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Utilisation of transluminal extraction atherectomy in the treatment of saphenous vein graft disease: two case reports
International Journal of Cardiology 66 (1998) 11–15
Utilisation of transluminal extraction atherectomy in the treatment of saphenous vein graft disease: two case reports H.L. White, D.H. Roberts*, J.S. Wright Cardiology Department, Blackpool Victoria Hospital, Whinney Heys Road, Blackpool, Lancashire FY3 8 NR, UK Received 28 August 1997; accepted 30 June 1998
Abstract Saphenous vein graft disease is an increasing problem as more patients undergo bypass grafting and to date the most effective management strategy remains undefined. The major limitations of angioplasty for saphenous vein graft lesions are the risk of distal embolization and restenosis. Primary stenting in this situation results in superior lumen enlargement and higher procedural success but is still associated with significant restenosis. We describe two cases in which transluminal extraction (TEC) atherectomy is utilised for the treatment of vein graft disease with good immediate and long term angiographic results. The first case reports the use of TEC atherectomy for the primary treatment of a discrete eccentric filling defect, and the second case describes the use of this technique in the management of in-stent restenosis. 1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: In-stent restenosis; Saphenous vein graft; TEC atherectomy
1. Case one A 35 year old man underwent double coronary artery bypass grafting, receiving saphenous vein grafts (SVG) to his posterior descending (PDA) and obtuse marginal (OM) arteries. Four years later following the recurrence of angina his left internal mammary artery (LIMA) was grafted onto his left anterior descending artery. His chest pain, classically ischaemic in nature, returned within 6 months and a clinical diagnosis of recurrent angina was made. (The 12 lead resting electrocardiogram disclosed longstanding deep T wave inversion across the precordial leads thus making exercise testing difficult to interpret). This was initially managed with medical therapy. After 18 months he was re-investigated for class IV angina. Cardiac catheterisation demonstrated *Corresponding author.
a large 3.5 mm SVG to the PDA with an eccentric filling defect narrowing the lumen by 80% (Fig. 1a). The SVG to the OM was occluded and there was a significant 70% lesion in the native circumflex. A 50% stenosis at the anastamosis of the LIMA graft was demonstrated. A multipurpose 10 Fr guiding catheter was introduced into the SVG to the PDA and a TEC wire was advanced to the native vessel. A 2.5 mm TEC device was selected because this is the largest available size and was felt the most appropriate for such a large calibre vessel (3.5 mm). TEC atherectomy was performed involving several passes through the diseased segment and resulted in a 10% residual stenosis (Fig. 1b) so adjuvant angioplasty was not undertaken. At the same session he underwent successful PTCA of his native circumflex artery resulting in a ,10% residual stenosis. He was discharged home on aspirin and his usual anti-anginal medication.
0167-5273 / 98 / $19.00 1998 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 98 )00200-9
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H.L. White et al. / International Journal of Cardiology 66 (1998) 11 – 15
Fig. 1. Serial angiograms – case one. (a) Eccentric filling defect in the saphenous vein graft to the Posterior Descending Artery (LAO). (b) The same lesion following transluminal extraction atherectomy (LAO). (c) The saphenous vein graft 12 months later showing no evidence of restenosis. (RAO).
Twelve months later following the recurrence of further clinical angina repeat catheterisation was performed confirming no evidence of vein graft restenosis (Fig. 1c). The anastomotic LIMA / LAD lesion had progressed to a 70% luminal narrowing.
2. Case two A 61 year old man underwent coronary artery bypass grafting. At surgery he received a LIMA to his left anterior descending artery and SVGs to his intermediate, diagonal and right coronary arteries. He presented 4 months later with classical recurrent,
class III angina. Repeat cardiac catheterisation revealed an occluded SVG to the diagonal, an ostial 90% stenosis in the SVG to the intermediate (Fig. 2a), a normal SVG to the right coronary artery and a functioning (LIMA) to the left anterior descending. Both native intermediate and anterior descending arteries were occluded proximally, and the proximal circumflex had developed an 80% stenosis. Also of note was the presence of a large side branch arising from the proximal LIMA. The patient underwent successful primary PTCA / stenting of the ostial SVG stenosis with a Palmaz Schatz biliary stent (PS154 Johnson and Johnson Cordis) with a final high pressure (16 atm) inflation
H.L. White et al. / International Journal of Cardiology 66 (1998) 11 – 15
13
Fig. 2. Serial angiograms – case two. (a) Ostial stenosis in the saphenous vein graft to intermediate artery. (b) Saphenous vein graft following angioplasty and stenting of ostial lesion. (c) Ostial in-stent restenosis within saphenous vein graft 6 months later. (d) Saphenous vein graft ostium following TEC atherectomy. (e) Saphenous vein graft ostium following adjunctive angioplasty.
