Direct Stenting and Placement of a Distal Protection Device after Laser Angioplasty in a Saphenous Vein Graft with Severe Stenos

Patients with recurring symptoms of angina due to saphenous vein graft (SVG) disease pose a difficult and increasingly frequent challenge. In general, these patients are older and have more extensive and diffuse disease of both the native circulation and the SVGs than do patients who have not undergone coronary bypass surgery. Repeat coronary bypass surgery is an option, but it is technically more demanding, is associated with higher mortality and morbidity, and has less optimal, long-term clinical results when compared with first-time bypass operations.¹ Favorable results have been achieved by using balloon angioplasty for the treatment of discrete, short lesions in relatively new bypass grafts. However, the results are less favorable in the treatment of older, diffusely diseased SVGs, wherein balloon angioplasty often results in inadequate dilatation, a high restenosis rate, and an increased likelihood of distal embolization associated with mortality and significant morbidity.^2,3 Percutaneous excimer laser angioplasty has been approved by the U.S. Food and Drug Administration for treatment of recurrent stenosis of SVGs. Results from industry-sponsored registries in approximately 1,000 patients with SVG lesions have shown that laser angioplasty can be performed successfully in 88–99% of patients and major complications (in-hospital death and Q-wave MI) were low (1.2% and 0.7%, respectively).4 In addition to debulking the atherosclerotic plaque and increasing the compliance of the lesion, we believe laser angioplasty can be utilized to ablate plaque and thrombus in critical graft lesions, allowing for safer passage of a distal protection device. Case Report. In August 2003, a 74-year-old white man with a history of triple-vessel coronary artery disease and multiple coronary artery bypass surgeries presented to the emergency department at our hospital after experiencing several episodes of chest pain and shortness of breath. Twenty-two years ago, the patient underwent triple coronary artery bypass surgery with a sequential saphenous vein graft to the first diagonal branch and the left anterior descending (LAD) artery and a saphenous vein graft to the left circumflex (LCX) artery. In 2001, a second bypass operation was performed by grafting the left internal mammary artery (LIMA) to the first obtuse marginal artery, and transluminal myocardial laser revascularization was performed in an effort to control his severe stable angina. His post-operative ejection fraction was 28%. The patient remained angina-free for two years. Three weeks before admission to our hospital, the patient experienced an episode of chest pain and was admitted to a local hospital, where he underwent coronary angiography. Unfortunately, the sequential graft to the diagonal branch and the LAD was not visualized on the angiogram. The patient was treated conservatively with intravenous heparin and nitroglycerin and was discharged home with a prescription of long-acting oral nitrates and calcium-channel blockers. He continued to experience frequent chest pain upon minimal exertion, despite the use of long-acting nitrates. The day before admission, he experienced 10/10-scaled severe left-sided chest pain which radiated to the right arm, as well as nausea, vomiting, and diaphoresis at rest. He came to our emergency department the next day. His blood pressure was 107/59 and his heart rate was regular (76 beats/min). The cardiovascular examination was otherwise unremarkable. Laboratory tests included a complete blood count (CBC) and coagulation and electrolyte panels, the results of which were all within normal limits. The results of the cardiac enzymes showed an elevated troponin I and an MB isoenzyme fraction of creatine kinase consistent with acute non-Q-wave myocardial infarction (MI). An electrocardiogram showed Q-waves in the inferior leads and a T-wave inversion in the anterior leads, which was also present in the previous examination. The patient had a history of hypertension and hypercholesterolemia. His current medications included aspirin (325 mg/day), clopidogrel (75 mg/day), carvedilol (25 mg, twice daily), losartan (25 mg/day), digitalis (0.25 mg/day), simvastatin (10 mg/day), amlodipine (5 mg/day), famotidine (10 mg, twice daily), and isosorbide mononitrate (60 mg/day). The patient did not smoke or drink alcohol. The coronary angiogram showed a 99% stenosis in the middle portion of a tortuous sequential SVG to the diagonal and LAD artery at the site of the diagonal graft anastomosis (TIMI grade II; Figure 1A). All native coronary arteries were occluded. The ejection fraction was 