Cutting Balloon Angioplasty

Michael S. Lee, MD, Varinder Singh, MD, Thomas J. Nero, MD, James R. Wilentz, MD
Michael S. Lee, MD, Varinder Singh, MD, Thomas J. Nero, MD, James R. Wilentz, MD
The cutting balloon was first designed by Barath et al.1 Approved for use outside the United States since 1995, the cutting balloon (InterVentional Technologies Inc., San Diego, California) has been recently approved as a treatment modality for interventional cardiologists for “high-pressure balloon resistant lesions” including de novo lesions and in-stent restenosis (ISR).2 Cutting balloon angioplasty (CBA) features three or four atherotomes (microsurgical blades), which are 3–5 times sharper than conventional surgical blades.3 The atherotomes, which are fixed longitudinally on the outer surface of a non-complaint balloon, expand radially and deliver longitudinal incisions in the plaque and vessel, relieving its hoop stress. The atherotomes, which measure 10 or 15 millimeters in length by 0.011–0.013´´ in height by 0.004–0.006´´ in width, are mounted along the length of the cutting balloon. Balloon sizes of 2.00–3.25 mm are provided with 3 atherotomes; those of 3.50–4.00 mm have 4 atherotomes. The unique design of the cutting balloon is engineered to protect the vessel from the edges of the atherotomes when it is deflated. This minimizes the risk of trauma to the vessel as the balloon is passed to and from the target lesion. With CBA, lower balloon inflation pressures (4–8 atmospheres) are recommended. The atherotomes deliver a controlled fault line during dilatation to ensure that the crack propagation ensues in an orderly fashion.3 CBA dilates the target vessel with less force to decrease the risk of a neoproliferative response and restenosis. Currently, CBA is indicated for the dilatation of coronary artery stenosis to improve myocardial perfusion in high-pressure balloon resistant lesions (Table 1). The target lesion should be discrete (CBA versus balloon angioplasty in de novo lesions. CBA has a different mechanism of action than plain old balloon angioplasty (POBA) in the dilatation of coronary artery stenosis. With POBA, dilatation of the target lesion occurs with force directed in a random manner that is converted to circumferential shear stress because of the artery-balloon geometry. Differential resistance to radial force within the lesion, due to varying degrees of fibrosis, may result in multiple arcs of dissection, rather than the radially directed fissures delivered by the longitudinal atherotomes of CBA.4 Intravascular ultrasound (IVUS) performed on 24 lesions (12 with CBA and 12 with POBA) has shown that CBA and its longitudinal incisions of plaque and vessel wall decrease the rate of dissection.5 Aorto-ostial lesions, either in native vessels or grafts, are particularly difficult to treat successfully with POBA despite high-pressure inflations because of the atherosclerosis, fibrosis and calcification present in the aortic wall.6 There is also a tendency for the target vessel to recoil after balloon inflation with POBA due to the higher concentration of muscle and elastic fibers around the ostium. Kurbaan and colleagues showed that aorto-ostial lesions, which were resistant to dilatation with POBA at high pressures, were successfully dilated with CBA to facilitate the insertion of a stent.6 In another study of mechanisms, sixty-three percent of the luminal enlargement produced by CBA was due to plaque compression and 37% was due to vessel expansion.7 With POBA, twenty-seven percent was due to plaque compression and 73% was due to vessel expansion. Hence, it appears that a more organized disruption of plaque due to the longitudinal atherotomes of CBA increases the luminal cross-sectional area by compression of the plaque rather than vessel expansion. The adhesion molecule, Mac-1 (CD11b/CD18), is upregulated on the surface of neutrophils after POBA and may reflect vessel wall injury or serve as a predictor of restenosis.8 These changes were seen to a lesser degree with CBA than with POBA.9 In animal models, platelet-derived growth factor A, mRNA expression and DNA synthesis were localized to the incisional segments after dilatation with CBA but were observed circumferentially after POBA.10 This suggests that CBA may result in less of the vessel wall trauma that is associated with balloon dilatation and, subsequently, reduced neutrophil activation, which may account for lower rates of restenosis. Percutaneous