Highlights
In chronic lung disease, a lower CT-derived BV5art/TAV ratio, representing reduced small-artery volume relative to total arterial volume, was associated with hemodynamically confirmed severe pulmonary hypertension.
This signal was strongest in COPD, where severe pulmonary hypertension also coincided with larger central vessel volumes, supporting a pattern of intrapulmonary vascular volume redistribution.
Parenchymal destruction and pulmonary hypertension were partly dissociated: emphysema extent in COPD did not correlate with hemodynamic severity or small-vessel volume, while fibrosis extent in ILD correlated with reduced small-vessel volumes but not with hemodynamic impairment.
The findings suggest that pulmonary hypertension in COPD and fibrosing ILD does not arise from a single anatomic pathway and that CT vascular phenotyping may add clinically useful information beyond visual assessment of emphysema or fibrosis.
Background
Pulmonary hypertension associated with chronic lung disease is a major determinant of exercise limitation, right ventricular stress, hospitalization risk, transplant candidacy, and mortality. Yet in routine practice, distinguishing the vascular component of disease from the parenchymal component remains difficult. In both COPD and fibrosing interstitial lung disease, pulmonary vascular remodeling has long been recognized histologically, but bedside quantification is challenging. Right heart catheterization remains the reference standard for diagnosis and grading of pulmonary hypertension, although it is invasive and generally reserved for selected patients with disproportionate symptoms, transplant evaluation, or suspected severe pulmonary vascular disease.
Chest CT is already central to the evaluation of chronic lung disease. Traditionally, CT has been used to define emphysema, fibrosis pattern, airway abnormalities, and indirect markers of pulmonary hypertension such as main pulmonary artery diameter. More recently, automated or semi-automated CT analysis has enabled volumetric assessment of pulmonary vessels. These methods allow separation of arteries and veins and quantification of small-vessel compartments that may reflect distal vascular pruning, remodeling, or altered blood distribution. Such measurements have generated interest as imaging biomarkers of pulmonary vascular disease, but their clinical meaning in chronic lung disease, especially across distinct phenotypes such as COPD and fibrosing ILD, has remained uncertain.
The study by Garcia and colleagues addresses this gap by asking a focused and clinically relevant question: are CT-assessed pulmonary vascular abnormalities associated with the presence and severity of pulmonary hypertension in COPD and fibrosing ILD, and how do these abnormalities relate to the burden of parenchymal damage?
Study Design and Methods
Design and population
This was an observational imaging-physiology study that included 117 patients with chronic lung disease: 63 with COPD and 54 with fibrosing ILD. The investigators also evaluated 38 subjects with idiopathic pulmonary arterial hypertension as a comparator group, which is a useful reference because idiopathic pulmonary arterial hypertension represents a pulmonary vascular disease with relatively preserved lung parenchyma.
Patients with COPD and ILD were stratified according to the presence and severity of pulmonary hypertension using right heart catheterization, the diagnostic gold standard. This is an important methodological strength because many prior CT studies have relied on echocardiography or clinical surrogates.
Imaging assessment
All participants underwent volumetric non-contrast chest CT. The investigators quantified pulmonary vessel volumes and stratified them into arterial and venous compartments. They also assessed the extent of emphysema in COPD and fibrosis in ILD. Of particular interest was the ratio of small arterial blood volume to total arterial volume, termed BV5art/TAV. Although the abstract does not define the exact diameter threshold in detail, BV5-based metrics generally refer to the volume of vessels with a cross-sectional area less than 5 mm2, a commonly used CT marker of the peripheral small-vessel compartment.
Clinical question and endpoints
The primary clinical objective was to determine whether CT-derived vascular measures were associated with hemodynamically defined pulmonary hypertension severity in COPD and fibrosing ILD. A second objective was mechanistic: to evaluate whether vascular abnormalities tracked with the extent of emphysema or fibrosis, which might clarify whether pulmonary hypertension mainly reflects parenchymal destruction, vascular remodeling, or a combination of both.
Key Findings
Baseline vascular morphology differed substantially between COPD and ILD
Patients with COPD had greater absolute vascular and lung volumes than patients with ILD. This is not surprising anatomically, since hyperinflation and larger thoracic volumes are common in COPD, whereas fibrosing ILD is typically associated with restricted lungs and lower total lung volumes. However, when small-vessel volume was normalized to lung volume, COPD showed lower values than ILD. This suggests that despite larger lungs and larger absolute vessel volumes, the effective density of distal vascular volume is reduced in COPD, consistent with pulmonary vascular pruning or loss of the peripheral vascular bed.
This distinction matters clinically because absolute vessel volume can be misleading when diseases differ so markedly in lung size. A normalized metric better captures whether the vascular tree is proportionate to the available lung parenchyma.
Severe pulmonary hypertension was associated with lower BV5art/TAV in both chronic lung diseases
In both COPD and fibrosing ILD, severe pulmonary hypertension was linked to a reduced volume of small arteries normalized to total arterial volume, that is, a lower BV5art/TAV ratio. The signal was more pronounced in COPD. This result is central to the paper because it identifies a CT marker that tracks with invasive hemodynamic severity across two major chronic lung disease populations.
