Is pulmonary hypertension still a contraindication for lung volume reduction?—a narrative review of contemporary evidence

Introduction

Chronic obstructive pulmonary disease (COPD) with severe emphysema can lead to lung hyperinflation and respiratory failure, and it is often complicated by secondary pulmonary hypertension (PH) due to chronic hypoxemia and loss of pulmonary vascular bed (1). PH in COPD is heterogenous: most cases are mild-to-moderate pre-capillary PH associated with chronic lung disease (group 3), but a small minority exhibit disproportionately severe haemodynamics (“pulmonary vascular phenotype”), which has different risk implications. PH is defined by a mean pulmonary artery pressure (mPAP) greater than 20 mmHg at rest measured by right-heart catheterization (2). Pre-capillary pulmonary arterial hypertension (PAH), which is the predominant phenotype in COPD, is distinguished by an mPAP >20 mmHg together with a pulmonary capillary wedge pressure ≤15 mmHg and pulmonary vascular resistance >2 Wood units (3). These definitions matter for lung volume reduction (LVR) decision-making because many surgical and bronchoscopic series use echocardiographic estimates, which are screening tools but not equivalent to invasive measurements (3).

It is also important to recognise that the haemodynamic definition of PH has changed substantially over time. Earlier LVR studies and early emphysema cohorts commonly defined PH as mPAP ≥25 mmHg, whereas contemporary European Society of Cardiology (ESC)/European Respiratory Society (ERS) guidelines lowered the diagnostic threshold to mPAP >20 mmHg together with PVR >2 Woods unit for pre-capillary disease (3). This shift has practical implications when interpreting older Lung volume reduction surgery (LVRS) and bronchoscopic lung volume reduction (BLVR) studies: a proportion of patients previously classified as having “no PH” would now meet the new diagnostic criteria. Consequently, many cohorts included in the LVR literature likely contain patients who would today be classified as having mild PH. Awareness of this definitional evolution is essential when comparing earlier studies with contemporary series and when extrapolating their conclusion to current clinical practice.

LVRS and BLVR are established treatments for selected patients with severe emphysema, providing improvements in lung function, exercise capacity, and quality of life (4). By removing or collapsing diseased, hyperinflated lung regions, LVRS/BLVR improves respiratory mechanics, which may indirectly benefit cardiovascular function by reducing right ventricular (RV) afterload and improving filling (1,5).

However, the presence of PH has been previously considered a contraindication to LVRS (1,6) out of concern that resecting lung tissue (and thus pulmonary vasculature) could acutely worsen pulmonary haemodynamics and precipitate right heart failure (1,6). These concerns led the National Emphysema Treatment Trial (NETT) and most early LVRS programs to exclude patients with moderate-to-severe PH (7). NETT excluded mPAP ≥35 mmHg or systolic PAP (sPAP) ≥45 mmHg on right-heart catheterization (8). In practice, this creates a therapeutic gap for symptomatic emphysema patients with borderline mild-moderate PH who may be excluded despite potentially favourable mechanics-driven haemodynamic effects of hyperinflation reduction.

In recent years, small studies and registry cohorts have challenged this exclusion, suggesting that mild-to-moderate PH may not preclude the benefits of LVR. Improved respiratory mechanics after LVRS or BLVR could favourably influence pulmonary haemodynamics by reducing dynamic hyperinflation and improving oxygenation (1). Indeed, case series of EBV therapy in emphysema reported improved pulmonary artery pressures (PAPs) and RV function with no increase in morbidity or mortality (9,10). This review therefore examines contemporary evidence regarding the safety, feasibility, and haemodynamic effects of LVR in patients with emphysema-associated PH. We present this article in accordance with the Narrative Review reporting checklist (available at https://atm.amegroups.com/article/view/10.21037/atm-2026-1-0028/rc).

Methods

Search strategy

We conducted an extensive literature search (through January 2026) using PubMed, MEDLINE, and Web of Science for publications on LVRS or BLVR in patients with PH and emphysema. Search terms included combinations of “lung volume reduction”, “LVRS”, “bronchoscopic lung volume reduction”, “emphysema”, “COPD”, and “pulmonary hypertension”. We also reviewed reference lists of relevant articles to identify additional studies. Both prospective and retrospective studies, clinical trials, and case series were included. We included the earliest reports from the 1990s through the most recent data. Only studies involving human subjects were considered (full example provided in Tables 1,2).

