Pulmonary Artery Banding (PAB) — Series: #1–6

Pulmonary Artery Banding #0: Overview of Physiologic Goals and Clinical Pathways

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Pulmonary artery banding (PAB) is a palliative operation that deliberately introduces resistance into the pulmonary arterial circulation. Its purpose is not to correct the underlying congenital anatomy, but to modify pulmonary blood flow and pressure so that the patient can safely reach a later definitive or staged operation. In contemporary practice, PAB is therefore best understood as a selective bridge: it may control pulmonary overcirculation in biventricular or single-ventricle lesions, stabilize high-risk neonates with ductal-dependent systemic circulation, or provide left-ventricular retraining before anatomic repair.

The physiologic problem addressed by PAB is usually excessive pulmonary blood flow. As pulmonary vascular resistance falls after birth, a large intracardiac communication or common ventricular output can direct a disproportionate fraction of cardiac output to the lungs. Pulmonary overcirculation increases pulmonary venous return, produces atrial and ventricular volume loading, worsens heart-failure physiology, and may compromise effective systemic perfusion. Chronic exposure of the pulmonary vascular bed to excessive flow and pressure also promotes pulmonary vascular remodeling. PAB creates a controlled obstruction that reduces pulmonary flow and limits transmission of proximal ventricular pressure to the distal pulmonary arteries.

The desired degree of restriction depends on the intended circulation. In biventricular physiology, traditional guidance has been to reduce distal pulmonary artery pressure to approximately 30–50% of systemic pressure. In single-ventricle physiology, the distal pressure target should be substantially lower and conceptually closer to the low-pressure pulmonary circuit required for later cavopulmonary palliation, with a mean pressure of approximately 15 mmHg cited as a practical reference [1]. These targets are physiologic guides rather than stand-alone endpoints; systemic pressure, oxygen saturation, ventricular loading, perfusion, and the underlying anatomy must be interpreted together.

1. Main Pulmonary Artery Banding

Main PAB places a circumferential band around the main pulmonary artery. The operation can be applied to either biventricular or single-ventricle circulation, but the reason for banding differs between the two pathways.

In biventricular lesions, the usual indication is a large left-to-right shunt with pulmonary overcirculation when immediate complete repair is undesirable because of severe comorbidity, low body weight, clinical instability, or anatomic complexity. Examples include selected large ventricular septal defects, atrioventricular septal defects, multiple ventricular septal defects, and other lesions in which pulmonary flow reduction can provide time before definitive repair. A contemporary staged-repair cohort of 125 high-risk patients undergoing PAB for biventricular shunt lesions reported hospital mortality of 7.2%, interstage mortality of 4.8%, and unplanned interstage reintervention in 14.4%; only 74.4% ultimately underwent complete repair during the reported follow-up [2]. These results emphasize that PAB is not a benign substitute for early repair but a strategy reserved for patients in whom the expected benefit of staging outweighs the additional interstage risk.

The hemodynamic effect of main PAB in biventricular physiology is straightforward: pulmonary blood flow falls, pulmonary venous return decreases, and ventricular volume loading is reduced. Distal pulmonary artery pressure also falls because the band partially isolates the pulmonary vascular bed from ventricular systolic pressure. Systemic arterial saturation should generally remain relatively high. In practice, oxygen saturation may be used as an adjunct during tightening, but no single saturation value should define an adequate band. The band must be restrictive enough to relieve pulmonary overcirculation without creating clinically important hypoxemia or excessive proximal ventricular pressure loading.

2. Main PAB in Single-Ventricle Physiology

In single-ventricle circulation, pulmonary and systemic vascular beds compete for a common ventricular output. When pulmonary vascular resistance is low and pulmonary blood flow is unrestricted, excessive Qp may occur at the expense of systemic flow. A relatively high systemic arterial saturation can therefore coexist with poor systemic oxygen delivery because too much total cardiac output is recirculating through the lungs.

Main PAB in this setting is intended to rebalance Qp and Qs. Restricting pulmonary flow reduces pulmonary venous return and single-ventricle volume loading while preserving more ventricular output for the systemic circulation. The long-term objective is also important: future Glenn and Fontan physiology requires a low-pressure, low-resistance pulmonary vascular bed. Preventing prolonged exposure to excessive pulmonary flow and pressure is therefore part of preparing the patient for cavopulmonary palliation.

Contemporary data support PAB as an acceptable initial strategy in selected single-ventricle patients with unrestricted pulmonary blood flow. In a cohort of 73 patients, hospital mortality was 4%; 88% had reached a Glenn procedure by 2 years, overall 5-year survival after PAB was 86%, and 71% of Glenn survivors had reached Fontan by 5 years [3]. However, 22% required reoperation before Glenn. Outcomes were worse in patients with genetic or extracardiac anomalies and in high-risk morphologies including heterotaxy, unbalanced atrioventricular septal defect, and mitral atresia [3]. Thus, successful PAB depends not only on technical banding but also on the underlying substrate and the feasibility of the entire staged pathway.

