Endovascular interventions in cancer patients with compromise of the mediastinal vasculature: a review

Introduction

Endovascular interventions have emerged as a critical tool for treating various vascular diseases. For cancer patients, vascular compromise can occur from extrinsic or intrinsic tumor compression, tumor erosion of the vascular wall, and malignant tumor or bland thrombus. Such vascular issues can lead to a wide variety of severe symptoms and signs, which include facial swelling, cerebral edema, poor cardiac output, or bleeding, to name a few. When compared to conventional surgical options, minimally invasive interventions offer quicker recovery periods, fewer side effects, and rapid symptomatic relief.

Endovascular procedures exploit the body’s preexisting vasculature to reach the mediastinum, where specialists use catheters in combination with other devices to provide treatment. The majority of endovascular procedures for mediastinal vascular compromise will involve treatment for vascular obstruction. Balloon dilatation, termed angioplasty or venoplasty depending on the vessel, is performed to dilate the stenotic or occluded vessel. A self-expanding stent can be placed to maintain the vessel’s patency. Depending on the clinical scenario, other treatment options include cytoreduction of thrombus with catheter-directed thrombolysis, mechanical thrombectomy, or embolectomy, which are minimally invasive interventions to remove thrombus or embolus from the mediastinal vasculature. Lastly, some endovascular procedures are performed for damaged vasculature in the setting of active bleeding or concern for impending bleeding risk. For this scenario, endovascular procedures include embolization and covered stent placement.

This review aims to highlight and address the most common endovascular interventions for vascular compromise based on the vessel or site affected within the mediastinum.

Section 1: characterization and planning

When clinical symptoms suggest concern for mediastinal vascular compromise, the first step to endovascular treatment is to characterize the vessel injury with imaging (1). While two-view chest radiographs may be diagnostic, cross-sectional imaging provides additional important details that assist treatment planning. The proceduralist typically requests a contrast-enhanced computed tomography (CT) to confirm the diagnosis, assess the extent of injury, validate the necessity for intervention, and ensure that all appropriate equipment is available. If compromise of the superior vena cava (SVC), heart, or pulmonary vasculature is suspected, then a CT pulmonary embolus protocol is most helpful so as to time the contrast bolus for opacification of the SVC and pulmonary vasculature. If compromise of the aorta or supra-aortic vessels are suspected, then a CT angiogram is most helpful to time the contrast bolus for opacification of these arteries. Occasionally, contrast-enhanced magnetic resonance imaging (MRI) can be helpful to better evaluate the cardiac and aortic walls, or characterize flow dynamics. Lastly, a fluoroscopic venogram or angiogram may be performed; however with advancements in cross-sectional imaging over the last few decades, the traditional diagnostic fluoroscopic study is typically reserved for situations where cross-sectional imaging is non-diagnostic, indications for endovascular treatment are uncertain, or when the patient cannot obtain cross-sectional imaging due to rapid clinical deterioration (2). When fluoroscopic imaging is indicated, an adjunctive intravascular ultrasound can be helpful during the venogram or angiogram to help characterize and measure vascular stenosis and possibly assist in treatment (Figure 1) (3).

Figure 1 Contrast enhanced CT image in the coronal view demonstrates a mediastinal mass with compression of the SVC (A, arrow). Removal of the intraluminal tumor thrombus may be performed with the use of intravascular ultrasound and mechanical thrombectomy. For example, in another patient with hepatic IVC compression and concern for tumor thrombus, intravascular ultrasound images confirmed tumor thrombus within the IVC (B, arrow) and absence of the thrombus after successful endovascular mechanical thrombectomy (C, arrow). The gross specimen was consistent with tumor thrombus from the patient’s known prostate cancer (D, arrow). CT, computed tomography; SVC, superior vena cava; IVC, inferior vena cava.

Once the affected vessel is identified, endovascular treatment selection largely depends on the nature and degree of injury (Table 1). At times, more than one endovascular treatment may be applied. In these situations, selecting the most appropriate treatment can be confusing if the technical considerations are not understood. One treatment might be favored over another depending on the specifics of the cancer, anticipated response of systemic or radiation therapies, patient comorbidities, or proceduralist experience. The following three comparative scenarios provide some examples of common clinical considerations when tailoring endovascular treatments.

