Pulmonary arterial diameter remains dilated despite a reduction of pulmonary arterial pressure post lung transplantation: a retrospective study
Original Article

Pulmonary arterial diameter remains dilated despite a reduction of pulmonary arterial pressure post lung transplantation: a retrospective study

Gil Herzberg1,2, Mordechai R. Kramer1,2, Eviatar Naamany1,2, Moshe Heching1,2, Yuri Peysakhovich2,3, Yaron Barac2,3, Dror Rosengarten1,2, Tzippy Shochat4, Ahuva Grubstein2,5 ORCID logo

1Pulmonary Division Rabin Medical Center - Beilinson Hospital, Petah Tikva, Israel; 2Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv, Israel; 3Department of Thoracic Surgery, Rabin Medical Center - Beilinson Hospital, Petah Tikva, Israel; 4Statistical Service, Rabin Medical Center - Beilinson Hospital, Petah Tikva, Israel; 5Department of Radiology, Rabin Medical Center - Beilinson Hospital, Petah Tikva, Israel

Contributions: (I) Conception and design: G Herzberg, MR Kramer; (II) Administrative support: G Herzberg, MR Kramer, A Grubstein; (III) Provision of study materials or patients: G Herzberg, MR Kramer, E Naamany, Y Peysakhovich, Y Barac; (IV) Collection and assembly of data: G Herzberg, MR Kramer, M Heching, D Rosengarten; (V) Data analysis and interpretation: G Herzberg, MR Kramer, M Heching, D Rosengarten, T Shochat, A Grubstein; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Ahuva Grubstein, MD. Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv, Israel; Department of Radiology, Rabin Medical Center - Beilinson Hospital, Kaplan 1st, Petah Tikva 49100, Israel. Email: Ahuvag@clalit.org.il.

Background: Pulmonary artery (PA) dilatation is a common feature of pulmonary hypertension (PH). While lung transplantation (LTx) leads to significant hemodynamic improvements, the effect on PA diameter remains unclear. This study aims to evaluate changes in PA diameter following LTx in patients with preexisting PH and determine whether structural vascular changes regress alongside pulmonary pressure normalization.

Methods: We retrospectively assessed 18 patients with PH who underwent LTx between 2002 and 2023. Main PA, right PA (RPA), and left PA (LPA) diameters were measured via computed tomography (CT) imaging pre-transplant and annually post-transplant (up to 12 years). Systolic pulmonary arterial pressure (SPAP) was assessed by echocardiography.

Results: Despite a significant reduction in SPAP, PA diameter remained largely unchanged (mean pre-LTx: 29.7 mm; post-LTx: 30.0 mm, P=0.670). The aorta diameter increased slightly (P=0.0027), and the PA-to-aorta (PA/Ao) ratio decreased (from 1.08 to 1.00; P=0.027). RPA and LPA showed no significant dimensional changes. Correlation between PA size and SPAP was weak and not significant both pre- and post-LTx (r=0.087 and 0.388, respectively).

Conclusions: In contrast to some previous reports suggesting vascular remodeling post-LTx, our findings suggest that PA diameter may remain dilated in some PH patients, even after normalization of pulmonary pressures. This could reflect the presence of structural changes that are less responsive to hemodynamic improvements and warrants a careful interpretation of persistent PA dilation on chest CTs following LTx.

Keywords: Lung transplantation (LTx); pulmonary hypertension (PH); computed tomography (CT)

Submitted May 04, 2025. Accepted for publication Sep 23, 2025. Published online Oct 21, 2025.

doi: 10.21037/qims-2025-1052

Introduction

Pulmonary hypertension (PH) leads to progressive remodeling and dilatation of the pulmonary vasculature, particularly the pulmonary artery (PA). The PA-to-aorta (PA/Ao) diameter ratio, as demonstrated on chest computed tomography (CT), is a widely used noninvasive method to quantify PA dilatation and this metric is considered a marker of disease severity (1-5). However, it is unclear whether it regresses following lung transplantation (LTx), which effectively reduces pulmonary pressure (6-8).

Several prior studies suggest that pulmonary vascular and right ventricular remodeling may reverse after LTx (6-9). Based on this, we hypothesized that LTx may reduce PA dilation demonstrated on chest CT in PH patients. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1052/rc).

Methods

Study design and population

This retrospective study included all patients who underwent LTx between 2002 and 2023 for PH, defined as a mean PA pressure (mPAP) ≥25 mmHg until 2022 (10-12), and >20 mmHg thereafter, as measured by right heart catheterization (13,14). The study was approved by the IRB of Rabin Medical Center, campus Beilinson (No. 0059-09-RMC), individual consent for this retrospective analysis was waived. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. Inclusion required the availability of pre- and post-transplant CT imaging and echocardiographic systolic PA pressure (SPAP) data.

Imaging and measurements

PA, aorta, right PA (RPA), and left PA (LPA) diameters were measured from high-resolution CT scans at the level of bifurcation. Measurements were taken pre-transplant and annually post-transplant (Figure 1). The PA/Ao ratio was calculated.

