Small vessel disease in chronic thromboembolic pulmonary hypertension: a comprehensive narrative review of multimodality imaging evaluation

Introduction

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare form of pulmonary hypertension (PH) that results from unresolved organized thromboemboli in the pulmonary arterial tree and is often precipitated by an acute pulmonary embolic event (1). Currently classified as Group 4 in the World Health Organization’s clinical classification of PH (2), CTEPH is characterized by thrombotic obstruction of pulmonary artery (PA) and subsequent vascular remodeling, leading to increased pulmonary vascular resistance (PVR) and eventual development of PH. The exact pathobiological mechanisms leading to CTEPH are still not completely elucidated. While predisposing conditions such as malignancy, chronic inflammatory disease, pacing wires and ventriculo-atrial shunts, antiphospholipid antibodies, splenectomy, thrombophilic disorder, and non-O blood group are known to increase the risk for CTEPH development, the exact transition from acute pulmonary embolism (PE) event to subsequent CTEPH development is still not fully understood (3). A unique feature of CTEPH is the development of secondary microvascular or small vessel disease (SVD). It is well known that microvascular disease is associated with poor surgical outcomes and persistent PH post-surgery (3). Imaging has proven to be transformative in diagnosis and treatment of CTEPH, with modalities such as ventilation-perfusion (V/Q) scanning and computed tomography angiography (CTA) being the mainstays in establishing the diagnosis (Figure 1). While macrovascular disease is well evaluated with imaging, preoperative evaluation of SVD still remains a diagnostic challenge. Many indirect findings on imaging studies can point to the presence of SVD although direct mapping of SVD still remains the holy grail in the management of CTEPH patients. This focused review aims to provide insights into imaging of SVD in the setting of CTEPH and highlight the challenges and future possibilities. We present this article in accordance with the Narrative Review reporting checklist (available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-1-652/rc).

Figure 1 Imaging of SVD in CTEPH. Diagram flowchart for imaging evaluation when SVD is suspected in CTEPH patients. 4D, four-dimensional; CT, computed tomography; CTEPH, chronic thromboembolic pulmonary hypertension; DECT, dual-energy computed tomography; PA, pulmonary artery; PC-MRI, phase-contrast magnetic resonance imaging; PVR, pulmonary vascular resistance; RVOT, right ventricular outflow tract; SVD, small vessel disease.

Methods

A broad electronic search was performed primarily using PubMed/MEDLINE and Scopus, with supplementary screening of references from relevant articles. The search strategy combined controlled vocabulary and free-text terms related to CTEPH, microvasculopathy or SVD, and imaging modalities. We focused mainly on recent literature published within the last 10 years, while selectively including a few earlier studies when essential for context. Only English-language publications were included, and priority was given to peer-reviewed articles. Eligible study designs comprised prospective and retrospective cohort studies, cross-sectional imaging studies, case-control studies, systematic reviews, and technically focused imaging papers; case series were included when they provided meaningful radiological characterization of microvascular disease. The identified studies were narratively synthesized with emphasis on imaging modality, radiologic patterns of microvascular involvement, and their clinical and pathophysiological relevance in CTEPH (Table 1).

Pathophysiology of SVD in CTEPH

As noted above, the pathophysiology in CTEPH is complex; several questions remain unanswered such as why some patients do not have prior history of acute PE (4). In this context, CTEPH has been described as a “two-vessel compartment model” with a large vessel component caused by chronic unresolved clot and a small vessel microvasculopathy (4). First described by Moser and Bloor, SVD in CTEPH is marked by complex alterations in the pulmonary microvasculature similar to idiopathic PA hypertension (5). These changes include intimal fibrosis, plexiform lesions and obliteration of arterioles, which collectively increase PVR. Notably, these microvascular changes are not limited to the regions distal to thromboembolic occlusion but can also affect unobstructed areas, suggesting a global pulmonary vascular response (4,5). In some cases, distal thrombosis involving the microvasculature is also seen that can be diffuse; this is typically seen in those patients where bronchial collaterals and anastomoses fail to develop (4).

