Quantitative imaging features of pulmonary artery involvement in Takayasu arteritis on computed tomography pulmonary angiography in patients with and without pulmonary hypertension

Introduction

Takayasu arteritis (TA) is a chronic granulomatous vasculitis that preferentially affects the aorta and its major branches in young women, but pulmonary artery involvement (PAI) is increasingly recognized as a clinically important extension of the disease. Autopsy and cross-sectional imaging series indicate that 20–86% of patients with TA show some degree of PAI (1). Hemodynamic loading imposed by pulmonary artery stenosis or occlusion drives right-heart stress, and roughly half of TA-PAI patients ultimately develop pulmonary hypertension (PH) (1-3). Once established, PH portends a markedly worse prognosis: multicenter cohorts demonstrate higher rehospitalization rates, more frequent invasive cardiovascular interventions, and significantly reduced survival compared with TA-PAI patients without PH (4,5).

The clinical recognition of TA-PAI is challenging. Dyspnea, chest discomfort, and nonspecific constitutional symptoms frequently mimic pulmonary infection, tuberculosis, embolism, or idiopathic PH, leading to diagnostic lags of 3–72 months in many series (6-9). Since misclassification at first presentation is common, imaging plays a decisive role in case detection. Multiple imaging modalities—including digital subtraction angiography (DSA), magnetic resonance angiography (MRA), ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) positron emission tomography/computed tomography (PET/CT) and ventilation perfusion scintigraphy—can depict pulmonary vascular involvement (10-12). Computed tomography pulmonary angiography (CTPA), however, uniquely combines non-invasiveness, wide availability, and high spatial resolution to deliver reproducible three-dimensional mapping of the pulmonary arterial tree. Conventional CTPA evaluation relies on qualitative descriptors—luminal narrowing or occlusion, post-stenotic dilatation, aneurysmal change, and concentric wall thickening—that may be subtle, asymmetric, or obscured by motion artefact; moreover, semi-quantitative grading of stenosis is labor-intensive and reader-dependent, contributing to the well-documented diagnostic delay.

Automated post-processing now permits rapid, objective quantification of pulmonary-vascular volume on CT, and such metrics sensitively track vascular remodeling in PH and fibrotic interstitial lung disease (13,14). Whether similar volumetric signatures exist in TA-PAI has not been investigated, and the spatial pattern of pulmonary artery remodeling in TA remains undefined.

Accordingly, we quantified pulmonary arterial volumes (PAVs) across predefined diameter strata in TA-PAI patients versus matched controls. We hypothesized that TA-PAI would exhibit preferential PAV loss in specific arterial segments and that these quantitative signatures would differ according to PH status. Establishing reproducible volumetric benchmarks could shorten the diagnostic interval, standardize disease-burden assessment, and improve longitudinal follow-up in this vulnerable population. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0082/rc).

Methods

Patients

This retrospective study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of Peking Union Medical College Hospital, China (No. I-23PJ2181), and the requirement for individual consent for this retrospective analysis was waived. All patients who underwent CTPA at Peking Union Medical College Hospital between April 2022 and March 2024 were retrospectively screened (Figure 1). The diagnosis of TA was completed according to the modified Ishikawa diagnostic criteria (15). TA-PAI was confirmed on CTPA by characteristic pulmonary lesions including stenosis, occlusion, dilation, or aneurysm. We excluded patients with pulmonary lesions caused by non-TA, such as other types of vasculitis (e.g., Behcet’s disease, antineutrophil cytoplasmic antibody associated-vasculitis, and systemic lupus erythematosus-related vasculitis), chronic thromboembolic PH, and sarcoidosis.

Figure 1 Flowchart of patient selection for the study. CTPA, computed tomography pulmonary angiography; PAI, pulmonary artery involvement; TA, Takayasu arteritis.

