Abstract
Background
Bronchial artery embolization (BAE) is an established treatment for hemoptysis in bronchiectasis, yet the risk of post-procedural recurrence remains significant. This study aimed to investigate the clinical and hemodynamic predictors of hemoptysis recurrence in patients with bronchiectasis following BAE.
Methods
We retrospectively analyzed 426 patients with bronchiectasis-related hemoptysis who underwent BAE between 2019 and 2022. Patients were followed for a median of 2 years to monitor recurrence. Baseline clinical data, angiographic findings, and hemodynamic parameters obtained via right heart catheterization were compared between recurrence and non-recurrence groups. Multivariate Cox proportional hazards regression was employed to identify independent risk factors for recurrence.
Results
Among the 426 patients, 113 (26.53%) experienced recurrence during the follow-up period. The recurrence group exhibited more severe imaging findings, including a higher prevalence of multilobar involvement (≥3 lobes: 47.79% vs. 36.10%, P=0.03) and lung destruction (27.43% vs. 14.70%, P=0.003). Angiographically, the recurrence group had significantly more non-bronchial systemic artery (NBSA) branches and total embolized vessels (P<0.001). Hemodynamically, the recurrence group showed significantly higher mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), and total pulmonary resistance (TPR) (all P<0.05). Multivariate Cox regression identified the presence of systemic-to-pulmonary shunts (SPS) [hazard ratio (HR) =2.434; 95% confidence interval (CI): 1.173–5.049; P=0.02] and increased TPR (HR =1.123; 95% CI: 1.014–1.242; P=0.03) as independent predictors of recurrence.
Conclusions
BAE is an effective intervention for hemoptysis in bronchiectasis, but recurrence is common. The presence of SPS and elevated TPR are key independent risk factors for post-BAE recurrence, highlighting the importance of hemodynamic assessment in predicting long-term outcomes.
Keywords: Bronchiectasis, bronchial artery embolization (BAE), recurrence, total pulmonary resistance (TPR), systemic-to-pulmonary shunts (SPS)
Highlight box.
Key findings
• Higher total pulmonary resistance and systemic-to-pulmonary shunts were related to an increased risk of recurrence in patients with bronchiectasis and hemoptysis after bronchial artery embolization (BAE).
What is known and what is new?
• BAE is an effective method for treating bronchiectasis with hemoptysis.
• There were significant differences in hemodynamic parameters and digital subtraction angiography imaging findings between the recurrence and non-recurrence groups.
What is the implication, and what should change now?
• Vigilant monitoring for shunts and close follow-up of patients with high pulmonary vascular resistance (PVR) are crucial for preventing recurrence.
• Further clinical investigation is warranted to determine if reducing pulmonary arterial pressure and PVR through pharmacological or non-pharmacological interventions can effectively lower the hemoptysis recurrence rate.
Introduction
Bronchiectasis is a chronic respiratory disease characterized by irreversible pathological dilation of the airways and progressive structural destruction of the bronchial walls (1). Persistent infection and chronic inflammation within the dilated bronchi trigger tissue remodeling and regional hypoxia. These processes upregulate pro-angiogenic mediators—such as vascular endothelial growth factor (VEGF)—driving the hypertrophy and neovascularization of the bronchial circulation (2). The resulting vessels are typically fragile and prone to rupture under inflammatory or hemodynamic stress, forming the primary anatomical basis for hemoptysis.
Currently, bronchial artery embolization (BAE) has emerged as the first-line intervention for managing clinically significant hemoptysis due to its minimally invasive nature, safety, and repeatability (3,4). Despite achieving high rates of initial hemostasis, recurrent bleeding remains a formidable clinical challenge, with reported recurrence rates reaching approximately 30% (5-8). While repeat BAE is often effective, the high economic burden and mortality associated with massive hemoptysis necessitate a deeper understanding of the factors predisposing patients to recurrence.