coronary intervention (PCI) of small vessel lesions is particularly challenging because of the high rates of restenosis despite current devices including the Rotablator and coronary stents. In an editorial recounting his experience since the initial days of coronary angioplasty, Meier notes that in small vessels POBA was associated with higher rates of both restenosis and dissection, which can lead to abrupt closure of the target vessel.11 In general, the findings of Kuntz and Baim as well as those of earlier studies have tied the restenosis rates closely to both reference vessel diameter and post-procedural diameter regardless of treatment modality.12,13 Even in the recent stenting literature, such as the ISAR small arteries study, restenosis remained higher in small vessels treated with stent implantation,14 although the BESMART small randomized study in vessels with a reference diameter of 2.24 mm found an advantage for stenting over POBA.15 The CAPAS study, which assessed CBA in small vessel lesions, demonstrated that CBA was associated with a significantly lower rate of angiographic restenosis than POBA (25.2% versus 41.5%, respectively; p = 0.009) at 3 months.16 Hence, CBA may have both a restenosis and acute procedural result advantage over POBA in small (fibrotic and calcified) vessels that may have a tendency to dissect as well as when the use of stents is associated with a higher rate of recurrence (long lesion, branch stenosis).17 Table 1. Lesion characteristics amenable for the cutting balloon3 • Resistant to high-pressure balloon inflation • Reference vessel 2.0–4.0 mm • Discrete (Table 2. Inclusion criteria for the Global Randomized Trial • De novo type A and B lesions • Native coronary arteries • Lesion length Reprinted with permission from InterVentional Technologies, Inc. Table 3. Exclusion criteria for the Global Randomized Trial • Untreated severe hypertension (diastolic blood pressure >= 115 mmHg) • Systolic blood pressure = 2.0 mg/dl • Known and symptomatic carotid artery stenosis Reprinted with permission from InterVentional Technologies, Inc. The Global Randomized Trial. The Global Randomized Trial was the largest multicenter randomized clinical trial that compared CBA with POBA in the treatment of de novo type A or B lesions in native coronary arteries up to 20 mm in length.18 The vessel size inclusion criterion was 2.0–4.0 mm. A total of 1,238 patients (1,385 lesions) from 5 countries and 31 centers throughout the United States, Canada, and Europe were enrolled and randomly assigned to CBA (n = 617) or POBA (n = 621). Inclusion and exclusion criteria are described in Tables 2 and 3. The major efficacy endpoints were angiographic restenosis rates at 6 months and target lesion revascularization (TLR) at 9 months. The safety endpoint was major adverse cardiac events (MACE), consisting of death, emergent coronary artery bypass surgery, Q-wave myocardial infarction and TLR at 9 months. Repeat coronary angiograms at 6 months were performed on 88.7% of all eligible patients, with clinical follow-up at 9 months on 83.3%. There was no significant difference between CBA and POBA at 6-month follow-up in angiographic and clinical results. The primary endpoint of angiographic restenosis at 6 months was 31.4% in the CBA group versus 30.4% in the POBA group (relative risk, 1.03; 95% confidence interval, 0.87–1.23). The secondary endpoints of 9-month TLR and MACE were also not statistically significantly. MACE beyond 30 days was 10.0% in the CBA group versus 12.9% in the POBA group (relative risk, 0.78; 95% confidence interval, 0.57–1.06). This trial showed that CBA was equivalent in safety and efficacy endpoints to POBA, but did not prove superiority for the general pool of PCI patients. Further investigation was thus warranted to assess the role of the device in particular situations. In-stent restenosis. Restenosis is the major limitation of PCI. Although coronary stenting has decreased the incidence of acute vessel thrombosis and restenosis compared with POBA, stenting does not ensure long-term vessel patency.19,20 Since coronary stenting is the most common PCI, with over 800,000 stents deployed per year in the United States, the most common form of restenosis is ISR. ISR is primarily caused by smooth muscle cell proliferation and extracellular matrix formation and neointimal hyperplasia, as opposed to balloon angioplasty in which restenosis is due to a combination of neointimal