Inclusion criteria

Studies were included if they reported on outcomes of LVRS or BLVR in patients with PH. We included human studies that assessed hemodynamic outcomes (e.g., PAP, pulmonary vascular resistance) and/or clinical outcomes (lung function, exercise capacity, survival) in PH patients undergoing LVR. Both surgical and bronchoscopic approaches were considered. We included all study designs (randomized trials, observational studies, and case series) given the ethical and logistical challenges of randomized trials in this specific population.

Language handling

English full texts were prioritized for feasibility and accuracy of appraisal; this is acknowledged as a limitation. Potentially relevant non-English studies with English abstracts were screened at abstract level but full multilingual extraction was not performed.

Data extraction

From each study, we extracted key details: sample size and patient characteristics (including severity of emphysema and PH), type of intervention (surgical LVRS or specific BLVR modality), hemodynamic measurements (e.g., PAPs pre- and post-intervention, right heart function indices), perioperative outcomes (morbidity, mortality), and longer-term results [lung function changes, 6-minute walk distance (6MWD), quality of life, etc.]. Where available, we noted whether PH was considered a contraindication or risk factor by the authors.

Synthesis

We organized the findings to address specific research questions formulated a priori. These questions include: Is PH an absolute contraindication to LVR? What effect does LVR have on pulmonary haemodynamics in PH (does it improve or worsen PH)? How does LVR impact RV function and exercise capacity in PH patients? What are the risks (e.g., mortality, right heart failure) of performing LVR in PH patients? Does the evidence differ by the type of intervention (surgical vs. bronchoscopic) or by PH etiology? We attempted to answer each question by collating evidence across studies. A narrative synthesis is provided for each question, supported by tabulated data (see Table 3 for a summary of major clinical studies). All source citations have been preserved in the required format.

Review

Rationale and mechanisms

The rationale for LVR in emphysema-associated PH rests on competing physiologic effects. On one hand, emphysema destroys alveolar-capillary units and chronic hypoxia promotes vasoconstriction and vascular remodelling, all of which increase pulmonary vascular load (24). Chronic hyperinflation further impairs RV filling by increasing intrathoracic pressure and flattening the interventricular septum. On the other hand, LVR may improve respiratory mechanics and gas exchange, thereby alleviating hypoxic vasoconstriction in pulmonary arterioles and relieving the burden on the right heart by reducing intrathoracic pressure and hyperinflation. In theory, removing the most diseased, non-functional lung regions (via LVRS or blocking them via BLVR) allows the remaining lung to expand and function more efficiently. Improved oxygenation and lung compliance can reduce PAP by mitigating hypoxia-driven vasoconstriction and lowering pulmonary vascular resistance (1,4,5,24).

Early evidence of these mechanisms comes from physiological studies. Improvements in stroke volume and oxygen pulse during exercise have been observed after LVRS, implying better cardiac performance post-surgery due to reduced hyperinflation and thus reduced extrinsic cardiac compression (12,16,25). Pathology studies also show that emphysema leads to pulmonary vessel loss and intimal thickening, which can stabilize or partially reverse if gas exchange and lung mechanics improve. Thus, LVR may interrupt the vicious cycle of hypoxia, elevated pulmonary pressures, and progressive RV strain, potentially stabilizing or lowering pulmonary vascular load and protecting the right ventricle (Figure 1) (15,20,21).

Figure 1 Conceptual mechanism through which lung volume reduction may benefit patients with PH. Hyperinflated lungs compress the heart and pulmonary vasculature, increasing intrathoracic pressure and reducing venous return. LVRS or BLVR reduces lung volume, thereby relieving cardiac compression, enhancing RV preload, and potentially lowering pulmonary artery pressures (Image made with FigureLabs). BLVR, bronchoscopic lung volume reduction; LVRS, lung volume reduction surgery; PH, pulmonary hypertension; RV, right ventricle.