Existing literature has largely attributed post-BAE recurrence to technical and anatomical factors, such as the recruitment of non-bronchial systemic arteries (NBSAs) or incomplete initial embolization (9,10). However, the role of pulmonary vascular lesions and systemic-to-pulmonary shunts (SPS)—frequently observed in advanced bronchiectasis—has not been systematically clarified. The formation of SPS creates a high-to-low pressure gradient between the systemic and pulmonary arterial systems, potentially inducing pulmonary hemodynamic alterations. Total pulmonary resistance (TPR), an indirect measure of pulmonary vascular resistance (PVR), may reflect these hemodynamic shifts and the extent of vascular remodeling. Nevertheless, robust clinical evidence linking these hemodynamic parameters to BAE outcomes remains limited.
Therefore, this study enrolled a cohort of 426 patients with bronchiectasis-related hemoptysis at The Affiliated Hospital of Jianghan University to (I) assess the clinical efficacy of BAE and (II) specifically investigate the contribution of pulmonary hemodynamic characteristics, such as TPR and SPS, to post-procedural recurrence. By identifying these physiological predictors, we aim to enhance risk stratification and support individualized follow-up strategies for this patient population. We present this article in accordance with the STROBE reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0039/rc).
Methods
Study population and design
This retrospective cohort study was conducted at The Affiliated Hospital of Jianghan University (Wuhan, China). We screened anonymized clinical data of patients with bronchiectasis and hemoptysis who underwent BAE between January 2019 and December 2022. A total of 426 patients were enrolled based on the following inclusion criteria: (I) age ≥18 years; (II) diagnosis of bronchiectasis according to the 2019 British Thoracic Society guidelines (11); and (III) underwent initial BAE for hemoptysis control. Exclusion criteria included: (I) incomplete clinical or imaging data; (II) absence of chest computed tomography angiography (CTA); (III) previously received interventional or surgical treatment for hemoptysis; (IV) lack of qualified sputum or bronchoalveolar lavage fluid (BALF) culture; and (V) inability to tolerate BAE due to severe cardiopulmonary comorbidities. This study was approved by the Institutional Ethics Committee of The Affiliated Hospital of Jianghan University (No. WHISHIRB-G-2024002), and the requirement for informed consent was waived due to its retrospective nature. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.
Data collection and severity assessment
Clinical characteristics, including laboratory findings from peripheral blood samples obtained prior to BAE, were extracted from electronic medical records. All patients underwent high-resolution computed tomography (HRCT) and bronchial artery (BA) CTA before the BAE procedure to evaluate pulmonary infection and identify culprit vessels. During the BAE intervention, concurrent bronchoscopy was performed to collect BALF for microbial metagenomic next-generation sequencing (mNGS) and standard microbiological cultures. For common pathogens (e.g., Pseudomonas aeruginosa, Klebsiella pneumoniae), a single positive culture from BALF or sputum was recorded. For non-tuberculous mycobacteria (NTM), diagnosis was strictly based on the presence of either two positive sputum cultures or a single positive BALF culture, combined with characteristic HRCT findings (e.g., tree-in-bud opacities or bronchiectatic changes), to distinguish true infection from transient colonization. The severity of hemoptysis was categorized by daily blood loss volume: mild (<100 mL), moderate (100–300 mL), and severe (>300 mL) (12).
BAE procedure and hemodynamic measurement
BAE was performed by experienced pulmonologists (10–20 years of experience) using the modified Seldinger technique via femoral access. Culprit vessels (dilatation, tortuosity, hypervascularity, or contrast extravasation) were identified via CTA and confirmed by digital subtraction angiography (DSA) using a 5-F catheter (Cobra, RLG, MIK; Cook, Bloomington, IN, USA) (13). A 1.98-F microcatheter (ASAHI Co., Ltd., Seto, Japan) was super selectively advanced for embolization using polyvinyl alcohol (PVA) particles (300–500 µm; Cook) combined with gelatin sponge particles (560–1,400 µm; Hangzhou Alicon Pharmaceutical Co., Ltd., Hangzhou, China). For patients with suspected pulmonary hypertension, right heart catheterization was performed using a 7-F floating catheter (Edwards, Irvine, CA, USA). Hemodynamic parameters, including central venous pressure (CVP), mean pulmonary arterial pressure (mPAP), right atrial pressure (RAP), right ventricular pressure (RVP), cardiac output (CO), and pulmonary capillary wedge pressure (PCWP), using the thermodilution method. Derived parameters were calculated as follows: cardiac index = CO/body surface area, PVR = (mPAP − PAWP)/CO, TPR = mPAP/CO.