hyperplasia along with elastic recoil and negative vascular remodeling.21–24 The incidence of ISR is 20–50%.25 ISR was initially managed with POBA. However, POBA was associated with a recurrent restenosis rate of 30–60%.25–27 In the U.S. Multicenter Palmaz-Schatz stent registry, there was a 30% rate of restenosis in the 1,189 patients.25 Of the 39.7% of patients treated with POBA for ISR, fifty-four percent had recurrent restenosis of the target vessel. It was then proposed that atheroablation using rotational, directional or excimer laser atherectomy might have clinical utility in the treatment of ISR.28–30 However, the search for therapies to prevent restenosis has been largely disappointing. No single form of PCI has emerged as the superior treatment modality. Mehran et al.31 reported that POBA, rotational ablation, laser therapy and restenting had essentially the same re-restenosis rates for the treatment of ISR. POBA did not lead to satisfactory results, with a high recurrence rate.32 Restenting of the in-stent restenotic lesion showed no advantage. Although acutely beneficial in re-expanding the stenotic lesion, improved long-term outcome was not maintained.33–35 Vom Dahl et al.36 showed no beneficial effect of rotational atherectomy and excimer laser angioplasty in decreasing the rate of recurrence. Endovascular brachytherapy in combination with other modalities has emerged as an effective treatment for ISR. The GAMMA-137 and SCRIPPS trials,38 which used gamma radiation, and the START trial,39 which used beta radiation, showed that the rate of re-restenosis was significantly reduced by delivering radiation therapy to in-stent restenotic lesions treated with conventional PCI. Despite promising results, concerns remain over potential long-term effects of radiation in a coronary artery. Thus, brachytherapy may be reserved only for those patients with recurrent restenosis. CBA offers another option for ISR. CBA confers several potential advantages over POBA in the treatment of ISR. Because the longitudinal atherotomes can concentrate the dilatation force, the cutting balloon enables more resistant lesions to be overcome. Shallow cuts force the plaque to break apart evenly. Lumen dilatation with CBA for ISR may be related to the extrusion of the fibrous residual neointimal plaque out of the stent struts,40,41 with less tissue injury when compared to other PCI types.42 During dilatation, elastic recoil may be reduced by the surgical incisions from the atherotomes.43–45 Scoring the neointimal plaque seems to lessen the elastic and fibrotic continuity of the internal fibrous layer, allowing the tissue to be pushed outward through the stent struts.40 IVUS revealed that overexpansion of the stent is the principal mechanism of action of high-pressure (greater than 15 atm) POBA for ISR.17 IVUS also demonstrated that CBA is superior to POBA in the extrusion of the neointimal plaque outside the stent.46 CBA, when compared with POBA, was associated with a greater acute gain but a smaller increase in stent area, which suggests that a higher quantity of neointimal plaque extruded outside the stent. Lower inflation pressures with CBA (8.8 ± 1.6 atm) lead to better results than with POBA (16.7 ± 4.0 atm).47 CBA achieved a better and more stable angiographic result than POBA and was associated with a lower rate of TVR at 9 months (12% vs. 20%, respectively).48 In addition, the “watermelon seeding effect” seen with other percutaneous techniques is not usually seen with CBA for ISR. In the treatment of ISR, Muramatsu et al.49 demonstrated with IVUS that there was a larger luminal area acute gain in patients treated with CBA (2.5 ± 0.8 mm2) compared with patients treated with POBA (1.8 ± 1.0 mm2). There was a smaller late lumen loss in patients treated with CBA (0.5 ± 0.4 mm2) compared with patients treated with POBA (1.3 ± 0.5 mm2). At follow-up (mean follow-up, 5.4 months), the rate of restenosis was lower in patients treated with CBA (24%) compared with patients treated with PTCA (59%). The IVUS findings suggested that the dilatation mechanism is the reduction of plaque through horizontal redistribution and compression because there was no increase in stent area or total vessel area. This leads to the hypothesis that CBA may minimize intimal membrane injury, thus suppressing neointimal hyperplasia. IVUS was used in another study to clarify the mechanism of lumen enlargement during CBA. Ahmed et al. studied the pre- and