Abstract
Background
A surgical-side pulmonary artery diameter (ssPAD) ≥23 mm has been linked to postoperative complications after lobectomy for non-small cell lung cancer (NSCLC), but its prognostic significance remains unclear. This study evaluated whether ssPAD ≥23 mm serves as an independent prognostic factor and a useful indicator for preoperative risk assessment.
Methods
We retrospectively analyzed 438 patients who underwent lobectomy for NSCLC between 2016 and 2017. Patients were classified by ssPAD: ≥23 mm (n=116) and <23 mm (n=322). Survival outcomes and clinicopathological variables were compared. The prognostic performance of ssPAD was assessed using C-statistics against main pulmonary artery diameter (MPAD) ≥28 mm and pulmonary artery-to-aorta (PA/A) ratio >1.
Results
The ssPAD ≥23 mm group showed lower 5-year recurrence-free survival (RFS; 61% vs. 71%, P=0.047) and overall survival (OS; 69% vs. 81%, P=0.001). Lung cancer-specific mortality (24% vs. 13%, P=0.03) and non-cancer mortality (15% vs. 7.1%, P=0.042) were higher, while adjuvant therapy was less frequent due to dyspnea. In multivariable analysis, ssPAD ≥23 mm remained an independent predictor of OS [hazard ratio (HR) 1.84, 95% confidence interval (CI): 1.22–2.79, P=0.004].
Conclusions
Preoperative ssPAD ≥23 mm may be an independent prognostic marker after lobectomy for NSCLC and a simple computed tomography (CT)-based tool for risk stratification.
Keywords: Surgical-side pulmonary artery diameter (ssPAD), non-small cell lung cancer (NSCLC), pulmonary hypertension (pHTN)
Highlight box.
Key findings
• Preoperative surgical-side pulmonary artery diameter (ssPAD) ≥23 mm was associated with worse overall survival after lung cancer resection.
• ssPAD ≥23 mm remained an independent prognostic factor in multivariable analysis (hazard ratio 1.59, 95% confidence interval: 1.06–2.39).
What is known and what is new?
• Pulmonary artery enlargement has been associated with adverse cardiopulmonary outcomes.
• This study demonstrates the prognostic value of ssPAD in resected non-small cell lung cancer.
What is the implication, and what should change now?
• ssPAD can be easily measured on routine preoperative computed tomography.
• ssPAD may aid preoperative risk stratification in patients undergoing lung cancer resection.
Introduction
Pulmonary hypertension (pHTN) is a known risk factor for postoperative respiratory failure, arrhythmia, and congestive heart failure in non-cardiac surgery (1-5). Right heart catheterization remains the gold standard for diagnosing pHTN, with elevated systolic pulmonary artery pressure (sPAP) ≥35 mmHg associated with poor prognosis and sPAP ≥45 mmHg linked to increased perioperative mortality (3). In patients with non-small cell lung cancer (NSCLC), both preoperative and postoperative pHTN significantly increases mortality risk (4,6).
The most common causes of pHTN are left heart diseases, such as left ventricular dysfunction and mitral valve disease (7,8). Although right heart catheterization and transesophageal echocardiography are key diagnostic tools, their invasive nature limits their routine preoperative use in lung cancer surgery. Conversely, chest computed tomography (CT) offers a non-invasive alternative for assessing pHTN, with main pulmonary artery diameter (MPAD) ≥28 mm and a pulmonary artery-to-aorta (PA/A) ratio >1 serving as reliable indicators (9,10). Similarly, the surgical-side pulmonary artery diameter (ssPAD) can be easily measured using preoperative chest CT, providing an additional marker for evaluating perioperative risk (11).
Previous studies have identified ssPAD ≥23 mm as an independent predictor of severe perioperative complications in patients undergoing lobectomy, with >10% of patients experiencing complications. However, the association between ssPAD and long-term prognosis, including overall survival (OS) and postoperative treatment decisions remains unclear.