Radiographic assessment
All pre-procedural CTA images were independently reviewed by two senior radiologists (with 10 and 15 years of experience, respectively) who were blinded to the clinical outcomes. While CTA provided initial vascular mapping, the definitive identification and quantification of culprit vessels were established during the DSA procedure.
The presence of SPS was primarily suspected on CTA by observing early pulmonary artery enhancement or filling defects. However, the final diagnosis of SPS was confirmed only when systemic-to-pulmonary communication was directly visualized via DSA, appearing as the opacification of the pulmonary artery following the injection of contrast medium into a systemic artery (14).
The final count of BAs was based on DSA findings, defined as any vessel arising from the aorta or its branches that showed enlargement, tortuosity, or hypervascularity and was successfully catheterized during the procedure.
Lung destruction was assessed on HRCT and defined as irreversible parenchymal damage characterized by extensive pleural adhesions, cavitation, and significant lung volume loss (15).
Follow-up and recurrence
After discharge, patients were followed up by outpatient clinic during 1–3 months and then underwent telephone interview for the first 2 years. The primary endpoint of the study was the recurrence of hemoptysis. The recurrent hemoptysis was defined as the occurrence of hemoptysis requiring medical intervention (e.g., medicine, hospitalization, BAE, or lung resection) or death due to hemoptysis following an initial successful BAE procedure, including mild, moderate, or massive (16). Recurrence-free time was defined as the duration between the date of hemostasis during this hospitalization to the date of recurrence or the date of last follow-up.
Statistical analysis
Data were presented as follows: number (percentage) for categorical variables, mean ± standard deviation (SD) for normally distributed data, and median [interquartile range (IQR)] for skewed distributions. T-test, Chi-squared test, or one-way analysis of variance (ANOVA) were used to compare differences. The incidence of the outcome during the follow-up period was assessed using Kaplan-Meier analysis, and log-rank tests were used to compare survival between groups. Univariate and multivariate Cox regression analysis were performed to identify independent predictors of recurrent hemoptysis post-BAE. Prior to constructing the multivariable model, collinearity among predictor variables was formally assessed. Variance inflation factors (VIFs) were calculated for all continuous and categorical predictors. A VIF threshold of <5 was used to indicate acceptable levels of multicollinearity. The selection of candidate variables was primarily guided by clinical relevance and a thorough review of the existing literature. All selected variables were included simultaneously in the multivariable model to adjust for potential confounding, irrespective of their statistical significance in univariate analyses. This approach ensures that variable selection is grounded in clinical knowledge rather than solely data-driven criteria. All statistical analyses were performed using SPSS (version 24) with two-tailed P<0.05 as statistically significant.
Results
Baseline characteristics and follow-up
During a median follow-up period of 24 months (IQR, 12–34 months), 15 patients (3.52%) were lost to follow-up. Among the remaining 426 patients, 113 (26.53%) experienced recurrent hemoptysis. As shown in Table 1, there were no significant differences between the recurrence and non-recurrence groups regarding age (P=0.73), sex (P=0.37), body mass index (P=0.09), or smoking history (P=0.06).