Age- and sex-matched controls were identified from the same period among individuals who underwent CTPA but had radiologically normal pulmonary arteries. Controls were excluded for the following reasons: (I) pulmonary nodules (diameter >5 mm); (II) lung diseases including chronic obstructive pulmonary disease, pulmonary emphysema, pulmonary embolism, pulmonary infection, interstitial lung disease, and thoracic tumors; (III) systemic disorders with potential pulmonary involvement (e.g., vasculitis); (IV) PH-related conditions: obstructive sleep apnea-hypopnea syndrome, left heart disease; (V) prior lung resection; and (VI) suboptimal image quality, defined as diaphragmatic domes above the tenth posterior rib, motion artifact, or inadequate contrast enhancement [<250 Hounsfield units (HU) in the main pulmonary artery].

Clinical characteristics

Demographic characteristics (including age, sex, height, and weight) and laboratory parameters were extracted from the electronic medical record via telephone follow-up by one investigator blinded to CTPA results. The disease activity markers for TA the most widely used in clinical are erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) (16). Laboratory tests obtained within 7 days before or after the index CTPA were recorded, including ESR (reference interval: 0–20 mm/h), CRP, IL-6 (reference interval: <5.9 pg/mL), and TNF-α (reference interval: <15.2 pg/mL).

All TA patients underwent echocardiography (ECHO) by certified echocardiologists. Each ECHO result was systematically reviewed by a senior echocardiologist. According to the European Society of Cardiology/European Respiratory Society (ESC/ERS) PH guidelines (1,17), TA-PAI patients were classified as high-probability PH cases if either: (I) peak tricuspid regurgitation velocity (TRV) reached 3.4 m/s (regardless of other ECHO PH signs), or (II) peak TRV measured 2.9–3.4 m/s on the presence of additional pre-specified ECHO variables suggestive of PH. When the peak TRV measured 2.9–3.4 m/s without other ECHO signs of PH, or when the peak TRV was ≤2.8 m/s or not measurable, ECHO suggested a low or intermediate probability of PH. Additional ECHO signs of PH included abnormalities in three categories: pulmonary artery (e.g., pulmonary artery diameter >25 mm), inferior vena cava and right atrium (e.g., right atrial area >18 cm²), and the ventricles (e.g., right ventricle/left ventricle basal diameter ratio >1.0). ECHO signs from at least two different categories above should be present. Missing laboratory or ECHO data were handled by case-wise exclusion.

Image acquisition

Cases underwent CTPA examinations on SOMATOM Force and SOMATOM Definition Flash (Siemens Healthcare, Forchheim, Germany). The scanning parameters were as follows: detector number of 192×0.6 mm (SOMATOM Force) and 128×0.6 mm (SOMATOM Definition Flash), tube voltage of 100 kVp, automatic tube current, rotation time of 0.5 s/circle, acquisition matrix of 512×512, slice thickness of 1.0 mm, and slice spacing of 0.7 mm. Iodinated contrast media (370 mgI/mL) was injected through the elbow median vein at 4 mL/s, with a dose of 40–45 mL, followed by an injection of saline at the same flow rate of 30 mL. Scanning was performed from pulmonary apex to costophrenic angle. A bolus-tracking technique was used with a trigger threshold of 120 HU in pulmonary artery trunk.

Qualitative image analysis

The CTPA images were independently evaluated by two thoracic radiologists (5 and 15 years of respective experience) who were blinded to the clinical data. Any discrepancies in interpretation were resolved through consensus discussion incorporating the clinical data. The assessment covered the main pulmonary artery, left and right pulmonary arteries, lobar pulmonary arteries, segmental arteries, and subsegmental branches. The pulmonary arteries of the patients were evaluated for the presence or absence of any of the following vascular abnormalities: wall thickening (wall thickness > 2 mm), stenosis (>25% reduction in the diameter of the diseased artery compared with the normal pulmonary artery), dilatation (>25% but <50% increase in the diameter of the diseased artery compared with the normal pulmonary artery), aneurysm (>50% increase in the diameter of the diseased artery compared with the normal pulmonary artery), occlusion, and in situ thrombosis (18). The main pulmonary artery diameter was measured in every patient.

