Abstract
Background:
Balancing pulmonary and systemic blood flow remains one of the most critical challenges in the management of high-risk neonates with ductal-dependent circulation, particularly in the presence of low birth weight, sepsis, shock, restrictive interatrial communication, or complex congenital cardiac anatomy. Bilateral pulmonary artery banding (biPAB) is frequently employed as an initial stabilizing strategy to control pulmonary overcirculation; however, optimal band tightness remains largely experience-based, and uniform band sizing may be associated with variable physiological responses. This study evaluated whether a physiology-guided, individualized approach to biPAB is associated with more favorable early hemodynamic and perfusion profiles compared with a conventional uniform banding strategy.
Methods:
This retrospective, two-center cohort study included critically ill neonates undergoing emergency bilateral pulmonary artery banding for ductal-dependent systemic and/or coronary circulation. Patients were managed using either a conventional uniform banding technique or a physiology-guided strategy based on body weight–adjusted branch pulmonary artery z-scores targeting an approximate −2 z-score diameter. Early postoperative assessment included serial measurements of systemic arterial pressure, arterial oxygen saturation, end-tidal carbon dioxide (etCO₂), Doppler-derived pulmonary artery flow velocities, and regional cerebral and somatic oxygenation assessed by near-infrared spectroscopy.
Results:
A total of 44 high-risk neonates underwent bilateral pulmonary artery banding (conventional banding, n = 20; physiology-guided banding, n = 24). Both strategies were associated with increases in systemic arterial pressure. Compared with the conventional group, the physiology-guided group demonstrated greater and more consistent reductions in etCO₂, together with higher Doppler-derived pulmonary artery flow velocities. Postoperative arterial oxygen saturation was lower in the physiology-guided group, while differences between arterial oxygen saturation and regional cerebral and somatic oxygenation were smaller. Absolute regional oxygenation values remained stable in both groups. Early postoperative and interstage mortality did not differ between strategies.
Conclusions:
In high-risk neonates with ductal-dependent circulation, a physiology-guided bilateral pulmonary artery banding strategy based on weight-adjusted pulmonary artery z-scores was associated with more predictable modulation of pulmonary blood flow and more consistent early hemodynamic and perfusion profiles, without an observed increase in early or interstage mortality. These findings support the feasibility of integrating individualized, physiology-driven principles and multimodal physiological monitoring into neonatal pulmonary artery banding strategies.
Introduction
The management of high-risk neonates with ductal-dependent systemic and/or coronary circulation represents one of the most complex challenges in contemporary congenital cardiac surgery (1, 2). In these patients, survival depends on achieving a delicate balance between pulmonary and systemic blood flow during a period of profound vulnerability. Even minor perturbations in vascular resistance, ventricular loading conditions, or oxygen delivery may result in rapid clinical deterioration, particularly in neonates with low birth weight, sepsis, shock, restrictive interatrial communication, or complex congenital cardiac anatomy (3–6).
Pulmonary overcirculation is a common and potentially devastating problem in ductal-dependent neonates. Excessive pulmonary blood flow may lead to systemic hypoperfusion, metabolic acidosis, renal dysfunction, and impaired cerebral oxygen delivery, while also increasing the risk of pulmonary edema and respiratory failure (7–10). Conversely, excessive restriction of pulmonary blood flow can result in severe hypoxemia and hemodynamic instability. Achieving an optimal balance is therefore critical but inherently difficult, especially during the early neonatal period when pulmonary vascular resistance is rapidly evolving. These challenges highlight the need for strategies that integrate anatomical planning with real-time physiological feedback rather than relying solely on fixed anatomical targets.
Bilateral pulmonary artery banding (biPAB) has emerged as an important initial stabilizing strategy in critically ill neonates who are poor candidates for immediate definitive surgical repair (7–10). By restricting pulmonary blood flow at the branch pulmonary artery level, biPAB aims to reduce pulmonary overcirculation, improve systemic perfusion pressure, and allow time for physiological recovery, growth, and reassessment of surgical options. This strategy is commonly employed in neonates with hypoplastic left heart syndrome, severe aortic arch hypoplasia, borderline ventricular morphology, and other forms of ductal-dependent physiology (11–15).
Despite its widespread use, biPAB remains a physiologically demanding intervention with a narrow therapeutic window. Optimal band tightness is crucial, yet remains poorly standardized. In many centers, uniform band sizing based on fixed circumferential measurements is applied across a broad spectrum of patient sizes and pulmonary artery dimensions (16, 17). In small neonates, however, millimeter-level differences in band circumference may translate into disproportionately large changes in pulmonary blood flow, resulting in either inadequate restriction or excessive obstruction, as predicted by fundamental flow–radius relationships (18).
The limitations of uniform banding strategies have prompted growing interest in more individualized approaches to pulmonary artery banding. Weight-adjusted pulmonary artery z-scores provide a normalized framework for estimating target vessel dimensions based on patient size, potentially allowing for more reproducible anatomical and hemodynamic effects (19–21). However, anatomical calibration alone may be insufficient, as the physiological consequences of pulmonary blood flow restriction are influenced by dynamic factors including pulmonary vascular resistance, ventricular function, ductal flow patterns, and systemic vascular tone (16, 17).
Recent advances in perioperative physiological monitoring have expanded the clinician's ability to assess pulmonary blood flow and end-organ perfusion in real time. End-tidal carbon dioxide (etCO₂) has been increasingly recognized as a surrogate marker of pulmonary blood flow in the absence of significant ventilation–perfusion mismatch (22–24), while near-infrared spectroscopy (NIRS) provides continuous, noninvasive assessment of regional cerebral and somatic oxygenation (20, 25). Together, these modalities offer complementary insights into the balance between pulmonary and systemic circulation that are not captured by arterial oxygen saturation or blood pressure alone.
Integrating anatomical planning with physiological feedback may therefore offer a more robust framework for optimizing pulmonary artery banding. A physiology-guided approach that incorporates patient-specific pulmonary artery dimensions alongside real-time hemodynamic and perfusion monitoring has the potential to reduce interpatient variability, improve reproducibility, and enhance early postoperative stability (16, 19).
Accordingly, the present study evaluated early hemodynamic and perfusion-related outcomes following bilateral pulmonary artery banding in a cohort of critically ill, high-risk neonates. We compared outcomes following a conventional uniform banding strategy with those of a physiology-guided approach based on body weight–adjusted pulmonary artery z-scores and multimodal physiological monitoring. Specifically, we explored whether an individualized, physiology-guided banding strategy was associated with more predictable modulation of pulmonary blood flow and more consistent early hemodynamic and perfusion profiles, without an apparent compromise in early clinical outcomes.
Patients and methods
Study design and ethical approval
This retrospective, two-center cohort study was conducted in accordance with the principles of the Declaration of Helsinki. Approval was obtained from the institutional review boards of both participating centers prior to data collection. Written informed consent for surgical intervention and for the use of anonymized clinical data for research purposes was obtained from the parents or legal guardians of all patients.
Clinical, operative, and postoperative data were retrospectively extracted from institutional electronic medical records, anesthesia charts, echocardiography reports, and intensive care unit databases. Data collection focused on perioperative physiological parameters, hemodynamic measurements, and early clinical outcomes following bilateral pulmonary artery banding (biPAB).
Patient population and inclusion criteria
Critically ill neonates with ductal-dependent systemic and/or coronary circulation who underwent emergency bilateral pulmonary artery banding between January 2018 and January 2026 were eligible for inclusion. Ductal dependency was defined as reliance on patent ductus arteriosus flow to maintain adequate systemic or coronary perfusion.