The central concern is that LVR also removes part of the pulmonary vasculature. Early studies raised the possibility that LVRS might acutely worsen PH in some patients by reducing the total cross-sectional area of the pulmonary vascular bed (13-15). In most of those patients the increase in PAP was attributed to higher pulmonary vascular resistance not to volume overload, as wedge pressure remained unchanged (14). The overall literature now suggests that this theoretical risk is real but usually outweighed by the favourable effects of improved mechanics and gas exchange in carefully selected patients. The balance between these effects is likely to depend on emphysema distribution, baseline hyperinflation, PH severity, gas-exchange reserve, and the presence of cardiac disease.

Safety and feasibility

Historically, PH was considered an exclusion criterion for LVR, largely based on expert opinion and concerns rather than extensive data (19). NETT initially excluded patients with systolic PAP >45 mmHg by echocardiography from enrolment, reflecting this cautious stance. Many BLVR trials have similarly excluded patients with more than mild PH. The key question is whether this conservative approach remains justified in light of emerging evidence.

Recent studies suggest that mild-to-moderate PH does not preclude safe LVR when patients are selected in experienced multidisciplinary programs (1,10,19,22,23,26). Observational surgical cohorts have generally reported perioperative mortality, prolonged air leak rates, intensive care use, and length of stay that are broadly comparable between emphysema patients with and without PH, provided severe PH and overt right heart failure are uncommon in the cohort (1,19). At the same time, PH should not be regarded as irrelevant. Registry-level data suggest that PH may increase perioperative risk after LVRS, indicating that careful preoperative phenotyping, anaesthetic planning, and postoperative monitoring remain important (18).

It should be noted that these favourable safety signals apply to mild-to-moderate PH, often defined as systolic PAP 35–50 mmHg on echo, or mean PAP <35 mmHg on right heart catheterization. Patients with severe PH; systolic PAP >60 mmHg or mean PAP ≥40 mmHg; were rare in these series. In one cohort, only 8 of 56 PH patients had “severe PH”, and while outcomes were not separately detailed for them, no obvious safety signal emerged (19). However, caution is still advised in extreme PH cases—careful hemodynamic assessment and possibly perioperative hemodynamic support may be needed.

Evidence for BLVR is smaller but directionally similar. Pilot and observational studies of endobronchial valve therapy in emphysema patients with PH report procedural feasibility without a consistent signal for acute haemodynamic collapse or right heart failure (9,10,20,26). An international consensus statement recommends that BLVR be considered carefully in patients with moderate PH (26). The same consensus advises against endoscopic valve therapy in patients with severe PH or decompensated right heart failure and emphasizes a multidisciplinary evaluation to balance risks and benefits

In summary, the available evidence indicates that LVR is feasible and reasonably safe in selected patients with mild-to-moderate PH, particularly when performed in experienced centres (22). The most defensible interpretation is therefore that PH is a risk modifier, rather than an absolute contraindication, that merits optimization, for example supplemental oxygen to reduce hypoxia, or PH-specific medications in select cases and possibly the use of intraoperative precautions like standby cardiopulmonary support. This framing better reflects current evidence than the former binary approach of universal exclusion. On that note, some centres have reported using veno-venous extracorporeal membrane oxygenation (ECMO) as prophylactic support during LVRS in PH patients, for example, Akil et al. used ECMO in high-risk cases to get them through the perioperative period safely (21). With these strategies, even patients with significant PH have undergone successful LVR.

Haemodynamic outcomes

Beyond safety, a critical question is whether LVR actually improves pulmonary haemodynamics or right heart function in patients with existing/documented PH. The evidence here is nuanced. Broadly, LVR tends not to worsen resting pulmonary haemodynamics and may even improve them in some cases, especially by reducing pulmonary capillary wedge pressure, whereas effects on PAP depend on the context (rest vs. exercise).