Measurement of PAV

Automated PAV extraction was carried out by the AZE Virtual Place workstation (Canon Medical Systems, Tokyo, Japan). The method incorporates the 3D U-Net network augmented with the Vessel-Lumen-Structure Optimization Module detailed by Ming et al. (19,20). The model was trained on 427 fully annotated CT volumes from four vendors (213 CTPA, 214 non-contrast CT) and, on an internal hold-out set, achieved Cl-DICE/Cl-Recall scores of 0.892/0.861 for CTPA and 0.925/0.903 for non-contrast CT. For every study in our cohort, lung-field cropping was first applied, after which the sub-volume was resampled to 0.726×0.726×0.8 mm and voxel intensities were clipped to the 0.5–99.5th percentile before z-score normalization. Segmentation was performed in sliding windows, with Gaussian weighting of overlaps; a C-library routine then removed isolated artefacts (<800 voxels) and re-connected fragmented branches before the mask was mapped back to native space. Two thoracic radiologists (5 and 15 years of respective experience), blinded to clinical data, reviewed every arterial mask and evaluated PAV extraction results using five-point scales across all cases in the study for accuracy and robustness, branch abundance, assistance for diagnosis, and vascular continuity (20). The average score for accuracy and robustness, branch abundance, assistance for diagnosis, and vascular continuity were 4.15, 4.03, 4.27, and 3.93, respectively. Inter-observer agreement was assessed using Cohen’s kappa test and the kappa values of accuracy and robustness, branch abundance, assistance for diagnosis, and vascular continuity were 0.887, 0.755, 0.683, and 0.815, respectively. Manual refinement of the arterial masks was performed when necessary.

The absolute PAVs of six non-overlapping diameter (D) strata (D ≤0.8, 0.8< D ≤1.6, 1.6< D ≤2.4, 2.4< D ≤3.2, 3.2< D ≤4.0, D >4.0 mm) were first measured (Figure 2). Based on these primary measurements, cumulative PAVs below different maximal diameter thresholds (≤0.8, ≤1.6, ≤2.4, ≤3.2, and ≤4.0 mm) as well as the total intraparenchymal PAV were calculated by sequential summation to assess overall PAV alteration. In addition, the proportional distribution of PAV across the non-overlapping diameter strata was calculated as a percentage of total intraparenchymal PAV to determine whether volume changes were disproportionately distributed across specific vessel-size ranges. PAVs were normalized to body surface area, which was calculated using the DuBois formula.

Figure 2 Computed tomography pulmonary arteries across different diameter ranges from Takayasu arteritis patient with pulmonary artery involvement (A) and control individual (B). D, diameter.

Statistical analysis

In this study, the software SPSS 27.0 (IBM Corp., Armonk, NY, USA) was used to perform statistical analysis for variables. The Shapiro-Wilk test was employed to assess whether continuous variables (expressed as mean or median values) followed a normal distribution. Normally distributed continuous variables were compared using independent samples t-tests, whereas non-normally distributed continuous variables were analyzed with the Mann-Whitney U test. Categorical variables were presented as frequencies (percentages), with unordered categorical variables compared using Chi-squared tests or Fisher’s exact tests. Double-sided P values <0.05 were considered indicative of a statistically significant difference.

Results

Demographics

This study ultimately enrolled a total of 90 patients with TA-PAI (TA-PAI group) and 47 individuals in the control group (Table 1). There were no significant differences in sex distribution or age between the two groups. The TA-PAI group included 82 females (91.1%), whereas the control group included 39 females (83.0%) (P=0.159). The median age was 33 years [interquartile range (IQR), 27–43] in the TA-PAI group and 36 (IQR, 30–50) years in the control group (P=0.089). The control group had significantly greater height (cm) [162.0 (IQR,160.0–168.0) vs. 160.0 (IQR, 158.8–165.0) cm, P=0.037] and weight (kg) [65.4 (IQR, 57.0–71.0) vs. 60.0 (IQR, 52.0–65.0) kg, P=0.002] than the TA-PAI group.