post-IVUS of 10 patients with native artery ISR and revealed that lumen cross-sectional area enlargement after CBA was almost entirely due to stent-lumen extrusion through stent struts (decrease in stent-lumen cross-sectional area with an increase in external elastic membrane and peri-stent plaque and media cross-sectional area), rather than additional stent expansion.50 In a matched comparison study, Adamian et al.42 showed that patients with ISR treated with CBA had a lumen loss that was lower at follow-up (at 6.2 ± 3.2 months) when compared to rotational atherectomy and additional stent implantation (0.63 ± 0.6 mm vs. 1.30 ± 0.8 mm and 1.36 ± 0.8 mm, respectively; p CBA and endovascular brachytherapy. With the proven efficacy of endovascular brachytherapy, the use of CBA may complement brachytherapy in the treatment of ISR, especially for diffuse lesions. CBA may be used to dilate the target lesion before a more definitive therapy like brachytherapy because of its accurate positioning and resistance to slip (“watermelon seeding”) during balloon inflation of fibrotic in-stent restenotic lesions.56 When compared with rotablation, where the burr must start proximally and may jump distal to the desired treatment length, this would limit the injury to the proximal or distal vessel that is a crucial aspect of the “edge effect” restenotic lesions that can be seen with brachytherapy.55 Summary. Studies thus far have shown that the cutting balloon is equivalent in safety and efficacy to POBA in the overall PCI population, and may afford an advantage over POBA in decreasing the incidence of restenosis and TLR in particular groups of interventional patients, although this has yet to be proven. The supportive evidence for CBA comprises a few small IVUS and non-randomized studies (except for CAPAS). The only large clinical trial performed with CBA, the Global Randomized Trial, showed that it was not superior to POBA in the treatment of de novo lesions. One group of patients who may benefit from CBA is those with small vessels less than 3.0 mm in diameter. A second group is those with difficult to dilate aorto-ostial lesions. Finally, those with fibrous but not highly calcified lesions may respond. Coronary artery stenting has decreased the rate of restenosis in PCI, but has brought about the new phenomenon of ISR.19 ISR remains the major limitation to PCI with stenting. The application of antimetabolite-coated stents is likely to substantially decrease this phenomenon, as has been shown in initial findings with sirolimus coating.57 In as much as ISR remains a clinical problem, its optimal treatment remains unclear. Although much of the data on CBA in ISR come from a few small nonrandomized studies, CBA offers another option alone or when applied along with brachytherapy in the armamentarium for the treatment of ISR, especially for focal lesions. Because of the atherotomes in CBA, dilatation is achieved with less injury to the intima, thus potentially suppressing neointimal hyperplasia. It may also be used to prepare diffuse ISR lesions prior to treatment with brachytherapy. If endovascular brachytherapy remains a mainstay in the treatment of ISR, a prospective trial will be needed to compare CBA to POBA as preparation for brachytherapy.
1. Barath P, Fishbein MC, Vari S, Forrester JS. cutting balloon: A novel approach to percutaneous angioplasty. Am J Cardiol 1991;68:1249–1251. 2. Muramatsu T, Tsukahara R, Ho M, et al. Efficacy of cutting balloon angioplasty for in-stent restenosis: An intravascular ultrasound evaluation. J Invas Cardiol 2001;13:439–444. 3. Ajani AE, Kim HS, Castagna M, et al. Clinical utility of the cutting balloon. J Invas Cardiol 2001;13:554–557. 4. Kurbaan AS, Foale RA, Sigwart U. cutting balloon angioplasty for in-stent restenosis. Cathet Cardiovasc Intervent 2000;50:480–483. 5. Martinez D, Goicolea J, Alfonzo F, et al. Intravascular ultrasound findings after cutting balloon angioplasty (Abstr). Eur Heart J 1996;17(Suppl):188. 6. Kurbaan AS, Kelly PA, Sigwart U. cutting balloon angioplasty and stenting for aorto-ostial lesions. Heart 1997;77:350–352. 7. Suzuki T, Nakamura M, Matsuda K, et al. Plaque compression without plaque shift is the mechanism of stenting after cutting balloon angioplasty. Am J Cardiol 1999;84(Suppl):56P. 8. Inoue T, Sakai Y, Morooka S, et al. Expression of polymorphonuclear leukocyte adhesion molecules and its clinical significance in patients treated with percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1996;28:1127–1133. 