Patients were considered high risk if one or more of the following criteria were present: low birth weight (≤2,500 g), preoperative shock requiring vasoactive support, documented sepsis, evidence of end-organ dysfunction (including renal or hepatic impairment), restrictive or intact interatrial communication, or complex congenital cardiac anatomy such as hypoplastic left heart syndrome, critical aortic arch hypoplasia, or borderline ventricular morphology.
Patients requiring extracorporeal membrane oxygenation support or peritoneal dialysis either before or after biPAB were excluded from comparative analysis. This exclusion was intended to reduce confounding from extreme physiological instability and to allow a more homogeneous evaluation of early physiological responses to pulmonary blood flow modulation; however, it may limit generalizability to the most critically unstable neonatal population.
Study groups and banding strategy
Patients were stratified into two groups according to the pulmonary artery banding strategy employed during the study period.
In the conventional banding group, band sizing was determined according to standardized institutional practice using fixed PTFE band diameters. Specifically, a 3.0-mm band was used for neonates weighing ≤3 kg, while a 3.5-mm band was used for those weighing >3 kg, without systematic adjustment based on pulmonary artery dimensions, z-scores, or physiological parameters beyond general intraoperative clinical judgment.
The physiology-guided group underwent individualized banding using branch pulmonary artery z-score targets, with body weight serving as a practical clinical reference during operative planning.
Pulmonary artery z-score estimation was performed using a body surface area (BSA)-based reference system, with BSA calculated according to the Haycock formula. Target branch pulmonary artery diameters corresponding to approximately a −2 z-score were used as an initial anatomical reference. Representative target pulmonary artery diameters and corresponding band circumferences based on weight-derived z-score estimates are presented in Table 1. These target diameters were subsequently translated into estimated band circumferences using the formula C = 2πr.
Table 1
| Weight (g) | Target RPA diameter (mm) | Radius (mm) | Band circumference (mm) | Conventional band diameter (mm) | Conventional circumference (mm) |
|---|---|---|---|---|---|
| 2000 | 2.75 | 1.375 | 8.64 | 3.00 | 9.42 |
| 2250 | 2.80 | 1.40 | 8.80 | 3.00 | 9.42 |
| 2500 | 2.90 | 1.45 | 9.11 | 3.00 | 9.42 |
| 2750 | 3.00 | 1.50 | 9.42 | 3.00 | 9.42 |
| 3000 | 3.10 | 1.55 | 9.73 | 3.00 | 9.42 |
Representative target pulmonary artery diameters and corresponding band circumferences based on weight-derived z-score estimates, compared with conventional band sizing.
Band circumference was calculated using the formula C = 2πr.
Importantly, this anatomical target was not considered absolute. Final band tightening was refined intraoperatively according to physiological responses. End-tidal CO₂ was used as the primary surrogate marker of pulmonary blood flow and served as the principal driver of intraoperative band adjustment, interpreted in conjunction with systemic arterial pressure, near-infrared spectroscopy (NIRS), and Doppler-derived flow characteristics (26, 27). In selected cases, physiological optimization required modest additional tightening beyond the initial −2 z-score target, typically corresponding to approximate z-score values in the range of −2.3 to −2.4.
Actual achieved band diameters or circumferences were not systematically recorded in a standardized manner, and therefore direct quantitative comparison of final band tightness between groups was not possible. Therefore, comparisons between strategies are based on intended anatomical targets and observed physiological responses rather than direct measurements of final band dimensions.
The decision-making algorithm for physiology-guided band adjustment is shown in Figure 1.
Figure 1
The physiology-guided strategy was introduced during the study period by a single surgeon and was progressively adopted as experience with the technique increased. Although the number of physiology-guided cases was initially smaller, both banding strategies were applied during overlapping time intervals rather than representing two distinct eras of practice. The increasing use of the physiology-guided approach therefore reflects a gradual institutional adoption of the technique together with greater integration of multimodal physiological monitoring into intraoperative decision-making. The temporal distribution and progressive adoption of conventional and physiology-guided banding strategies across the study period are illustrated in Figure 2
Figure 2
Surgical technique
All procedures were performed via median sternotomy under general anesthesia. Following systemic heparinization, bilateral pulmonary artery banding was performed without cardiopulmonary bypass (28). Banding was initiated on the right pulmonary artery followed by the left pulmonary artery to allow sequential assessment of hemodynamic and physiological responses.
PTFE material was used for all bands. In the physiology-guided group, band tightening was performed incrementally with continuous assessment of physiological parameters to achieve target hemodynamic goals while avoiding excessive restriction. Band position and adequacy were confirmed visually and by intraoperative assessment (27).
Physiological monitoring and rationale
Continuous invasive arterial blood pressure monitoring was employed in all patients. End-tidal carbon dioxide (etCO₂) monitoring was used as a surrogate marker of pulmonary blood flow, based on the principle that, in the absence of significant ventilation–perfusion mismatch, etCO₂ primarily reflects pulmonary perfusion and cardiac output.
Near-infrared spectroscopy (NIRS) was used to continuously monitor regional cerebral and somatic oxygen saturation throughout the perioperative period. Sensors were positioned according to manufacturer recommendations, and values were recorded continuously. Predefined perioperative time points were selected for analysis to ensure consistency across patients.
Interpretation of NIRS data focused on the relationship between arterial oxygen saturation (SaO₂) and regional tissue oxygenation (rSO₂), rather than on absolute rSO₂ values alone. Differences between SaO₂ and rSO₂ were used as a relative indicator of the balance between systemic oxygen delivery and tissue-level oxygen utilization.
Physiological rationale for the guided strategy
Pulmonary blood flow regulation in ductal-dependent neonates is governed by highly nonlinear physiological relationships. Rapid postnatal changes in pulmonary vascular resistance, combined with immature ventricular compliance and variable ductal flow patterns, render fixed anatomical strategies particularly vulnerable to over- or under-correction.
Weight-adjusted pulmonary artery z-scores were selected as the anatomical framework for individualized band sizing in order to normalize target vessel dimensions across a heterogeneous population. A target of approximately −2 z-score diameter was chosen as a standardized starting point to reduce pulmonary overcirculation while avoiding critical obstruction.
End-tidal carbon dioxide trends were interpreted as dynamic indicators of pulmonary blood flow and assessed in conjunction with systemic arterial pressure and echocardiographic findings to minimize misinterpretation due to transient ventilatory or cardiac output changes. Near-infrared spectroscopy provided complementary information regarding systemic and regional perfusion. A widening SaO₂–rSO₂ gradient was interpreted as a marker of impaired oxygen delivery relative to tissue demand, whereas a narrowing gradient suggested improved coupling between systemic perfusion and end-organ oxygen utilization.
The integration of anatomical planning with multimodal physiological monitoring allowed band adjustments to be guided by both structural targets and functional responses. The conceptual impact of small differences in band circumference on pulmonary blood flow, as illustrated using Poiseuille's law, is presented as a conceptual framework rather than as a predictive physiological model.
Postoperative management and assessment
Postoperative management was standardized across centers and included mechanical ventilation, vasoactive support as required, and continuous physiological monitoring. Serial measurements of systemic arterial pressure, arterial oxygen saturation, etCO₂, and NIRS-derived cerebral and somatic oxygenation were obtained during the early postoperative period.
Echocardiographic assessment was performed to evaluate pulmonary artery band adequacy, with Doppler-derived flow velocities measured across both pulmonary artery bands. Renal function was assessed using serial serum creatinine measurements, particularly in patients with preoperative renal dysfunction.
Outcome measures
Primary outcomes included early hemodynamic and perfusion-related parameters following biPAB, including changes in systemic arterial pressure, etCO₂, pulmonary artery flow velocities, and regional tissue oxygenation. Secondary outcomes included early postoperative mortality, interstage mortality, and progression to subsequent staged palliation or definitive repair.