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H.L. White et al. / International Journal of Cardiology 66 (1998) 11 – 15
using a 4.5 mm (Schneider Chubby) balloon (Fig. 2b). The final post-procedural stenosis measured 20%. At the same session he also underwent successful PTCA to the native circumflex resulting in a residual 10% stenosis. His medication on discharge was aspirin and warfarin in addition to his usual anti-anginal therapy. Six months later he again developed classical angina on minimal exertion, and was re-investigated. This revealed a 90% in-stent restenosis (Fig. 2c). A 10 Fr hockey stick TEC guiding catheter was introduced into the saphenous vein graft and a TEC wire advanced to the distal native vessel. TEC atherectomy was initially performed cautiously using a smaller 1.5 mm catheter involving several passes through the stent, then followed by a 2.5 mm TEC device, leaving only a 20% residual stenosis (Fig. 2d). Finally, PTCA was performed using a 4.5 mm Schneider Chubby balloon inflated to 16 atm. The post-procedural stenosis measured 10% (Fig. 2e). He was discharged on aspirin 300 mg daily and his previous anti-anginal medication. Further cardiac catheterisation was undertaken 5 months later which revealed no evidence of in-stent restenosis (Fig. 3). The side branch of the IMA appeared of large calibre and was felt to be accountable for his residual angina (‘steal’ effect).
Fig. 3. Serial angiograms – case two. Saphenous vein graft 5 months later showing no evidence of restenosis (all projections RAO).
3. Discussion Primary stenting is the treatment of choice for lesions in SVGs greater than 3 mm in diameter because of its favourable impact on restenosis compared to PTCA alone [1–4]. However, the event-free survival for stented aorto-ostial lesions is only approximately 50% [5]. The use of TEC for SVG stenoses has previously been described but adjunctive angioplasty is required in over 90% of cases to achieve a satisfactory luminal diameter [6]. Studies involving angiographic follow-up after TEC have demonstrated restenosis rates of 69%, but some of the patients included in this series had diffuse disease within degenerated SVGs and complex lesion morphology was frequently identified [6]. Our first case, however, demonstrates that for a discrete eccentric SVG lesion TEC atherectomy alone can produce a good immediate and long term result. Recently, the role of atherectomy devices has been extended to the treatment of in-stent restenosis in both native vessels and SVGs [7,8]. TEC relies on cutting and aspiration and is particularly suited for thrombus-containing lesions in stented SVGs. There was no suggestion of thrombus in our second case but TEC was chosen rather than directional atherectomy because of the slower rotating co-axial cutting mechanism which is less likely to damage the stent or SVG wall, especially if a small cutter is used initially. This risk can be reduced further by the prior use of IVUS (Intravascular Ultrasound) to exclude incomplete stent strut expansion, but this was unavailable in our laboratory at the time. Rotablation would be a difficult technique to use in this ostial location and also carries the risk of distal embolisation. Histological studies reveal that by 6 months following stent deployment smooth muscle cells and an extracellular matrix form the bulk of the re-stenotic material [9]. The TEC is able to extract this material and thus increase the luminal diameter. This is supported by the findings of MacDonald et al. suggesting that the luminal diameter achieved by PTCA within restenotic stents is predominantly the result of compression and extrusion of material rather than stent expansion [10]. Goods et al. successfully treated a restenotic stented segment in the native LAD with the TEC device followed by adjuvant PTCA [7]. Patel et al. have already reported the successful use of this
H.L. White et al. / International Journal of Cardiology 66 (1998) 11 – 15
combination in re-stenotic stented segments of SVGs [10]. We describe a further case, with follow-up angiography, supporting the theory that the debulking mechanism of TEC, followed by adjuvant PTCA, may be the best available treatment for the management of SVG in-stent re-stenosis.
4. Conclusion This case illustrates the value of TEC atherectomy in the primary treatment of eccentric filling defects in saphenous vein grafts, and demonstrates that adjuvant PTCA is not always required to attain an adequate post-procedure luminal diameter and a satisfactory long term angiographic result. This debulking technique also appears safe and effective in the management of in-stent restenosis within SVGs.
References [1] de Feyter PJ, van Suylen RJ, de Jaegure PPT, Topol EJ, Serruys PW. Balloon angioplasty for the treatment of lesions in Saphenous Vein Grafts. J Am Coll Cardiol 1993;21:1539–49. [2] Hirshfield JW, Schwartz JS, Jugo R, McDonald RG, Goldberg S, Savage MT, Bass T, Vetrovel G, Cowley M, Taussig AS, Whitworth HB, Margolis JR, Hill JA, Pepine C., the M-HEART investigators. Restenosis after coronary angioplasty: a multivariate statistical model to relate lesion and procedure variables to restenosis. J Am Coll Cardiol 1991;18:647–56.
