ABSTRACT: Stenting of saphenous vein graft (SVG) lesions is associated with a high risk of periprocedural myocardial infarction, due primarily to distal embolization. Although embolic protection devices are the only clinical trial-proven therapy for preventing periprocedural myocardial infarction during SVG interventions, they are currently used in only a small proportion of eligible patients. In this review, we present an update on the clinical data and practical recommendations for using the currently available embolic protection devices during SVG interventions.
Key Words: embolic protection; saphenous vein graft
J INVASIVE CARDIOL 2009;21:415–417
Periprocedural myocardial infarction (MI) occurs in up to 28% of all saphenous vein graft (SVG) percutaneous coronary interventions (PCI)1 and is associated with higher morbidity and mortality.2 Although several pharmacologic (administration of calcium channel blockers,3 nitrates,4 adenosine,5 thrombolytics6 and glycoprotein IIb/IIIa inhibitors7) and mechanical (direct stenting8, use of undersized stents9 or covered stents to trap debris against the SVG wall10 and embolic protection devices EPD2) strategies have been evaluated over the last two decades to address this problem, only EPDs have been shown to decrease periprocedural MI in SVG interventions.
SVG Degeneration Score
Although no-reflow is more likely with PCI of diffusely diseased SVGs, it can also occur in PCI of focally diseased SVGs.11 A degeneration score was recently developed to quantify the extent of lumen irregularity and ectasia (> 20% of the reference normal segment) within the SVG.12 The cumulative length (in millimeters or mm) of SVG luminal irregularities or ectasia is divided by the length of the entire SVG and presented as a percent. If the ratio is 75%. Along with SVG plaque volume, the SVG degeneration score has been shown to be the strongest predictor of 30-day major adverse cardiac events (MACE) following an SVG PCI.12 Although SVGs with a higher degeneration score have a higher risk of post-PCI MI, the use of an EPD provided a similar relative risk reduction (approximately 40%) in all categories of the SVG degeneration score.
Although the current PCI guidelines give a Class I recommendation for the use of an EPD in SVG PCI when technically feasible, in an analysis of the American College of Cardiology National Cardiovascular Data Registry (ACC NCDR), Mehta et al reported that EPDs were only used in 22% of SVG PCI procedures.13 We believe that this review of contemporary EPDs available for use during SVG PCI will prompt greater adoption of EPD use during SVG PCI.
Available EPDs for SVG PCI
Most SVG lesions are located in the mid-body of the graft (38%), followed by proximal (30%) and distal graft (23%) locations.14 Ostial and anastomotic lesions account for 15 mm from the graft ostium, and distal protection for lesions located ≤ 15 mm of the ostium. It is worth noting that in the control arm, 24% of patients remained unprotected, compared to 2% in the test arm, and 82% patients in the test arm were protected by the Proxis alone.
Conclusion
In conclusion, the evidence base for use of EPDs during SVG PCI is compelling, and its use is a Class I indication of the American College of Cardiology and American Heart Association guidelines. We hope that our review provides this evidence in a readily accessible format to the interventional community and promotes universal adoption of embolic protection during SVG PCI.
Acknowledgements. The authors wish to acknowledge the generous support of the Clark Gregg Fund of the Harris Methodist Foundation, Forth Worth, Texas, and the technical assistance of Avantika Banerjee in the preparation of this manuscript.
From the VA North Texas Healthcare System, Dallas, Texas, and the University of Texas Southwestern Medical Center, Dallas, Texas.
Disclosures: Dr. Banerjee has received speaker honoraria from Boston Scientific Corp., Cordis Corp., St. Jude Medical, and Medtronic, Inc., and research grants from Boston Scientific and The Medicines Company. Dr. Brilakis has received speaker honoraria from St. Jude Medical and Medicure.
Manuscript submitted June 2, 2009 and final version accepted June 11, 2009.
Address for correspondence: Subhash Banerjee, MD, 4500 S. Lancaster Road (111a), Dallas, TX 75216. E-mail: subhash.banerjee@utsouthwestern.edu
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