Based on ECHO results, 17 and 73 TA-PAI patients were classified into the PH group and non-pulmonary hypertension (NPH) group, respectively (Table 1). Although no significant sex differences were observed between the PH and NPH subgroups, the PH group exhibited a significantly higher median age [43 (IQR, 29–50) years] compared with the NPH group [33 (IQR, 26.5–39.5) years] (P=0.015). Height (cm) did not differ significantly between the PH and NPH groups [160.0 (IQR, 156.5–163.0) vs. 160.0 (IQR, 159.0–166.0) cm, P=0.588]. Weight (kg) also showed no significant difference [59.1±9.5 vs. 60.0 (IQR, 51.5–66.0) kg, P=0.922].

Qualitative imaging and laboratory findings

Laboratory parameters, including ESR, CRP, TNF-α, and IL-6, showed no significant differences between the PH and NPH groups (Table 1).

CTPA revealed that the main pulmonary artery diameter was significantly larger in the PH group (32.3±5.4 mm) compared with the NPH group (26.9±5.3 mm) (P<0.001). Radiological features demonstrated that the PH group had significantly higher rates of pulmonary artery stenosis (88% vs. 63%, P=0.045), dilation (71% vs. 29%, P=0.001), and aneurysm formation (24% vs. 4%, P=0.007) compared with the NPH group (Figure 3). However, no significant differences were observed in pulmonary artery wall thickening, occlusion, or in situ thrombosis between the two subgroups. TRV significantly elevated in the PH group [3.2 (IQR, 3.0–3.3) m/s] compared with the NPH group [2.3 (IQR, 2.2–2.5) m/s] (P<0.001) (Table 1).

Figure 3 Pulmonary arterial manifestations in Takayasu arteritis patients with pulmonary hypertension. (A) Stenosis and wall thickening of the right pulmonary artery (white arrow) in a 24-year-old female patient. (B) Posterior volume-rendered technique image in a 29-year-old female patient showing aneurysmal dilatation of the left upper lobe pulmonary artery with dilatation of its branches (white arrow).

PAV in patients versus controls

Based on the cumulative PAVs obtained by sequential summation of the measured non-overlapping diameter strata, comparative analysis of PAVs (mL) between the TA-PAI and control groups revealed significant reductions in the TA-PAI group for arteries with diameters ≤3.2 mm [52.8 (IQR, 45.8–57.7) vs. 56.6±11.2 mL, P=0.047] and ≤4.0 mm [59.5 (IQR, 52.2–65.0) vs. 63.7±11.6 mL, P=0.028]. No significant differences were observed for arteries ≤1.6, ≤2.4, >4.0 mm, or the total pulmonary artery within the pulmonary parenchyma. Measurements of PAVs for arteries with diameters ≤0.8 mm were also obtained; however, because this size range is close to the lower technical limit of CT-based vessel segmentation, these data were not further interpreted (Table 2).

The proportional distribution of PAVs was calculated for both TA-PAI and control groups according to non-overlapping pulmonary artery diameter categories (D ≤0.8, 0.8< D ≤1.6, 1.6< D ≤2.4, 2.4< D ≤3.2, 3.2< D ≤4.0, D >4.0 mm) as percentages of total PAV within the pulmonary parenchyma (Table 3). Proportional distribution analysis showed that the TA-PAI group had significantly higher contributions from 0.8< D ≤1.6 mm (23.6%±5.7% vs. 20.8%±3.4%, P<0.001) arteries, but lower contributions from 1.6< D ≤2.4 mm (26.1%±5.5% vs. 28.6%±6.3%, P=0.021) and 2.4< D ≤3.2 mm (21.6%±3.5% vs. 23.6%±3.4%, P=0.001) arteries compared with control group. No significant differences were noted for 3.2< D ≤4.0 or D >4.0 mm arteries.

PAV in patients with versus without PH

Comparative evaluation of cumulative PAVs between PH and NPH subgroups within the TA-PAI cohort revealed no statistically significant differences across all arterial diameter categories (≤0.8, ≤1.6, ≤2.4, ≤3.2, ≤4.0, >4.0 mm) or in total intraparenchymal PAV (Table 4).