Table 1. The baseline characteristics of the study population.
| Variables | No recurrence (n=313) | Recurrence (n=113) | P |
|---|---|---|---|
| Age (years) | 61.16±12.35 | 61.61±10.58 | 0.73 |
| Male | 187 (59.74) | 62 (54.87) | 0.37 |
| BMI (kg/m2) | 22.34±3.69 | 21.63±3.70 | 0.09 |
| History of smoking | 86 (27.48) | 21 (18.58) | 0.06 |
| Comorbidities | |||
| Hypertension | 98 (31.31) | 30 (26.55) | 0.34 |
| Coronary artery disease | 24 (7.67) | 10 (8.85) | 0.69 |
| Atrial fibrillation | 12 (3.83) | 5 (4.42) | >0.99 |
| Diabetes | 32 (10.22) | 16 (14.16) | 0.26 |
| Antithrombotic therapy | |||
| Oral anticoagulants | 6 (1.92) | 2 (1.77) | >0.99 |
| Antiplatelet therapy | 22 (7.03) | 6 (5.31) | 0.53 |
| Hemoptysis profile | |||
| Duration of hemoptysis (years) | 7.00 (3.00, 16.00) | 5.00 (3.00, 16.50) | 0.53 |
| 24-h hemoptysis volume (mL) | 50.00 (15.00, 200.00) | 40.00 (10.00, 100.00) | 0.09 |
| Severity of hemoptysis | 0.23 | ||
| Mild (<100 mL/day) | 181 (57.82) | 70 (61.95) | |
| Moderate (100–300 mL/day) | 89 (28.43) | 36 (31.86) | |
| Severe (>300 mL/day) | 43 (13.74) | 7 (6.19) | |
| Imaging and angiographic data | |||
| Destroyed lung | 46 (14.70) | 31 (27.43) | 0.003 |
| Extent of bronchiectasis (number of lobes) | 2.00 (1.00, 3.00) | 2.00 (2.00, 3.00) | 0.02 |
| Number of bronchiectatic lobes ≥3 | 113 (36.10) | 54 (47.79) | 0.03 |
| Pulmonary atelectasis | 104 (33.23) | 42 (37.17) | 0.45 |
| Number of BAs | 2.00 (2.00, 3.00) | 2.00 (2.00, 3.00) | 0.50 |
| Number of NBSAs | 3.50 (2.00, 6.00) | 5.50 (3.00, 9.00) | <0.001 |
| Number of ectopic BAs | 1.00 (1.00, 1.00) | 2.00 (1.00, 2.00) | 0.001 |
| Total number of embolized vessels | 6.00 (4.00, 9.00) | 8.00 (5.00, 12.00) | <0.001 |
| SPS | 203 (64.86) | 97 (85.84) | <0.001 |
| Etiology for bronchiectasis | |||
| Post-infective | 167 (53.35) | 53 (46.90) | 0.24 |
| Idiopathic | 98 (31.31) | 41 (36.28) | 0.33 |
| Tuberculosis | 16 (5.11) | 6 (5.31) | 0.94 |
| NTM | 8 (2.56) | 3 (2.65) | >0.99 |
| ABPA | 3 (0.96) | 1 (0.88) | >0.99 |
| COPD | 15 (4.79) | 5 (4.42) | 0.87 |
| Asthma | 2 (0.64) | 1 (0.88) | >0.99 |
| Other cause | 4 (1.28) | 3 (2.65) | 0.58 |
| Microbial detection | |||
| Pseudomonas aeruginosa | 36 (11.50) | 15 (13.27) | 0.62 |
| Aspergillus | 17 (5.43) | 11 (9.73) | 0.11 |
| NTM | 7 (2.23) | 1 (0.88) | 0.62 |
| Klebsiella pneumoniae | 8 (2.56) | 1 (0.88) | 0.50 |
| Escherichia coli | 2 (0.64) | 1 (0.88) | >0.99 |
| Haemophilus influenzae | 15 (4.79) | 5 (4.42) | 0.87 |
| Laboratory data | |||
| WBC (×109/L) | 7.56±3.00 | 7.18±2.59 | 0.23 |
| CRP (mg/L) | 3.15 (1.13, 15.2) | 5.45 (1.54, 18.94) | 0.08 |
| Length of hospital stay (days) | 8.45±3.10 | 8.98±3.39 | 0.13 |
Data are presented as mean ± SD, n (%), or median (IQR). ABPA, allergic bronchopulmonary aspergillosis; BA, bronchial artery; BMI, body mass index; COPD, chronic obstructive pulmonary disease; CRP, C-reactive protein; IQR, interquartile range; NBSA, non-bronchial systemic artery; NTM, non-tuberculous mycobacteria; SD, standard deviation; SPS, systemic-to-pulmonary shunts; WBC, white blood cell.