To further evaluate this association and determine the prognostic significance of ssPAD, a retrospective study was conducted on 438 patients with NSCLC who underwent lobectomy. The objective was to determine whether ssPAD is an independent prognostic factor and explore its potential role in preoperative risk assessment. We present this article in accordance with the STROBE reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1627/rc).
Methods
Patients
As shown in Figure 1, this retrospective study initially included 466 patients with NSCLC who underwent lobectomy (R0 resection) and were pathologically staged from IA1 to IIIB between January 2016 and December 2017 at the National Cancer Center Hospital East, Japan. Exclusion criteria included patients with multiple synchronous or metachronous cancers (n=23), those who received neoadjuvant therapy (n=3), and those enrolled in clinical trials involving treatment (n=2). Following these exclusions, 438 patients were included in the final analysis.
Figure 1.

Patient selection flowchart. Flowchart illustrating patient inclusion and exclusion criteria, ultimately leading to the final study population analyzed. NSCLC, non-small cell lung cancer; ssPAD, surgical side pulmonary artery diameter; TSCT, thin section computed tomography.
The cutoff value for ssPAD was set at 23 mm, based on previous reports indicating an increased incidence of major postoperative complications when ssPAD exceeds 23 mm (6). Patients were stratified into two groups: ssPAD ≥23 mm (n=116) and ssPAD <23 mm (n=322). This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Institutional Review Board of National Cancer Center (No. 2017-418; date of approval: March 16, 2018), and informed consent was obtained from all participants.
ssPAD evaluation
Plain or contrast-enhanced thin-section CT using the mediastinal window setting was performed within three months before surgery. As shown in Figure 2, the MPAD and aortic diameter were measured at the level of pulmonary artery division. The right and left pulmonary artery diameters were defined as the maximum diameters measured between the point of division and the origin of the first branch of each respective pulmonary artery. All measurements were performed by a single investigator to ensure consistency.
Figure 2.

Pulmonary artery and aortic measurements on chest CT. Measurements of MPAD and aortic diameter obtained at the level of pulmonary artery bifurcation. The right and left pulmonary artery diameters were assessed at their widest points between the bifurcation and first branch origin. Blue arrows indicate MPAD and AoD; red arrows indicate RPAD and LPAD pulmonary artery diameters. AoD, aortic diameter; CT, computed tomography; LPAD, light pulmonary artery diameter; MPAD, main pulmonary artery diameter; RPAD, right pulmonary artery diameter.
Statistical analysis
The data cut-off date was September 30, 2024. Continuous variables were expressed as median and interquartile range and compared using the Mann-Whitney U test. Categorical clinicopathological characteristics were assessed using the Chi-squared test or Fisher’s exact test, as appropriate. Postoperative complications were classified according to the Clavien-Dindo classification system (12).
OS was defined as the duration from surgery to the last follow-up or death from any cause. Recurrence-free survival (RFS) was defined as the duration from surgery to disease recurrence or death. Local recurrence was defined as recurrence involving the surgical margin, ipsilateral/contralateral hilar and mediastinal lymph nodes, ipsilateral lungs, or pleura. Distant recurrence was defined as metastasis to the contralateral lung, distant organs (brain, bone, liver, and adrenal glands), supraclavicular lymph nodes, or pericardium.
OS and RFS were estimated using the Kaplan-Meier method, with group differences assessed using the log-rank test. Propensity score matching (PSM) was applied to adjust for baseline characteristics using a 1:3 nearest-neighbor matching algorithm with a caliper width of 0.2. Covariates included age (≥70 years), sex, body surface area, smoking history, forced expiratory volume in 1 s as a percentage ≤70%, pathological stage, ischemic heart disease, and interstitial pneumonia.