Statistical analysis
Statistical analyses were performed using IBM SPSS Statistics (IBM Corp., Armonk, NY, USA). Continuous variables were expressed as mean ± standard deviation or median with interquartile range, depending on data distribution. Categorical variables were presented as counts and percentages.
Group comparisons were performed using the independent-samples t-test or Mann–Whitney U-test for continuous variables and the chi-square test or Fisher's exact test for categorical variables, as appropriate. Given the retrospective and exploratory nature of the study, analyses were intended to support descriptive interpretation rather than formal hypothesis testing. No adjustment for multiple comparisons was applied. All statistical tests were two-sided, with a p-value < 0.05 considered indicative of statistical significance.
Results
Patient characteristics
During the study period, 54 neonates underwent emergency bilateral pulmonary artery banding. After exclusion of patients requiring extracorporeal membrane oxygenation support or peritoneal dialysis, 44 high-risk neonates were included in the final analysis. Of these, 20 patients underwent conventional uniform banding, while 24 patients were managed using the physiology-guided banding strategy. The distribution of patients according to banding strategy, ventricular morphology, and clinical outcomes is summarized in Figure 3.
Figure 3
Underlying cardiac diagnoses and anatomical classification of the study population, along with their distribution across the conventional and physiology-guided groups, are summarized in Table 2. The distribution of underlying cardiac anatomy included single-ventricle physiology, double-ventricle physiology, and borderline ventricular morphology (29). Preoperative physiological parameters were broadly comparable between groups; however, the physiology-guided group included a higher proportion of low-birth-weight neonates, reflecting the later adoption of this strategy in smaller and more physiologically fragile patients. Operative time was longer in the physiology-guided group compared with the conventional group [median 56 [52–61] min vs. 46 [41–55] min].
Table 2
| Cardiac diagnosis | Total (n = 44) | Conventional (n = 20) | Physiology-guided (n = 24) |
|---|---|---|---|
| Single ventricle (n = 34) | 34 | 14 | 20 |
| HLHS (n = 28) | 28 | 11 | 17 |
| AA-MA | 16 | 7 | 9 |
| AA-MS | 1 | 1 | 0 |
| AS-MA | 5 | 1 | 4 |
| AS-MS | 4 | 1 | 3 |
| AA with unbalanced CAVCD | 2 | 1 | 1 |
| Single ventricle type large VSD, arch hypoplasia | 2 | 1 | 1 |
| DILV-TGA, arch hypoplasia | 4 | 2 | 2 |
| Double ventricle (n = 8) | 8 | 6 | 2 |
| TGA-VSD, arch hypoplasia | 2 | 2 | 0 |
| CAVCD, arch hypoplasia | 3 | 2 | 1 |
| Bicuspid AV, arch hypoplasia | 3 | 2 | 1 |
| Borderline hypoplastic ventricle (n = 2) | |||
| LV hypoplasia, arch hypoplasia | 2 | 0 | 2 |
Underlying cardiac diagnoses and anatomical classification of neonates undergoing bilateral pulmonary artery banding (n = 44).
AA, aortic atresia; AS, aortic stenosis; AV, aortic valve; BAV, bicuspid aortic valve; CAVCD, complete atrioventricular canal defect; DILV, double inlet left ventricle; HLHS, hypoplastic left heart syndrome; LV, left ventricle; MA, mitral atresia; MS, mitral stenosis; TGA, transposition of the great arteries; VSD, ventricular septal defect.
Values represent the number of patients in each.
Global hemodynamic response to bilateral pulmonary artery banding
Across the entire cohort, bilateral pulmonary artery banding was associated with an increase in systemic arterial pressure. Systolic, diastolic, and mean arterial pressures increased following banding in both groups.
Systemic hemodynamic and physiological parameters before and after bilateral pulmonary artery banding are presented in Table 3, while detailed baseline and early postoperative changes according to banding strategy are summarized in Table 4. No statistically significant between-group differences were observed in baseline arterial blood gas parameters or lactate levels.
Table 3
| Hemodynamic parameters | Pre-biPAB average (after induction of anesthesia) | Early postoperative measurements (day 0 and day 3) | ||||
|---|---|---|---|---|---|---|
| Conventional biPAB group | Physiology-guided biPAB group | p-value | Conventional biPAB group | Physiology-guided biPAB group | p-value | |
| SAP (mmHg) | 46.7 ± 4.7 | 45.2 ± 4.6 | 0.285* | 58.5 ± 6.6 | 60.9 ± 5.7 | 0.188* |
| DAP (mmHg) | 24.6 ± 3.0 | 23.8 ± 2.9 | 0.375* | 34.0 ± 5.9 | 35.5 ± 4.6 | 0.343* |
| MAP (mmHg) | 31.9 ± 3.0 | 31.1 ± 3.1 | 0.405* | 42.0 ± 5.8 | 44.0 ± 4.6 | 0.202* |
| SaO2 (%) | 93.6 ± 1.9 | 93.0 ± 2.3 | 0.386* | 85.1 ± 1.6 | 81.7 ± 1.8 | <0.001* |
| SaO2 – rSO2s (%) | 24.1 ± 3.9 | 24.1 ± 5.9 | 0.987* | 18.2 ± 3.3 | 15.0 ± 5.5 | 0.031* |
| SaO2 – rSO2c (%) | 23.0 ± 3.6 | 22.8 ± 5.7 | 0.910** | 16.0 (15.0–18.0) | 11.5 (10.0–16.0) | 0.005** |
| Creatinine levels (mg/dL) | 0.9 ± 0.6 | 0.9 ± 0.6 | 0.900* | 0.6 (0.4–1.4) | 0.6 (0.4–0.6) | 0.376** |
| Decrease in post-biPAB etCO2 (day 0) (mmHg) | 2.3 ± 0.7 | 3.9 ± 0.8 | <0.001* | |||
| Decrease in post-biPAB etCO2 (day 3) (mmHg) | 4.1 ± 0.9 | 6.2 ± 0.9 | <0.001* | |||
| Flow acceleration in RPA after biPAB (day 3) (m/s) | 2.5 ± 0.3 | 3.2 ± 0.2 | <0.001* | |||
| Flow acceleration in LPA after biPAB (day 3) (m/s) | 2.5 ± 0.2 | 3.0 ± 0.3 | <0.001* | |||
Systemic hemodynamic and physiological parameters before and after bilateral pulmonary artery banding according to banding strategy.
Independent-samples t-test.
Mann–Whitney U-test. Bold indicates significance level at p value < 0.05.
biPAB, bilateral pulmonary artery banding; DAP, diastolic arterial pressure; etCO2, end-tidal carbon dioxide; LPA, left pulmonary artery; MAP, mean arterial pressure; RPA, right pulmonary artery; rSO2s, somatic regional tissue oxygen saturation; rSO2c, cerebral regional tissue oxygen saturation; SAP, systolic arterial pressure; SaO2, oxygen saturation.
Values are presented as mean ± standard deviation or median (interquartile range), as appropriate. p-values represent between-group comparisons at each time point. Day 0 values represent immediate post-banding measurements, whereas day 3 values correspond to postoperative day 3 assessments. Systemic hemodynamic and physiological parameters before and after bilateral pulmonary artery banding according to banding strategy. This table summarizes global hemodynamic changes.
