Saphenous Vein Graft Aneurysms

Introduction
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.
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
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.
Clinical
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.
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.

http://emedicine.medscape.com/article/161328-overview