Mechanisms, Prevention and Treatment of Saphenous Vein Graft Disease
Section snippets
Pathophysiology
The continuum of SVG failure begins with harvesting, which causes vessel ischemia followed by reperfusion injury ultimately, leading to endothelial damage.3 Extracellular matrix proteins become exposed to blood flow, inducing adhesion and activation of platelets. Activated platelets generate thrombogenic, chemotactic and vasoconstricting agents, as well as express superficial adhesion molecules that bind circulating leukocytes, that facilitate their migration into the vessel wall.3
Symptoms and Sequelae of SVG Failure
The risk of SVG disease progression, ultimately leading to graft occlusion, is highest in the grafts already showing evidence of disease.5 The patency of angiographically normal or mildly changed SVGs is favorable and absence of graft disease is a strong predictor of survival after CABG. Importantly, while not every SVG occlusion is symptomatic, there is an association of SVG failure with increased rates of adverse cardiac events. A retrospective study with 7-year follow-up (n = 1243), revealed
Prevention of SVG Failure
CABG performed on a beating heart without the use of cardiopulmonary bypass (off-pump) has been proposed as an alternative to a conventional procedure. However, as extracorporeal oxygenation induces platelet dysfunction, it may be paradoxically beneficial in terms of early vein graft patency. Conversely, off-pump CABG induces a transient state of hypercoagulability and aspirin resistance in post-operative period. In a metaanalysis of 12 RCTs SVG patency was higher after on-pump (RR = 1.41; 1.24
Interventional Treatment of SVG Failure
Diffuse nature of SVG degeneration challenges the possibilities of interventional treatment. PCI to the most diseased segment is an effective strategy to relieve ischemic symptoms, but has no influence on the course of SVG degeneration in non-stented segments. Majority of ischemic events following PCI to SVG result from disease progression in non-treated SVG segments. SOS trial subanalysis reported rapid progression of untreated intermediate SVG lesions to obstructive disease (28, 47 and 84% at
Conflict of Interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
References (45)
- et al.
Long-term patency of saphenous vein and left internal mammary artery grafts after coronary artery bypass surgery: results from a Department of Veterans Affairs Cooperative Study
J Am Coll Cardiol
(2004) - et al.
Coronary bypass graft fate and patient outcome: angiographic follow-up of 5,065 grafts related to survival and reoperation in 1,388 patients during 25 years
J Am Coll Cardiol
(1996) - et al.
Disease progression in nonintervened saphenous vein graft segments: a serial intravascular ultrasound analysis
J Am Coll Cardiol
(2009) - et al.
Pathology of drug-eluting versus bare-metal stents in saphenous vein bypass graft lesions
JACC Cardiovasc Interv
(2012) - et al.
Incidence and clinical correlates of ruptured plaques in saphenous vein grafts: an intravascular ultrasound study
J Am Coll Cardiol
(2005) - et al.
Management of patients with aortocoronary saphenous vein graft aneurysms: JACC State-of-the-Art review
J Am Coll Cardiol
(2021) - et al.
Relation of early saphenous vein graft failure to outcomes following coronary artery bypass surgery
Am J Cardiol
(2005) - et al.
Clinical presentation and angiographic characteristics of saphenous vein graft failure after stenting: insights from the SOS (Stenting Of Saphenous Vein Grafts) trial
JACC Cardiovasc Interv
(2009) - et al.
Comparison of graft patency between off-pump and on-pump coronary artery bypass grafting: an updated meta-analysis
Ann Thorac Surg
(2014) - et al.
The no-touch saphenous vein for coronary artery bypass grafting maintains a patency, after 16 years, comparable to the left internal thoracic artery: a randomized trial
J Thorac Cardiovasc Surg
(2015)