Clinical scenarios

• In one comparative treatment scenario, active bleeding from tumor erosion or damage to the vascular wall can be treated with either embolization or placement of a covered stent. Embolization is highly effective for small vessel damage, such as bronchial artery injury or peripheral pulmonary artery pseudoaneurysms, as embolization provides occlusion of the injured small vessels with precise injection of particles or liquid embolic (4-7). While small and low-profile stents are manufactured and more readily available, the physical constraints of the small diameter vessel may prevent satisfactory positioning of the stent and may even increase the risk of bleeding complications after stent deployment. For large vessel damage, however, such as a central pulmonary artery or thoracic aorta pseudoaneurysm, covered stents are the main endovascular method to isolate the damaged portion of the vessel with a stent of specified diameter and length (4).
• In another comparative treatment scenario, vascular compression caused by an extrinsic tumor can be treated with endovascular balloon dilatation and placement of a stent or by embolization of the extrinsic tumor. If the compression of the vasculature results in life-threatening or severe symptoms, or if the tumor is hypovascular, then embolization might not be appropriate. In this scenario, immediate symptomatic relief can be achieved with endovascular balloon dilation of the stenotic region and stent placement to provide a physical framework to prevent repeat stenosis (8). Stent placement, however, can also have drawbacks depending on the clinical presentation. Stents are generally non-retrievable once deployed and may occlude with time, both factors which might not be ideal if the extrinsic tumor is expected to decrease in size with chemotherapy or radiation, if the patient has a long life expectancy or in the setting of contradiction to the anticoagulation that is often recommended to prevent future occlusion of the stent (9-11). In these settings, the alternative treatment of tumor embolization may provide sufficient symptomatic relief, particularly if the extrinsic compressive tumor is hypervascular and hence expected to respond well to embolization, and symptoms are mild and not immediately life-threating as the symptomatic relief after embolization often requires weeks to be achieved. After embolization of the tumor arteries, patients expect to have symptomatic improvement over 2 months as the tumor volume responds to devascularization (12).
• In a third comparative treatment scenario, intravascular thrombus can be treated with either thrombolysis, vacuum aspiration, mechanical retrieval, or stent placement (13-16). Thrombolysis involves the injection of a potent thrombolytic agent, which might be highly effective but contraindicated in cancer patients with coagulopathy or intracranial lesions. Alternatively, vacuum retrieval of thrombus might be highly effective for acute thrombus, but less ideal for benign chronic thrombus or tumor thrombus both of which can adhere firmly to the vessel wall to the vessel wall (15,17). For benign chronic thrombus or tumor thrombus, mechanical retrieval or placement of a covered stent may be appropriate for definitive treatment (13,18,19). In consideration for stent placement, this treatment option often requires the patient to maintain lifelong anticoagulation to prevent future stent occlusion, which again might not be appropriate in contraindications to anticoagulation or long life expectancy (20).

The above three scenarios are meant to convey a general sense of the multitude of considerations that an interventionalist will weigh during triage of a patient with mediastinal vascular compromise. The access and type of treatment varies greatly based upon the type and location of injury, the injury characteristic, and patient comorbidities. The article has been structured based upon anatomical site of vascular compromise, as this often is the first factor that affects the treatment triage and technical approach.

Access and approach

The percutaneous access is planned once the most appropriate endovascular treatment is selected. Most endovascular treatments are performed with 5–8 French access sheaths due to their low profile and broad availability. Larger access sheaths of up to 24 French may be required for venous mechanical endovascular thrombectomy or stent placement. An assist from vascular surgery for open arterial access may be necessary to place large stents within the aorta. The location of vascular access is planned based upon the mediastinal vessel affected, any patient-specific anatomical variants, and preference of the proceduralist. Interventions in the SVC or pulmonary arteries are performed from venous access through the internal jugular, brachial, or femoral veins. Pulmonary venous interventions are also typically performed via a transvenous approach, but may require a trans-septal cardiac puncture (21). Endovascular procedures for the aorta or supra-aortic vessels are typically performed with percutaneous access via the common femoral artery, but can also be approach via radial or brachial artery access.

Contraindications

Absolute and relative contraindications to endovascular procedures should be considered within the clinical context. Treatments are typically postponed in the event of active infection; however, exceptions are made for life-saving interventions in the event of severe vascular compromise. For instance, active hemorrhage caused by a fungal pseudoaneurysm may warrant emergent embolization. Other relative contraindications that can frequently present in cancer patients include significant thrombocytopenia or other bleeding disorders, which might warrant pre-procedure correction of bleeding diathesis with infusion of platelets, fresh frozen plasma, or packed red blood cell blood products. Typically acceptable lab parameters for venous access procedures are platelet count greater than 20,000 and an international normalized ratio (INR) below 2–3 (22). Arterial access procedures are safer for patients with a platelet count greater than 50,000 and an INR below 1.5–1.8. Finally, standard contraindications for thrombolytics apply for thromboembolism treatment with catheter-directed thrombolytic injection, including absolute contraindications for intracranial hemorrhage, cerebral neoplasm, recent stroke, and active bleeding or bleeding diathesis (23).