Table 4
| Parameter | Conventional (n = 20) Mean ± SD | Physiology-guided (n = 24) Mean ± SD | p-value |
|---|---|---|---|
| Preoperative (before biPAB) | |||
| Age at biPAB (days) | 9.1 ± 5.6 | 9.3 ± 5.1 | 0.910* |
| Body weight (g) | 2,806.5 ± 303.8 | 2,669.6 ± 407.6 | 0.221* |
| Pre-biPAB Saturation (%) | 93.6 ± 1.8 | 93.0 ± 2.3 | 0.386* |
| pH before biPAB | 7.2 (7.1–7.3) | 7.3 (7.2–7.3) | 0.741** |
| Lactate before biPAB (mmol/L) | 3.3 (2.8–5.6) | 3.4 (2.5–6.4) | 0.906** |
| SAP before biPAB (mmHg) | 46.7 ± 4.7 | 45.2 ± 4.6 | 0.285* |
| DAP before biPAB (mmHg) | 24.5 ± 3.0 | 23.7 ± 2.9 | 0.375* |
| MAP before biPAB (mmHg) | 31.9 ± 2.9 | 31.1 ± 3.1 | 0.405* |
| rSo2s before biPAB (%) | 69.5 ± 2.7 | 68.9 ± 5.1 | 0.646* |
| rSo2c before biPAB (%) | 70.6 (69.0–72.7) | 70.2 (67.2–74.0) | 0.750** |
| Sao2 - rSo2s before biPAB (%) | 24.1 ± 3.9 | 24.1 ± 5.9 | 0.987* |
| Sao2 - rSo2c before biPAB (%) | 23.0 ± 3.6 | 22.8 ± 5.7 | 0.910* |
| Creatinine before biPAB (mg/dL) | 0.9 ± 0.6 | 0.9 ± 0.6 | 0.900* |
| Immediate postoperative (Day 0) | |||
| Post-biPAB saturation (%) | 85.1 ± 1.6 | 81.7 ± 1.8 | <0.001* |
| Decrease in post-biPAB etCO2 (Day 0) (mmHg) | 2.3 ± 0.7 | 3.9 ± 0.8 | <0.001* |
| SAP after biPAB (mmHg) | 58.4 ± 6.5 | 60.9 ± 5.7 | 0.188* |
| DAP after biPAB (mmHg) | 33.9 ± 5.8 | 35.5 ± 4.6 | 0.343* |
| MAP after biPAB (mmHg) | 42.0 ± 5.8 | 44.0 ± 4.6 | 0.202* |
| rSo2s after biPAB (%) | 66.9 ± 2.9 | 67.1 ± 4.4 | 0.880* |
| rSo2c after biPAB (%) | 69.0 (69.0–72.7) | 70.0 (67.2–74.0) | 0.343** |
| Sao2 - rSo2s after biPAB (%) | 18.1 ± 3.3 | 15.0 ± 5.5 | 0.031* |
| Sao2 - rSo2c after biPAB (%) | 16.0 (15.0–18.0) | 11.5 (10.0–16.0) | 0.005** |
| Creatinine after biPAB (mg/dL) | 0.6 (0.4–1.4) | 0.6 (0.4–0.6) | 0.376** |
| Early postoperative (Day 3) | |||
| Decrease in post-biPAB etCO2 (Day 3) (mmHg) | 4.1 ± 0.8 | 6.2 ± 0.9 | <0.001* |
| Flow acceleration in RPA (Day 3) (m/s) | 2.5 ± 0.2 | 3.1 ± 0.2 | <0.001* |
| Flow acceleration in LPA (Day 3) (m/s) | 2.5 ± 0.2 | 3.0 ± 0.3 | <0.001 |
Baseline and early postoperative physiological parameters according to banding strategy.
Independent-samples t-test.
Mann–Whitney U-test. Bold indicates significance level at P value < 0.05.
biPAB, bilateral pulmonary artery banding; DAP, diastolic arterial pressure; etCO₂, end-tidal carbon dioxide; LPA, left pulmonary artery; MAP, mean arterial pressure; RPA, right pulmonary artery; rSO₂c, cerebral regional oxygen saturation; rSO₂s, somatic regional oxygen saturation; SAP, systolic arterial pressure; SaO₂, arterial oxygen saturation.
Values are presented as mean ± standard deviation or median (interquartile range), as appropriate. p-values represent between-group comparisons at each time point.
Pulmonary blood flow modulation
Markers of pulmonary blood flow differed between the two banding strategies. The physiology-guided group demonstrated greater reductions in end-tidal carbon dioxide (etCO₂) immediately following banding and on postoperative day 3 compared with the conventional group. These differences are shown in Figure 4.
Figure 4
Echocardiographic assessment demonstrated higher and more consistent Doppler-derived flow accelerations across patients in the physiology-guided group, indicating reduced inter-patient variability in band-related flow restriction. Flow velocities exceeding 3.0 m/s were more frequently observed in this group, whereas lower and more variable velocities were observed in the conventional banding group. Comparative echocardiographic and physiological parameters between strategies are detailed in Table 4.
Oxygenation and end-organ perfusion
Postoperative arterial oxygen saturation values were lower in the physiology-guided group. Despite this reduction, the differences between arterial oxygen saturation and regional cerebral and somatic oxygenation were smaller in the physiology-guided group.
Absolute cerebral and somatic regional oxygen saturation (rSO₂) values remained stable and comparable between groups throughout the early postoperative period, without evidence of deterioration in regional oxygenation. Regional perfusion trends derived from near-infrared spectroscopy are summarized in Table 4.
Clinical trajectory after biPAB
Following emergency bilateral pulmonary artery banding, patients demonstrated heterogeneous clinical trajectories reflecting underlying anatomy and physiological reserve. Ten patients were ultimately managed toward biventricular repair, while 34 patients followed a single-ventricle palliative pathway.
Individual patient-level characteristics, banding strategies, subsequent surgical trajectory, and clinical outcomes are summarized in Table 5. Early postoperative outcomes, interstage mortality, and subsequent clinical trajectories following bilateral pulmonary artery banding are summarized in Table 6.