3. Bilateral Pulmonary Artery Banding

Bilateral PAB is anatomically and physiologically distinct from conventional main PAB. Separate bands are placed around the right and left branch pulmonary arteries while leaving the main pulmonary artery and ductal pathway unobstructed. This configuration is particularly useful when systemic perfusion depends on flow from the pulmonary artery through the patent ductus arteriosus.

The classic setting is hypoplastic left heart syndrome or another form of ductal-dependent systemic circulation in which a conventional main PAB would impede the route from the right ventricle to the ductus and systemic arteries. Bilateral branch restriction allows pulmonary blood flow to be controlled while ductal patency is maintained with prostaglandin E₁ or ductal stenting. Atrial-level restriction must also be assessed because inadequate pulmonary venous egress across the atrial septum can become a separate source of instability.

Bilateral PAB is also used as a resuscitative bridge in neonates considered too high risk for immediate Norwood or other cardiopulmonary-bypass-dependent reconstruction. In a series of 24 high-risk single-ventricle neonates and infants treated with bilateral PAB plus ductal stenting or prostaglandin support, 15 patients (62.5%) survived to subsequent Norwood, stage II palliation, or transplantation [4]. Another rescue series of 10 neonates with ductal-dependent systemic outflow obstruction documented improvement in organ function in 9 patients before later definitive surgery [5]. A broader 66-patient experience demonstrated that bilateral PAB could be applied across complex single- and biventricular anatomy, particularly in patients with arch abnormalities, although hospital mortality remained 11% overall [6].

These data support bilateral PAB as a stabilization strategy rather than evidence that it is superior to primary neonatal reconstruction. Patient selection strongly influences reported outcomes, and available studies are retrospective.

4. Pulmonary Artery Consequences of Bilateral PAB

The major tradeoff of bilateral PAB is branch pulmonary artery morbidity. The bands are intentionally placed directly on the branch pulmonary arteries, and subsequent focal stenosis, distortion, or the need for patch augmentation or catheter intervention is common.

In a comparison of 50 patients treated with bilateral PAB and 53 patients undergoing Norwood palliation, pulmonary artery growth and Fontan candidacy were similar, but the bilateral-PAB group required earlier and more frequent pulmonary artery interventions [7]. Only 20% were alive and free from pulmonary artery intervention 5 years after band removal. Smaller band diameter and band duration greater than 90 days were associated with increased intervention risk [7].

This observation is clinically important when choosing a hybrid or rescue pathway. Restricting pulmonary flow may stabilize the circulation, but the pulmonary arteries must later become an unobstructed, low-resistance vascular bed. Surveillance after bilateral PAB should therefore specifically evaluate branch pulmonary artery geometry and gradients, and the subsequent operation should anticipate the possibility of pulmonary artery reconstruction.

5. PAB for Left-Ventricular Training in ccTGA

A different application of PAB is ventricular retraining rather than pulmonary-flow control. In congenitally corrected transposition of the great arteries without significant pulmonary stenosis, the morphologic left ventricle functions as the subpulmonary ventricle. As pulmonary vascular resistance falls, the LV becomes progressively exposed to a low afterload and may lose the pressure-generating capacity required to support the systemic circulation.

When an anatomic repair is planned, PAB can increase LV afterload and systolic pressure before a double-switch strategy. In an intention-to-treat cohort of patients with ccTGA or a prior atrial-switch circulation, PAB provided effective morphologic-LV training before anatomic repair and also served as palliation in patients who did not proceed to repair [8]. Outcomes were less favorable with increasing age, and preserved morphologic-LV function was central to successful progression toward anatomic repair [8].

The objective is not simply to generate a high instantaneous LV pressure. The trained ventricle must develop an adequate and durable pressure reserve without prohibitive dysfunction or maladaptive hypertrophy. Serial assessment therefore includes LV systolic function, wall thickness, geometry, septal position, atrioventricular valve function, and pressure response during the training period.

6. Technical and Intraoperative Principles

For main PAB, the band is generally positioned around the mid-main pulmonary artery, leaving sufficient distance from the pulmonary valve proximally and the pulmonary artery bifurcation distally. This reduces the risks of pulmonary-valve impingement and branch pulmonary artery distortion. Fixation sutures are commonly used to reduce band migration.

Traditional circumference formulas, including weight-based rules, can provide an initial estimate, but final tightness should be physiology guided. The supplied contemporary evidence does not establish a universally optimal band circumference, pressure gradient, or oxygen-saturation target. The most defensible approach is therefore to integrate distal pulmonary artery pressure, systemic arterial pressure, oxygen saturation, ventricular pressure loading, perfusion, and the intended surgical pathway rather than relying on a single numeric criterion.