Figure 1 Comparison of mean metrics before and after transplant. This figure displays the mean values of PA diameter, aorta diameter, PA ratio, RPA diameter, and LPA diameter measured before and after LTx. The overlay of these values provides a visual comparison of changes across vascular metrics, highlighting significant reductions in PA ratio and increases in aorta diameter post-transplant, with other measurements showing minimal changes. LPA, left PA; LTx, lung transplantation; PA, pulmonary artery; RPA, right PA.

Right heart catheterization is the standard method for diagnosing PH and was used to establish the diagnosis in most of our patients prior to LTx. In follow-up studies, and for the minority of patients unable to undergo catheterization, SPAP was estimated via transthoracic echocardiography using Doppler-based measurement of tricuspid regurgitation velocity as the sole method for assessing pulmonary pressures. Therefore, SPAP was used as the primary measurement for follow-up evaluation.

Statistical analysis

Continuous variables were analyzed using paired t-tests or Wilcoxon signed-rank tests. Correlations between PA diameter and SPAP were assessed via Pearson correlation and linear regression. A P value <0.05 was considered significant. All analyses were performed using SAS, version 9.0 (SAS Institute, Cary, NC, USA).

Results

A total of 18 patients with a confirmed diagnosis of PH who underwent LTx and had annual follow-up CT and echocardiographic imaging were included in the analysis (Table 1). The majority were women, and the mean age at LTx was 45±17 years. Follow-up duration ranged from 3 to 12 years. Most patients (12/18, 67%) underwent double-LTx, while 4/18 (22%) received a single-lung transplant and 2/18 (11%) underwent combined heart-LTx (these were excluded from PA diameter calculations due to donor-derived PA).

Table 1

Characteristics of the study group

Patient Diagnosis Age at LTx (years) Gender Type of transplantation Follow-up (years) Weight (kg) Height (cm) BMI (kg/m2) SPAP pre-transplant (mmHg) SPAP post-transplant (mmHg) pre mPAP (mmHg) post mPAP (mmHg)/years
1 PH 47 Male Double lung 10 80 183 24 89 20
2 SSc-PH 57 Female Single lung R 12 95 162 36 60 29 45
3 PH 52 Female Double lung 12 57 170 19 39 20 75 28/11 years
4 PH 34 Male Double lung 7 83 185 25 41 20 49
5 SSc-PH 58 Male Double lung 6 78 168 28 43 20 80 30/6 years
6 SSc-PH 68 Male Double lung 6 77 188 22 101 20 22
7 SSc-PH 65 Female Double lung 5 51 158 20 37 20 37
8 PVOD-PH 35 Female Double lung 6 50 158 20 107 20
9 CTD-ILD 65 Female Double lung 5 62 165 23 91 31 95
10 SSc-PH 55 Female Single lung L 3 75 160 29 48 20 31
11 PH 43 Female Double lung 7 61 176 19 93 34 43
12 IPF 32 Male Double lung 3 72 168 25 66 20 59
13 PH 36 Male Heart-lung 12 75 174 25 90 26
14 SSc-PH 52 Female Single lung L 12 66 153 28 60 30
15 SSc-PH 31 Female Double 12 70 167 25 90 22
16 SSc-PH 61 Female Single lung L 12 72 152 31 60 37
17 PH 9 Female Heart-lung 12 19 143 29 60 20
18 PH 12 Female Double 12 112 20

BMI, body mass index; CTD-ILD, connective tissue disease-associated interstitial lung disease; IPF, idiopathic pulmonary fibrosis; L, left; LTx, lung transplantation; mPAP, mean pulmonary artery pressure; PH, pulmonary hypertension; PVOD, pulmonary veno-occlusive disease; R, right; SPAP, systolic pulmonary arterial pressure; SSc, systemic sclerosis.

Systolic PA pressure (SPAP) decreased significantly at 10–12 years post-LTx (Table 2), indicating a notable hemodynamic response.

Table 2

Echocardiographic measurements before and after the LTx

Measurement Before LTx Up to 12 years post LTx P value
SPAP (mmHg) 72.05±25.84 24.05±5.84 0.00000105

Normally distributed continuous variables are presented as mean ± standard deviation. Paired t-tests were used to compare pre- and post-transplant values. LTx, lung transplantation; SPAP, systolic pulmonary arterial pressure.

Vascular measurements showed that the diameter of the main PA remained essentially unchanged, measuring 29.7±6.0 mm pre-transplant versus 30.0±5.1 mm post-transplant (P=0.670). The RPA diameter increased slightly from 24.1±3.9 to 24.4±3.7 mm (P=0.693), while the LPA demonstrated a similar modest increase, from 23.7±4.8 to 24.4±5.1 mm (P=0.874). In contrast, the ascending aortic diameter increased significantly, from 27.8 to 30.1 mm (P=0.002), resulting in a significant reduction in the PA/Ao ratio, from 1.08 to 1.00 (P=0.0276) (Table 3). Of note, in the two patients who underwent heart-LTx, the diameter of the main PA increased by 2–4 mm (from 32 to 36 mm and from 22 to 24 mm, respectively) over a 12-year follow-up period, reflecting the donor-derived PA changes.