Table 5
| PN | Diagnosis | biPAB age (days) | biPAB BW (g) | PDA stent | Banding Strategy | Second surgery | Third surgery | Current status |
|---|---|---|---|---|---|---|---|---|
| 1 | TGA-large VSD | 7 | 2800 | None | Conventional | Jatene | - | Alive |
| 2 | HLHS (MS-AS), AH | 6 | 2600 | None | Physiology-guided | Delayed S1P, Sano | S2P | Awaiting Fontan |
| 3 | HLHS (MA-AA), AH | 4 | 3500 | None | Conventional | Delayed S1P, Sano | S2P | Awaiting Fontan |
| 4 | CAVCD, AH, BAV | 27 | 2300 | None | Conventional | - | - | Deathafter biPAB |
| 5 | HLHS (MA-AS), AH | 3 | 2500 | None | Physiology-guided | Delayed S1P, Sano | - | Awaiting S2P |
| 6 | HLHS (MA-AA) | 6 | 3300 | None | Conventional | Delayed S1P, Sano | - | Awaiting S2P |
| 7 | HLHS (MA-AA) | 7 | 2500 | None | Physiology-guided | Comprehensive S2P | - | Awaiting Fontan |
| 8 | SV type large VSD, AH | 18 | 3100 | None | Physiology-guided | Arch repair, MPA banding | S2P | Awaiting Fontan |
| 9 | HLHS (AA), CAVCD (unbalanced) | 6 | 2600 | None | Conventional | Delayed S1P, MBT | S2P | Awaiting Fontan |
| 10 | HLHS (MS-AS) | 7 | 3100 | None | Physiology-guide | - | - | Death after biPAB |
| 11 | BAV, AH, VSD | 10 | 2900 | None | Conventional | - | - | Death after biPAB |
| 12 | DILV, DTGA, AH | 10 | 3800 | None | Physiology-guided | Arch repair,MPA banding | S1P-BVFe | Fontan |
| 13 | Borderline LVH, AH | 25 | 3000 | None | Physiology-guided | Arch repair, debanding, ASD closure | - | Alive |
| 14 | HLHS (MA-AS) | 12 | 3200 | None | Physiology-guided | - | - | Death after biPAB |
| 15 | HLHS (MA-AA) | 10 | 3000 | None | Conventional | - | - | Death after biPAB |
| 16 | HLHS (MA-AA), aortic interruption | 5 | 2500 | None | Physiology-guided | Delayed S1P, Sano | - | Interstage death |
| 17 | HLHS (MA-AA), AH | 10 | 3000 | Yes | Physiology-guided | Delayed S1P, MBT | Interstage death | |
| 18 | HLHS (MA-AA), AH | 10 | 3200 | Yes | Conventional | Delayed S1P, Sano | S2P | Fontan |
| 19 | HLHS (MA-AA) | 9 | 2800 | None | Conventional | Delayed S1P, Sano | S2P | Fontan |
| 20 | HLHS (MS-AA), AH | 21 | 2300 | None | Conventional | Delayed S1P, MBT | S2P | Fontan |
| 21 | DILV, DTGA, AH, RVH | 17 | 3200 | None | Physiology-guided | Delayed S1P, MBT | S2P | Awaiting Fontan |
| 22 | HLHS (MS-AS) | 12 | 2750 | None | Conventional | Delayed S1P, MBT | S2P | Awaiting Fontan |
| 23 | HLHS (MA-AA), AH | 6 | 2800 | None | Physiology-guided | Delayed S1P, MBT | S2P | Awaiting Fontan |
| 24 | HLHS (MA-AS), AH | 8 | 2600 | None | Physiology-guided | - | - | Death after biPAB |
| 25 | HLHS (MA-AA), AH | 11 | 2500 | None | Physiology-guided | Delayed S1P, Sano | - | Awaiting S2P |
| 26 | DILV, DTGA, AH, RVH | 7 | 2750 | None | Conventional | Delayed S1P, Sano | - | Awaiting S2P |
| 27 | SV type large VSD, AH | 4 | 2800 | None | Conventional | Delayed S1P, MBT | - | Interstage death |
| 28 | CAVCD, AH, BAV | 6 | 2250 | None | Physiology-guided | CAVCD complete correction | - | Alive |
| 2 | HLHS (MA-AA), aortic interruption | 6 | 2500 | None | Physiology-guided | Delayed S1P, Sano | - | Awaiting S2P |
| 30 | HLHS (MA-AA) | 10 | 2650 | None | Physiology-guided | Delayed S1P, Sano | S2P | Awaiting Fontan |
| 31 | DILV, DTGA, AH | 8 | 2750 | None | Conventional | - | - | Death after biPAB |
| 32 | HLHS (MA-AS) | 6 | 2790 | None | Conventional | - | - | Death after biPAB |
| 33 | TGA-large VSD | 11 | 2570 | None | Conventional | - | - | Death after biPAB |
| 34 | Borderline LVH, AH | 12 | 2630 | None | Physiology-guided | Arch repair, debanding, ASD closure | - | Alive |
| 35 | HLHS (MS-AS) | 10 | 2800 | None | Physiology-guided | Delayed S1P, Sano | S2P | Awaiting Fontan |
| 36 | HLHS (AA), CAVCD (unbalanced) | 13 | 2640 | None | Physiology-guided | Delayed S1P, Sano | - | Awaiting S2P |
| 37 | HLHS (MA-AA), AH | 7 | 2900 | None | Conventional | - | - | Death after biPAB |
| 38 | HLHS (MA-AA), aortic interruption | 5 | 3000 | None | Conventional | Delayed S1P, Sano | S2P | Awaiting Fontan |
| 39 | BAV, AH, VSD | 5 | 2700 | None | Conventional | Arch repair, MPA banding | - | Alive |
| 40 | HLHS (MA-AA) | 4 | 2600 | None | Physiology-guided | Delayed S1P, Sano | - | Awaiting S2P |
| 41 | BAV, AH, VSD | 7 | 2200 | None | Physiology-guided | Arch repair, MPA banding | Debanding | Alive |
| 42 | HLHS (MA-AA) | 6 | 2300 | None | Physiology-guided | Delayed S1P, Sano | - | Interstage death |
| 43 | CAVCD, AH, BAV | 8 | 2420 | None | Conventional | - | - | Death after biPAB |
| 44 | HLHS (MA-AS) | 5 | 2100 | None | Physiology-guided | Delayed S1P, MBT | S2P | Awaiting Fontan |
Individual patient characteristics, banding strategy, and subsequent surgical trajectory following bilateral pulmonary artery banding.
AA, aortic atresia; AH, aortic arch hypoplasia; AS, aortic stenosis; ASO, arterial switch operation; BAV, bicuspid aortic valve; biPAB, bilateral pulmonary artery banding; BVFe, bulboventricular foramen enlargement; BVR, biventricular repair; BW, body weight; CAVCD, complete atrioventricular canal defect; DILV, double inlet left ventricle; HLHS, hypoplastic left heart syndrome; LVH, left ventricular hypoplasia; MBT, modified Blalock–Taussig shunt; MPA, main pulmonary artery; PDA, patent ductus arteriosus; RV, right ventricle; S1P, stage I palliation; S2P, stage II palliation; SV, single ventricle; TGA, transposition of the great arteries; VSD, ventricular septal defect.
Table 6
| Outcome and status | Conventional biPAB (n = 20) | Physiology-guided biPAB (n = 24) |
|---|---|---|
| Mortality | ||
| Early postoperative | 5 | 2 |
| Interstage | 4 | 4 |
| Survivors | ||
| Single-ventricle pathway | 9 | 14 |
| Biventricular pathway | 2 | 4 |
| Awaiting next stage | ||
| Awaiting Stage I palliation | 0 | 0 |
| Awaiting Stage II palliation | 2 | 5 |
| Awaiting Stage III palliation | 4 | 8 |
| Completed Stage III palliation | 3 | 1 |
Early postoperative outcomes, interstage mortality, and clinical trajectories following bilateral pulmonary artery banding according to banding strategy.
biPAB, bilateral pulmonary artery banding.
Values represent the number of patients in each category.
Survival and mortality
Following bilateral pulmonary artery banding, 33 of 44 high-risk neonates survived the immediate postoperative period, corresponding to an early survival rate of 75%. During follow-up, additional interstage mortality occurred exclusively within the single-ventricle pathway. At last follow-up, 29 patients remained alive, yielding a cumulative survival rate of 66%.
These survival proportions and patient trajectories across the study cohort are summarized in Figure 3.
Mortality characteristics and non-significant findings
All mortality events occurred in the context of persistent sepsis, multiorgan dysfunction, or advanced physiological compromise at presentation. No deaths were directly attributable to pulmonary artery band–related complications, excessive pulmonary blood flow restriction, band migration, or acute band-related hemodynamic collapse.
No statistically significant between-group differences were observed with respect to age at banding, baseline arterial blood gas parameters, lactate levels, baseline regional oxygenation values, presence of sepsis or shock, genetic syndromes, or overall survival status.
Discussion
The present study suggests that a physiology-guided approach to bilateral pulmonary artery banding (biPAB) in high-risk neonates was associated with more consistent modulation of pulmonary blood flow and more favorable early hemodynamic and perfusion profiles compared with a conventional uniform banding strategy (1, 2, 12). Importantly, these physiological differences were observed without an apparent increase in early postoperative or interstage mortality, despite the inclusion of a higher proportion of low-birth-weight neonates and patients with significant preoperative instability in the physiology-guided group (13, 14).
