Saphenous Vein Graft Aneurysms

Coronary artery revascularization with saphenous vein grafts (SVGs) has become a surgical standard for treatment of coronary artery disease since Favaloro first described it in 1967. Riahi and associates described the rare complication of saphenous vein graft aneurysm (SVGA) in 1975.[1]

SVGA is defined as a localized dilation of the vessel to 1.5 times the expected normal diameter. These are classified as true and false aneurysms (or pseudoaneurysms): true aneurysms involve all 3 layers of the vessel wall, whereas false aneurysms involve disruption of 1 or more layers of the vessel wall with a well-defined collection of blood or hematoma outside the endothelium. True aneurysms present twice as often as pseudoaneurysms.[2]  Further classification of SVGAs as large or small is not well defined, although dilation to more than 2 cm has generally led to consideration for surgical therapy. SVGAs reported in literature range from 1-14 cm in diameter.

The most common site for saphenous vein graft aneurysm (SVGA) formation appears to be the right coronary artery (38.0%), followed by the left anterior descending (25.3%), obtuse marginal (10.9%), and left circumflex (10.5%), according to a systematic review of published cases by Ramirez et al.[3]  True aneurysms develop in the body of the vein graft and are typically fusiform. Early presentation of SVGA is attributed to an inherent weakness of the venous wall due to lack of circular muscle at the site of venous valves. Late presentation of SVGA is thought to be due to developing atherosclerosis and thrombus related to hyperlipidemia, hypertension, defects to the vein graft, and trauma.[4, 5, 6]

The initial event in SVGA formation is thought to be atheroma formation followed by plaque rupture, resulting in injury to the vessel wall. This cascade of events is exacerbated by arterial pressures within the vein graft.  Valve insertion points along the vein graft are especially prone to true SVGA formation, where smooth muscle in the media changes from circular to a weaker longitudinal orientation. Other possible contributing factors include varicosities with impaired elastic tissue integrity not detected at the time of harvesting, vascular injury from previous percutaneous intervention (PCI), and trauma to the graft at the time of surgery. Underlying collagen vascular disease may play a role in the occurrence of SVGA.[7]

False aneurysms are saccular and typically located at the proximal SVG anastomosis, although they have been reported in the body and at the distal anastomosis. These are thought to occur because of tension on the anastomosis with suture rupture, or from technical issues in suture placement. Infection, particularly postoperative mediastinal sepsis involving Staphylococcus aureus, is commonly associated with false aneurysm formation because of suture line dehiscence. SVGA formation in the body of the graft has been reported to occur at the site of previous PCI and in the setting of chronic corticosteroid use.

The mechanism responsible for the formation of saphenous vein graft aneurysm (SVGA) is poorly understood. Late formation of SVGA (>5 years after coronary artery bypass grafting [CABG]) is likely related to atherosclerotic degeneration leading to vessel wall weakening and resulting graft dilatation. Other factors contributing to SVGA formation include vessel wall ischemia after disruption of the vasa vasorum during the harvesting and grafting process. The high pressure and pulsatile flow of the arterial system may also contribute to SVGA formation.

Some combination of these entities likely explains late aneurysm development. Conversely, early SVGA formation likely occurs via different pathophysiology. Contributing factors leading to the formation of early SVGA include infection, intrinsic weakness of the venous wall utilized, and technical complications related to CABG surgery itself.[3]

Incidence

Aneurysmal dilation of saphenous vein grafts (SVGs) is thought to be relatively common; however, putting a number to the incidence remains a challenge. Some literature reports estimate the number to be as high as 14% at 6 to 12 years,[8]  whereas one case series suggested a much lower incidence of 0.07%.[9]

The true incidence of significant saphenous vein graft aneurysm (SVGA) is likely underestimated because the initial presentation may be rupture leading to sudden death, the aneurysm may not appear on angiography if it contains a significant thrombus and, importantly, many patients with SVGA do not have symptoms. It has been reported that one third of SVGA cases are found in asymptomatic patients.[3]

Race-, sex- and age-related demographics

Among reported cases of SVGA in which race was identified, the patients were White. Additionally, men represent 87% of the SVGA cases.[10]  The sex difference may be, in part, because men have a higher rate of atherosclerotic disease and more men than women undergo coronary artery bypass surgery.[3]

SVGAs present on average within the sixth decade of life. Women tend to be older than men at presentation, probably because they generally develop coronary artery disease later in life and therefore undergo coronary artery revascularization later than men.

