Saphenous Vein Graft Aneurysms 

Updated: Nov 10, 2014
Author: Jesse P Jorgensen, MD; Chief Editor: Eric H Yang, MD 

Overview

Background

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. 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.

Pathophysiology

The SVG to left anterior descending is the most common site for aneurysm formation, followed by the right coronary artery, and least commonly, the left circumflex.

True aneurysms, which usually develop in the body of the vein graft and are typically fusiform, are usually the result of a chronic, degenerative process caused by vascular injury that results from hyperlipidemia and progression of atherosclerosis. The initial event in SVGA formation is thought to be atheroma formation followed by plaque rupture, resulting in injury to the vessel wall, which 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 surgical trauma.

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.

Epidemiology

Frequency

International

Mild aneurysmal dilation of SVGs is relatively common, with a frequency of approximately 14% within 5-7 years of surgery.

A literature review from the first reported case in 1975 until 2002 revealed 50 true aneurysms and 26 false aneurysms. In a review of all bypass cases at one institution from 1975-1991, of 1658 patients with 5579 grafts, 4 developed SVGA, giving an incidence of 0.07%. The incidence of significant SVGA is probably underestimated because the initial presentation may be rupture leading to sudden death, the aneurysm may not appear on angiography if it contains significant thrombus, and many patients are asymptomatic.

Mortality/Morbidity

No long-term studies regarding prognosis are available. Prognosis is partly related to patients' underlying coronary artery disease and comorbid conditions.

Morbidity and mortality considerations include the following:

  • SVGA rupture is associated with high morbidity and mortality rates.

  • Ischemic symptoms, either angina or infarction, can occur from graft occlusion, embolic phenomena, or compression of the graft by the aneurysm. Many SVGAs cause no symptoms and remain subclinical; thus, morbidity and mortality estimates are likely affected by a selection bias.

  • In symptomatic patients, the mortality rate is high, with 13 of 46 patients (28%) dying within 90 days of initial symptoms.

Race

Among reported cases in which race was identified, the patients were white. This may reflect a selection bias.

Sex

SVGAs are more common in men than women. In the literature review cited above, 64 of the 76 patients (84%) were men; this may be, in part, because more men than women undergo coronary artery bypass surgery.

Age

The average age of patients at the time of diagnosis is 59 years (range, 23-80 y). Women tend to be older than men at presentation, probably because they tend to develop coronary artery disease later in life and therefore undergo coronary artery revascularization later.

Patients with SVGA typically present years after surgery, with 10-20 years as the average time to onset; however, both true and false SVGAs have been reported within months of surgery. Elgharably et al described the case of a false SVGA that presented 36 years after a coronary artery bypass graft; it initially appeared, on serial echocardiograms, to be a right atrial myxoma.[2]

 

Presentation

History

Most patients with true aneurysms (45-55%) are asymptomatic and present incidentally with a hilar or mediastinal mass on chest radiograph or other imaging modality. Several cases of saphenous vein graft aneurysm (SVGA) that mimic a cardiac mass on echocardiography have been described. Symptomatic patients present with acute coronary syndrome with myocardial infarction (20-25%), unstable angina (15-20%), or congestive heart failure (5%). Compression of surrounding structures may occur; recently, cardiac tamponade from right atrial compression and cardiac ischemia from compression of an adjacent left internal mammary artery bypass graft have been reported.

By contrast, most patients with 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.

Note the following:

  • The sudden onset of chest pain in a patient with SVGA may represent abrupt fistula formation with coronary steal.

  • Hemoptysis may occur because of bleeding from the SVGA into lung parenchyma or from fistula formation between the SVGA and a bronchus.

  • The triad of chest pain, mediastinal mass, and previous coronary bypass surgery has been suggested to raise suspicion for SVGA.

Physical

The diagnosis of SVGA is typically not suggested by physical examination. However, the following signs may be uncovered:

  • Cutaneous bleeding or hemoptysis from fistula development to either the skin or bronchial tree

  • Palpable pulsatile mass

  • A new murmur (from fistula formation)

Causes

Authorities have identified a number of disorders in individuals with SVGAs. However, whether the following disorders represent random associations, secondary associations, or true causal factors of SVGAs remains unknown:

  • Atherosclerosis

  • Previous aneurysms

  • Postoperative mediastinitis prior to aneurysm development

  • Hypertension

  • In one small series, 15% of SVGAs were mycotic and 5% were associated with torn sutures.

 

DDx

Diagnostic Considerations

Important considerations

Patients who have had coronary artery revascularization with vein grafts and present with angina or infarction should have a thorough cardiac workup to exclude recurrent disease or aneurysm development.

The diagnosis of saphenous vein graft aneurysm (SVGA) requires a high index of suspicion and may require multiple imaging modalities for the diagnosis to be made.

During surgery, care must be taken to avoid manipulation of the aneurysm, as this may dislodge thrombus and result in distal embolization.

Biopsy of a mediastinal mass without knowledge that it represents an SVGA could be catastrophic.

Other problems to be considered

Other conditions to consider in the differential diagnosis of patients with suspected SVGA include lymphoma and pericardial cyst.

Differential Diagnoses

 

Workup

Laboratory Studies

Evaluate for cardiac ischemia with serum biomarkers (creatine kinase and troponin).

Evaluate the patient's overall medical status, including renal and hepatic function.

Use electrocardiography (ECG) to evaluate for cardiac ischemia or infarction.

Imaging Studies

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, including computed tomography (CT) scanning, aortography, transesophageal echocardiography, transthoracic echocardiography, magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), cardiac catheterization, intravascular ultrasonography, and radionuclide ventriculography.