Multivariate analysis of OS was performed using the Cox proportional hazards model to identify independent prognostic factors. The prognostic performance of vascular parameters was evaluated using the concordance index (C-index). Pairwise comparisons of C-index values were performed using the survcomp package. Statistical significance was set at P<0.05. All statistical analyses were conducted using R software (version 4.3.3; The R Foundation for Statistical Computing, Vienna, Austria) and EZR (version 1.55; Saitama Medical Center, Jichi Medical University, Saitama, Japan).
Results
Patient characteristics
A total of 438 patients were included in this analysis, with 116 patients in the ssPAD ≥23 mm group and 322 patients in the ssPAD <23 mm group. The baseline characteristics are summarized in Table 1. Patients in the ssPAD ≥23 mm group were significantly older, with a higher proportion of males and greater body surface area than those in the ssPAD <23 mm group (P<0.05). Body weight and body mass index (BMI) were also higher in this group, indicating a tendency toward larger body size (P<0.05). Additionally, a higher prevalence of smoking history and lower forced expiratory volume in 1 s as a percentage were observed in the ssPAD ≥23 mm group. Among comorbidities, ischemic heart disease was significantly more frequent (P=0.049).
Table 1. Clinicopathological findings in patients.
| Variables | ssPAD ≥23 (n=116) | ssPAD <23 (n=322) | P value |
|---|---|---|---|
| Age (years) | 72 [52–87] | 69 [30–87] | <0.001 |
| Sex, male | 79 [68] | 185 [58] | 0.047 |
| Height (cm) | 163.5 [136.0–183.6] | 160.3 [133.6–181.5] | 0.06 |
| Weight (kg) | 62.4 [31.8–88.8] | 57.7 [30.1–99.7] | <0.001 |
| BMI (kg/m2) | 23.3 [15.0–31.7] | 22.1 [14.4–38.2] | 0.001 |
| Body surface area (m2) | 1.67 [1.16–2.03] | 1.60 [1.07–2.17] | 0.001 |
| PS, 1 or 2 | 10 [9] | 16 [5] | 0.11 |
| Smoking | |||
| Never | 28 [24] | 105 [33] | 0.09 |
| Ever | 88 [75] | 217 [67] | |
| Clinical stage | |||
| I | 81 [70] | 246 [78] | 0.19 |
| II | 26 [22] | 56 [18] | |
| III | 9 [8] | 15 [4] | |
| FEV1.0% | 74.1 [32–97] | 76.5 [34–97] | 0.08 |
| Comorbidities | |||
| Hypertension | 57 [49] | 131 [41] | 0.13 |
| DM | 21 [18] | 53 [17] | 0.67 |
| COPD | 21 [18] | 53 [17] | 0.67 |
| IP | 11 [9] | 19 [6] | 0.20 |
| Ischemic heart disease | 12 [10] | 16 [5] | 0.049 |
| Cerebrovascular disease | 10 [8] | 16 [5] | 0.17 |
| Surgical side | |||
| Right | 81 [69] | 198 [61] | 0.14 |
| Left | 35 [30] | 124 [38] | |
| ssPAD | 25.0 [23.0–30.3] | 20.1 [13.5– 22.9] | <0.001 |
| pT | |||
| 1 | 55 [47] | 205 [64] | 0.009 |
| 2 | 40 [35] | 86 [27] | |
| 3 | 13 [11] | 22 [6] | |
| 4 | 8 [7] | 9 [3] | |
| pN | |||
| 0 | 88 [76] | 260 [80] | 0.02 |
| 1 | 22 [19] | 31 [10] | |
| 2 | 6 [5] | 31 [10] | |
| pStage | |||
| I | 72 [62] | 238 [74] | 0.04 |
| II | 26 [22] | 43 [13] | |
| III | 18 [16] | 41 [13] | |
| Histological type | |||
| Adenocarcinoma | 77 [66] | 242 [75] | 0.09 |
| Squamous cell carcinoma | 26 [22] | 62 [19] | 0.50 |
| Others | 13 [12] | 19 [6] | |
| Vascular invasion | 46 [40] | 101 [31] | 0.14 |
| Lymphatic permeation | 8 [6] | 28 [8] | 0.69 |
| Pleural invasion | 43 [37] | 72 [23] | 0.003 |
| EGFR mutation, yes | 26 [32] | 110 [44] | 0.052 |
Data are presented as median [range] or n [%]. BMI, body mass index; COPD, chronic obstructive pulmonary disease; DM, diabetes mellitus; EGFR, epidermal growth factor receptor; FEV, forced expiratory volume; IP, idiopathic pulmonary fibrosis; PS, performance status; ssPAD, surgical side pulmonary artery diameter.