Nearly 70% of SVGAs occur 10 years after coronary artery bypass surgery.[3]  However, time to onset has been reported over a wide range. Both true and false SVGAs have been reported within months of surgery. Baydoun et al described a SVGA presenting as abdominal pain compressing the adjacent liver 43 years after surgery.[11]

Morbidity/mortality

No long-term studies regarding prognosis are available, but saphenous vein graft aneurysm (SVGA) is thought to carry a poor prognosis, with survival suggested to be around 2 years.[3]  Underlying coronary artery disease, hyperlipidemia, and hypertension have negative effects on patient prognosis.[5]  Increasing aneurysm size is associated not only with higher risk of rupture but also with high morbidity and mortality.[3]  Ischemic symptoms occur from graft occlusion, embolic phenomena, or compression of the graft by the aneurysm. As previously mentioned, many SVGAs remain subclinical, thus morbidity and mortality estimates are likely affected by selection bias. In symptomatic patients, mortality is high, with 13 of 46 patients (28%) dying within 90 days of initial symptoms. Furthermore, in-hospital mortality for giant SVGA has been reported at greater than 15%.[12]  

Complications

Complications of SVGAs include the following:

• Sudden aneurysm rupture leading to hemothorax, hemopericardium, or sudden death

• Thrombus formation within the aneurysm is very common and may result in embolization to the bypassed vessel with ischemia or infarction.

• Compression and mass effect on adjacent cardiac and mediastinal structures

• Fistula formation between the aneurysm and right atrium, left atrium, right ventricle, pulmonary artery, bronchus, or chest wall

• Superior vena cava (SVC) syndrome has been reported in association with SVGA to right atrial fistulas and with false aneurysm rupture.

Saphenous vein graft aneurysm (SVGAs) are usually suspected after abnormalities are noted on chest radiographs.[6]  Most patients with true aneurysms (45-55%) are asymptomatic. According to reported cases, mean aneurysm size at diagnosis was 60.4 mm, with reports of pseudoaneurysms being even larger. Although aneurysm growth is commonly reported, rates of growth vary.[3]

Symptomatic patients with true aneurysms present with myocardial infarction (20-25%), unstable angina (15-20%), or congestive heart failure (5%). By contrast, most patients having false aneurysm present with symptoms, including unstable angina (45-50%), myocardial infarction (15%), bleeding (10%), hemoptysis (6%), and infection (4%). Only 15% of patients with false SVGA are asymptomatic.

The size of SVGAs and their proximity to intrathoracic structures causes a variety of mechanical complications that are well documented in the literature. Acute coronary syndrome and congestive heart failure are common findings associated with SVGA. More rare and/or severe complications include rupture, severe tricuspid stenosis, right atrial fistula formation, fistula formation leading to isolated right heart failure, cardiac compression and subsequent atrial flutter, pulmonary artery compression, high-gradient right ventricular outflow tract obstruction, and cardiac tamponade caused by a leaking SVGA.[13, 14, 15, 16, 17, 18, 19, 20]

 

The diagnosis of saphenous vein graft aneurysm (SVGA) is typically not suggested by physical examination. However, the literature has provided cases with a variety of findings includin: cutaneous bleeding or hemoptysis from fistula development to the skin or bronchial tree; palpable pulsatile anterior chest wall mass[13] ; a new murmur from fistula formation, abdominal pain from compression of upper abdominal organs[11] ; and stridor.[21]

Patients suspected to have a saphenous vein graft aneurysm (SVGA) should be evaluated for cardiac ischemia with serum biomarkers (creatinine kinase and troponin). The patient’s overall medical status should be considered, including their renal and hepatic function. Electrocardiography (ECG) should be utilized to evaluate for cardiac ischemia or infarction.