Clinical relevance of SVD

Currently the main treatment options for CTEPH patients include surgical pulmonary thromboendarterectomy (PTE) for proximal fibrotic lesions and interventional balloon pulmonary angioplasty (BPA) for more distal organized clots. Presence of SVD and its preprocedural assessment is crucial since it is a predictor of residual or persistent PH after success full PTE (3,6). Extensive SVD has also been suspected in patients that exhibit residual PH after multiple repeated BPA sessions and described as an independent factor contributing to worst prognosis (3). The hemodynamic impact of SVD has also been evaluated by PA occlusion technique using to estimate effective pulmonary capillary pressure. Based on the PA decay curve, it estimates pulmonary capillary pressure, which allows PVR to be separated into upstream resistance—attributable to organized proximal fibrotic thrombi—and downstream resistance, reflecting distal microvasculopathy. Gerges et al. showed that downstream resistance correlated with histomorphometric indices of small-vessel disease, establishing this invasive technique as gold standard for microvasculopathy diagnosis. Furthermore, the group provided further evidence that a lower preoperative upstream resistance was an independent predictor of more extensive microvascular disease, associated with persistent PH and higher mortality following PTE (3).

Radiological assessment of SVD

Clinically, presence of SVD in CTEPH patients is suspected when there is discrepancy in the extent of the mechanical obstruction by proximal fibrotic clots and the degree of increase in PVR. The extent of mechanical obstruction in the large pulmonary arteries can be evaluated using V/Q scanning, which is typically used as the first line imaging exam in evaluation of intermediate to high probability CTEPH patients. In large vessel disease related to CTEPH, one or more mismatched defects are classically seen (6). Further evaluation of the presence of mechanical obstruction can also be comprehensively assessed by CTA, that demonstrates a spectrum of lesions such as organized thrombi lining in the proximal pulmonary vessels, abrupt tapering of vessels, or intraluminal fibrous webs (7,8). In computed tomography (CT) assessment of SVD, one of the typical findings include presence of mosaic attenuation. However, this finding alone is nonspecific and can be associated with a multitude of associated vascular and airway diseases. Often, multiple imaging tools need to be utilized to identify potential patients with SVD.

V/Q scanning

V/Q scintigraphy remains the initial test of choice for diagnosis of CTEPH. Ease of availability, extensive validation and high sensitivity are some of the obvious advantages that make V/Q scanning a robust tool for diagnosis of CTEPH (7). Early studies have shown that V/Q scanning is more sensitive than CTA in diagnosis of CTEPH (7). While this might have changed over the years with newer and improved CT scanning tools, there is no doubt that V/Q scan offers a quick way to diagnose CTEPH. Typically characterized by large, mismatched perfusion defects, a normal scan effectively rules out CTEPH. V/Q scan is not without limitations and false positive defects can be seen with numerous other conditions such as vasculitis, fibrosing mediastinitis and neoplastic lesions such as sarcoma. In one study on 150 patients comparing various V/Q scanning techniques with CTA (9), both V/Q scanning techniques were more sensitive [V/Q single-photon emission computed tomography (SPECT): 85%, P<0.001 vs. CTA: 67%; V/Q planar scintigraphy: 83%, P<0.001 vs. CTA: 67%], and less specific (V/Q planar scintigraphy: 51%, P=0.03 vs. CTA: 60%; V/Q SPECT: 42%, P<0.01 vs. CTA: 60%) than was CTA for segmental analysis. Poor subpleural perfusion (PSP) in the capillary phase of pulmonary angiography is considered one of the direct imaging signs of underlying SVD (10) (Figure 2). This finding can be evaluated with V/Q scanning although can be limited with planar imaging due to shine-through effect as well as due to limitations in spatial resolution. As noted above, SVD is suspected in patients with discordant imaging and hemodynamic findings. This has also been shown with V/Q scanning; in one study on 76 patients, it was shown that CTEPH patients had higher mean pulmonary arterial pressure (mPAP) and total pulmonary resistance (TPR) as compared to patients with acute PE for similar degrees of vascular obstruction as measured on V/Q scanning (11). Another longitudinal analysis of V/Q scans in patients with unoperated CTEPH has shown that the classic findings of segmental mismatched perfusion defects change progressively over time and evolve into a more homogenous perfusion pattern, something that can be attributed to development of secondary microvasculopathy (12).