Significant differences were observed in the pathological T and N descriptors, as well as in overall tumor stage. The ssPAD ≥23 mm group exhibited a lower prevalence of adenocarcinoma, a significantly higher rate of pleural invasion, and less frequent epidermal growth factor receptor gene mutations.
Survival curve analysis
The median follow-up duration for the entire cohort was 72.0 months. Univariate and multivariate analyses are shown in Table 2. In the univariable analysis, age ≥70 years, male sex, BMI, smoking history, interstitial pneumonia, stage III disease, vascular invasion, lymphatic permeation, pleural invasion, and ssPAD ≥23 mm were significantly associated with OS (P=0.001). In the multivariable analysis, age ≥70 years, BMI, interstitial pneumonia, stage III disease, vascular invasion, and ssPAD ≥23 mm remained significant, with ssPAD ≥23 mm identified as an independent poor prognostic factor (P=0.004).
Table 2. Cox proportional hazards model for OS.
| Variables | Reference | Univariable | Multivariable | ||
|---|---|---|---|---|---|
| Hazard ratio (95% CI) | P value | P value | |||
| ≥70 years old | <70 years old | 2.22 (1.48–3.33) | <0.001 | 1.74 (1.12–2.73) | 0.01 |
| Male | Female | 2.43 (1.57–3.75) | <0.001 | 1.73 (1.01–2.94) | 0.045 |
| BMI (per 1 kg/m2 increase) | – | 0.95 (0.90–1.01) | 0.10 | 0.89 (0.83–0.95) | <0.001 |
| Smoking history | Non-smoker | 2.95 (1.73–5.01) | <0.001 | 1.47 (0.77–2.79) | 0.24 |
| IP present | absent | 4.90 (3.00–7.98) | <0.001 | 3.66 (2.17–6.20) | <0.001 |
| FEV1.0% <70% | FEV1.0% ≥70% | 0.92 (0.61–1.37) | 0.68 | 0.63 (0.40–0.97) | 0.04 |
| pStage III | pStage I/II | 3.11 (2.04–4.73) | <0.001 | 2.12 (1.34–3.35) | 0.001 |
| Vascular invasion | No vascular invasion | 3.61 (2.47–5.19) | <0.001 | 1.82 (1.15–2.88) | 0.01 |
| Lymphatic permeation | No lymphatic permeation | 2.29 (1.34–3.90) | 0.002 | 1.69 (0.97–2.94) | 0.06 |
| Pleural invasion | No pleural invasion | 3.46 (2.38–5.02) | <0.001 | 1.70 (1.08–2.70) | 0.02 |
| Adjuvant | No adjuvant therapy | 0.94 (0.61–1.46) | 0.80 | 0.81 (0.50–1.32) | 0.39 |
| ssPAD ≥23 mm | ssPAD <23 mm | 2.21 (1.52–3.23) | <0.001 | 1.84 (1.22–2.79) | 0.004 |
BMI, body mass index; CI, confidence interval; FEV, forced expiratory volume; IP, interstitial pneumonia; OS, overall survival; ssPAD, surgical side pulmonary artery diameter.
Due to significant baseline differences, PSM was performed. Table S1 shows the clinicopathological characteristics post-PSM, with the ssPAD ≥23 mm group consisting of 80 patients, while the ssPAD <23 mm group consisting of 240 patients. Following matching, no significant differences remained between groups.
