Pathophysiology of Saphenous Vein Graft Disease

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Several factors contribute to stenosis of saphenous vein grafts, including intimal hyperplasia, plaque formation, and graft remodeling. Additionally, arterialization of the graft accelerates atherosclerosis. Furthermore, atheroma found in SVGs are more friable (easily break into small pieces) and more prone to thrombus than plaques found in native vessels. Another reason why SVGs are more susceptible to thrombotic occlusion is that they lack side branches^[1].

Saphenous Vein Graft Aneurysms[edit | edit source]

It is also known as SVGA, aortocoronary saphenous vein graft aneurysms, saphenous vein graft aneurysm disease and saphenous vein graft aneurysmal dilatation.

Causes of Saphenous Vein Graft Aneurysms[edit | edit source]

• Atherosclerosis
• Hypertension
• Mycotic
• Postoperative mediastinitis
• Previous aneurysms
• Torn sutures

Amyloidosis of Saphenous Coronary Bypass Grafts[edit | edit source]

Amyloid has been associated with accelarated disease in saphenous vein grafts.^{[2] [3] [4] [5] [6]}

Rupture of the Saphenous Vein Coronary Artery Bypass Grafts[edit | edit source]

Aspergillus species causing a necrotizing vasculitis have been associated with rupture of a saphenous vein grafts.

Phlebitis in the Implanted SVG[edit | edit source]

Acute postoperative phlebitis is a rare complication of SVG implantation which can be associated with SVG thombosis, and a purulent pericarditis and mediastinitis^[7][8].

Potential for Pre-Operative SVG Failure[edit | edit source]

It should be noted that studies of SVGs that are not implanted show that about 1% of veins are already stenosed by > 50% before implantation^[9].

References[edit | edit source]

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