SVC syndrome (SVCS)

As the major draining vein of the upper body, obstruction of the SVC can lead to a constellation of symptoms known as SVCS. Until 50 years ago, infectious diseases such as syphilis and tuberculosis accounted for the majority of SVCS. With advancements in the prevention and treatment of these infectious etiologies over the last few decades, most SVCS today result from iatrogenic factors and cancer. Approximately 40% of SVCS cases are caused by thrombosis or stenosis secondary to central venous catheters and other medical devices, while malignant tumors are the cause of the majority of the remaining 60% of cases (24).

In cancer patients, SVCS can be caused by external tumor compression, direct tumor invasion, tumor thrombosis, benign thrombosis, or iatrogenic lines and devices. The most common malignant causes for SVCS are non-small cell lung cancer (NSCLC; 50%), small-cell lung cancer (SCLC; 25%), non-Hodgkin’s lymphoma (NHL; 12%), metastases (9%), germ-cell tumor (3%), thymoma (2%), mesothelioma (1%), and other cancers (1%) (12,25-27).

Compression of the SVC leads to decreased venous return to the heart and resultant increased venous pressure in the upper torso. The severity of symptoms is directly related to the degree of venous obstruction and inversely related to the presence of venous collaterals (18,28,29). If the compression occurs gradually, collateral veins may redirect venous return to the heart, and symptoms may be limited to mild swelling and distended subcutaneous vessels in the upper torso, upper extremities, and neck that may be partially or completely relieved with inclined or upright positioning. If the collateral circulation cannot compensate for the obstruction or if SVC obstruction is rapid in onset, the patient may experience debilitating and potentially life-threatening sequela.

The constellation of clinical symptoms associated with SVCS can initially include upper extremity and facial swelling but, in more severe cases, may progress to include cyanosis, plethora, or functional compromise of the larynx and pharynx that manifests as cough, hoarseness, dysphagia, stridor, and respiratory distress. In severe cases, cerebral edema may lead to headaches, visual disturbances, and altered mental status. Although the presentation of severe SVCS can be striking and debilitating, most cases are not fatal. Ahmann et al. documented only one death in 1986 patients with SVCS (19). Patients tend to develop symptoms over two weeks or longer, which can afford time to receive treatment.

The multidisciplinary approach to SVCS is tailored based on the etiology of the obstruction and the patient’s clinical presentation. A clinical exam identifies the urgency for intervention and allows the provider to track the progression of clinical symptoms. Cross-sectional imaging is important to identify the etiology of disease. Optimally, CT or MRI is performed with contrast. A fluoroscopic venogram can be performed for definitive diagnosis and also allows for measurement of blood flow gradients across the stenosis and treatment planning.

Various classification schemes have been advanced to help guide the clinical discussion for endovascular intervention. Some of these classification systems rely upon imaging findings. For example, the Stanford and Doty classification system stratifies patients based on the degree of SVC obstruction and flow within the azygous vein (30). Most recommendations, however, focus predominantly on the clinical presentation to guide the indication for endovascular treatment, while radiologic imaging provides invaluable information to identify the etiology of the stenosis and assist the proceduralist in treatment planning.

Several causes for symptomatic SVCS might not warrant endovascular intervention. If the vascular compromise is related to an indwelling central line, this offending device can be removed to improve venous flow (31,32). If a mediastinal or lung tumor is the cause for SVCS compression, then biopsy is critical for triage as the underlying malignancy plays a large part in identifying the optimal treatment plan. For example, in patients with SVCS caused by lymphoma and germ cell tumors, SVCS is often relieved with chemotherapy or radiation alone (18). It is important to note that the initial clinical response to chemotherapy or radiation therapy does not obviate the need for endovascular procedures in the future. In patients with SVCS treated with chemotherapy, radiation, or both, approximately 20% can have symptomatic recurrence (33).

Endovascular intervention for SVCS includes venoplasty and stent placement. Stent placement is indicated for thrombus in the case of severe acute symptoms such as respiratory compromise or altered mental status (Figure 2) (1). Stent placement is also indicated to treat symptomatic SVCS caused by cancers such as mesothelioma that are known to not respond well to chemotherapy and radiation (34). Balloon venoplasty is typically performed during stent placement rather than as a standalone treatment. Venoplasty alone can be insufficient to provide long-term patency to a vessel, particularly if tumor compression is the etiology for SVCS, as continued tumor growth can overcome the temporary effects of venoplasty. Conversely, venoplasty may be attempted as a first-line measure in focal or short-segment stenosis from a prior central line (35). In addition, venoplasty alone might be preferred in patients who are not good candidates for anticoagulation or those with long life expectancy, as stent deployment often necessitates life-long anticoagulation to prevent future thrombosis and occlusion.