The 5-year RFS and OS curves post-PSM are shown in Figure 3, respectively. The 5-year RFS rate was 61% [95% confidence interval (CI): 49–70%] in the ssPAD ≥23 mm group and 71% (95% CI: 65–77%) in the ssPAD <23 mm group (P=0.047). The 5-year OS was 69% (95% CI: 57–78%) in the ssPAD ≥23 mm group and 81% (95% CI: 75–85%) in the ssPAD <23 mm group (P=0.001).
Figure 3.

Kaplan-Meier curves for recurrence-free survival (A) and overall survival (B) based on ssPAD groups following propensity score matching. Patients were categorized into two groups: ssPAD ≥23 mm and ssPAD <23 mm.. The ssPAD ≥23 mm group showed significantly poorer recurrence-free survival (P=0.047) and overall survival (P=0.001) than the ssPAD <23 mm group. ssPAD, surgical side pulmonary artery diameter.
Table 3 summarizes the perioperative outcomes, including 30-day complications, adjuvant chemotherapy, recurrence rates, and causes of death. The 30-day complication rate was 27% in the ssPAD ≥23 mm group and 22% in the ssPAD <23 mm group, with no significant difference (P=0.36). For grade ≥2 complications, the rates were 23% and 17%, respectively, with no significant difference (P=0.32). Atrial fibrillation showed a trend toward higher incidence in the ssPAD ≥23 mm group.
Table 3. Perioperative outcomes after propensity score matching.
| Variable | ssPAD ≥23 mm (n=80) | ssPAD <23 mm (n=240) | P value |
|---|---|---|---|
| 30-day complication | |||
| Total | 22 [27] | 53 [22] | 0.36 |
| ≥ Grade 2 | 18 [23] | 41 [17] | 0.32 |
| Atrial fibrillation | 6 [7.5] | 6 [2.5] | 0.08 |
| Adjuvant therapy | 9 [11] | 66 [27] | 0.002 |
| Recurrence | |||
| Total | 21 [26] | 54 [22] | 0.54 |
| Local | 7 [8.8] | 16 [6.7] | 0.62 |
| Distant | 14 [17] | 38 [16] | 0.73 |
| Cause of death | |||
| Lung cancer | 19 [24] | 32 [13] | 0.03 |
| Causes other than lung cancer | 12 [15] | 17 [7.1] | 0.042 |
| Cardiopulmonary disease | 7 [8.8] | 9 [3.8] | 0.13 |
Data are presented as n [%]. ssPAD, surgical side pulmonary artery diameter.
Adjuvant chemotherapy was administered significantly less frequently in the ssPAD ≥23 mm group (11% vs. 27%, P=0.002). Recurrence rates (total, local, and distant) showed no significant differences between groups. However, both cancer-specific and other-cause mortality rates were significantly higher in the ssPAD ≥23 mm group than in the ssPAD <23 mm group. Cancer-specific mortality was 24% vs. 13% (P=0.03), and other-cause mortality was 15% vs. 7.1% (P=0.042). Mortality due to cardiopulmonary complications was 8.8% in the ssPAD ≥23 mm group vs. 3.8% in the ssPAD <23 mm group (P=0.13).
Previous studies have reported that MPAD ≥28 mm and pulmonary artery to aorta ratio (PA/A ratio) >1 are associated with OS in patients with lung cancer (13). Therefore, to evaluate the prognostic performance of the three vascular indicators (MPAD ≥28 mm, PA/A ratio >1, and ssPAD ≥23 mm), the C-index was used for OS assessment. As shown in Table 4, the highest C-index was observed for ssPAD ≥23 mm (0.68), followed by PA/A ratio >1 (0.64) and MPAD ≥28 mm (0.56). Statistically, the C-index for ssPAD ≥23 mm was significantly higher than that for MPAD ≥28 mm (P=0.01), whereas the difference between ssPAD ≥23 mm and PA/A >1 was not statistically significant (P=0.34). Furthermore, ssPAD ≥23 mm demonstrated a higher hazard ratio (HR) compared to the other indicators, suggesting greater clinical utility in predicting poor survival outcomes.