Figure 2 Angiogram and perfusion V/Q scan. A 78-year-old female with CTEPH status post PTE, with recurrent PH. (A) Digital subtraction angiogram image of left lung demonstrates PSP in the capillary phase with poor intraluminal filling of distal segmental and subsegmental arteries represented by a subpleural area as ≤1.5 cm (approximately one rib width) from the lateral pleura. (B) Perfusion image from V/Q scan of the same patient in AP projection demonstrates near normal perfusion to the left lung. Discrepancy between the V/Q and pulmonary angiogram findings could be attributed to differences in spatial resolution and ability of angiogram to assess perfusion in multiple phases. This image is published with the patient/participant’s consent. AP, anteroposterior; CTEPH, chronic thromboembolic pulmonary hypertension; PH, pulmonary hypertension; PSP, poor subpleural perfusion; PTE, pulmonary thromboendarterectomy; V/Q, ventilation-perfusion.

CTA

CTA is an established frontline imaging in evaluation of CTEPH. Excellent spatial resolution, high contrast-to-noise ratio, and detailed assessment of pulmonary arteries down to the subsegmental levels are some of the advantages that make CTA a premier tool in evaluation of CTEPH. Another advantage of CTA is the ability to simultaneously evaluate alternate causes of perfusion defects, thus limiting the differential diagnoses. CTA is the test of choice for anatomic mapping of disease and characterization of CTEPH lesions, which can help in surgical planning or targeting lesions for BPA. One of the limitations of CTA is that CTEPH lesions can be subtle and can be missed if not carefully evaluated; this has accounted for lower sensitivity of CTA in CTEPH detection as compared to V/Q scanning (9). CTA offers several insights into evaluation of SVD, although none are specific. One of the commonly used marker is the presence of mosaic attenuation. This is a nonspecific finding in isolation, although associated findings such as segmental vessel caliber reduction, presence of bronchial artery and systemic collaterals and parenchymal densities point to CTEPH as likely cause (13) (Figure 3). In context of CTEPH, mosaic attenuation also termed as “mosaic perfusion” refers to patchwork of increased CT attenuation (reflecting redistributed vascular flow) and decreased CT attenuation (which are areas of obstructed vessels or microvessel disease). Newer tools such as photon counting CT can provide further insights into evaluation of mosaic perfusion. In a small study on 29 CTEPH patients with mosaic perfusion evaluated with photon counting CT (14), significant differences in the diameters of the most distal pulmonary vessels were noted with higher frequency of dilated arterioles (91.9%) and venules (70.9%) in areas of ground-glass opacity (GGO), while thin arterioles (69.8%) and venules (55.8%) were the dominant findings in areas of hypoattenuation. In areas of GGO, findings similar to Group 1 PH were seen such as ill-defined micronodules, and areas of lobular GGO. Systemic-to-pulmonary anastomoses were depicted more frequently in the periphery of hypoattenuated areas (36%) versus hyperattenuated areas (25.6%) (Figure 3); these have been shown to be contributors to SVD (14). Presence of bronchial artery (BA) collaterals is known to be associated with a good postoperative response and likely represents a protective response in maintaining the viability of lung parenchyma distal to the PA occlusive lesions (15). In a study by Shimizu et al., total cross-sectional area of BA measured with CTA correlated with extent of central disease, and the area was significantly higher than in patients with distal microvascular disease (16). Quantitative CTA assessment of small vessels can provide functional insights for CTEPH patients and might help identify patients with SVD, although data is sparse. Shahin et al. evaluated different subgroups of PH using quantitative CT and found that patients with CTEPH had reduced volume of peel vessels and small vessel volume correlated with pulmonary function tests (17).