9. Inoue T, Sakai Y, Hoshi K, et al. Lower expression of neutrophil adhesion molecule indicates less vessel wall injury and might explain lower restenosis rate after cutting balloon angioplasty. Circulation 1998;97:2511–2518. 10. Barath P. Microsurgical dilatation concept: Animal data. J Invas Cardiol 1996;8:2A–5A. 11. Meier B. How to treat small coronary vessels with angioplasty. Heart 1998;79:215–216. 12. Schwarz F, Preusler W, Reifart N, et al. Long term results of coronary angioplasty in relation to vessel size. Deutsch Med Wochenschr 1991;116:1857–1861. 13. Hirschfeld JW, Schwartz JS, Jugo R, et al., and the M-Heart Investigators. A multivariate model statistical model to relate lesion and procedure variables to restenosis. J Am Coll Cardiol 1991;18:647–656. 14. Kastrati A, Schöming A, Dirshinger J, et al. A randomized trial comparing stent with balloon angioplasty in small vessels in patients with symptomatic coronary artery disease: ISAR-SMART Study Investigators: Intracoronary stenting or angioplasty for restenosis reduction in small arteries. Circulation 2000;102:2593–2598. 15. Koning R, Eltchaninoff H, Commeau R, et al., for the BESMART (BeStent in Small Arteries) Trial Investigators. Stent placement compared with balloon angioplasty for small coronary arteries: In-hospital and 6-month clinical and angiographic results. Circulation 2001;104:1604–1608. 16. Izumi M, Tsuchikane E, Funamoto M, et al. Final results of the CAPAS trial. Am Heart J 2001;142:782–789. 17. Schiele F, Meneveau N, Vuillemenot A, et al. Intracoronary ultrasound assessment of balloon angioplasty in intrastent restenosis (Abstr). J Am Coll Cardiol 1997;29:240A. 18. Bonan R, Roose P, Suttorp M, et al. cutting balloon global randomized trial: Restenosis and revascularization rate (Abstr). Circulation 1997;96:I-324. 19. Fischman DL, Leon MB, Baim DS, et al. A randomized comparison of coronary stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med 1994;331:496–501. 20. Serruys PW, de Jaegere P, Kiemeneiji F, et al. A comparison of balloon expandable stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994;331:489–495. 21. Hoffman R, Mintz GS, Dussaillant GR, et al. Patterns and mechanisms of in-stent restenosis. A serial intravascular ultrasound study. Circulation 1996;94:1247–1254. 22. Kornowski R, Mintz GS, Kent KM, et al. Increased restenosis in diabetes mellitus after coronary interventions is due to exaggerated intimal hyperplasia. A serial intravascular ultrasound study. Circulation 1997;95:1366–1369. 23. Strauss BH, Umans VA, van Suylen RJ, et al. Directional atherectomy for the treatment of restenosis within coronary stents: Clinical, angiographic and histologic results. J Am Coll Cardiol 1992;20:1465–1473. 24. Kearney M, Pieczek A, Haley L, et al. Histopathology of in-stent restenosis in patients with peripheral artery disease. Circulation 1997;95:1998–2002. 25. Baim DS, Levine MJ, Leon MB, et al. Management of restenosis within the Palmaz-Schatz coronary stent (the U.S. multicenter experience). The U.S. Palmaz-Schatz Stent Investigators. Am J Cardiol 1993;71:364–366. 26. Gordon PC, Gibson M, Cohen DC, et al. Mechanism of restenosis and redilatation within coronary stents: Quantitative angiographic assessment. J Am Coll Cardiol 1993;21:1166–1174. 27. Macander PJ, Roubin GS, Agrawal SK, et al. Balloon angioplasty for the treatment of in-stent restenosis: Feasibility of, safety, and efficacy. Cathet Cardiovasc Diagn 1994;32:125–131. 28. Mintz GS, Hoffmann R, Mehran R, et al. In-stent restenosis: The Washington Hospital Center experience. Am J Cardiol 1998;81:7E–13E. 29. Dauerman HL, Baim DS, Cutlip DE, et al. Mechanical debulking versus balloon angioplasty for the treatment of diffuse in-stent restenosis. Am J Cardiol 1998;82:277–284. 30. Mehran R, Mintz GS, Satler LF, et al. Treatment of in-stent restenosis with excimer laser coronary angioplasty: Mechanisms and results compared with PTCA alone. Circulation 1997;96:2183–2189. 31. Mehran R, Dangas G, Mintz GS, et al. In-stent restenosis: “Rhe great equalizer” — Disappointing outcomes with all interventional strategies (Abstr). J Am Coll Cardiol 1993;33(Suppl A):63A. 32. Eltchaninoff H, Koning R, Tron C, et al. Balloon angioplasty for the treatment of coronary in-stent restenosis: Immediate results and 6-month angiographic recurrent restenosis rate. J Am Coll Cardiol 1998;32:980–984. 