Figure 2 JenyA 61-year-old woman with lung adenocarcinoma. A mediastinal metastasis caused compression upon the SVC (A, arrow) that was initially planned to be treated with radiation therapy. Unfortunately, the patient developed worsening headaches, shortness of breath, and dysphasia that were all exacerbated when the patient reclined. A venogram performed from the right upper extremity confirmed complete occlusion of the SVC with minimal collateral venous development (B, arrow). The obstruction was crossed with an endovascular catheter and a non-covered stent was placed across the SVC to improve venous return to the heart (C, arrow). The patient’s symptoms improved overnight. SVC, superior vena cava.

Stenting for SVCS with life-threatening symptoms has been well documented to have good immediate and long-term effectiveness and a low complication rate. In a review of 44 studies with a total of 1,437 patients, Léon et al. found immediate clinical effectiveness within 48–72 hours of 90.50% (95% CI: 88.86–91.97%) (24). Symptomatic recurrences occurred in 11%, of which 78% were successfully treated with repeat intravascular intervention. The non-fatal complication rate was 8.28% (95% CI: 6.91–9.83%), which consisted of stent migration (18.80%), tumor invasion of the stent (13.68%), early post-stent thrombosis (10.26%), and hemoptysis (7.69%). The overall fatal complication rate was 1.46% (95% CI: 0.91–2.23%), nearly all occurring immediately or within 24 hours post-intervention. The most common fatal complications included hemoptysis (19.05%), ruptured SVC (19.05%), hemopericardium (9.25%), and respiratory failure (9.52%).

Right atrium

Cancer patients can present with pathology that extends or propagates from the SVC or inferior vena cava (IVC) into the right atrium. For example, iatrogenic devices such as fragmented central catheters or thromboembolic filters may migrate from the SVC or IVC (36). Similarly, tumor thrombus may extend from the SVC or IVC into the right atrium (37). Yet again, cross-sectional imaging is helpful for the diagnosis of the pathology and to ascertain the presence of damage to the cardiac wall or pericardial effusion. A transthoracic or transesophageal echocardiogram can be obtained to identify the impact on cardiac function and characterize flow dynamics.

Foreign bodies within the heart can be treated with endovascular retrieval (Figure 3). The indications and risks are determined based on the foreign body material composition, size, and shape. Fragments of central catheters are generally easily removed under fluoroscopic guidance via access through the internal jugular or femoral veins (38). Attempts to retrieve metallic objects can be more challenging, and a multidisciplinary discussion that includes representatives from surgery and cardiology is recommended. During the retrieval of metallic objects, damage to the cardiac valves or wall may result in permanent cardiac dysfunction or life-threatening hemorrhagic pericardial effusion.

Figure 3 JenyA 59-year-old man with history of metastatic rectal cancer presented with severe stenosis of the IVC due to liver metastasis (A, arrow), which resulted in recurrent high volume ascites despite multiple paracenteses. Simultaneous venograms through catheters in the IVC and the right middle hepatic vein redemonstrated the stenosis (B, arrow). A metallic stent was placed at the location of stenosis (C, arrow). Unfortunately, the metallic stent migrated to the right atrium. The stent was retrieved with snares from an internal jugular approach (D, arrow maintains location of IVC stenosis comparable to prior imaging, while the arrowhead identifies snare capture of the stent). The stent could not be removed through a sheath, and was instead safely deployed in the SVC (E, arrow maintains location of IVC stenosis, while the arrowhead identifies stent deployed in SVC). IVC, inferior vena cava; SVC, superior vena cava.

Tumor thrombus may extend from the IVC or SVC into the right atrium, compromising venous return to the heart and potentially resulting in tumor emboli to the pulmonary artery or lung parenchyma. The most common tumor emboli originate from renal cell carcoma and hepatocelluar carcinoma extension into the IVC (39). Treatment of the tumor thrombus can be approached through three different mechanisms. The tumor can be embolized, with resultant decrease in the size and extent of the tumor and the associated tumor thrombus. Alternatively, stent deployment can be used to trap the tumor between the stent and the vessel wall (IVC vs. SVC). Lastly, mechanical thrombectomy can be used to aspirate or snare any residual uncontained tumor. Arterial embolization can be performed with selective, catheter-directed injection of small particles or liquid embolic into the arteries supplying the tumor (40). The treatment effects are typically realized up to 2 months after embolization, as the tumor slowly responds to devascularization. Embolization can be performed as an adjunctive therapy before surgical resection or as a standalone treatment when surgery is contraindicated. Placement of a covered stent of a covered stent into the SVC or IVC may be undertaken to trap the tumor embolus along the vascular wall, effectively decreasing obstruction and mitigating the risk for embolization to the atrium and pulmonary arteries. When placed within vessels compromised by tumors, covered stents have been suggested for improved long-term patency at 3, 6, and 12 months compared to uncovered stents due to decreased tumor overgrowth of the stent (41).