Regarding comorbidities and medications, the prevalence of hypertension, coronary artery disease, atrial fibrillation, and diabetes was comparable between groups (all P>0.05). Notably, the use of oral anticoagulants (P>0.99) and antiplatelet therapy (P=0.53) also showed no significant disparity. Furthermore, no statistically significant differences were observed in hemoptysis severity (P=0.23), etiology of bronchiectasis (P>0.05), microbial detection rates (P>0.05), or laboratory data (P>0.05).
Imaging and angiographic findings
Imaging analysis revealed that the recurrence group had a significantly higher number of involved lobes [median: 2 (IQR, 2, 3) vs. 2 (IQR, 1, 3), P=0.02] and a higher prevalence of multilobar involvement (≥3 lobes: 47.79% vs. 36.10%, P=0.03) compared with the non-recurrence group. The incidence of destroyed lung was also significantly higher in patients with recurrence (27.43% vs. 14.70%, P=0.003).
During BAE, the recurrence group demonstrated a greater number of NBSAs (P<0.001), ectopic BAs (P=0.001), and a higher total number of embolized vessels (P<0.001). Crucially, the presence of SPS was significantly more frequent in the recurrence group (85.84% vs. 64.86%, P<0.001; Table 1, Figure 1).
Figure 1.
SPS imaging findings. (A) Pulmonary enhanced CT shows filling defects in the pulmonary arteries (arrow). (B) DSA indicates tortuous, chaotic, and increased BAs in the right lung, with pulmonary artery visualization, indicating the presence. The arrow indicates the SPS. BAs, bronchial arteries; CT, computed tomography; DSA, digital subtraction angiography; SPS, systemic-to-pulmonary shunts.
Hemodynamic profiles
Based on the echocardiographic examinations, all study participants subsequently underwent right heart catheterization. Right heart catheterization results are summarized in Table 2. Compared with the non-recurrence group, patients in the recurrence group exhibited significantly higher mPAP (20.31±6.68 vs. 18.88±5.87 mmHg, P=0.03) and lower CO (5.01±1.21 vs. 5.40±1.23 L/min, P=0.009). Furthermore, both PVR (1.95±1.15 vs. 1.68±0.93 Wood, P=0.046) and TPR (4.42±2.58 vs. 3.58±1.38 Wood, P=0.006) were significantly elevated in the recurrence group.
Table 2. Comparison of hemodynamic characteristics between patients with and without hemoptysis recurrence after BAE.
| Characteristics | No recurrence (n=313) | Recurrence (n=113) | P |
|---|---|---|---|
| mPAP (mmHg) | 18.88±5.87 | 20.31±6.68 | 0.03 |
| CO (L/min) | 5.40±1.23 | 5.01±1.21 | 0.009 |
| Cardiac index (L/min/m2) | 3.28±0.65 | 3.17±0.82 | 0.22 |
| CVP (mmHg) | 6.57±2.89 | 6.26±3.72 | 0.40 |
| RAP (mmHg) | 6.23±3.17 | 6.01±3.82 | 0.55 |
| RVP (mmHg) | 10.99±5.21 | 11.69±5.82 | 0.25 |
| PAWP (mmHg) | 10.35±4.67 | 10.97±4.80 | 0.23 |
| PVR (Wood) | 1.68±0.93 | 1.95±1.15 | 0.046 |
| TPR (Wood) | 3.58±1.38 | 4.42±2.58 | 0.006 |
Data are presented as mean ± SD. BAE, bronchial artery embolization; CO, cardiac output; CVP, superior vena cava pressure; mPAP, mean pulmonary arterial pressure; PAWP, pulmonary artery wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVP, right ventricular pressure; SD, standard deviation; TPR, total pulmonary resistance.