Table 4. Evaluation of risk factors by Harrell’s C-index.
| Predictor | C-index (95% CI) | HR (95% CI) | P value (OS) | P value (vs. ssPAD) |
|---|---|---|---|---|
| ssPAD ≥23 mm | 0.68 (0.60–0.76) | 2.21 (1.52–3.23) | <0.001 | Reference |
| MPAD ≥28 mm | 0.56 (0.47–0.66) | 1.30 (0.89–1.89) | 0.18 | 0.01 |
| PA/A >1 | 0.64 (0.50–0.79) | 1.77 (0.95–3.29) | 0.07 | 0.34 |
CI, confidence interval; HR, hazard ratio; MPAD, main pulmonary artery diameter; OS, overall survival; PA/A, pulmonary artery to aorta ratio; ssPAD, surgical side pulmonary artery diameter.
Discussion
This study is the first to demonstrate that the ssPAD measured on preoperative CT serves as an independent prognostic factor for poor outcomes in patients with NSCLC undergoing lobectomy. Among patients with completely resected stage IA1–IIIB NSCLC, ssPAD ≥23 mm was independently associated with reduced OS. Even after PSM, OS remained significantly lower in the ssPAD ≥23 mm group, confirming its association with poor prognosis. Moreover, ssPAD showed superior prognostic predictive ability compared to conventional pulmonary artery indicators, such as MPAD ≥28 mm and PA/A ratio >1.
Previous studies have suggested that preoperative enlargement of the ssPAD may be associated with an increased risk of perioperative complications. Kneuertz et al. reported that in patients undergoing lobectomy, those with ssPAD ≥23 mm had a major complication rate exceeding 10% and found an association between ssPAD enlargement and major perioperative complications (11). However, in this study, aside from a significantly higher incidence of atrial fibrillation, no significant differences were observed in other perioperative complications. This discrepancy may be attributed to variations in patient background or perioperative management strategies.
One potential explanation for the poor prognosis in the ssPAD ≥23 mm group is the significantly lower rate of adjuvant chemotherapy administration. As shown in Table S2, approximately 40% of patients eligible for adjuvant chemotherapy declined treatment due to their poor general condition, possibly influenced by exertional dyspnea, an early symptom of pHTN. In patients with preexisting pHTN, the development of iatrogenic pHTN following lung resection may further exacerbate respiratory symptoms, potentially making continuation of adjuvant therapy challenging.
Regarding post-recurrence treatment, patients with ssPAD ≥23 mm received fewer interventions and were likely to opt for best supportive care (52% vs. 31%). Notably, none of the patients in this group underwent surgery or radiotherapy after recurrence, suggesting potential barriers to aggressive treatment (Table S3). The post-recurrence mortality rate was significantly higher in the ssPAD ≥23 mm group than in the ssPAD <23 mm group (85% vs. 59%; P<0.05), indicating that impaired performance status and respiratory symptoms may hinder treatment options and contribute to poorer outcomes.
pHTN is closely associated with pulmonary artery enlargement. CT-based indicators such as PA/A >1 and MPAD ≥28 mm have been widely recognized as simple and sensitive markers. A PA/A ratio >1 has been associated with acute exacerbations, cardiac injury, and increased mortality in patients with chronic obstructive pulmonary disease (11,14-16). Similarly, MPAD ≥28 mm has been identified as a poor prognostic factor in patients with NSCLC (13). In this study, ssPAD ≥23 mm outperformed PA/A >1 and MPAD ≥28 mm in prognostic prediction, based on the C-statistic analysis.