Acute pulmonary artery embolism

In the United States, venous thromboembolism with pulmonary embolism (PE) is estimated to result in 150,000–250,000 hospitalizations and 60,000–100,000 deaths yearly (42). Non-endovascular treatments include systemic anticoagulation, peripheral thrombolysis, surgical embolectomy, and mechanical circulatory support. The endovascular interventions are catheter-directed thrombolysis and catheter embolectomy (43). Triage within a multidisciplinary group setting is recommended to provide the most appropriate therapy depending on the patient’s symptoms, cardiac strain, and contradictions to anticoagulation such as thrombocytopenia, recent surgery, or brain metastases (44).

Catheter-directed thrombolysis for pulmonary artery thromboembolism is performed by inserting a 4–6 French catheter via the right atrium and ventricle into the pulmonary artery (Figure 4). The thrombolytic agent is thus delivered directly into the embolus. Most commonly, tissue plasminogen activator is infused at a rate of 0.5–1.0 mg/hour for a total dose of 12–24 mg over a 12–24 hour infusion. Catheter-directed mechanical fragmentation or thrombectomy can be performed immediately before or after catheter-directed thrombolysis (Figure 5) (45). Fragmentation is performed by mechanical agitation of a major thrombus in the main pulmonary arteries using a catheter or wire. It is typically followed by attempts to quickly push the fragmented small clots from the main pulmonary artery into distal segmental branches to restore blood flow through the larger mainstem pulmonary artery and decrease right heart strain. Thrombectomy typically involves a larger diameter catheter (8–24 French), with either vacuum aspiration and/or nitinol metallic discs that capture the clot to allow mechanical retrieval (46,47). Thrombectomy can be performed without thrombolytics, which provides a means to treat patients with contraindications to thrombolytic agents.

Figure 4 JenyA 60-year-old man with multiple myeloma presented with bilateral pulmonary embolus in the mainstem and segmental branches (A, arrows). Endovascular access was performed via right internal jugular access. Pulmonary artery pressures were 70/22 mmHg with mean of 37 mmHg (B and C, arrows designate right and left pulmonary artery catheters respectively). Overnight infusion of tissue plasminogen activator via both catheters provided symptomatic relieve, decreased thrombus burden on subsequent pulmonary angiogram the next afternoon (D), and decreased pulmonary artery pressures to 51/22 mmHg with mean of 33 mmHg.

Figure 5 JenyA 46-year-old woman with history of metastatic colon cancer presented with bilateral segmental pulmonary emboli within the lower lobes, greater in the right (A, arrow). She was determined to be a high-intermediate risk with tachycardia, elevated troponin-T and BNP, and enlarged right ventricle on CT-angiogram. Catheter directed angiogram confirmed absence of blood flow to the bilateral lower lobes (B, arrow demonstrates right segmental artery cut off) and main pulmonary artery pressure measured 25 mmHg. Mechanical thrombectomy was performed bilaterally with restoration of the blood flow (C, arrow demonstrated reconstituted right pulmonary artery). BNP, b-type natriuretic peptide; CT, computed tomography.

Clinical outcomes for catheter-directed PE treatment vary based on clinical presentation, underlying patient factors, and technique employed. In a multicenter study that treated 101 patients with massive or submassive PE, clinical success as defined by stabilization of hemodynamics, improvement in pulmonary hypertension or right heart strain, and survival to hospital discharge was achieved in 86% and 97%, respectively (48). Notably, patients with massive PE were treated with the addition and combination of catheter-directed fragmentation and aspiration immediately before and after catheter-directed infusion. In a multicenter registry with 137 patients and a meta-analysis with 860, the catheter-directed thrombolysis complication rate included intracerebral hemorrhage in 1.5% and 0.35%, respectively and major complications in 9.4% and 4.65%, respectively. Major complications included fatality, intracranial hemorrhage, and any bleeding that required transfusion or surgical repair (49). Lastly, the use of ultrasound-accelerated thrombolysis has been pursued as a potential means to improve outcomes with some suggestions of similar treatment efficacy with reduced thrombolytic infusion time and treatment-related complications (50).