Table 3

Radiologic measurements before and after LTx

Measurement Before LTx Up to 12 years post LTx P value
PA diameter (mm) 29.72±6.01 30.00±5.11 0.67
Aorta diameter (mm) 27.83±5.15 30.06±4.12 0.002
PA/Ao ratio 1.08±0.18 1.00±0.14 0.027
Right PA diameter (mm) 24.06±3.93 24.44±3.75 0.693
Left PA diameter (mm) 23.72±4.81 24.44±5.06 0.874

Normally distributed continuous variables are presented as mean ± standard deviation. Paired t-tests were used to compare pre- and post-transplant values. Ao, aorta; LTx, lung transplantation; PA, pulmonary artery.

Weak, non-significant correlations were observed between PA diameter and SPAP both before (r=0.087) and after (r=0.388) LTx. Linear regression analysis demonstrated limited predictive value of PA size for SPAP, with R2 values of 0.008 pre-transplant and 0.150 post-transplant (Figure 2).

Figure 2 Average pulmonary artery diameter and estimated pulmonary artery systolic pressure. PA, pulmonary artery.

Discussion

This study reveals that while pulmonary pressures normalize after LTx, PA dilation persists in our patients after years of follow-up. Several studies (6-8) have reported ventricular improvements post-transplant. Katz et al. provided early evidence that LTx results in immediate decreases in PA pressures and right ventricular size, with normalization of septal geometry (6). Sarashina et al. demonstrated remodeling of the right ventricle (8). Kayawake et al. demonstrated that the main PA diameter significantly decreases within three months post-LTx, decreasing from a mean of 32.4 mm preoperatively to 26.9 mm postoperatively (P<0.001). This is the only study we found that directly and systematically quantifies the main PA diameter changes in these patients’ population (10). The reduction found was followed within three months; the PA diameter in PH patients was similar to those without PH, in a follow-up time of three months. In contrast, we observed the opposite when our patients were followed for a substantially longer period. This finding may indicate a more complex pattern, potentially reflecting changes that occur closer to the time of surgery but do not necessarily persist over the long term. Sakuma et al. reviewed the role of inflammation in the pathogenesis of PH (15), where inflammation is a central driver of pulmonary vascular remodeling. Key mechanisms include infiltration of inflammatory cells into the pulmonary arterial wall and elevated levels of circulating cytokines and chemokines, which correlate with disease severity and progression. These inflammatory processes contribute to endothelial dysfunction, smooth muscle proliferation, and extracellular matrix remodeling, all of which underlie the structural changes, including PA dilation. In the context of patients with PH who have undergone LTx, either the change is permanent or the removal of the diseased pulmonary vasculature through transplantation eliminates chronic inflammation, leading to reversal of vascular remodelling and reduction in main PA diameter. Our long-term follow-up findings (years after LTx) suggest that the PA may demonstrate persistent dilation which may reflect prior structural changes rather than ongoing PH. This, together with LTx as a treatment option for PH patients refractory to maximal medical therapy (15-18), may help explain the observed outcomes. Our findings indicate that PA size is not a reliable surrogate for the current hemodynamic status following LTx. Moreover, the significant decrease in the PA/Ao ratio appears to be driven primarily by changes in the aorta. These observations underscore the importance of interpreting post-transplant imaging within the broader context of both structural and functional parameters.

Major limitations of the study are its retrospective design, which may introduce selection bias, the small cohort size, and the absence of a control group. Additionally, the long follow-up period includes cases treated during earlier eras, when medical management strategies were considered standard but are now outdated. These factors may increase the risk of a Type II error (false negative), potentially limiting the ability to detect significant associations. However, this also represents a strength of the study, as the cohort included patients with severe, treatment-refractory PH, in whom the observed findings were pronounced and consistent despite the limited sample size.

Conclusions

Despite significant improvements in pulmonary hemodynamics post-LTx, PA diameter may remain dilated, which may be attributed to irreversible vascular remodeling. Persistent PA dilation should not be interpreted as indicative of active PH in transplant recipients.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1052/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1052/dss

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1052/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 approved by the IRB of Rabin Medical Center, campus Beilinson (No. 0059-09-RMC), individual consent for this retrospective analysis was waived. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

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: Herzberg G, Kramer MR, Naamany E, Heching M, Peysakhovich Y, Barac Y, Rosengarten D, Shochat T, Grubstein A. Pulmonary arterial diameter remains dilated despite a reduction of pulmonary arterial pressure post lung transplantation: a retrospective study. Quant Imaging Med Surg 2025;15(12):11743-11748. doi: 10.21037/qims-2025-1052

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