The most robust data come from the NETT cardiovascular substudy, which was a controlled trial setting. That study found no increase in resting PAP after LVRS compared with medical therapy and suggested more favourable wedge-pressure behaviour in the surgical group (post-LVRS wedge change –1.8 vs. +3.5 mmHg in controls, P=0.04) (5). The conclusion was clearly stated: “LVRS was not associated with an increase in pulmonary artery pressures”, providing level I evidence that lung reduction does not acutely exacerbate PH in moderate cases. Observational data from surgical series broadly support this conclusion. Across cohorts, PAPs are generally unchanged or modestly reduced after LVRS, particularly in patients with heterogeneous emphysema nd measurable baseline hyperinflation (1,19,21,23).

Studies that examined filling pressure and cardiac performance provide additional mechanistic support. PCWP often remains stable or decreases after LVR, while cardiac index, stroke volume, ventricular preload, and exercise oxygen pulse may improve (5,10,12,15,16,20,25). Advanced imaging studies after BLVR with cardiac MRI similarly demonstrated increased right- and left-ventricular end-diastolic volumes and cardiac output, consistent with improved preload and stroke volume without worsening PH (20).

Beyond pressure numbers, RV function can be assessed by echocardiographic metrics. A BLVR found that RV longitudinal strain (apical segment) improved significantly 8 weeks after BLVR (strain changed from –7.9% to –13.3%, P=0.04; more negative strain indicates better contractility) (9). Moreover, in patients who clinically responded to BLVR (i.e., had lobar atelectasis and FEV₁ gain), there was a significant drop in NT-proBNP levels correlating with 6-minute walk improvement (9). This implies unloading of the right ventricle in responders. In surgical series, although formal RV ejection fraction measurements are rarely reported, clinical indicators of RV function (exercise capacity, BNP levels, echo estimates) generally improved. For example, one study noted improved oxygen pulse and exercise capacity post-LVRS, consistent with enhanced stroke volume output by the heart after reducing hyperinflation (25).

An important conceptual framework for interpreting these findings is right-ventricle-pulmonary artery (RV-PA) coupling. LVR may improve RV-PA coupling even if PAPs do not change substantially. By reducing hyperinflation and improving cardiac preload, LVRS and BLVR can increase stroke volume and RV efficiency, allowing the RV to operate at a more favourable point on the pressure-volume relationship. This may explain why several studies report improved exercise capacity, oxygen pulse, or RV strain despite minimal changes in resting PAP (9,20,25). Figure 2 summarises haemodynamic responses to LVR interventions.

Figure 2 Haemodynamic effects of lung-volume-reduction interventions. (A) Surgical LVRS lowered median sPAP from 41 to 37 mmHg three months post-operatively in patients with pulmonary hypertension (1). (B) BLVR improved right-ventricular function, with increased right-ventricular end-diastolic volume index and enhanced ventricular strain; pulmonary artery pressures did not rise (9). (C) In the NETT cardiovascular substudy, end-expiratory PCWP decreased after LVRS (–1.76±7.1 mmHg) but increased in patients receiving medical therapy (+3.46±11.1 mmHg; P=0.04) (5). BLVR, bronchoscopic lung volume reduction; LVRS, lung volume reduction surgery; NETT, National Emphysema Treatment Trial; PCWP, pulmonary capillary wedge pressure; sPAP, systolic pulmonary artery pressure.

Not all studies are uniformly positive. Earlier reports described increases in PAP or PVR after surgery in some patients (13-15). The discrepancy in these early findings likely relates to differences in patient selection and measurement conditions (rest vs. exercise). This is supported by a study that found that after LVRS, resting PAP did not change and exercise PAP was not significantly elevated compared to pre-op (15), whereas after lobectomy, PAP rose significantly during exercise (15). In the LVRS group, the key change was an amelioration of exercise-induced PCWP elevation (post-LVRS exercise wedge was much lower than pre-op) (15). Additionally, advances in operative technique may partly explain the improved outcomes in contemporary series. Early LVRS was predominantly performed via median sternotomy or thoracotomy, whereas modern practice favors video-assisted thoracoscopic surgery (VATS), which is associated with reduced surgical trauma and faster recovery (27-29).

Functional gains and survival

Functional benefit is a prerequisite for justifying intervention in this high-risk population. The literature indicates that yes, appropriately selected emphysema patients with PH improve to a similar extent in lung function, exercise capacity, and quality of life as those without PH (1,10,19,20). Reported gains include higher FEV₁, lower residual volume, better 6MWD, and improved quality of life measures.