Figure 3 Chest CT MIP. A 35-year-old female with CTEPH status post PTE with persistent PH. (A) Lung window image illustrating interspersed hypo and hyperattenuating areas, representing mosaic attenuation. Note the increased centrilobular nodules within the areas of increased attenuation (arrows). (B) MIP demonstrating increased tortuous vessels (arrow) in area of increased attenuation in the left lower lobe. Adjacent area of decreased attenuation demonstrates reduced caliber of vessels. (C,D) MIP images demonstrating tortuous vessels extending to the fissures and pleural surfaces (arrows), illustrating systemic to pulmonary anastomosis. This image is published with the patient/participant’s consent. CT, computed tomography; CTEPH, chronic thromboembolic pulmonary hypertension; MIP, maximum intensity projection; PH, pulmonary hypertension; PTE, positron emission tomography.

Dual-energy CT (DECT)

DECT has revolutionized the imaging of CTEPH over the last decade. Using differences in iodine attenuation over different kilovoltages, DECT allows quantification of iodine within a voxel of lung tissue, termed as “perfused blood volume (PBV)”. Studies have shown PBV to be a good surrogate marker of lung perfusion (18). By allowing assessment of anatomic and perfusion information on a single scan, DECT has emerged as one of the frontline tools for assessment of CTEPH. Several studies have shown that perfusion information from DECT correlates with hemodynamic parameters and can help in prediction of post-operative outcomes (19-21). Qualitative assessment of PBV images can help identify areas of PSP and potentially identify patients with microvasculopathy (Figure 4). In a study 93 patients evaluated with DECT, pulmonary perfusion of blood volume in the normally perfused group showed an inverse correlation with PVR, while that of patients in the poorly perfused group did not. Patients with PSP on DECT had a lower diffusing capacity of the lungs for carbon monoxide (DL_CO), which might be the strongest predictor of microvasculopathy including diffuse distal thrombosis (22,23). Another study demonstrated that PSP was present in 51% of patients with CTEPH, although this finding improved after BPA. Quantitative assessment of DECT-based vascular parameters might further insights into the presence of SVD, although data is lacking (24).

Figure 4 DECT iodine perfusion map. PBV image from the same patient (mentioned in Figure 2) demonstrates mottled perfusion abnormalities, typical of SVD. This image is published with the patient/participant’s consent. DECT, dual-energy computed tomography; PBV, perfused blood volume; SVD, small vessel disease.

Magnetic resonance imaging (MRI)

MRI offers considerable potential in evaluation of CTEPH, although this has not yet translated into clinical practice. Currently, MRI is the gold standard for evaluation of right ventricle (RV) function and morphology. Phase contrast-MRI (PC-MRI) velocity mapping of PA provide valuable insights into pulmonary flow and vascular resistance and are proven biomarkers for noninvasive monitoring and for assessment of response to therapy. Systolic notching along the time course of mean pulmonary velocity is a known finding in PH and Hardziyenka et al. proposed that an echocardiographic timing of this notch can provide insights into the presence of SVD (25); the later the notch in systole, the greater the downstream resistance. Similar such findings can be assessed with two-dimensional (2D) PC-MRI and can be used to assess response to therapy (26) (Figure 5). Newer tools such as four-dimensional (4D) flow MRI allow comprehensive assessment of PA flow dynamics. Novel markers of increased PA pressures and PVR such as vortex, pulsed-wave velocity and wall shear stress (WSS) can provide unique noninvasive insights into the hemodynamics and the status of underlying microvasculature (27). Dynamic contrast enhanced MRI and DECT have been demonstrated to have comparable assessments of perfusion defects and similar abilities to detect perfusion improvement following PTE (28). There is a lot of interest in noninvasive assessment of lung perfusion and ventilation using techniques such as phase resolved functional lung (PREFUL) MRI. In one study on 42 CTEPH patients, quantitative parameters obtained using PREFUL MRI correlated with hemodynamic parameters highlighting the potential benefits (29). While these techniques are promising and might provide valuable clues to the presence of SVD, technical challenges remain and most of these tools are still in their nascent stage. Further research and prospective trials might shed light on the future of MRI in assessment of SVD.

Figure 5 Phase contrast velocity encoded MRI of the PA. A 61-year-old male with CTEPH. Phase contrast velocity encoded MRI of the PA demonstrates systolic notching (arrow), a finding typically seen with increased pulmonary vascular resistance. The timing of the systolic notch can help partition large vessel versus small vessel disease. This image is published with the patient/participant’s consent. CTEPH, chronic thromboembolic pulmonary hypertension; MRI, magnetic resonance imaging; PA, pulmonary artery.