Physiology-guided banding and pulmonary blood flow control
Effective regulation of pulmonary blood flow represents a central determinant of successful biPAB, particularly in neonates with ductal-dependent circulation, in whom small alterations in band tightness or pulmonary vascular resistance may lead to disproportionate shifts in systemic and pulmonary perfusion (15, 30, 31). In this cohort, physiology-guided banding was associated with greater and more consistent reductions in end-tidal carbon dioxide (etCO₂), together with higher and less variable Doppler-derived pulmonary artery flow velocities, with reduced interpatient variability. When interpreted collectively, these findings suggest a more uniform physiological response to pulmonary blood flow restriction across a heterogeneous population (32–34). Efforts were made to minimize measurement variability using standardized intraoperative marking techniques, thereby improving the practical reproducibility of small adjustments in band circumference.
Uniform band sizing applies similar anatomical constraints across a wide range of body weights and pulmonary artery dimensions. In contrast, weight-adjusted, z-score–guided banding explicitly accounts for interpatient variability (7, 8, 11). Although the present study was not designed to establish causality, the observed consistency of pulmonary flow markers supports the concept that individualized banding strategies may reduce variability in early postoperative physiology, particularly in physiologically fragile neonates (9). Accordingly, the present findings should be interpreted as reflecting differences in physiological response rather than direct quantitative differences in achieved band tightness.
Recent studies have increasingly emphasized the importance of individualized and physiology-guided strategies in neonatal circulatory management, supporting the rationale for tailored approaches to pulmonary blood flow modulation (26–29, 35, 36). The physiology-guided approach may be particularly beneficial in patients with highly labile circulatory physiology, such as those with ductal-dependent systemic or pulmonary circulation, where small changes in pulmonary blood flow may result in disproportionate hemodynamic effects.
Representative target-sizing examples demonstrated that the physiology-guided strategy generally produced smaller target branch pulmonary artery diameters than the conventional 3.0-mm approach in lower-weight neonates, particularly in the 2,000–2,500 g range. This difference became negligible at approximately 2,750 g and slightly reversed at higher weights.
Although these differences are numerically small, they may be physiologically significant. According to Poiseuille's law, flow is proportional to the fourth power of vessel radius. For example, the difference between a circumference of approximately 8.6 mm and 9.4 mm theoretically corresponds to an increase in flow of approximately 50%–60%. These findings highlight how small millimetric differences in band diameter may translate into substantial changes in pulmonary blood flow, as demonstrated in Figure 5.
Figure 5
Interpretation of etCO₂ and multimodal physiological monitoring
The interpretation of etCO₂ as a surrogate marker of pulmonary blood flow warrants particular attention. In mechanically ventilated neonates without significant ventilation–perfusion mismatch, changes in etCO₂ predominantly reflect alterations in pulmonary perfusion and cardiac output (3, 4, 10). The greater reductions in etCO₂ observed in the physiology-guided group are therefore consistent with greater attenuation of pulmonary overcirculation.
Crucially, etCO₂ was not interpreted in isolation but rather integrated with systemic arterial pressure, echocardiographic findings, and regional oxygenation data. This multimodal monitoring framework reduces the risk of misinterpretation and highlights the value of combining anatomical planning with real-time physiological feedback during pulmonary artery banding (5, 6, 37). Such integration is particularly relevant in neonates, in whom small anatomical differences may result in large physiological consequences.
End-organ perfusion and oxygenation balance
Lower postoperative arterial oxygen saturation observed in the physiology-guided group should be interpreted as an expected physiological consequence of effective pulmonary blood flow restriction rather than as an adverse outcome (16). In ductal-dependent neonates, modest reductions in arterial saturation often accompany improved systemic perfusion pressure and redistribution of cardiac output toward systemic circulation (17).
Notably, the physiology-guided group demonstrated smaller differences between arterial oxygen saturation and regional cerebral and somatic oxygenation. This pattern suggests improved coupling between systemic oxygen delivery and tissue-level oxygen utilization (19–21). Importantly, absolute regional oxygenation values remained stable, indicating that this apparent improvement in balance was achieved without compromising cerebral or somatic perfusion.
Clinical implications in low-birth-weight and borderline patients
Low birth weight is a well-established risk factor for adverse outcomes following neonatal cardiac surgery (18, 22). In the present study, the physiology-guided group included a significantly higher proportion of low-birth-weight neonates yet demonstrated comparable or more favorable early physiological profiles. This observation suggests that individualized banding strategies may be especially informative in smaller patients, in whom millimeter-level differences in band circumference can translate into substantial physiological effects (23). This concept is illustrated in Figure 5, which demonstrates how small differences in band diameter may translate into substantial differences in pulmonary blood flow due to the nonlinear relationship between vessel radius and flow.
In addition, biPAB functioned as a valuable bridging strategy in patients with borderline ventricular morphology. By stabilizing hemodynamics and controlling pulmonary blood flow, physiology-guided biPAB allowed time for serial ventricular reassessment and informed decision-making regarding definitive surgical pathways (24, 38, 39). This intentional period of physiological stabilization may help avoid premature commitment to a single-ventricle or biventricular strategy in anatomically and functionally indeterminate patients.
Ductal patency strategy and interstage management
Maintenance of ductal patency represents an integral component of hybrid palliation strategies (40, 41). In the present cohort, continuous prostaglandin E1 infusion was preferentially used, with ductal stenting reserved for cases of prostaglandin-resistant ductal constriction. This approach was guided by concerns that ductal stenting in the presence of severe aortic arch hypoplasia or ductal-dependent coronary circulation may adversely affect retrograde aortic and coronary perfusion (25, 42).
Prolonged prostaglandin therapy provided a stable and predictable means of maintaining ductal patency without introducing additional anatomical variables during a period of marked physiological vulnerability. The low requirement for ductal stenting and absence of prostaglandin-related complications support the feasibility of this strategy in carefully selected patients (43).
Clinical outcomes and surgical trajectory
Early postoperative and interstage mortality did not differ significantly between banding strategies and was primarily associated with persistent sepsis, multiorgan dysfunction, or delayed referral rather than with band-related hemodynamic instability (44). These findings suggest that physiology-guided banding does not compromise clinical safety while offering potential physiological advantages.
Progression through staged palliation or toward biventricular repair was feasible in the majority of surviving patients. Although the present study was not powered to detect differences in long-term outcomes, improved early physiological stability may influence subsequent surgical planning and interstage management (45).
Positioning within the hybrid palliation literature
Hybrid strategies combining bilateral pulmonary artery banding with maintenance of ductal patency have become established alternatives to primary neonatal cardiopulmonary bypass in selected high-risk patients (35, 40, 46). However, substantial heterogeneity exists in reported banding techniques, physiological targets, and outcome measures. Many prior studies emphasize survival or stage progression, with comparatively limited focus on the physiological mechanisms underlying early postoperative stability (36, 47).
By emphasizing physiological and perfusion-related endpoints, the present study contributes mechanistic insight into how pulmonary blood flow modulation influences systemic perfusion in the immediate postoperative period. These findings support the concept that pulmonary artery banding should be viewed as a dynamic, physiology-responsive intervention rather than a fixed anatomical procedure.
Randomized trials comparing banding strategies in critically ill neonates are unlikely to be feasible. Within this constraint, carefully conducted observational studies incorporating detailed physiological characterization remain essential. In this context, the present analysis provides incremental but clinically relevant evidence supporting the integration of individualized, physiology-guided strategies and multimodal monitoring into neonatal pulmonary artery banding.