These benefits are clinically relevant because PH patients often begin from a more compromised cardiopulmonary baseline. The available comparatice cohorts suggest that PH does not eliminate the functional response to LVRS, although absolute performance may remain lower than in patients without PH (1,19).

Longer-term survical data remain limited. Existing series suggest that selected PH patients can have medium-term survival comparable to non-PH patients after LVRS, but these findings should be interpreted cautiously because of small sample sizes and selection bias (1,22). In higher-risk cohorts, early deaths still occur, usually in the setting of advanced disease, severe PH, or major perioperative complications (21). Thus functional benefit appears reproducible, whereas survival signal remains less certain.

Does the effect of LVR differ by intervention type?

As for the intervention type, differences may exist between surgical and bronchoscopic approaches in PH patients, though direct comparisons are lacking. Conceptually, both approaches aim to reduce hyperinflation and improve mechanics, but they differ in invasiveness, magnitude of volume reduction, and candidate selection (4,26,30). Recent studies including a propensity matched study and a randomized trial in general emphysema patients found surgical LVRS and endobronchial valves produced comparable improvements in lung function and exercise capacity at 1 year (30,31). Extrapolating cautiously, BLVR may be favoured in PH patients with high operative risk, whereas LVRS may provide greater benefit in those able to tolerate surgery.

Limitations

Limitations include the narrative (non-meta-analytic) design and the feasibility-driven prioritization of English full texts. The literature consists predominantly of single-center retrospective cohorts with modest sample sizes. Only one RCT provides level I evidence and this study excluded patients with mPAP ≥35 mmHg. The severe PH subgroup is particularly underrepresented, with most studies containing fewer than 10 such patients. Furthermore, PH assessment methods vary considerably across studies; while right heart catheterisation is gold standard, many studies rely on echocardiographic estimates, which may be inaccurate in hyperinflated lungs. Another challenge in interpreting the existing literature is that comparisons between studies often become “apples-to-oranges” in the context of the evolution of PH definition. These limitations must be considered when interpreting the findings presented.

Conclusions

In patients with emphysema and coexisting PH, LVR interventions can confer significant benefits in lung function, symptoms, and even pulmonary hemodynamics, challenging the old dogma that PH is an absolute contraindication. The available literature suggests that carefully selected patients with mild-to-moderate PH can undergo LVRS or BLVR with meaningful improvements in exercise capacity, quality of life, and cardiopulmonary function, without consistent evidence of haemodynamic deterioration.

Key findings include the following: LVRS does not increase resting PAP and can reduce PH severity in some cases; it improves cardiac function, notably increasing RV output during exercise, likely by relieving hyperinflation and improving oxygenation; PH patients have higher surgical risk, but in experienced centers perioperative mortality remains low comparable to standard LVRS in mild PH, though higher in severe PH.

That said, caution is warranted. Patients with very severe PH or overt right heart failure were underrepresented in the successful series and may fare poorly with any intervention short of lung transplantation. In clinical practice, invasive haemodynamic assessment and multidisciplinary evaluation may help guide decision-making in patients with suspected PH who are being considered for LVR.

Future studies should focus on identifying optimal patient selection criteria, including haemodynamic thresholds, and on clarifying the comparative effects of LVRS vs. BLVR on survival, functional status, PAP, echocardiographic right-heart indices, and patient-reported outcomes. Future studies should also incorporate perioperative haemodynamic monitoring and longitudinal follow-up to evaluate longer-term effects. Additionally, as PH-targeted medications improve, an interdisciplinary approach combining contemporary medical optimisation, including oxygen therapy and diuretics when clinically indicated, and selected PH-directed therapy, with LVR could yield better outcomes and should be explored.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://atm.amegroups.com/article/view/10.21037/atm-2026-1-0028/rc

Peer Review File: Available at https://atm.amegroups.com/article/view/10.21037/atm-2026-1-0028/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-2026-1-0028/coif). V.K. serves as an unpaid editorial board member of Annals of Translational Medicine from December 2025 to December 2027. V.K. is also a proctor for Intuitive. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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