Discussion

This study demonstrated that TA-PAI patients exhibited significant reductions in PAVs for arteries ≤3.2 and ≤4.0 mm compared with controls. The reductions in PAVs were particularly prominent in pulmonary arteries with diameters ranging from 1.6 to 3.2 mm. TA-PAI patients with PH showed larger main pulmonary artery diameters and higher rates of stenosis, dilation, and aneurysms, but no significant differences in PAV metrics compared with non-PH patients. Significant changes in volume of pulmonary arteries of specific diameters were observed between TA-PAI patients and controls, which could potentially serve as a quantitative imaging biomarker for early detection and disease monitoring.

TA, a large-vessel vasculitis affecting the aorta and its major branches, promotes intimal hyperplasia, adventitial thickening, and intramural neovascularization through granulomatous inflammation and maladaptive immune responses, ultimately compromising vascular integrity and tissue perfusion (21). TA causes vascular dilation and aneurysms as a result of more severe or rapid inflammatory destruction of the arterial wall, causing medial weakening and loss of structural integrity. It also induces stenosis and occlusion through intimal thickening, fibrosis, and thrombus formation in response to chronic inflammation (22). In this study, TA-PAI patients commonly exhibited imaging manifestations including pulmonary arterial wall thickening, stenosis, and occlusion, whereas dilation, aneurysms, and in situ thrombosis were relatively less frequent. In most previous studies, pulmonary arterial stenosis and occlusion were the most common findings, whereas wall thickening, dilation, aneurysms, and in-situ thrombosis were relatively rare (1,5,18,23). In another study, the imaging manifestations of TA-PAI were predominantly stenosis and dilation (3). Even among studies based on the Chinese population, the reported frequencies of different imaging manifestations varied. Earlier research has demonstrated that active disease states were more frequently associated with pulmonary arterial wall thickening, whereas aneurysms tended to be less common in this phase compared with inactive disease (24). Further subgroup analysis in our study revealed that TA-PAI patients in the PH group exhibited a higher prevalence of pulmonary artery stenosis, dilation, and aneurysms compared with the NPH group. This finding is consistent with previous reports indicating a greater incidence of aneurysms in TA-PAI patients with PH than in those without (5). The observed variations in imaging manifestations among TA-PAI patients across studies could potentially be explained by differences in disease status and the proportion of PH cases in study cohorts.

This study measured PAV within the lung parenchyma. Compared with the control group, the TA-PAI group showed a significant reduction in the volumes of pulmonary arteries with diameters ≤3.2 and ≤4.0 mm. This suggests that, in the TA-PAI cohort, volume loss predominantly occurred in relatively large-sized pulmonary arteries.

Further analysis comparing the percentages of PAVs across different diameter segments revealed that TA-PAI patients had significantly lower percentages in the 1.6< D ≤2.4 and 2.4< D ≤3.2 mm ranges but higher percentages in smaller diameters, with no significant difference in larger diameters. This indicates that volume reduction in TA-PAI was most pronounced in pulmonary arteries measuring 1.6–3.2 mm in diameter. Previous studies have reported that the main pulmonary artery lesions mainly included thickening and stenosis; Lobar pulmonary artery lesions mainly included stenosis and occlusion; Occlusion was dominant in segmental pulmonary artery (18), which aligns with our findings. As noted earlier, PAI in TA often presents with insidious and nonspecific clinical features, leading to delayed diagnosis. Quantifying PAV loss may help clinicians to identify vascular abnormalities earlier. The preferential reduction in specific diameter ranges could serve as a potential indicator of TA-PAI. Moreover, converting visual assessments into quantitative measurements may improve follow-up evaluations for TA-PAI patients.