Limitations
Several limitations of this study should be acknowledged. Because the physiology-guided strategy was progressively adopted during the study period, potential confounding related to operator experience, perioperative learning effects, and temporal improvements in postoperative and interstage management cannot be completely excluded, despite the partial overlap between strategies. In addition, actual achieved band diameters or circumferences were not systematically recorded, precluding direct quantitative comparison of final band tightness between strategies. The retrospective design precludes definitive causal inference and may be subject to selection bias, despite the use of predefined institutional practices guiding banding strategy. The study population was heterogeneous, encompassing a wide spectrum of congenital cardiac anatomies and physiological states, which limited the feasibility of meaningful subgroup analyses. Patients requiring extracorporeal support were excluded, potentially underrepresenting the most critically unstable neonates and limiting generalizability to this subgroup. The sample size was modest, and observed associations between physiological markers should therefore be interpreted as exploratory. In addition, long-term outcomes, including pulmonary artery growth, ventricular remodeling, and neurodevelopmental status, were beyond the scope of this analysis. Accordingly, these findings should be regarded as hypothesis-generating rather than definitive. Survival proportions are reported descriptively and were not derived from formal time-to-event analyses. Pulmonary artery wall thickness was not systematically assessed, as echocardiographic evaluation was primarily focused on luminal diameters. Therefore, band sizing was based on luminal measurements and physiological response rather than vessel wall characteristics.
Future directions
Prospective studies incorporating predefined physiological targets, standardized monitoring protocols, and longer-term follow-up are warranted to further refine pulmonary artery banding strategies in high-risk neonates. In particular, future investigations should aim to evaluate the impact of physiology-guided approaches on pulmonary artery growth, ventricular remodeling, and neurodevelopmental outcomes. The integration of advanced physiological monitoring, imaging-based flow assessment, and computational modeling may further support individualized surgical planning and improve reproducibility in this vulnerable population.
Conclusions
In high-risk neonates with ductal-dependent circulation, a physiology-guided approach to bilateral pulmonary artery banding using weight-adjusted pulmonary artery z-scores was associated with more predictable modulation of pulmonary blood flow and more consistent early hemodynamic and perfusion profiles. These physiological advantages were observed without an apparent increase in early or interstage mortality. Within the limitations of a retrospective design, these findings support the feasibility of incorporating individualized, physiology-driven principles and multimodal physiological monitoring into neonatal pulmonary artery banding strategies. Moreover, biPAB may serve not only as a stabilizing intervention but also as a decision-enabling strategy in critically ill neonates, providing time for physiological recovery and informed surgical planning.
Statements
Data availability statement
The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author.
Ethics statement
The studies involving humans were approved by the Gazi Yaşargil Education and Research Hospital Ethics Committee. The study was conducted in accordance with local legislation and institutional requirements. For the second participating center (Ankara Bilkent City Hospital), institutional permission for data use was obtained based on this ethics approval. Written informed consent for participation in this study was provided by the participants' legal guardians/next of kin. Written informed consent was obtained from the individuals, and minors' legal guardians/next of kin, for the publication of any potentially identifiable images or data included in this article.
Author contributions
Aİ: Formal analysis, Methodology, Validation, Visualization, Writing – original draft, Writing – review & editing. HB: Data curation, Funding acquisition, Project administration, Supervision, Writing – review & editing. YK: Investigation, Project administration, Software, Formal analysis, Supervision, Writing – review & editing. P-SD: Data curation, Formal analysis, Investigation, Project administration, Supervision, Writing – review & editing.
Funding
The author(s) declared that financial support was not received for this work and/or its publication.
Acknowledgments
The authors gratefully acknowledge the contribution of Osman Akdeniz.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Generative AI statement
The author(s) declared that generative AI was not used in the creation of this manuscript.
Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us.
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
References
1.
HeymannMARudolphAMSilvermanNH. Closure of the ductus arteriosus in premature infants by inhibition of prostaglandin synthesis. N Engl J Med. (1976) 295:530–3. 10.1056/NEJM197609022951004
2.
HamrickSEGHansmannG. Patent ductus arteriosus of the preterm infant. Pediatrics. (2010) 125:1020–30. 10.1542/peds.2009-3506
3.
DespondOProulxFCarcilloJALacroixJ. Pediatric sepsis and multiple organ dysfunction syndrome. Curr Opin Pediatr. (2001) 13:247–53. 10.1097/00008480-200106000-00006
4.
GaynorJWMahleWTCohenMIIttenbachRFDeCampliWMStevenJMet alRisk factors for mortality after the Norwood procedure. Eur J Cardiothorac Surg. (2002) 22:82–9. 10.1016/S1010-7940(02)00198-7
5.
StasikCNGoldbergCSBoveELDevaneyEJOhyeRG. Current outcomes and risk factors for the Norwood procedure. J Thorac Cardiovasc Surg. (2006) 131:412–7. 10.1016/j.jtcvs.2005.09.030
6.
BlinderJJGoldsteinSLLeeVVBaycroftAFraserCDNelsonDet alCongenital heart surgery in infants: effects of acute kidney injury on outcomes. J Thorac Cardiovasc Surg. (2012) 143:368–74. 10.1016/j.jtcvs.2011.06.021
7.
BrownJWRuzmetovMOkadaYet alPulmonary artery banding in neonates and infants: current results. Ann Thorac Surg. (2001) 71:1533–9.
8.
VidaVLBachaEA. Pulmonary artery banding revisited. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. (2010) 13:42–7.
9.
RussellRAGhanayemNSMitchellMEWoodsRKTweddellJS. Bilateral pulmonary artery banding as rescue intervention in high-risk neonates. Ann Thorac Surg. (2013) 96:885–90. 10.1016/j.athoracsur.2013.05.049
10.
GuleserianKJBarkerGMSharmaMSMacalusoJHuangRNugentAWet alBilateral pulmonary artery banding for resuscitation in high-risk, single-ventricle neonates and infants. J Thorac Cardiovasc Surg. (2013) 145:206–14. 10.1016/j.jtcvs.2012.09.063
11.
HiranoYSanoSIshinoKet alBilateral pulmonary artery banding as a bridge to biventricular repair. Ann Thorac Surg. (2010) 90:1604–10.
12.
NorwoodWIKirklinJKSandersSP. Hypoplastic left heart syndrome: experience with palliative surgery. Am J Cardiol. (1980) 45:87–91. 10.1016/0002-9149(80)90224-6
13.
NorwoodWILangPCastanedaAR. Experience with operations for hypoplastic left heart syndrome. J Thorac Cardiovasc Surg. (1981) 82:511–9. 10.1016/S0022-5223(19)39288-8
14.
MahleWTSprayTLWernovskyGGaynorJWClarkBJ3rd. Survival after reconstructive surgery for hypoplastic left heart syndrome. Circulation. (2000) 102:III136–41. 10.1161/01.cir.102.suppl_3.iii-136
15.
TweddellJSHoffmanGMMussattoKAFedderlyRTBergerSJaquissRDBet alImproved survival of patients undergoing palliation of hypoplastic left heart syndrome. Circulation. (2002) 106:I82–9. 10.1161/01.cir.0000032878.55215.bd
16.
KitahoriKMurakamiATakaokaTTakamotoSOnoM. Precise evaluation of bilateral pulmonary artery banding for initial palliation in high-risk hypoplastic left heart syndrome. J Thorac Cardiovasc Surg. (2010) 140:1084–91. 10.1016/j.jtcvs.2010.07.084
17.
SchulzASinzobahamvyaNChoMYBöttcherWMieraORedlinMet alBilateral pulmonary artery banding before Norwood procedure: survival of high-risk patients. Thorac Cardiovasc Surg. (2020) 68:30–7. 10.1055/s-0038-1676617
18.
PoiseuilleJLM. Recherches expérimentales sur le mouvement des liquides dans les tubes de très petits diamètres. C R Acad Sci Paris. (1840) 11:961–7.
19.
PettersenMDDuWSkeensMEHumesRA. Regression equations for calculation of z-scores of cardiac structures in a large cohort of healthy infants, children, and adolescents. J Am Soc Echocardiogr. (2008) 21:922–34. 10.1016/j.echo.2008.02.006
20.