Positron emission tomography (PET)

PET imaging, particularly with fluorodeoxyglucose (FDG), is an emerging tool in CTEPH. It can be used to assess metabolic activity and inflammation in the pulmonary arteries. Increased FDG uptake has been observed in patients with CTEPH, and it may be a marker of inflammation and vascular remodeling. In one study, FDG uptake in the lung parenchyma was found to be higher in patients with distal disease than in proximal disease, suggesting potential role in assessing peripheral vasculopathy (30).

Emerging techniques and future directions

As noted above, newer CT tools such as photon counting CT offer promise in evaluation of detailed morphology of the lung parenchyma and better understanding of vascular changes (14). Similarly newer MRI tools such as 4D flow and PREFUL MRI can offer promise in evaluation of SVD (29).

Emerging artificial intelligence (AI) and machine learning for automated segmentation and analysis of cardiopulmonary and vascular structures has the potential to harness the full diagnostic value of medical imaging (31). Recent advances in quantitative evaluation of CTEPH increasingly leverage computational hemodynamics and AI-driven imaging to elucidate microvascular involvement and its relationship with impaired hemodynamics. DECT and AI-based perfusion quantification, such as the PerAIDE model described by Xi et al. (32) provide detailed maps of lung perfusion abnormalities that correlate with PVR and mean PA pressure, reflecting microvascular impairment beyond visible macrovascular obstruction. Similarly, automated metrics derived from CT pulmonary angiography correlate with invasive hemodynamic parameters, enhancing diagnostic accuracy and linking vascular morphologic changes to pulmonary circulation dysfunction (33). Complementing these imaging biomarkers, patient-specific blood flow dynamics models using computational fluid dynamics (CFD) reveal altered pulmonary arterial flow in CTEPH: compared with controls, patients exhibit reduced flow velocity, decreased WSS, increased oscillatory shear index (OSI), and greater blood stagnation, factors implicated in endothelial dysfunction, thrombogenicity, and vascular remodeling that may extend into the microvasculature (34). These hemodynamic disturbances, quantifiable through simulation of patient-specific anatomy and hemodynamics, provide mechanistic insight into how altered flow patterns contribute to disease progression and may serve as emerging markers for SVD severity in CTEPH.

In parallel, synchrotron radiation-based pulmonary microangiography offers an experimental method to visualize the microvascular architecture and dynamic blood flow at very high spatial and contrast resolution (35), suggesting potential for in-depth characterization of microvasculopathy and real-time pulmonary blood flow distribution. Lastly, patient-specific hemodynamic modeling has been introduced by Ebrahimi et al. providing a non-invasive computational framework to estimate the extent of microvascular remodeling and simulate individual responses to PTE. By integrating CTA geometries with right heart catheterization (RHC) data, these multiscale models can potentially estimate the extend of SVD and simulate post-surgical outcomes (36).

Conclusions

Management of CTEPH is a complex task, requiring a personalized, multimodal treatment strategy involving multidisciplinary teams. Imaging plays a crucial role in diagnosis and risk stratification of these patients. Preoperative imaging using various tools allows confident diagnosis of CTEPH and determines patients’ surgical suitability for PTE or BPA. Assessment of SVD still continues to be a challenge, although significant progress has been made. The presence of distal PA obstructions and PVR out of proportion to the degree of mechanical obstruction, are strongly suggestive of underlying microvascular disease. Preoperative recognition of SVD is crucial as these are associated with worse clinical outcomes and may result in recurrent/residual PH following surgery. Several imaging findings on various imaging modalities can provide clue to the presence of microvascular disease, although requires careful assessment and multidisciplinary input (Table 2). Advanced imaging tools and continued research into novel imaging techniques can enhance our understanding of SVD and help in earlier detection and help targeted therapy. Finally, AI development as well as hemodynamic simulation, and high-resolution imaging may converge to quantify microvasculopathy and guide personalized assessment and treatment in CTEPH.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-1-652/rc

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Funding: None.

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