Overtightening may cause inadequate pulmonary blood flow, hypoxemia, excessive proximal ventricular pressure, or ventricular dysfunction. Undertightening leaves persistent pulmonary overcirculation, ventricular volume loading, and pulmonary vascular exposure. A technically successful band is one that achieves the intended circulatory balance and remains appropriate until the planned next stage.

7. Outcomes, Complications, and Clinical Perspective

Contemporary multicenter registry data reinforce the selective nature of PAB. An analysis of 3,367 procedures in the Society of Thoracic Surgeons Congenital Heart Surgery Database identified operative mortality of 8% after main PAB and 26% after bilateral PAB [9]. These figures should not be interpreted as a direct comparison of procedures because bilateral PAB is disproportionately used in neonates with complex ductal-dependent systemic circulation and major preoperative risk. Nevertheless, they demonstrate that PAB remains associated with meaningful mortality.

Important complications include residual pulmonary overcirculation, excessive restriction, band migration, pulmonary-valve distortion, branch pulmonary artery stenosis, need for band adjustment, ductal obstruction in hybrid physiology, and later pulmonary artery intervention. Additional risk arises during the interstage period and at subsequent complete repair, including conduction injury and heart block in complex biventricular repairs [2].

PAB should therefore be integrated into a longitudinal surgical plan. Before banding, the team should define the immediate physiologic objective, the intended duration of palliation, the criteria for proceeding to the next stage, and the potential downstream consequences of the band itself.

The central principle is that PAB is not an anatomic repair but a deliberate restructuring of cardiovascular physiology. In biventricular shunt lesions, it reduces pulmonary overcirculation and ventricular volume loading while allowing delayed repair. In single-ventricle physiology, it balances pulmonary and systemic flow and protects the pulmonary vascular bed for later cavopulmonary circulation. In ductal-dependent systemic circulation, bilateral PAB controls pulmonary flow while ductal flow sustains systemic perfusion. In ccTGA, PAB can instead serve as a controlled afterload intervention to retrain the morphologic LV.

Appropriate use therefore depends on understanding anatomy, Qp/Qs, distal pulmonary pressure, ventricular loading, systemic oxygen delivery, and the next intended operation. The band is only the mechanical instrument; the true therapeutic target is a safer and more durable physiologic state from which the patient can progress to definitive or staged reconstruction.

References

[1] Sharma R. Pulmonary artery banding: rationale and possible indications in the current era. Ann Pediatr Cardiol. 2012;5(1):40-43.

[2] Afifi ARSA, Seale AN, Chaudhari M, Khan NE, Jones TJ, Stumper O, Botha P. Pulmonary artery banding: still a role for staged bi-ventricular repair of intracardiac shunts? Cardiol Young. 2023;33(9):1627-1633.

[3] Alsoufi B, Manlhiot C, Ehrlich A, Oster M, Kogon B, Mahle WT, Maher K, McCrindle BW, Kanter K. Results of palliation with an initial pulmonary artery band in patients with single ventricle associated with unrestricted pulmonary blood flow. J Thorac Cardiovasc Surg. 2015;149(1):213-220.

[4] Guleserian KJ, Barker GM, Sharma MS, Macaluso J, Huang R, Nugent AW, Forbess JM. Bilateral pulmonary artery banding for resuscitation in high-risk, single-ventricle neonates and infants: a single-center experience. J Thorac Cardiovasc Surg. 2013;145(1):206-214.

[5] Russell RA, Ghanayem NS, Mitchell ME, Woods RK, Tweddell JS. Bilateral pulmonary artery banding as rescue intervention in high-risk neonates. Ann Thorac Surg. 2013;96(3):885-890.

[6] Sakurai T, Sakurai H, Yamana K, Nonaka T, Noda R, Otsuka R, Osawa T. Expectations and limitations after bilateral pulmonary artery banding. Eur J Cardiothorac Surg. 2016;50(4):626-631.

[7] Davies RR, Radtke WA, Klenk D, Pizarro C. Bilateral pulmonary arterial banding results in an increased need for subsequent pulmonary artery interventions. J Thorac Cardiovasc Surg. 2014;147(2):706-712.

[8] Winlaw DS, McGuirk SP, Balmer C, Langley SM, Griselli M, Stumper O, De Giovanni JV, Wright JG, Thorne S, Barron DJ, Brawn WJ. Intention-to-treat analysis of pulmonary artery banding in conditions with a morphological right ventricle in the systemic circulation with a view to anatomic biventricular repair. Circulation. 2005;111(4):405-411.

[9] Devlin PJ, Argo M, Habib RH, McCrindle BW, Jegatheeswaran A, Jacobs ML, Jacobs JP, Backer CL, Overman DM, Karamlou T. Contemporary applications and outcomes of pulmonary artery banding: an analysis of The Society of Thoracic Surgeons Congenital Heart Surgery Database. Ann Thorac Surg. 2024;117(1):128-135.