The main pulmonary artery diameter was significantly larger in the PH subgroup compared with the NPH group, which is consistent with the result of previous study (25). No significant differences in PAVs were observed between the NPH and PH subgroups in TA-PAI, whereas visual assessment suggests a higher proportion of pulmonary artery stenosis, dilation, and aneurysms in PH cases. Extensive studies have documented characteristic pulmonary vascular remodeling patterns across various PH subtypes. The majority of studies reported dilation and increased volume of large pulmonary arteries in PH populations; several PH subtypes—including PH secondary to left heart disease, pulmonary arterial hypertension, PH associated with interstitial lung disease, and chronic thromboembolic PH—demonstrate reduction in small vessel volume (13,26-30). Multiple studies have demonstrated correlations between these vascular remodeling patterns and disease severity parameters (26,27,29,30). Previous studies have suggested that TA-PH may exhibit characteristics of both pre-capillary PH, sharing pathophysiological similarities with chronic thromboembolic PH through vascular obstruction and remodeling, as well as post-capillary PH secondary to left ventricular dysfunction from systemic hypertension (2). In our study, the PH cases were predominantly mild (median TRV 3.2 m/s) with small PH sample size (17 cases), which may have contributed to the negative findings. Furthermore, the coexistence of pulmonary artery stenosis, dilation, and aneurysms in the PH group might have resulted in counterbalancing volumetric changes. Future studies could analyze pulmonary vascular changes at the lobar/segmental level in combination with morphological features such as stenosis, occlusion, dilatation, and aneurysm and include larger PH cohorts to further investigate these findings.

This study has several limitations. This was a single-center study with a relatively small sample size. The TA-PAI cohort consisted of patients receiving long-term regular treatment and follow-up, which may represent a selected population with less severe disease manifestations. Notably, the small sample size of PH cases in our cohort, predominantly with mild disease severity, may limit the generalizability of findings related to pulmonary vascular remodeling. Due to the case-control design, case definition partially relied on qualitative imaging findings, which may introduce incorporation bias when imaging-derived quantitative parameters are compared between groups. In addition, diameter-based categorization may compare vessels from different anatomical generations across individuals, which could influence subgroup comparisons; future methodological developments may enable more robust generation- or bifurcation-based analysis. Furthermore, very small peripheral pulmonary arteries—particularly relevant in PH—could not be reliably evaluated on CT. In the present study, PAVs for arteries ≤0.8 mm were not further interpreted, as this range is close to the lower limit of reliable vessel segmentation. Finally, the retrospective design necessitated reliance on ECHO for PH diagnosis rather than the gold standard right heart catheterization, potentially affecting the accuracy of hemodynamic assessments.

Conclusions

This study quantified the PAV reduction on CTPA, and demonstrated that TA-PAI patients exhibited significant reductions of PAV, particularly in specific diameter ranges, compared with controls. PAV might be beneficial for detecting TA.

Acknowledgments

The authors thank all those individuals who have contributed to the preparation of this research study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0082/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0082/dss

Funding: This work was supported by the National High Level Hospital Clinical Research Funding (No. 2022-PUMCH-B-069) and the National Natural Science Foundation of China (No. 82173623).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0082/coif). B.L. and Z.M. are employees of Canon Medical Systems (China). The other 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 and its subsequent amendments. The study was approved by the Institutional Review Board of Peking Union Medical College Hospital, China (No. I-23PJ2181), 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/.