Pulmonary artery stenosis (PAS)

PAS is primarily seen in children with congenital heart disease but has been reported in adults. Rarely, mediastinal tumors cause extrinsic compression of the pulmonary arteries to produce hemodynamically significant obstruction. Teratomas and Hodgkin’s disease are the most common causes of extrinsic pulmonary artery compression in cancer patients (51). Additional causes for PAS include inflammatory processes such as Takayasu arteritis and Behcet disease, mediastinal fibrosis (most commonly seen after Histoplasma infection) and chronic thromboembolism (52,53). Clinical manifestations are often nonspecific and include chest pain and dyspnea. Cross-sectional imaging with contrast-enhanced CT or MRI often provides a definitive diagnosis. Transthoracic echocardiogram (TTE) can provide a useful non-invasive modality to measure blood velocity within the pulmonary arteries. A pulmonary angiogram with pressure measurements can also be pursued for a definitive diagnosis if cross sectional imaging is inconclusive (54).

Due to very limited data, the decision to treat PAS with an endovascular approach should be made on a case-by-case basis. Percutaneous angioplasty and stenting can be considered in patients with severe PAS that results in right ventricular dysfunction, severe pulmonary valvular regurgitation, or hemodynamic instability (55). In these patients, stenting provides rapid symptom relief compared to radiation and chemotherapy. Gutzeit et al. describe a case of NSCLC-causing PAS that manifested as severe shortness of breath and orthopnea (56). Angioplasty and stenting of the pulmonary artery resulted in immediate improvement of symptoms. Similarly, Fierro-Renoy et al. describe a case of bilateral PAS in a patient with NSCLC who was treated with bilateral angioplasty and stenting, resulting in the resolution of symptoms (55). Two additional case reports by Hirota et al. and Meckel et al. describe similar clinical scenarios with successful pulmonary artery stenting in right-sided heart failure due to malignant pulmonary artery obstruction (57,58).

Pulmonary artery pseudoaneurysm

A pulmonary artery pseudoaneurysm can develop in cancer patients as a sequela of prior treatments, including cardiac catheterization, surgery, radiation therapy, or percutaneous lung biopsy and ablation (59-63). In addition, pseudoaneurysms in the pulmonary artery may arise in immune-compromised cancer patients with fungal or tuberculosis lung infections, termed Rasmussen aneurysms.

Pseudoaneurysms are associated with a high mortality rate due to the potential to rupture and cause massive hemoptysis. The patient may present clinically with new or intermittent hemoptysis or asymptomatic with an incidental imaging finding. Cross-sectional contrast-enhanced CT is diagnostic; however, pulmonary arteriography may identify pseudoaneurysms not well seen on cross-sectional imaging (64).

Endovascular treatment options include embolization with coils or liquid embolic agents and covered stent placement. While embolization is often the most convenient and safest treatment option, particularly for pseudoaneurysms in distal pulmonary artery segments, stent placement may be pursued for more proximal locations to preserve distal pulmonary artery perfusion (Figure 6). A high mortality rate is reported due to the high risk for rupture of the pseudoaneurysm during instrumentation (65). Multidisciplinary precautions should be coordinated between the proceduralist, anesthesiology, and thoracic surgery. In the event that endovascular access is challenging and deemed too high a risk, then pseudoaneurysms in distal segments can also be treated with injection of an embolic agent via a CT-guided percutaneous access (66).

Figure 6 JenyA 28-year-old woman with a cavitary right lower lobe lung lesion that was biopsied at an outside hospital (A, arrow). Approximately 3 months after the biopsy, the patient presented with progressively worsening shortness of breath and chest imaging confirmed pneumonia. An incidental finding of a pseudoaneurysm was noted in the right lower lobe (B, arrow), which was likely a complication of the prior biopsy. After completion of antibiotics and resolution of pneumonia, the patient presented for endovascular treatment given the risk for life-threatening bleeding if the pseudoaneurysm were to rupture. A selective angiogram in the right lower lobe pulmonary artery demonstrated the pseudoaneurysm arose from the basilar segmental branch and contained a large neck (C, arrow). A covered stent was placed across the pseudoaneurysm to provide complete occlusion of the pseudoaneurysm while maintaining distal patency of the artery (D, arrow). A follow up CT scan 6 years later confirms complete resolution of the pseudoaneurysm and persistent patency of the stent (E, arrow). CT, computed tomography.