Although preoperative ssPAD enlargement has not been previously emphasized, findings suggest that it may serve as a surrogate marker for underlying pHTN, similar to PA/A >1 and MPAD ≥28 mm. Physiological changes following lobectomy may exacerbate pHTN in patients with enlarged preoperative ssPAD, potentially leading to postoperative deterioration. Thus, ssPAD may serve as more than an anatomical marker, potentially reflecting underlying cardiopulmonary vulnerability as well as pHTN. This interpretation is consistent with a recent study demonstrating that pulmonary artery enlargement was associated with increased non-lung cancer-related mortality after lung cancer resection, suggesting that pulmonary artery enlargement may reflect both impaired cardiopulmonary reserve and competing mortality risk (17).
Importantly, preoperative measurement of ssPAD may aid in identifying patients at risk of postoperative complications, those unsuitable for adjuvant therapy, and individuals likely to face challenges in post-recurrence treatment. Given that chest CT is a routine component of lung cancer evaluation (18), incorporating detailed preoperative ssPAD assessment could be a practical and informative enhancement to preoperative workups.
This study has some limitations. Firstly, as a retrospective single-center analysis, the findings may have limited generalizability. Prospective multicenter studies are required for validation. Secondly, right heart catheterization, the gold standard for diagnosing pHTN, was not performed, and transthoracic echocardiography was infrequently used; thus, the correlation between ssPAD and actual pHTN remains uncertain. Thirdly, postoperative ssPAD measurements were not obtained, leaving the relationship between ssPAD and postoperative pHTN unclear. Future prospective studies incorporating detailed cardiopulmonary function assessments are warranted to clarify the clinical significance of ssPAD. Additionally, comparative studies involving sublobar resections may provide further insight into the relationship between lung preservation, ssPAD, and prognosis.
Conclusions
Preoperative ssPAD ≥23 mm was an independent predictor of poor OS in patients with NSCLC undergoing lobectomy. Compared with conventional pulmonary artery parameters, ssPAD demonstrated superior prognostic performance. As a simple CT-based marker, ssPAD may help identify high-risk patients and facilitate individualized perioperative management.
Supplementary
The article’s supplementary files as
Acknowledgments
We thank the clinical staff of the National Cancer Center Hospital East for their valuable support. This paper was presented at the 65th Annual Meeting of the Japan Lung Cancer Society, held in Yokohama, Japan, from November 14–16, 2024.
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. It was approved by the Institutional Review Board of National Cancer Center (No. 2017-418; date of approval: March 16, 2018), and informed consent was obtained from all participants.
Footnotes
Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1627/rc
Funding: None.
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1627/coif). The authors have no conflicts of interest to declare.
Data Sharing Statement
Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1627/dss
References
- 1. Humbert M, Kovacs G, Hoeper MM, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J 2022;43:3618-731.. 10.1093/eurheartj/ehac237 [DOI] [PubMed] [Google Scholar]
- 2. Lai HC, Lai HC, Wang KY, et al. Severe pulmonary hypertension complicates postoperative outcome of non-cardiac surgery. Br J Anaesth 2007;99:184-90.. 10.1093/bja/aem126 [DOI] [PubMed] [Google Scholar]