35%, with evidence of an old inferior myocardial infarction. The LIMA graft was patent and the SVG-to-LCX graft was totally occluded from its origin. Given the critical nature of the lesion, we planned to perform laser angioplasty of the saphenous vein graft before inserting the distal protection device and stent to prevent distal embolization from the advancement of the protection device and to ablate any overlying thrombus. A 7 Fr sheath was inserted into the right femoral artery. Initially, the lesion was crossed with a 0.014 inch floppy guidewire (GT1 Floppy, Medtronic AVE, Santa Rosa, California). The concentric excimer laser catheter (0.9 mm, followed by 1.4 mm; Vitesse-COS, Spectranetics, Colorado Springs, Colordo) was advanced slowly over the wire, with saline flush used during ablation (Figure 1B). Two passes with each catheter were performed to achieve adequate recanalization. The distal protection device (FilterWire EX, Boston Scientific Corporation, Natick, Massachusetts) was delivered after laser angioplasty by using a buddy wire technique during advancement. The original guidewire was then withdrawn and a 4.0 x 23 mm Cypher coronary stent (Cordis, Miami Lakes, Florida) was deployed. Because the stenosis was a hard lesion that did not fully yield to stent placement, balloon inflation with a 4.0 x 18 mm balloon (Quantum Ranger, Boston Scientific/Scimed, Maple Grove, Minnesota) at 17 atm was performed. The angiogram showed TIMI grade III and only a 10% visual remaining residual stenosis (Figure 2). The distal protection device was removed using a delivery-retrieval sheath, and a large amount of embolic debris was seen within the filter. Eptifibatide was administered during the procedure. No complications were noted during or after the procedure. The patient’s post-procedural electrocardiogram revealed no significant changes. The post-procedural cardiac enzyme levels, including CPK and CK-MB, were within normal limits 18 hours after the procedure, and the patient was discharged home in good condition on the following day. The patient presented with atypical chest pain five months later and underwent repeat coronary angiography after a nuclear perfusion study suggested anterior ischemia. The origin of the graft, which had a moderate stenosis on the previous angiogram, had progressed. A stent was successfully placed using distal protection (Figure 3). We did not perform laser athero-ablation because the lesion was not critical and the risk associated with advancing the filter was deemed low. No significant restenosis was noted in the stented area. Discussion. Although the pathologic changes are similar in both, SVG disease does not parallel the severity of atherosclerotic progression in native vessels. Graft stenosis results from intimal hyperplasia, mostly within the first year, followed by atherosclerotic plaque build-up and graft remodeling in subsequent years.⁵ As a result of these processes, only about 80% of venous grafts remain patent five years after surgery, and approximately 60% at 7 to 10 years.⁶ Several features unique to venous grafts may be responsible for increasing the thrombogenic and proliferative response: 1) The endothelial cells in veins are larger, thinner, and less firmly anchored than in arteries; 2) the tunica intima is more permeable; and 3) the internal elastic lamina is poorly defined.⁷ Therefore, atherosclerotic plaques in SVGs are softer, more friable, and usually associated with thrombus and platelet activation when compared to plaques in the native coronary arteries. In addition, vein graft lesions tend to accumulate lipids because of increased lipid uptake, decreased lipolysis, and increased synthesis of complex lipids.⁸ Finally, many vein grafts are oversized relative to the distal vessel, and this size mismatch may result in sluggish flow in the graft that could promote thrombus formation. Coronary embolization, resulting in elevated cardiac enzymes and an ST-elevation or non-ST-elevation MI, is an important cause of morbidity and mortality after PTCA in SVGs. The likelihood of developing an elevation in serum CK-MB was evaluated in a report of 1,056 patients with successful dilation of an SVG lesion.⁹ A major increase in CK-MB occurred in 15% of patients. Mortality at one year was significantly greater in patients with a major increase in serum CK-MB compared to those with no increase or only a minor elevation. On multivariate analysis, major CK-MB elevation was the strongest independent predictor of late mortality. For this reason, a variety of embolic protection devices have been developed. Plaque debris can be retrieved and distal embolization minimized after percutaneous interventions with these devices, leading to a reduction in both MI and no-reflow.