Pulmonary vein stenosis (PVS)

PVS is a rare entity that primarily occurs in young children with congenital heart disease. Malignant causes are rare, but have been reported for bronchogenic carcinoma, esophageal tumors, lymphoma, and metastases (67). Non-malignant etiologies can also present in cancer patients, such post-radiation damage or from inflammatory and infectious causes such as fibrosing mediastinitis, sarcoidosis, or tuberculosis. Iatrogenic causes have also been documented from cardiology radiofrequency ablation procedures to treat atrial fibrillation (68,69).

Patients with PVS present with shortness of breath and radiographic evidence of localized pulmonary edema. Delayed diagnosis is common as the symptoms and radiographic findings are similar to those seen with pneumonia or cardiac disease. Cross-sectional imaging with contrast-enhanced CT or MRI can provide the definitive diagnosis and characterize the degree of vascular compromise. Normal pulmonary vein diameter is 10–15 mm. For symptoms of PVS to manifest, compression of the vessel diameter to 4–6 mm, or 60% vessel narrowing, is often necessary (68). When the diagnosis is uncertain, a pulmonary artery wedge angiography can be pursued for definitive diagnosis.

Although PVS is rare and data is limited, percutaneous angioplasty and stenting via trans-septal puncture has been pursued for acute symptomatic relief. In 34 patients with a benign etiology of PVS, balloon venoplasty alone provided immediate symptomatic relieve in 42%, while the combination of venoplasty and stenting provided acute symptomatic relief in 95% (70). The rate of re-stenosis has been reported between 33–72% and depends on the etiology of the stenosis, reference diameter of the pulmonary vein, and initial stent diameter. Complication rates range from 0–25% and include pulmonary vein perforation, stent dislodgment, hemoptysis, pulmonary hemorrhage, ST-elevation, and transient neurological deficits (71). In a series of 98 patients requiring 145 catheterizations, only two vein perforations and one stent dislodgement were reported (68). While the predominant experience with PVS stenting has been performed in patients with non-cancerous etiology, this endovascular option can be pursued in cancer patients in the appropriate clinical setting.

Bronchial arteries

Bronchial artery damage in cancer patients can result in hemorrhage into the mediastinum, lung parenchyma, or pleura. Patients can present with hemoptysis, chest pain, dyspnea, and fatigue. Both primary lung and metastatic tumors can precipitate this injury (72-74). In addition, bronchial artery injury can be the sequela of fungal or microbacterial infection in immunocompromised cancer patient, or a result of cancer related therapy including radiation therapy, surgery, or percutaneous ablation (75,76). Cross-sectional imaging with CT can help localize the pathology, although an angiogram may be necessary for definitive diagnosis due to the small caliber of the bronchial arteries. The endovascular treatment of bronchial artery injury is embolization with either particles or metallic coils and plugs. The immediate success rate is high, albeit recurrence of bleeding is common and repeat embolization may be required. In 21 cancer patients treated with bronchial artery embolization, immediate bleeding control was achieved in 96%, but the median time to recurrence of bleeding was 66 days, and recurrence-free survival was 34% after 1 year (77).

Vascular erosion or pseudoaneurysm of the bronchial arteries occurs most commonly within the lung parenchyma. Endovascular treatment with embolization can be performed with selective injection of small particles for partial to complete occlusion of the artery. Bleeding typically resolves immediately after embolization, although the patient may continue to have some hemoptysis for days after the procedure as the blood that accumulated before the embolization is cleared from the lung parenchyma. Embolization can also provide secondary benefits if a tumor caused the bronchial artery injury, as embolization can result in tumor necrosis (74,78). In rare situations, embolization of a distal pseudoaneurysm may not be possible due to the anatomy and distortion from a lung tumor. In these cases, percutaneous embolization under CT guidance or a combination of fluoroscopic and US guidance may be attempted (79).

Pseudoaneurysms in the mediastinal segment of the bronchial arteries can be treated with occlusive embolization. Typically, metallic coils or plugs are used to completely occlude the arterial component distal to and proximal to the pseudoaneurysm. Thus, collateral circulation that develops after embolization will not revascularize the aneurysm from the distal arterial component. Rarely, the pseudoaneurysm is located within the mediastinum in close proximity to the aorta. In this case, complete embolization may be challenging, and a thoracic aorta stent graft may be necessary to occlude the arterial flow to the pseudoaneurysm completely (62,80).

Aorta and supra-aortic arteries

Damage to the aorta or supra-aortic vessels can present in various mechanisms in cancer patents. Unlike for venous structures, extrinsic tumor growth does not typically cause compression of large diameter arteries in the mediastinum. Tumor expansion between the supra-aortic vessels can displace these vessels, which may present as imaging abnormalities. While the tumors themselves might not directly damage the supra-aortic arteries, cancer treatments such as radiation or surgery can result in arterial or cardiac valvular damage (81). Although rare, tumor invasion can result in pseudoaneurysm development, as seen in a lung cancer erosion case report into the aortic arch (7). Pseudoaneurysms can also be caused by fungal or mycobacterial infections, which are not uncommon in immunocompromised cancer patients. Historically, these patients were treated surgically, but there is growing evidence that endovascular treatments provide a minimally invasive treatment alternative (82).