- 3. Yang X, Wang L, Lin L, et al. Elevated Pulmonary Artery Systolic Pressure is Associated with Poor Survival of Patients with Non-Small Cell Lung Cancer. Cancer Manag Res 2020;12:6363-71.. 10.2147/CMAR.S260857 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Minai OA, Yared JP, Kaw R, et al. Perioperative risk and management in patients with pulmonary hypertension. Chest 2013;144:329-40.. 10.1378/chest.12-1752 [DOI] [PubMed] [Google Scholar]
- 5. Price LC, Martinez G, Brame A, et al. Perioperative management of patients with pulmonary hypertension undergoing non-cardiothoracic, non-obstetric surgery: a systematic review and expert consensus statement. Br J Anaesth 2021;126:774-90.. 10.1016/j.bja.2021.01.005 [DOI] [PubMed] [Google Scholar]
- 6. Nations JA, Lin J, Park AB, et al. Pulmonary Hypertension and Survival among Non-Small Cell Lung Cancer Patients: A Retrospective Cohort Study in the U.S. Military Health System. J Clin Med 2024;13:3217.. 10.3390/jcm13113217 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7. Simonneau G, Gatzoulis MA, Adatia I, et al. Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol 2013;62:D34-41.. 10.1016/j.jacc.2013.10.029 [DOI] [PubMed] [Google Scholar]
- 8. Al-Omary MS, Sugito S, Boyle AJ, et al. Pulmonary Hypertension Due to Left Heart Disease: Diagnosis, Pathophysiology, and Therapy. Hypertension 2020;75:1397-408.. 10.1161/HYPERTENSIONAHA.119.14330 [DOI] [PubMed] [Google Scholar]
- 9. Shen Y, Wan C, Tian P, et al. CT-base pulmonary artery measurement in the detection of pulmonary hypertension: a meta-analysis and systematic review. Medicine (Baltimore) 2014;93:e256.. 10.1097/MD.0000000000000256 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10. Iyer AS, Wells JM, Vishin S, et al. CT scan-measured pulmonary artery to aorta ratio and echocardiography for detecting pulmonary hypertension in severe COPD. Chest 2014;145:824-32.. 10.1378/chest.13-1422 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11. Kneuertz PJ, Yudovich MS, Amadi CC, et al. Pulmonary artery size on computed tomography is associated with major morbidity after pulmonary lobectomy. J Thorac Cardiovasc Surg 2022;163:1521-1529.e2.. 10.1016/j.jtcvs.2021.01.124 [DOI] [PubMed] [Google Scholar]
- 12. Clavien PA, Barkun J, de Oliveira ML, et al. The Clavien-Dindo classification of surgical complications: five-year experience. Ann Surg 2009;250:187-96.. 10.1097/SLA.0b013e3181b13ca2 [DOI] [PubMed] [Google Scholar]
- 13. Eul B, Cekay M, Pullamsetti SS, et al. Noninvasive Surrogate Markers of Pulmonary Hypertension Are Associated with Poor Survival in Patients with Lung Cancer. Am J Respir Crit Care Med 2021;203:1316-9.. 10.1164/rccm.202005-2023LE [DOI] [PubMed] [Google Scholar]
- 14. Wells JM, Washko GR, Han MK, et al. Pulmonary arterial enlargement and acute exacerbations of COPD. N Engl J Med 2012;367:913-21.. 10.1056/NEJMoa1203830 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15. Wells JM, Farris RF, Gosdin TA, et al. Pulmonary artery enlargement and cystic fibrosis pulmonary exacerbations: a cohort study. Lancet Respir Med 2016;4:636-45.. 10.1016/S2213-2600(16)30105-9 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16. Cheng Y, Li L, Tu X, et al. The Main Pulmonary Artery to the Ascending Aorta Diameter Ratio (PA/A) as a Predictor of Worse Outcomes in Hospitalized Patients with AECOPD. Int J Chron Obstruct Pulmon Dis 2022;17:1157-65.. 10.2147/COPD.S357696 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17. Nishikubo M, Kuroda S, Haga N, et al. Pulmonary artery enlargement as a predictor of long-term prognosis in patients with resected early-stage non-small cell lung cancer. JTCVS Open 2025;23:266-75.. 10.1016/j.xjon.2024.11.009 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18. Goldstraw P, Chansky K, Crowley J, et al. The IASLC Lung Cancer Staging Project: Proposals for Revision of the TNM Stage Groupings in the Forthcoming (Eighth) Edition of the TNM Classification for Lung Cancer. J Thorac Oncol 2016;11:39-51.. 10.1016/j.jtho.2015.09.009 [DOI] [PubMed] [Google Scholar]