References

1. He Y, Lv N, Dang A, Cheng N. Pulmonary Artery Involvement in Patients with Takayasu Arteritis. J Rheumatol 2020;47:264-72. [Crossref] [PubMed]
2. Jiang X, Zhu YJ, Zhou YP, Peng FH, Wang L, Ma W, et al. Clinical features and survival in Takayasu's arteritis-associated pulmonary hypertension: a nationwide study. Eur Heart J 2021;42:4298-305. [Crossref] [PubMed]
3. Kong X, Ma L, Lv P, Cui X, Chen R, Ji Z, Chen H, Lin J, Jiang L. Involvement of the pulmonary arteries in patients with Takayasu arteritis: a prospective study from a single centre in China. Arthritis Res Ther 2020;22:131. [Crossref] [PubMed]
4. Koster MJ, Warrington KJ, Matteson EL. Morbidity and Mortality of Large-Vessel Vasculitides. Curr Rheumatol Rep 2020;22:86. [Crossref] [PubMed]
5. Huang Z, Gao D, Liu Z, Liu X, Liang Y. Long-term outcomes and prognostic predictors of patients with Takayasu's arteritis along with pulmonary artery involvement. Clin Exp Rheumatol 2022;40:765-71. [Crossref] [PubMed]
6. Karadag B, Kilic H, Duman D, Ongen Z, Vural VA, Yazici H. Takayasu disease with prominent pulmonary artery involvement: confusion with pulmonary disease leading to delayed diagnosis. Mod Rheumatol 2008;18:507-10. [Crossref] [PubMed]
7. Jin SA, Lee JH, Park JH, Oh JK, Kim MS, Park YK, Kim JH, Kang SW, Kim SS. Endovascular treatment in a patient with left main coronary and pulmonary arterial stenoses as an initial manifestation of Takayasu's arteritis. Heart Lung Circ 2015;24:e26-30. [Crossref] [PubMed]
8. Hayashi K, Nagasaki M, Matsunaga N, Hombo Z, Imamura T. Initial pulmonary artery involvement in Takayasu arteritis. Radiology 1986;159:401-3. [Crossref] [PubMed]
9. Yang J, Peng M, Shi J, Zheng W, Yu X. Pulmonary artery involvement in Takayasu's arteritis: diagnosis before pulmonary hypertension. BMC Pulm Med 2019;19:225. [Crossref] [PubMed]
10. Maz M, Chung SA, Abril A, Langford CA, Gorelik M, Guyatt G, et al. 2021 American College of Rheumatology/Vasculitis Foundation Guideline for the Management of Giant Cell Arteritis and Takayasu Arteritis. Arthritis Rheumatol 2021;73:1349-65. [Crossref] [PubMed]
11. Direskeneli H. Clinical assessment in Takayasu's arteritis: major challenges and controversies. Clin Exp Rheumatol 2017;35:189-93.
12. Alibaz-Oner F, Direskeneli H. Update on Takayasu's arteritis. Presse Med 2015;44:e259-65. [Crossref] [PubMed]
13. Shahin Y, Alabed S, Alkhanfar D, Tschirren J, Rothman AMK, Condliffe R, Wild JM, Kiely DG, Swift AJ, Quantitative CT. Evaluation of Small Pulmonary Vessels Has Functional and Prognostic Value in Pulmonary Hypertension. Radiology 2022;305:431-40. [Crossref] [PubMed]
14. John J, Clark AR, Kumar H, et al. Pulmonary vessel volume in idiopathic pulmonary fibrosis compared with healthy controls aged > 50 years. Sci Rep 2023;13:4422. [Crossref] [PubMed]
15. Sharma BK, Jain S, Suri S, Numano F. Diagnostic criteria for Takayasu arteritis. Int J Cardiol 1996;54:S141-7.
16. Tian Y, Li J, Tian X, Zeng X. Using the co-expression network of T cell-activation-related genes to assess the disease activity in Takayasu's arteritis patients. Arthritis Res Ther 2021;23:303. [Crossref] [PubMed]
17. Galiè N, Humbert M, Vachiery JL, Gibbs S, Lang I, Torbicki A, et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). Eur Heart J 2016;37:67-119. [Crossref] [PubMed]
18. Liao H, Zhang N, Pan L, Du J, Liu J, Zheng Y. Predictors for pulmonary artery involvement in Takayasu arteritis and its cluster analysis. Arthritis Res Ther 2023;25:9. [Crossref] [PubMed]