A chest radiograph may suggest a saphenous vein graft aneurysm (SVGA) by revealing abnormalities of the mediastinum or other thoracic structures. Multiple modalities have been used to confirm the diagnosis of SVGA. Case reports seem to favor cardiac computed tomography (CT) angiography (CTA) for establishing the diagnosis, treatment planning, and posttreatment evaluation.[10]  Other diagnostic tools include aortography, transesophageal echocardiography, transthoracic echocardiography, magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), cardiac catheterization, and intravascular ultrasonography.

CT scanning of the chest shows an SVGA as an enhancing mass in the mediastinum. CT scanning, particularly high-resolution studies gated to the cardiac cycle, provides useful information, including determining the continuity of the mass with the saphenous vein graft (SVG), determining the presence of thrombi, differentiating between solid and cystic masses, and the mass effect on adjacent structures. See the image below

Coronary angiography is the criterion standard to delineate the anatomy of the aneurysm. However, a limitation of coronary angiography is impaired opacification of the SVGA if a thrombus is present within the aneurysm. See the following image.

Sherry and Harms described the ability of MRI to demonstrate the anatomy of the aneurysm and to assess the patency of the graft.[22]  Khabeishvili and associates demonstrated that transesophageal echocardiography (TEE) can also assist in diagnosing an SVGA.[23]  Benari et al revealed that SVGAs can be correctly identified with first-pass radionuclide ventriculography.[24]  Ennis and colleagues have diagnosed SVGAs with intravascular ultrasonography.[25]

See the videos below for more information on SVGAs.

 

Because saphenous vein graft aneurysms (SVGAs) are rare, the approach to management has been derived from case reports and case series. Dieter and colleagues reported the outcome of 13 patients, two of whom had surgical therapy, while the remainder were deemed poor surgical candidates due to comorbid conditions.[9] Eight patients had an uneventful follow-up course while being managed medically, and there was no survival benefit attributed to either surgical or conservative management.

No “safe” size for SVGA surveillance is known, as even "small" SVGAs measuring up to 20 mm treated conservatively were associated with adverse outcomes in one third of cases.[3]  Mortality for patients receiving conservative management was higher at 23.8% than in similar patients managed with surgery (13.9%) or percutaneous intervention (6.1%).[3]   Regardless, patients may be treated conservatively because of comorbid conditions precluding surgery or because of patient preference.

Medical therapy has also been pursued based on imaging characteristics suggesting low risk for rupture, such as a thick aneurysm wall or absence of flow into the aneurysm because of thrombus, especially in asymptomatic patients. Additional features that may support conservative management include aneurysm diameter less than 1 cm and brisk flow through the graft. This strategy should include surveillance imaging with magnetic resonance imaging (MRI), computed tomography (CT) scanning, or coronary angiography to monitor aneurysm growth over time.

Of note, antihypertensive and cholesterol-lowering therapy, such as with a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin), may be beneficial in slowing aneurysm progression but limited data are available. The benefit of anticoagulant therapy with warfarin (Coumadin) is not known. The role of beta-blockers in preventing further SVGA dilatation, in contrast to their role in treating aortic aneurysms, has not been well studied. However, many of these patients, particularly those with angina, left ventricular systolic dysfunction, and/or a history of myocardial infarction, benefit from beta-blocker therapy. Aspirin is generally recommended in most patients with SVGA based on the presence of underlying coronary artery disease.

Diet and activity

A heart-healthy diet should be followed to reduce risk factors for further cardiac disease; however, the influence of diet on subsequent aneurysm formation is unknown. Early mobilization followed by gradual resumption of normal activity is important for successful postoperative recovery.

Consultations

Careful monitoring in the intensive care unit is required during the initial postoperative period if surgical resection or percutaneous intervention is performed. The Heart Team approach involving cardiologists and cardiothoracic surgeons is recommended for thorough patient evaluation. 