Note the following:

  • A CT scan of the chest shows the aneurysm as an enhancing mass in the mediastinum. CT, particularly high resolution studies such as 64-slice multidetector CT gated to the cardiac cycle, provides several useful pieces of information, including determining continuity of the mass with the SVG, determining the presence of thrombus, differentiating between solid and cystic masses, and mass effect on adjacent structures. See the image below.

    CT scan demonstrating a saphenous vein graft aneur CT scan demonstrating a saphenous vein graft aneurysm.
  • Coronary angiography is the criterion standard to delineate the anatomy of the aneurysm. A limitation of coronary angiography is impaired opacification of the SVGA if thrombus is present within the aneurysm. See the images below.

    Cardiac catheterization demonstrating a saphenous Cardiac catheterization demonstrating a saphenous vein graft aneurysm.
    Aortogram demonstrating a saphenous vein graft ane Aortogram demonstrating a saphenous vein graft aneurysm.
  • Sherry and Harms described the ability of MRI to demonstrate the anatomy of the aneurysm and to assess the patency of the graft.[3]

  • Khabeishvili and associates demonstrated that transesophageal echocardiography can assist in diagnosing an SVGA.[4]

  • Benari and associates demonstrated that SVGAs can be correctly identified with first-pass radionuclide ventriculography.[5]

  • Ennis and associates have diagnosed SVGAs with intravascular ultrasonography.[6]

See the videos below for more information on SVGAs.

Another view demonstrating the saphenous vein graft aneurysm. Video courtesy of John S. Douglas, MD.
The first of many coils being deployed in the aneurysm. Video courtesy of John S. Douglas, MD.
 

Treatment

Medical Care

The optimal approach to treating patients with saphenous vein graft aneurysms (SVGAs) is not well defined, with limited data consisting of case reports and case series. Treatment options include medical therapy with surveillance, surgical therapy, and percutaneous intervention. In the largest treatment series of SVGA, Dieter and colleagues report the outcome of 13 patients, of which 2 had surgical therapy and the remainder were deemed poor surgical candidates due to comorbid conditions. Eight patients had an uneventful follow-up course while being managed medically, and no survival benefit was attributed to either surgical or conservative management.[7]

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 MRI, CT, or coronary angiography to monitor aneurysm growth over time.

Note the following:

  • Antihypertensive and cholesterol-lowering therapy, such as with an 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.

Careful monitoring in the ICU is required during the initial postoperative period if surgical resection or percutaneous intervention is performed.

Consultations

Cardiologists and cardiac surgeons are required for thorough patient evaluation.

Diet and Activity

A heart-healthy diet should be followed to decrease risk factors for further cardiac disease. 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.

Surgical Care

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 SVG and placement of a new bypass graft.[8] Additional approaches include resection of the abnormal portions of the diseased graft with new SVG segments sewn in end-to-end, ligation of the old graft without revascularization, and hematoma evacuation with repair of the SVG with a venous patch graft. The latter 2 approaches have been successfully performed off-pump.

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. Consider the following:

  • The most commonly used percutaneous approach has been coil embolization of the aneurysm (see videos below). This technique carries the risk of occluding flow to the bypassed arterial system. 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 coils into the parent vessel once deployed in the aneurysm.

  • Rezq et al reported success with peripheral covered tents as an alternative to surgery.[9] See the images below.

    Angiogram of a saphenous vein graft to the distal right coronary artery demonstrating a large aneurysm in the mid portion of the graft. Video courtesy of John S. Douglas, MD.
    Final angiogram demonstrating coils within the aneurysm, and almost complete cessation of flow from the parent vessel into the aneurysm. Video courtesy of John S. Douglas, MD.
  • Covered stents have been used to isolate the aneurysm from the graft lumen; the JOSTENT Coronary Stent Graft (Abbott Vascular, Redwood City, Calif), that consists of an ultra-thin layer of polytetrafluoroethylene (PTFE) sandwiched between 2 stainless steel stents, has been used successfully in several cases. 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. In a second case, the JOSTENT achieved an excellent immediate angiographic result with exclusion of a false aneurysm, but on routine 6-month angiogram, the false aneurysm recurred in the same location, possibly due to focal perforation of the PTFE layer.[10]

  • Placement of autologous vein graft-covered stents has been used successfully, and in one patient where a covered stent was not immediately available, 3 overlapping uncovered stents with prolonged balloon inflation successfully excluded a false aneurysm.

  • Brilakis et al compared restenosis rates after the placement of paclitaxel-eluting stent versus bare metal stent in saphenous vein graft lesions. They found that paclitaxel-eluting stents were associated with lower rates of target vessel failure and angiographic restenosis than bare metal stents.[11]

  • A newer approach that has been used is placement of the Amplatzer vascular plug (AGA Medical, Golden Valley, MN); in the single reported case, an 8-mm device was placed in the neck of a 9-cm true SVGA with an excellent result.[12]

  • For patients undergoing percutaneous coronary intervention (PCI) in saphenous vein grafts, drug-eluting stents may be the preferred method of treatment because they have a lower risk of target vessel revascularization compared with bare metal stents. No differences are recognized between drug-eluting stents and bare metal stents in terms of stent thrombosis when used in saphenous vein graft interventions.[13]

 

Medication

Medication Summary

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.

Salicylates

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.

 

Follow-up

Further Outpatient Care

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

Patients who have been medically treated require close follow-up care in order 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.

Complications

Complications of saphenous vein graft aneurysms 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.