LopezLColanSDFrommeltPCEnsingGJKendallKYounoszaiAKet alRecommendations for quantification methods during the performance of a pediatric echocardiogram. J Am Soc Echocardiogr. (2010) 23:465–95. 10.1016/j.echo.2010.03.019
21.
CantinottiMScaleseMMurziBAssantaNSpadoniIDe LuciaVet alEchocardiographic nomograms for chamber diameters and areas in Caucasian children. J Am Soc Echocardiogr. (2014) 27:1279–92. 10.1016/j.echo.2014.08.005
22.
TobiasJD. End-tidal carbon dioxide monitoring in infants and children. Paediatr Anaesth. (2009) 19:106–14. 10.1111/j.1460-9592.2009.02930.x
23.
ShibataSCWilsonDF. Pulmonary blood flow and end-tidal carbon dioxide monitoring. Anesthesiology. (2015) 123:57–65.
24.
NevinMAMcDonnellCMcShaneAJ. End-tidal CO₂ as a surrogate for pulmonary blood flow in pediatric cardiac surgery. Br J Anaesth. (2017) 119:1163–71.
25.
RychikJGoldbergDJ. Late consequences of single-ventricle palliation. Circulation. (2014) 129:1123–32.
26.
TakeiTKanekoYKondoRMorisakiNAchiwaI. Intraoperative echocardiographic indicator for optimal bilateral pulmonary artery banding. Gen Thorac Cardiovasc Surg. (2025) 73:811–8. 10.1007/s11748-025-02156-9
27.
ÇelikMCÇelikÖBKalçıkM. Reevaluating echocardiographic indicators in bilateral pulmonary artery banding. Gen Thorac Cardiovasc Surg. (2026) 74(1):99–100. 10.1007/s11748-025-02210-6
28.
HonguHNomuraKHamayaIUgakiSShimizuTYamagishiMet alLasso technique for bilateral pulmonary arterial banding. Interdiscip Cardiovasc Thorac Surg. (2025) 40:ivaf130. 10.1093/icvts/ivaf130
29.
YamasakiTUmezuKTobaSIshikawaRBesshoSItoHet alBilateral pulmonary artery banding facilitates the systemic ventricular outflow tract growth for biventricular and univentricular repair candidates of complex arch anomaly. Heart Vessels. (2024) 39:891–8. 10.1007/s00380-024-02412-7
30.
GibbsJLWrenCWattersonKGHunterSHamiltonJR. Stenting of the arterial duct combined with banding of the pulmonary arteries and atrial septostomy: a new approach to palliation for hypoplastic left heart syndrome. Br Heart J. (1993) 69:551–5. 10.1136/hrt.69.6.551
31.
AkintürkHMichel-BehnkeIValeskeKMuellerMThulJBauerJet alHybrid transcatheter–surgical palliation: basis for univentricular or biventricular repair—the giessen experience. Pediatr Cardiol. (2007) 28:79–87. 10.1007/s00246-006-1444-7
32.
GalantowiczMCheathamJP. Lessons learned from the development of a new hybrid strategy for the management of hypoplastic left heart syndrome. Pediatr Cardiol. (2005) 26:190–9. 10.1007/s00246-004-0962-4
33.
CaldaroneCABensonLNHoltbyHLiJRedingtonANVan ArsdellGS. Initial experience with hybrid palliation for neonates with hypoplastic left heart syndrome. Ann Thorac Surg. (2007) 84:201–8. 10.1016/j.athoracsur.2007.04.127
34.
PizarroCDerbyCDBaffaJMMurdisonKARadtkeWA. Improving the outcome of high-risk neonates with hypoplastic left heart syndrome: hybrid procedure or conventional surgical palliation?Eur J Cardiothorac Surg. (2008) 33:613–8. 10.1016/j.ejcts.2007.12.042
35.
BurkhartHMNakamuraYSalkiniASchwartzRMRanalloCDMakilESet alBilateral pulmonary artery banding in higher risk neonates with hypoplastic left heart syndrome. JTCVS Open. (2023) 16:689–97. 10.1016/j.xjon.2023.08.005
36.
WernovskyGOzturkMDiddleJWMuñozRd'UdekemYYerebakanC. Rapid bilateral pulmonary artery banding: a developmentally based proposal for the management of neonates with hypoplastic left heart. JTCVS Open. (2023) 14:398–406. 10.1016/j.xjon.2023.03.009
37.
DaveHRosserBKnirschWHublerMPretreRKretschmarO. Hybrid approach for hypoplastic left heart syndrome and its variants: the fate of the pulmonary arteries. Eur J Cardiothorac Surg. (2014) 46:14–9. 10.1093/ejcts/ezt604
38.
HickeyEJCaldaroneCAMcCrindleBW. Critical left ventricular outflow tract obstruction in neonates. J Thorac Cardiovasc Surg. (2011) 142:123–30.
39.
EmaniSMMcElhinneyDBTworetzkyWet alStaged left ventricular recruitment after single-ventricle palliation. Circulation. (2012) 126:S160–6.
40.
HiranoYInamuraNKawazuYAokiHKayataniFIwaiSet alFactors associated with achievement of biventricular repair after bilateral pulmonary artery banding in interrupted aortic arch. World J Pediatr Congenit Heart Surg. (2018) 9:54–9. 10.1177/2150135117737685
41.
OtaNMurataMTosakaYIdeYTachiMItoHet alIs routine rapid-staged bilateral pulmonary artery banding before stage I Norwood a viable strategy?J Thorac Cardiovasc Surg. (2014) 148:1519–25. 10.1016/j.jtcvs.2013.11.053
42.
RychikJRomeJJCollinsMHet alThe hypoplastic left heart syndrome: from fetus to fontan. Circulation. (2013) 128:170–9.
43.
GewilligMBrownSC. The fontan circulation after 45 years. Eur Heart J. (2016) 37:1–8.
44.
KarimiMFaroukAGoldenAGilkesonR. Hybrid palliation of interrupted aortic arch in a high-risk neonate. Ann Pediatr Cardiol. (2010) 3:74–6. 10.4103/0974-2069.64360
45.
AkintürkHYörükerUSchranzD. Hypoplastic left heart syndrome palliation: technical aspects and common pitfalls of the hybrid approach. World J Pediatr Congenit Heart Surg. (2022) 13:588–92. 10.1177/21501351221099935
46.
RussellHMPasqualiSKJacobsJPet alOutcomes of bilateral pulmonary artery banding in neonates with ductal-dependent circulation. Ann Thorac Surg. (2017) 103:147–54.
47.
GuleserianKJSharmaMSBarkerGMet alOutcomes after staged palliation following bilateral pulmonary artery banding. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. (2015) 18:50–7.
Summary
Keywords
bilateral pulmonary artery banding, ductal-dependent circulation, end-tidal carbon dioxide, high-risk neonates, near-infrared spectroscopy, physiology-guided pulmonary artery banding, pulmonary blood flow
Citation
İrdem AK, Balık H, Kılıç Y and Dinç PS (2026) Physiology-guided bilateral pulmonary artery banding in high-risk neonates: early hemodynamic and perfusion outcomes. Front. Cardiovasc. Med. 13:1803385. doi: 10.3389/fcvm.2026.1803385
Received
03 February 2026
Revised
01 April 2026
Accepted
02 April 2026
Published
04 May 2026
Volume
13 - 2026
Edited by
Ornella Milanesi, University of Padua, Italy
Reviewed by
Zakhia Saliba, Hôtel-Dieu de France, Lebanon
Shannen Kizilski, Boston Children's Hospital and Harvard Medical School, United States
Updates
Copyright
© 2026 İrdem, Balık, Kılıç and Dinç.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Ahmet Kuddusi İrdem drirdem@gmail.com
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.