19. Ming Y, Zhang Y, Xiao R, Zhao R, Wang J, Piao S, Song L, Xu Y, Sui X, Song W. Automated 3D Quantitative Analysis of Intrapulmonary Vessel Volume on Noncontrast CT in Healthy Individuals. Curr Med Imaging 2025;21:e15734056354924. [Crossref] [PubMed]
20. Ming Y, Luo S, Zhao L, Zhao R, Li B, Xu Q, Song W. High Accuracy Pulmonary Vessel Segmentation for Contrast and Non-contrast CT Images and Clinical Evaluation. arXiv:250316988v2 [Preprint] 2025 [cited 2025 May 19]. Available online: https://arxiv.org/abs/2503.16988
21. Pugh D, Karabayas M, Basu N, Cid MC, Goel R, Goodyear CS, Grayson PC, McAdoo SP, Mason JC, Owen C, Weyand CM, Youngstein T, Dhaun N. Large-vessel vasculitis. Nat Rev Dis Primers 2022;7:93. [Crossref] [PubMed]
22. Firouzi A, Khalilipur E, Khajali Z, Pouraliakbar H, Baay M, Abdi A, Panah MK, Zadeh LS, Kiani K, Rezaeian A, Hosseini Z. The Treatment Dilemma of Arteriopathy in Takayasu Arteritis- A State-of-the-Art Approach. Curr Probl Cardiol 2023;48:101359. [Crossref] [PubMed]
23. Xi X, Du J, Liu J, Zhu G, Qi G, Pan L. Pulmonary artery involvement in Takayasu arteritis: a retrospective study in Chinese population. Clin Rheumatol 2021;40:635-44. [Crossref] [PubMed]
24. Gong JN, Mao JJ, Kuang TG, Yang SQ, Li JF, Wang JF, Huang Q, Miao R, Guo XJ, Li YD, Yang YH. Analysis of clinical features between active and inactive patients of Takayasu's arteritis with pulmonary arteries involvement. Int J Cardiol 2023;381:88-93. [Crossref] [PubMed]
25. Boerrigter B, Mauritz GJ, Marcus JT, Helderman F, Postmus PE, Westerhof N, Vonk-Noordegraaf A. Progressive dilatation of the main pulmonary artery is a characteristic of pulmonary arterial hypertension and is not related to changes in pressure. Chest 2010;138:1395-401. [Crossref] [PubMed]
26. Xu W, Xi L, Ni Y, Wang J, Yang H, Liu A, Gao Q, Tao X, Huang Q, Liu X, Zhen Y, Xie W, Liu M. Artificial intelligence-driven quantitative analysis of CT morphological differences between chronic thromboembolic pulmonary hypertension and chronic thromboembolic disease. Quant Imaging Med Surg 2025;15:1101-13. [Crossref] [PubMed]
27. Melzig C, Weinheimer O, Egenlauf B, Do TD, Wielpütz MO, Grünig E, Kauczor HU, Heussel CP, Rengier F. Automated volumetry of core and peel intrapulmonary vasculature on computed tomography angiography for non-invasive estimation of hemodynamics in patients with pulmonary hypertension (2022 updated hemodynamic definition). Cardiovasc Diagn Ther 2024;14:1083-95. [Crossref] [PubMed]
28. Hei H, Zhao W, Dong N, Duan X, Shen C, Ding H. Quantitative assessment of pulmonary blood flow redistribution in the classification of group 1 and group 4 pulmonary hypertension. Quant Imaging Med Surg 2024;14:8658-71. [Crossref] [PubMed]
29. Zhao W, Guo J, Dong N, Hei H, Duan X, Shen C. Diagnostic value of 3D volume measurement of central pulmonary artery based on CTPA images in the pulmonary hypertension. BMC Med Imaging 2023;23:211. [Crossref] [PubMed]
30. Alkhanfar D, Shahin Y, Alandejani F, Dwivedi K, Alabed S, Johns C, Lawrie A, Thompson AAR, Rothman AMK, Tschirren J, Uthoff JM, Hoffman E, Condliffe R, Wild JM, Kiely DG, Swift AJ. Severe pulmonary hypertension associated with lung disease is characterised by a loss of small pulmonary vessels on quantitative computed tomography. ERJ Open Res 2022;8:00503-2021. [Crossref] [PubMed]