PGD-3 risk. It is helpful to guide the clinical discovery of LVDD high-risk groups and improve cardiac function in time may reduce the occurrence of PGD to some extent. In addition, the results suggest that LVDD is not an independent risk factor for mortality, which provides guidance for the selection criteria of LTx candidates to some extent.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1447/rc

Data Sharing Statement: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1447/dss

Peer Review File: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1447/prf

Funding: This study was supported by the Top Talent Support Program for Young and Middle-aged People of Wuxi Health Committee (No. HB2023025).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1447/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. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The Wuxi People’s Hospital Research Ethics Committee approved this study and waived the informed consent due to the retrospective nature of the study (approval No. KY24155; September 27, 2024).

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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