Endovascular treatment of arterial pathology in the aorta and supra-aortic vessels is predominantly performed with the placement of a covered stent. Arterial access is typically obtained via the common femoral arteries. An open surgical access to the common femoral arteries was traditionally necessary to advance the thoracic aorta stents. Percutaneous access has evolved with new closure devices that can facilitate stent advancement to a certain size without open surgical access (83). Injury or stenosis in the supra-aortic arteries can also be approached through brachial or radial artery access in certain situations, again depending upon the size of the stent required (Figure 7) (84).

Figure 7 JenyA 60-year-old man with epithelioid malignant mesothelioma status post left pleurectomy decortication, resection of the diaphragm, and posterior mediastinal lymph node dissection with adjuvant radiation to the left hemithorax. The patient presents to the emergency room with large volume hemoptysis, left shoulder pain, and left upper extremity pallor and numbness. A CT demonstrated a pseudoaneurysm in the left subclavian artery with bronchial fistula and pleural cutaneous fistula (A, arrow identifies pseudoaneurysm with adjacent mediastinal and parenchymal hematoma). Arterial access was achieved via both a femoral and left brachial access (B, arrow and arrowhead respectively). Angiograms through the bilateral accesses confirmed and further characterized the pseudoaneurysm (C, arrow). A stent was successfully placed via the left brachial artery access, with occlusion of the pseudoaneurysm and reconstitution of blood flow (D, arrow). CT, computed tomography.

Stent deployment for the aorta or supra-aortic arteries is performed under fluoroscopy, similar to stent deployment in other vascular locations. For complex aortic arch treatment, intra-procedural cross-sectional imaging can be used for additional information to confirm successful stent deployment (85). Complications include stent migration, endovascular leak, and arterial dissection (86). After stent placement, recommendations include anticoagulation with dual antiplatelet medications for several weeks to months and typically at least one antiplatelet lifelong (87,88). This need for anticoagulation is an important consideration when planning stent placement in cancer patients who might develop intracranial metastases or bleeding diathesis from tumor growth or systemic treatments in the near future. Follow-up with contrast-enhanced CT, MRI, or duplex ultrasound is routinely scheduled to monitor for endovascular leaks around the stent (88,89).

Conclusions

Compromise of mediastinal vasculature in cancer patients can be caused by a myriad of etiologies, including extrinsic tumor compression, erosion of the vascular wall, benign or malignant thrombus, and iatrogenic injury. While this review is comprehensive, the current level of evidence for the described treatment outcomes is limited due to the lack of large cohort studies or randomized control studies, data heterogeneity necessary to achieve high levels of literature evidence. This is perhaps due to the relative rarity of various disease processes affecting the mediastinum and the relative novel and burgeoning field of endovascular and interventional radiology. Furthermore, patients present with marked clinical variety based on the location, type, and degree of vascular injury. The decision for endovascular treatment is best pursued with a multidisciplinary discussion to tailor the treatment for the patient’s presenting symptoms, comorbidities, and future cancer treatment considerations.

Acknowledgments

Funding: None.

Footnote

Provenance and Peer Review: This article was commissioned by the Guest Editors (Bruce Sabath and Roberto F. Casal) for the series “Management of Airway and Vascular Invasion in the Mediastinum” published in Mediastinum. The article has undergone external peer review.

Peer Review File: Available at https://med.amegroups.com/article/view/10.21037/med-22-43/prf

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://med.amegroups.com/article/view/10.21037/med-22-43/coif). The series “Management of Airway and Vascular Invasion in the Mediastinum” was commissioned by the editorial office without any funding or sponsorship. J.K. reports grants from Linglife AI, Elekta and Trisalus, consulting fees from Boston Scientific, Johnson & Johnson, SIRTex and Argon, payments from Johnson & Johnson, meeting supports from Boston Scientific and Johnson & Johnson. J.K. serves as the board member for Johnson & Johnson, Boston Scientific and Linglife AI. J.K. holds stocks in Bayou Surgical. None of the conflicts is relate to the content of this manuscript. The authors have no other 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 or integrity of any part of the work are appropriately investigated and resolved. All clinical procedures described in this study were performed in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was not required as the provided images have no identification whatsoever that would identify any particular patient treated at MD Anderson.

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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