Sareyyupoglu et al retrospectively reviewed data from 16 patients who underwent surgical saphenous vein graft aneurysm (SVGA) repair. The authors recommended surgical revascularization for symptomatic patients, patients with aneurysms exceeding 1 cm in diameter, or patients with evidence of diminished graft flow.[2] Memon et al supported coil embolization as an alternative treatment option in patients with high surgical risk.[26]

A review of the literature suggests management ranges from surgical (58.4%) to percutaneous intervention (15.8%) to conservative management (20.1%).[3] Surgical therapy is generally considered when an SVGA is discovered, given the morbidity and mortality associated with aneurysm rupture. The optimal timing of surgery is unknown; however, in cases of symptomatic aneurysms, suspected mycotic aneurysm, fistula formation, and/or confirmed false aneurysm, urgent surgical intervention is strongly recommended. The traditional surgical approach has been ligation of the aneurysm-containing saphenous vein graft (SVG) and placement of a new bypass graft.[3]

Percutaneous options now include Amplatzer devices, covered stents, and coiling.[27, 28] Historically, percutaneous therapy has been reserved for patients who are poor surgical candidates. However, as percutaneous techniques evolve, these approaches are being considered as alternatives to surgical intervention. One such technique that has been described uses coil embolization of the aneurysm (see the videos below). However, this technique carries the risk of occluding flow to the bypassed arterial system. More recently, "stent-assisted" coil embolization has been described, whereby a stent is placed in the parent vessel across the mouth of the aneurysm, providing a scaffold to prevent prolapse of the coils into the parent vessel once deployed in the aneurysm. Rezq et al reported success with peripheral covered stents as an alternative to surgery.[27]

Covered stents have been used to isolate the aneurysm from the graft lumen; the JOSTENT Coronary Stent Graft, consisting of an ultra-thin layer of polytetrafluoroethylene (PTFE) sandwiched between two stainless steel stents, has been used successfully in several cases.[29] However, the results have been mixed due to technical issues. In one case, the JOSTENT migrated into the aneurysm, requiring placement of a second overlapping bare metal stent for repositioning, finally achieving a good result.[29] In a second case, the JOSTENT achieved an excellent immediate angiographic result with exclusion of a false aneurysm, but on routine 6-month angiography, the false aneurysm recurred in the same location, possibly due to focal perforation of the PTFE layer.[29]

Placement of autologous vein graft-covered stents has been used successfully, and in one patient in which a covered stent was not immediately available, three overlapping uncovered stents with prolonged balloon inflation successfully excluded a false aneurysm.[30]

In choosing between uncovered bare metal stents and drug-eluting stents, drug-eluting stents in SVGs yield superior long-term outcomes. For patients undergoing percutaneous coronary intervention (PCI) in SVGs, drug-eluting stents may be preferred to bare metal stents because they have a lower risk of target vessel revascularization. For example, Brilakis et al compared restenosis rates after the placement of paclitaxel-eluting stent versus bare metal stent in SVG lesions.[30] They found that paclitaxel-eluting stents were associated with lower rates of target vessel failure and angiographic restenosis than bare metal stents.[30] No differences are recognized between drug-eluting stents and bare metal stents in terms of stent thrombosis when used in SVG interventions.[31]

A newer approach that has been used is placement of the Amplatzer vascular plug; in a single reported case, an 8-mm device was placed in the neck of a 9-cm true SVGA with an excellent result.[32] Although reports suggest that surgery remains the preferred treatment strategy for SVGAs, morbidity and mortality are higher when compared with percutaneous approaches such as covered stents.[10, 13]

Endovascular stent graft repair of an SVGA by adapting an abdominal aortic graft to the ascending aorta has also been suggested in the setting of patients not candidates for traditional open repair for ascending aneurysms or dissections.[33]

Instruct patients to immediately return to the hospital if symptoms recur.

Patients who have been medically treated require close follow-up care to detect progression of saphenous vein graft aneurysm (SVGA) disease and emergence of other graft aneurysms.

Most importantly, patients need continued medical treatment of coronary artery disease and atherosclerosis.

No specific medications are recommended for treatment of symptomatic saphenous vein graft aneurysms (SVGAs). Many patients, because of their underlying coronary artery disease, benefit from beta-blockers and aspirin.

The role of antiplatelet and anticoagulant agents in the medical management of this entity is unknown.

Class Summary

Useful for prevention of ischemic events.

Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Treats mild to moderate pain and headache. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2. Acts on heat-regulating center of hypothalamus and vasodilates peripheral vessels to reduce fever.