Risk factors for recurrence and survival analysis
Univariate Cox regression identified several risk factors for recurrence, including number of bronchiectatic lobes ≥3, destroyed lung, number of NBSAs, SPS, and TPR (all P<0.05). Multicollinearity assessment confirmed that all variables had a VIF <5, indicating model stability (Table S1). In the multivariate Cox model, only the presence of SPS [hazard ratio (HR) =2.434; 95% confidence interval (CI): 1.173–5.049; P=0.02] and TPR (HR =1.123; 95% CI: 1.014–1.242; P=0.03) remained independent predictors of recurrent hemoptysis (Table 3).
Table 3. Univariate and multivariate Cox regression analysis of risk factors for recurrent hemoptysis after BAE.
| Variables | Univariable analysis | Multivariate analysis† | |||
|---|---|---|---|---|---|
| HR (95% CI) | P value | HR (95% CI) | P value | ||
| Age | 1.003 (0.987, 1.018) | 0.75 | 0.992 (0.973, 1.011) | 0.40 | |
| Male (vs. female) | 1.207 (0.833, 1.749) | 0.32 | 1.096 (0.663, 1.812) | 0.72 | |
| Number of bronchiectatic lobes ≥3 | 1.516 (1.048, 2.193) | 0.03 | 1.056 (0.644, 1.733) | 0.83 | |
| Destroyed lung | 1.806 (1.195, 2.731) | 0.005 | 0.981 (0.542, 1.776) | 0.95 | |
| Number of NBSAs | 1.072 (1.032, 1.113) | <0.001 | 1.041 (0.991, 1.093) | 0.11 | |
| SPS | 2.942 (1.732, 4.995) | <0.001 | 2.434 (1.173, 5.049) | 0.02 | |
| mPAP | 1.026 (0.999, 1.054) | 0.06 | 0.998 (0.953, 1.045) | 0.92 | |
| TPR | 1.141 (1.064, 1.223) | <0.001 | 1.123 (1.014, 1.242) | 0.03 | |
†, all covariates were age, sex, bronchiectasis ≥ 3 lobes, destroyed lung, the number of NBSA, SPS, mPAP, and TPR. Each group adjusted for the other covariates except itself. BAE, bronchial artery embolization; CI, confidence interval; HR, hazard ratio; mPAP, mean pulmonary arterial pressure; NBSA, non-bronchial systemic artery; SPS, systemic-to-pulmonary shunts; TPR, total pulmonary resistance.
Kaplan-Meier survival analysis revealed that the 1-, 2-, and 3-year hemoptysis-free survival rates were 90.50%, 88.50%, and 86.00% for the SPS group, compared with 74.00%, 66.90%, and 62.30% for the non-SPS group, respectively (log-rank P<0.001; Figure 2A). Similarly, patients with TPR <3 Wood had significantly higher 3-year survival rates than those with TPR ≥3 Wood (82.90% vs. 54.10%, log-rank P<0.001; Figure 2B).
Figure 2.
Kaplan-Meier analysis of hemoptysis-free survival. (A) Cumulative hemoptysis-free survival curves for patients in the SPS and non-SPS groups. The 1-, 2-, and 3-year hemoptysis-free survival rates were 90.50%, 88.50%, and 86.00% for the SPS group, compared with 74.00%, 66.90%, and 62.30% for the non-SPS group, respectively (log-rank P<0.001). (B) Cumulative hemoptysis-free survival curves stratified by TPR. The 1-, 2-, and 3-year hemoptysis-free survival rates were 88.00%, 85.20%, and 82.90% for the TPR <3 Wood group, and 68.70%, 60.30%, and 54.10% for the TPR ≥3 Wood group, respectively (log-rank P<0.001). SPS, systemic-to-pulmonary shunts; TPR, total pulmonary resistance.