^10,11 Despite their advantages, embolic protection devices are not without problems and complications. For example, the filters must be placed distally, beyond the lesion, and the profile of these devices, although small, still accounts for a small risk of embolization when crossing the lesion. In addition, the filters may become filled with debris, arresting flow in the SVG and inhibiting the function of the filter, which is dependent upon flow. If there is no flow, emboli are no longer trapped within the filter but rather within the static column of blood between the lesion and the filter. Unless the blood is vigorously aspirated, recapture of the filter will result in restitution of antegrade coronary blood flow and distal embolization of debris. Because of the potential for distal embolization and dissection resulting from advancement of a bulky distal protection device through a critical stenosis in an SVG, we chose laser angioplasty for atherothromboablation of the stenosed SVG and subsequently placed a stent in the vessel. In our experience, embolic debris is sometimes evident in the filter on angiography immediately after gentle lesion cross with deflated angioplasty balloons, stents, and even after advancement of the filter itself. This most likely represents filter-induced fragmentation of the atherothrombotic plaque during advancement. Laser thrombolysis is the selective removal of thrombus from occluded blood vessels using laser energy. The new, small laser catheters are capable of high energies and are easy to use. It has been observed from in vitro studies that the pulsed excimer laser can create deep, smooth-edged craters in hard, calcified atherosclerotic tissue, with minimal damage to adjacent normal tissue.¹² Results from studies of in vitro or in vivo animal models also suggest that the excimer lasers precisely cut through atheroma, without harmful thermal injury. The preliminary experience with atherosclerotic plaques in the aorta of human cadavers shows minimal damage to adjacent normal tissue, with sharp incision margins.¹³ In atherosclerotic rabbits, examination of the arterial wall one month after excimer laser angioplasty showed less intimal and medial tissue, and typical thermal effects were absent on microscopic examination.¹⁴ It has been suggested that pre-dilatation with a small-diameter balloon may allow for safer advancement of distal protection devices in critical lesions. We believe that predilation itself can also lead to distal embolization and no-reflow. Rogers et al. have recently shown that particulate retrieved with a vascular filtering device or an occlusion balloon was similar in amount and character.¹⁵ Therefore, we propose the use of laser atherothrombo-ablation to reduce the risk of this complication, because light can be transmitted without contacting the target thrombus. The laser tip need only be within 1 cm of the thrombus to work effectively. The use of laser angioplasty may be of particular value when obstructions can be crossed with a guidewire, but not with a conventional balloon catheter or distal protection device or when the occlusion is confirmed to be extremely long. An initial study of 535 stenosed SVGs suggests that excimer laser-facilitated angioplasty has the most favorable outcome for discrete lesions located at the ostium and in the body of smaller SVGs.¹⁶ For grafts with a mean age of 8 years, clinical success was achieved in 92% of the cases, with a 3% distal embolization rate. More recent experience at another institution has been excellent: 44 consecutive patients who underwent excimer laser coronary angioplasty in de novo saphenous venous graft lesions with a mean graft age of 10 years had 100% procedural success rate and 0% incidence of CPK greater than three times the upper limit.¹⁷ Of note, abciximab was used in 85% of the patients. Controversy still exists as to whether laser angioplasty provides benefits in addition to those of percutaneous techniques; retrospective comparisons have provided various results.^18,19 The data registry enrolling 151 patients with an acute myocardial infarction showed 0% distal embolization among the 31 patients with degenerated vein graft lesions when a laser catheter was used to debulk angiographically high-risk thrombi.²⁰ Which patients are the best candidates for this technique — with respect to safety and benefit — is a question that has yet to be answered. Any added costs for the technique (the laser catheter with the concomitant use of a distal protection device and a drug-eluting stent) may be offset by the potential decrease in complications and prolonged hospital stays. A larger series of patients is needed to further study the potential benefits of this technique.