Physiologically, a lower BV5art/TAV ratio suggests a relative loss or underfilling of the distal arterial compartment together with a proportionally greater contribution from larger proximal arteries. That pattern is compatible with peripheral vessel remodeling, pruning, or elevated downstream resistance. It also aligns with the concept that pulmonary hypertension in chronic lung disease may involve not only destruction of gas-exchanging units but also structural and functional reorganization of the vascular tree.
COPD showed a particularly strong pattern of distal loss and central enlargement
Among patients with COPD, severe pulmonary hypertension was associated not only with reduced small-artery proportion but also with larger central vessel volumes. This combination supports the authors’ interpretation of intravascular volume redistribution: less blood volume represented in the peripheral small arteries and more in the larger central vessels. Such a pattern may reflect increased proximal capacitance, altered flow dynamics, distal obliteration, or all three.
For clinicians, this is an intriguing observation because it suggests that pulmonary hypertension in COPD may be identifiable on CT as a vascular phenotype rather than inferred only from advanced emphysema, hypoxemia, or pulmonary artery enlargement. It also reinforces the concept that a subset of patients with COPD develops a disproportionately severe pulmonary vascular syndrome.
Emphysema extent did not explain pulmonary hypertension severity in COPD
One of the study’s most clinically provocative findings is that in COPD, the extent of emphysema did not correlate with hemodynamic impairment or with small-vessel volume. This argues against a simplistic model in which pulmonary hypertension severity is merely the direct consequence of alveolar and capillary bed destruction proportional to emphysema burden.
Instead, the data support a more complex pathobiology involving vascular remodeling that may be partially independent of radiographic emphysema severity. That interpretation is consistent with prior work showing endothelial dysfunction, intimal thickening, muscularization of small pulmonary arteries, cigarette smoke-related vascular injury, and hypoxic vasoconstriction in COPD, even in areas without severe emphysematous destruction.
In ILD, fibrosis related to vessel loss but not to hemodynamic severity
The ILD findings differed in an important way. The extent of fibrosis was inversely correlated with the volume of small arteries and veins, indicating that more extensive fibrotic remodeling is associated with reduced peripheral vascular volume. However, fibrosis extent was not related to hemodynamic impairment. This suggests that while fibrosis may physically reduce or distort the vascular bed, the severity of pulmonary hypertension cannot be inferred from fibrosis burden alone.
This is clinically relevant because fibrosing ILD patients with similar extents of radiographic fibrosis can have very different pulmonary vascular phenotypes. The implication is that CT vascular measurements may identify those with disproportionate vascular involvement beyond what parenchymal imaging alone suggests.
Comparison with idiopathic pulmonary arterial hypertension
The inclusion of idiopathic pulmonary arterial hypertension provides a conceptual anchor, even though the abstract does not provide detailed comparative statistics. The presence of a comparator group with primarily vascular rather than parenchymal disease helps situate the chronic lung disease findings along a spectrum of vascular remodeling. In practice, it underscores that CT vascular phenotyping may eventually help differentiate pulmonary hypertension driven mainly by parenchymal disease from pulmonary hypertension with a more dominant vascular component.
Clinical Interpretation
The most actionable message from this study is that BV5art/TAV appears to be a sensitive CT marker of severe pulmonary hypertension in chronic lung disease, especially in COPD. If validated externally, such a metric could enrich risk stratification in several settings: patients with COPD who have dyspnea out of proportion to spirometry, ILD patients with unexplained gas-exchange limitation, transplant evaluation, and selection of patients who warrant echocardiography or right heart catheterization.
At present, clinicians often rely on non-specific CT signs such as enlarged pulmonary artery diameter, right heart enlargement, or diffuse vascular attenuation. These markers are useful but imperfect. A quantitative marker that reflects the structure of the distal arterial tree may offer a more pathophysiologically grounded signal. Importantly, the study does not suggest CT can replace right heart catheterization for diagnosis. Rather, it supports CT as a noninvasive phenotyping tool that may identify a vascular endotype within chronic lung disease.
The findings also sharpen the mechanistic distinction between COPD and fibrosing ILD. In COPD, pulmonary hypertension seems less tied to the topographic extent of emphysema and more to a vascular remodeling pattern characterized by small-vessel depletion and central arterial prominence. In fibrosing ILD, peripheral vessel loss tracks with fibrosis burden, but pulmonary hypertension severity depends on additional factors beyond the amount of fibrosis visible on CT. These may include hypoxic vasoconstriction, endothelial dysfunction, vascular compression or obliteration at the microscopic level, comorbid left heart disease, thrombotic burden, and differences in right ventricular adaptation.