33. Elezi S, Kastrati A, Hadamitzky M, et al. Clinical and angiographic follow-up after balloon angioplasty with provisional stenting for coronary in-stent restenosis. Cathet Cardiovasc Intervent 1999;48:151–156. 34. Al-Sergani HS, Ho PC, Nesto RW, et al. Stenting for in-stent restenosis: A long-term clinical follow-up. Cathet Cardiovasc Intervent 1999;48:143–148. 35. Antoniucci D, Valenti R, Moschi G, et al. Stenting for in-stent restenosis. Cathet Cardiovasc Intervent 2000;49:376–381. 36. vom Dahl J, Radke PW, Haager PK, et al. Clinical and angiographic predictors of recurrent restenosis after percutaneous transluminal rotational atherectomy for treatment of diffuse in-stent restenosis. Am J Cardiol 1999;83:862–867. 37. Leon MB, Teirstein PS, Lansky A, et al. Intracoronary gamma radiation to reduce in-stent restenosis: The multicenter gamma-I randomized clinical trial. J Am Coll Cardiol 1999;33:19A. 38. Teirstein PS, Massullo V, Jani S, et al. Catheter-based radiotherapy to inhibit restenosis after coronary stenting. N Engl J Med 1997;336:1697. 39. Takagi A, Morino Y, Fox T, et al. Efficacy of intracoronary b-irradiation for the treatment on in-stent restenosis: Volumetric analysis by intravascular ultrasound. Circulation 2000;102(Suppl II):II-422. 40. Albiero R, Nishida T, Karvouni E, et al. cutting balloon angioplasty for the treatment of in-stent restenosis. Cathet Cardiovasc Intervent 2000;50:452–459. 41. Kinoshita Y, Matsuno Y, Ohta T, et al. Dilatation mechanism of cutting balloon angioplasty for in-stent restenosis: Comparison with plain old balloon angioplasty using volumetric intravascular ultrasound analysis (Abstr). Am J Cardiol 2000;86(Suppl 8A):120i. 42. Adamian M, Colombo A, Briguori C, et al. cutting balloon angioplasty for the treatment of in-stent restenosis: A matched comparison with rotational atherectomy, additional stent implantation and balloon angioplasty. J Am Coll Cardiol 2001;38:672–679. 43. Barath P, Fishbein MC, Vari S, Forrester JS. cutting balloon: A novel approach to percutaneous angioplasty. Am J Cardiol 1991;68:1249–1252. 44. Lary B. Coronary artery incision and dilation. Arch Surg 1980;115:1478–1480. 45. Barath P. Microsurgical dilatation concept: Animal data. J Invas Cardiol 1996;8:2A–5A. 46. Muramatsu T, Tsukahara R, Ho M, et al. Evaluation of mechanism of cutting balloon for in-stent restenosis by intravascular ultrasound. Am J Cardiol 1998;82(Suppl 7A):72S. 47. Kinoshita S, Suzuki T, Hosokawa H, et al. A comparison of initial and long-term results of cutting balloon and POBA in the treatment of in-stent restenosis. Jpn Intervent Meeting I-M029. 48. Chevalier B, Royer T, Guyon P, Glatt B. Treatment of in-stent restenosis: Short and midterm results of a pilot randomized study between balloon and cutting balloon (Abstr). J Am Coll Cardiol 1999;33(Suppl A):62A. 49. Muramatsu T, Tsukahara R, Ho M, et al. Efficacy of cutting balloon angioplasty for in-stent restenosis: An intravascular ultrasound evaluation. J Invas Cardiol 2001;13:439–444. 50. Ahmed JM, Mintz GS, Castagna M, et al. Mechanism of lumen enlargement during cutting balloon angioplasty for in-stent restenosis: An intravascular ultrasound study. J Am Coll Cardiol 2001;2(Suppl):78A. 51. Lousarian A, Akiyama T, Kobayashi Y, et al. Diffuse versus focal in-stent restenosis: Clinical angiographic and procedural determinants. Circulation 1997;96(Suppl 1):I-591. 52. Mehran R, Ito S, Abizaid A, et al. Does lesion length affect late outcome of patients with in-stent restenosis? Results of multicentre angioplasty for stent restenosis (LARS) registry. J Am Coll Cardiol 1998;31(Suppl A):142A. 53. Yokoi H, Kimura T, Nakagawa Y, et al. Long-term clinical and quantitative angiographic follow-up after the Palmaz-Schatz stent restenosis. J Am Coll Cardiol 1996;27(Suppl A):224A. 54. Iijima R, Nakamura M, Kitagawa Y, et al. The impact of cutting balloon angioplasty for the treatment of diffuse in-stent restenosis. Comparison with conventional balloon angioplasty. J Am Coll Cardiol 2001;2(Suppl):80A. 55. King SB. A cutting edge technology, or is it? J Am Coll Cardiol 2001;38:680–681. 56. Teirstein PS, Massullo V, Jani S, et al. Three-year clinical and angiographic follow-up after intracoronary radiation: Results of a randomized clinical trial. Circulation 2000;101:360–365. 57. Sousa JE, Costa MA, Abizaid A, et al. Lack of neointimal proliferation after implantation of sirolimus-coated stents in human coronary arteries. Circulation 2001;103:192–195.