Massive particulate atheromatous material was observed on histological examination of debris from a Percusurge embolization containment device, used in clinically uncomplicated direct stent coronary vein graft intervention. This is provided first to illustrate the severity of distal embolization that can go clinically unnoticed after direct stenting and second to support the case for routine use of distal protection devices for vein graft intervention Case Report. A 72-year-old male underwent percutaneous coronary intervention to a 95% lesion in a right coronary artery (RCA) vein graft (VG) (Figure 1A). He underwent 2 coronary artery bypass operations 22 and 14 years prior, with grafts placed to the left anterior descending (LAD), circumflex (CX) and RCA at the second operation. The RCA VG had undergone prior intervention, with an Ultra stent (Guidant Corporation, Santa Clara, California) placed proximal and a P154M stent (Cordis Corporation, Miami Lakes, Florida) placed distal. There was documented left ventricular impairment with an ejection fraction of 28%. He was admitted with a non-Q wave myocardial infarction, requiring intra-aortic balloon pump support, and coronary angiography revealed a culprit RCA VG lesion. Using 8 French guide support, a 300 cm length, 0.0014´´ High Torque Floppy II wire (Guidant Corporation) was advanced to the lesion, and crossed after “buddying” with the same wire in a 190 cm length. A Percusurge embolization containment device was advanced to the distal VG and the distal balloon inflated to 5.5 mm, after which the lesion was direct-stented using a 4.5 x 28 mm Ultra stent (Guidant Corporation) inflated at 12 atmospheres for 60 seconds (Figure 1B). The Percusurge system was then aspirated. The VG was also stented more proximally with two further 4.5 x 18 mm Ultra stents, inflated to 14 atmospheres for a total of 60 seconds, again under Percusurge protection. The final appearances were angiographically very satisfactory (Figure 1C) and there was no rise in cardiac enzymes. Fragments of the debris retrieved from the Percusurge device were embedded in OCT tissue medium (Labtek), and snap-frozen in liquid nitrogen. Five-micron sections were cut and treated with hematoxylin and eosin (H&E), oil-red-0, periodic acid-Schiff (PAS), trichrome, Verhoeff elastic, Alcian blue and von Kossa stains. Immunohistochemical stains included antibodies to CD68 (KP-1, Dako), smooth muscle actin (SMA, Sigma), CD3 and CD20 (L26, Dako). After blocking with horse serum, the tissue was treated with primary antibodies followed by horse anti-rabbit and mouse secondary antibody and streptavidin (BioGenex) for anti-CD3 or horse anti-rabbit and mouse secondary antibody and avidin-biotin horseradish peroxidase complex (Dako) for the other primary antibodies. Slides were developed with 3-amino-9-ethyl-carbazole (Sigma) and counterstained with Gill’s hematoxylin (Fisher Scientific). The histologic findings are shown in detail in Figure 2, and were consistent with atheromatous fragments, measuring up to 1,000 µm in maximal diameter, containing lipid, microcalcifications and some fibrin. There were histocytic foam cells, few T-cell lymphocytes and rare B-cell lymphocytes in the tissue. There was an apparent absence of smooth-muscle-like cells. Discussion. The Percusurge is one of a number of novel embolization containment devices. It relies on a distal balloon inflation to prevent downstream emboli during intervention, followed by manual aspiration of blood and atheromatous debris prior to distal balloon deflation and has recently been proposed for VG intervention.1 VG atherosclerosis is morphologically distinct from native coronary artery disease in that it is often diffuse and concentric, with little calcification or fibrous cap formation, whereas native disease tends to be focal and eccentric, often with marked calcification and a clearly defined fibrous cap.2–4 Importantly, VG lesions may also be more friable and associated with higher rates of procedure-related complications.5 The type of degenerated, aged vein graft as in this case is at high risk for “no reflow” during intervention, a phenomenon thought to be due to distal embolization, although other mechanisms such as the release of vasoconstrictor substances have also been proposed.6,7 In this case, it is possible that some degree of embolization occurred prior to Percusurge insertion, at the time of wire manipulation, although this would have been unlikely to have been aspirated. It is also clear that after Percusurge deployment the procedure went very smoothly, with no clinical suggestion of embolization or “no reflow” phenomenon. Histology of particulate debris from 3 of 15 patients undergoing VG intervention has previously shown cholesterol clefts, macrophages, lipid and fibrin, although the histological appearances of microcalcification, lipid-laden crystalline material and macrophages, and the T and B lymphocytes observed here, have not been previously reported.8,9 In a separate series, these debris particles were a mean of 204 ± 57 µm (range, 8–3,427 µm) in the major axis, and significantly less plaque material was observed when stents were used compared to angioplasty alone.9 The present findings, however — with fragments up to 1,000 µm — demonstrate that massive embolization of atheromatous debris can still occur, even after angiographically uncomplicated direct stent VG intervention. While these findings are clearly from only one case, the complexity of the debris and the sheer size of the particles are striking, given the apparently benign nature of the intervention, using minimal manipulation and contemporary direct stent techniques. The present study supports the previous histological reports,8,9 but also suggests that a large amount of debris still occurs despite improved interventional techniques, and also provides further insight into the histological complexity of this atheromatous material. These observations support the routine use of protection devices for treatment of VG lesions, and suggest that further clinical evaluation is warranted.
1. Oesterle SN, Hayase M, Baim DS, et al. An embolization containment device. Cathet Cardiovasc Intervent 1999;47:243‚Äì250. 2. Kalan JM, Roberts WC. Morphologic findings in saphenous veins used as coronary arterial bypass conduits for longer than 1 year: Necropsy analysis of 53 patients, 123 saphenous veins and 1,865 five-millimeter segments of veins. Am Heart J 1990;119:1164‚Äì1184. 3. Lie JT, Lawrie GM, Morris GC. Aortocoronary bypass saphenous vein graft atherosclerosis: Anatomic study of 99 vein grafts from normal and hyperlipoproteinemic patients up to 75 months postoperatively. Am J Cardiol 1977;40:906‚Äì914. 4. Motwani J, Topol EJ. Aortocoronary saphenous vein graft disease. Pathogenesis, predisposition and prevention. Circulation 1998;97:916‚Äì931. 5. Kereiakes DJ. Percutaneous transcatheter therapy of aorto-ostial stenoses. Cathet Cardiovasc Diagn 1996;38:292‚Äì300. 6. Hillegass WB, Dean NA, Liao L, et al. Treatment of no-reflow and impaired flow with nitric oxide donor nitroprusside following percutaneous coronary interventions: Initial human clinical experience. J Am Coll Cardiol 2001;37:1335‚Äì1343. 7.Baim DS, Carrozza JP Jr. Understanding the ‚Äúno reflow‚Äù problem. Cathet Cardiovasc Diagn 1996;1:7‚Äì8. 8. Carlino M, De Gregorino J, Di Mario C, et al. Prevention of distal embolization during saphenous vein graft angioplasty. Experience with a new temporary occlusion and aspiration system. Circulation 1999;99:3221‚Äì3223. 9. Webb JG, Carere RG, Virmani R, et al. Retrieval and analysis of particulate debris after saphenous vein graft intervention. J Am Coll Cardiol 1999;34:468‚Äì475.