Discussion
This study demonstrated that the presence of SPS and elevated TPR are independent predictors of recurrent hemoptysis in bronchiectasis patients following BAE. During a median follow-up of 24 months, the recurrence rate was 26.53%, which is consistent with previously reported rates. Notably, the hemoptysis-free survival was significantly lower in patients with SPS or high TPR (TPR ≥3 Wood). These findings emphasize that beyond the successful embolization of culprit vessels, underlying pulmonary hemodynamic status and vascular remodeling play critical roles in long-term outcomes.
The presence of SPS was a robust predictor of recurrence in our cohort (HR =2.434; P=0.02). In bronchiectasis, chronic airway inflammation and hypoxia trigger the proliferation of systemic collateral vessels and the formation of shunts between high-pressure systemic arteries and low-pressure pulmonary arteries (17-19). Although BAE effectively occludes the main culprit vessels, SPS often involves extensive and microscopic collateral networks that are difficult to fully embolize. The persistent high-to-low pressure gradient through these shunts can facilitate the rapid recruitment of new collateral vessels or the reopening of previously embolized pathways, eventually leading to re-bleeding. Our results support the view that SPS represents a more advanced stage of vascular remodeling in bronchiectasis, necessitating more meticulous angiographic evaluation and potentially more aggressive embolization strategies.
Another significant finding is the independent association between elevated TPR and recurrence (HR =1.123; P=0.03). Elevated TPR in our study group was likely a result of chronic parenchymal destruction, hypoxia-induced pulmonary vasoconstriction, and vascular bed obliteration (20-22). Patients in the recurrence group exhibited significantly higher mPAP and TPR compared to those without recurrence. This hemodynamic environment creates a “vicious cycle”: high pulmonary resistance increases the pressure within the pulmonary arterial system, which may impede the healing of the fragile bronchial-pulmonary capillary beds and promote the formation of new systemic collaterals to bypass the high-resistance pulmonary circulation (23-25). The clinical implication is that managing pulmonary hypertension and improving lung function may be as important as the embolization procedure itself in reducing long-term recurrence.
Furthermore, we found that traditional risk factors identified in previous literature (26-31), such as the number of involved lobes and the presence of destroyed lung, were significant in univariate analysis but lost independent predictive value in the multivariate model. This suggests that SPS and TPR may serve as more proximal or integrated markers of the disease’s vascular and hemodynamic severity. While previous studies have emphasized the importance of NBSAs, our data indicate that the physiological impact of these vessels (manifested as SPS and altered TPR) is the primary driver of recurrence.
There are some limitations in this study. First, the retrospective design may have introduced selection bias. Second, our definition of recurrence was based on events requiring medical intervention, which might have underestimated the incidence of minor, self-limiting bleeding. Finally, the 2-year follow-up period may not capture very late recurrence patterns. Prospective studies with longer follow-up and serial hemodynamic assessments are needed to validate these findings.
Conclusions
In conclusion, BAE is an effective treatment for hemoptysis in bronchiectasis, though recurrence remains common. The presence of SPS and elevated TPR are key independent predictors of recurrence. These findings provide a valuable tool for risk stratification, suggesting that patients with high TPR may benefit from a more comprehensive initial interventional approach and integrated management of their underlying pulmonary hemodynamic status to potentially improve long-term recurrence-free survival.
Supplementary
The article’s supplementary files as
Acknowledgments
We are grateful to all volunteers and staffs who participated in this study.
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 approved by the Institutional Ethics Committee of The Affiliated Hospital of Jianghan University (No. WHISHIRB-G-2024002), and the requirement for informed consent was waived due to its retrospective nature. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.
Footnotes
Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0039/rc
Funding: This work was supported by the Research Project of Wuhan Preventive Medicine Association (No. 2025GWYYFRH31), the National Natural Science Foundation of China (No. 82500066), and the Natural Science Foundation Exploration Plan of Wuhan (No. 2025040601020212).
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0039/coif). The authors have no conflicts of interest to declare.
Data Sharing Statement
Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-1-0039/dss
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