1. Lytle BW, Loop FD, Taylor PC, et al. The effect of coronary reoperation on the survival of patients with stenoses in saphenous vein bypass grafts to coronary arteries. J Thorac Cardiovasc Surg 1993;105:605–612;Discussion 612–614. 2. de Feyter PJ, van Suylen RJ, de Jaegere PP, et al. Balloon angioplasty for the treatment of lesions in saphenous vein bypass grafts. J Am Coll Cardiol 1993;21:1539–1549. 3. Douglas JS Jr, Gruentzig AR, King SB III, et al. Percutaneous transluminal coronary angioplasty in patients with prior coronary bypass surgery. J Am Coll Cardiol 1983;2:745–754. 4. Litvack F, Eigler N, Margolis J, et al. Percutaneous excimer laser coronary angioplasty: Results in the first consecutive 3,000 patients. The ELCA Investigators. J Am Coll Cardiol 1994;23:323–329. 5. Motwani JG, Topol EJ. Aortocoronary saphenous vein graft disease: Pathogenesis, predisposition, and prevention. Circulation 1998;97:916–931. 6. Loop FD, Lytle BW, Cosgrove DM, et al. Influence of the internal mammary artery graft on 10-year survival and other cardiac events. N Engl J Med 1986;314:1–6. 7. Smith SH, Geer JC. Morphology of saphenous vein-coronary artery bypass grafts: Seven to 116 months after surgery. Arch Pathol Lab Med 1983;107:13–18. 8. Cox JL, Chiasson DA, Gotlieb AI. Stranger in a strange land: The pathogenesis of saphenous vein graft stenosis with emphasis on structural and functional differences between veins and arteries. Prog Cardiovasc Dis 1991;34:45–68. 9. Mautner SL, Mautner GC, Hunsberger SA, Roberts WC. Comparison of composition of atherosclerotic plaques in saphenous veins used as aortocoronary bypass conduits with plaques in native coronary arteries in the same men. Am J Cardiol 1992;70:1380–1387. 10. Stone GW, Rogers C, Hermiller J, et al. Randomized comparison of distal protection with a filter-based catheter and a balloon occlusion and aspiration system during percutaneous intervention of diseased saphenous vein aorto-coronary bypass grafts. Circulation 2003;108:548–553. 11. Baim DS, Wahr D, George B, et al. Randomized trial of a distal embolic protection device during percutaneous intervention of saphenous vein aorto-coronary bypass grafts. Circulation 2002;105:1285–1290. 12. Tomaru T, Geschwind HJ, Boussignac G, et al. Comparison of ablation efficacy of excimer, pulsed-dye, and holmium-YAG lasers relevant to shock waves. Am Heart J 1992;123:886–895. 13. Grundfest WS, Litvack F, Forrester JS, et al. Laser ablation of human atherosclerotic plaque without adjacent tissue injury. J Am Coll Cardiol 1985;5:929–933. 14. Rosenfeldt FL, Chi L, Black AJ, et al. Excimer laser angioplasty in the atherosclerotic rabbit: Comparison with balloon angioplasty. Am Heart J 1992;124:349–355. 15. Rogers C, Huynh R, Seifert PA, et al. Embolic protection with filtering or occlusion balloons during saphenous vein graft stenting retrieves identical volumes and sizes of particulate debris. Circulation 2004;109:1735–1740 16. Bittl JA, Sanborn TA, Yardley DE, et al. Predictors of outcome of percutaneous excimer laser coronary angioplasty of saphenous vein bypass graft lesions. The Percutaneous Excimer Laser Coronary Angioplasty Registry. Am J Cardiol 1994;74:144–148. 17. Ebersole DG. Excimer laser for revascularisation of saphenous vein grafts. Lasers Med Sci 2001;16:78–83. 18. Strauss BH, Natarajan MK, Batchelor WB, et al. Early and late quantitative angiographic results of vein graft lesions treated by excimer laser with adjunctive balloon angioplasty. Circulation 1995;92:348–356. 19. Ahmed JM, Hong MK, Mehran R, et al. Comparison of debulking followed by stenting versus stenting alone for saphenous vein graft aortoostial lesions: Immediate and one-year clinical outcomes. J Am Coll Cardiol 2000;35:1560–1568. 20. Topaz O, Ebersole D, Das T, et al. Excimer laser angioplasty in acute myocardial infarction (The CARMEL Multicenter Trial). Am J Cardiol 2004; 93: 694–701.