Strengths and Limitations
Strengths
The study has several notable strengths. First, pulmonary hypertension classification was anchored to right heart catheterization rather than echocardiography. Second, the imaging analysis appears to have separated arteries from veins, which is methodologically more informative than whole-vessel metrics alone. Third, the investigators examined both COPD and fibrosing ILD, allowing disease-specific rather than disease-agnostic conclusions. Fourth, the inclusion of parenchymal quantification makes the paper more mechanistically informative, because it tests whether vascular abnormalities simply mirror parenchymal damage.
Limitations
As with most imaging biomarker studies, several limitations deserve attention. The sample size is moderate, particularly once subdivided by disease type and pulmonary hypertension severity, which may limit precision. The abstract does not provide effect sizes, confidence intervals, or discrimination statistics, so the incremental predictive value of BV5art/TAV over conventional clinical or CT markers cannot yet be judged. Because the design is observational and apparently cross-sectional, causality cannot be inferred; the study shows association, not temporal progression.
Technical generalizability is another issue. Quantitative vascular CT metrics can be influenced by CT acquisition parameters, inspiratory effort, contrast use or lack thereof, segmentation algorithms, and motion artifact. External validation across scanners, centers, and software pipelines will be essential before routine clinical use. In addition, the abstract does not detail the ILD subtypes represented, which matters because pulmonary vascular involvement may differ between idiopathic pulmonary fibrosis and other fibrosing ILDs. Finally, the study focuses on anatomic vascular volumes, which do not directly capture vascular compliance, endothelial function, or regional perfusion.
How This Fits With Existing Literature
The work aligns with a growing body of literature suggesting that CT-derived small-vessel metrics reflect clinically meaningful pulmonary vascular disease. In COPD, prior studies have linked reduced distal vessel volume or blood vessel counts to airflow limitation, emphysema, and outcomes, although associations with invasive pulmonary hemodynamics have been less consistently characterized. In ILD, pulmonary artery enlargement and vascular pruning have been associated with pulmonary hypertension risk, but quantitative separation of arterial and venous compartments has been less extensively explored.
Current pulmonary hypertension guidelines emphasize that pulmonary hypertension associated with lung disease requires integrated assessment, including symptoms, lung function, gas exchange, imaging, echocardiography, and when indicated right heart catheterization. This study supports the idea that CT may contribute more than structural diagnosis of lung disease alone; it may provide a vascular signature that helps identify severe pulmonary hypertension and better explain clinical heterogeneity.
Practical Implications for Clinicians
For pulmonologists and thoracic radiologists, the study suggests several practical considerations. First, severe pulmonary hypertension should be suspected in COPD even when emphysema burden does not appear extreme, particularly if symptoms, diffusion impairment, or oxygen needs seem disproportionate. Second, in fibrosing ILD, fibrosis extent alone should not reassure clinicians that pulmonary hypertension is absent or mild. Third, structured CT vascular analysis may eventually become a useful adjunct in multidisciplinary discussion, especially at referral centers that evaluate advanced lung disease and lung transplantation.
For researchers, BV5art/TAV appears promising as a trial enrichment biomarker. It may help identify patients with chronic lung disease who carry a stronger pulmonary vascular phenotype and who might benefit from more detailed physiologic testing, longitudinal monitoring, or enrollment in studies of pulmonary vascular-targeted strategies.
Conclusion
Garcia and colleagues provide compelling evidence that CT-derived pulmonary vascular morphology is meaningfully associated with severe pulmonary hypertension in chronic lung disease. The most informative marker in this analysis, the BV5art/TAV ratio, points to relative depletion of the small-artery compartment and is particularly sensitive in COPD. Just as importantly, the study shows that parenchymal damage and pulmonary hypertension are not tightly coupled: emphysema burden in COPD did not track with hemodynamic severity, while fibrosis burden in ILD related to peripheral vessel loss but not directly to pulmonary hypertension severity.
These findings support a shift from viewing pulmonary hypertension in chronic lung disease as merely a byproduct of damaged parenchyma toward recognizing distinct vascular phenotypes that CT can help define. Before adoption in routine care, the metrics require standardization, external validation, and demonstration of incremental value over existing tools. Even so, the study is a meaningful step toward noninvasive vascular phenotyping in COPD and fibrosing ILD.
Funding and ClinicalTrials.gov
The abstract provided does not report funding details or a ClinicalTrials.gov registration number. Readers should consult the full Chest article for complete disclosure statements and source of support.
Citation
Garcia AR, Vollmer I, Blanco I, San José Estepar R, Rodriguez-Chiaradía DA, López-Meseguer M, Martin-Ontiyuelo C, Nardelli P, Hernandez-Gonzalez F, Bosacoma A, Ribas J, Pomares X, Santos S, Molina-Molina M, Sellares J, Rahaghi FN, Washko G, San José Estepar R, Barberà JA. Characterization of CT-Derived Pulmonary Vascular Abnormalities Associated with Pulmonary Hypertension in Chronic Lung Disease. Chest. 2026-05-27. PMID: 42208731. https://pubmed.ncbi.nlm.nih.gov/42208731/
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