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[3] Urban P, Sigwart U, Golf S, Kaufman U, Sadeghi H, Kappenberger L. Intravascular stenting for stenosis of aortocoronary bypass grafts. J Am Coll Cardiol 1989;13:1085–91. [4] Strauss BH, Serruys PW, Bertrand ME, Peul J, Meier B, Goy JJ, Kappenberger L, Rickards AF, Sigwart U. Quantitative angiographic follow-up of the coronary wallstent in native vessels and bypass grafts (European experience – March 1986 to March 1990). Am J Cardiol 1992;69:475–81. [5] Chui Wong S, Popma J, Hong MK, Satler LF, Pichard AD, Kent KM, Chein Chuang Y, Bucher TA, Donovan K, Leon MB. Procedural results and long term clinical outcomes in aorto-ostial saphenous graft lesions after new device angioplasty. J Am Coll Cardiol 1995;25:394A. [6] Safian D, Grines CL, May MA, Lichtenberg A, Juran N, Schrieber TL, Pavlides G, Meany TB, Savas V, O’Neill WW. Clinical and angiographic results of transluminal extraction coronary atherectomy in Saphenous Vein Bypass Grafts. Circulation 1994;89:302–12. [7] Goods CM, Jain SP, Liu MW, Babu RB, Roubin GS. Intravascular ultrasound-guided transluminal extraction atherectomy for restenosis after Gianurco–Roubin coronary stent implantation. Catheter Cardiovasc Diagn 1996;37:317–9. [8] Patel JJ, Meadaa R, Cohen M, Adiraju R, Kussmaul III WG. Transluminal extraction atherectomy for aortosaphenous vein graft stenosis. Catheter Cardiovasc Diagn 1996;38:320–4. [9] Strauss BH, Umans VA, van Suylen RJ, de Feyter PJ, Marco J, Robertson GC, Renkin J, Heydrickx G, Vuzevski VD, Bosman FT, Serruys PW. Directional atherectomy for treatment of restenosis within coronary stents: clinical, angiographic and histological results. J Am Coll Cardiol 1992;20:1465–73. [10] MacDonald RG, O’Neill BJ, Creighton JE, Brown RIG, Slivocka JE, Penn IM. Is coronary stent expansion the mechanism for successful dilatation of stent restenosis? A quantitative angiographic study. Circulation 1991;II-84:196.
Utilisation of transluminal extraction atherectomy in the treatment of saphenous vein graft disease: two case reports H.L. White, D.H. Roberts*, J.S. Wright Cardiology Department, Blackpool Victoria Hospital, Whinney Heys Road, Blackpool, Lancashire FY3 8 NR, UK Received 28 August 1997; accepted 30 June 1998
Abstract Saphenous vein graft disease is an increasing problem as more patients undergo bypass grafting and to date the most effective management strategy remains undefined. The major limitations of angioplasty for saphenous vein graft lesions are the risk of distal embolization and restenosis. Primary stenting in this situation results in superior lumen enlargement and higher procedural success but is still associated with significant restenosis. We describe two cases in which transluminal extraction (TEC) atherectomy is utilised for the treatment of vein graft disease with good immediate and long term angiographic results. The first case reports the use of TEC atherectomy for the primary treatment of a discrete eccentric filling defect, and the second case describes the use of this technique in the management of in-stent restenosis. 1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: In-stent restenosis; Saphenous vein graft; TEC atherectomy
1. Case one A 35 year old man underwent double coronary artery bypass grafting, receiving saphenous vein grafts (SVG) to his posterior descending (PDA) and obtuse marginal (OM) arteries. Four years later following the recurrence of angina his left internal mammary artery (LIMA) was grafted onto his left anterior descending artery. His chest pain, classically ischaemic in nature, returned within 6 months and a clinical diagnosis of recurrent angina was made. (The 12 lead resting electrocardiogram disclosed longstanding deep T wave inversion across the precordial leads thus making exercise testing difficult to interpret). This was initially managed with medical therapy. After 18 months he was re-investigated for class IV angina. Cardiac catheterisation demonstrated *Corresponding author.
a large 3.5 mm SVG to the PDA with an eccentric filling defect narrowing the lumen by 80% (Fig. 1a). The SVG to the OM was occluded and there was a significant 70% lesion in the native circumflex. A 50% stenosis at the anastamosis of the LIMA graft was demonstrated. A multipurpose 10 Fr guiding catheter was introduced into the SVG to the PDA and a TEC wire was advanced to the native vessel. A 2.5 mm TEC device was selected because this is the largest available size and was felt the most appropriate for such a large calibre vessel (3.5 mm). TEC atherectomy was performed involving several passes through the diseased segment and resulted in a 10% residual stenosis (Fig. 1b) so adjuvant angioplasty was not undertaken. At the same session he underwent successful PTCA of his native circumflex artery resulting in a ,10% residual stenosis. He was discharged home on aspirin and his usual anti-anginal medication.
0167-5273 / 98 / $19.00 1998 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 98 )00200-9
12
H.L. White et al. / International Journal of Cardiology 66 (1998) 11 – 15
Fig. 1. Serial angiograms – case one. (a) Eccentric filling defect in the saphenous vein graft to the Posterior Descending Artery (LAO). (b) The same lesion following transluminal extraction atherectomy (LAO). (c) The saphenous vein graft 12 months later showing no evidence of restenosis. (RAO).
Twelve months later following the recurrence of further clinical angina repeat catheterisation was performed confirming no evidence of vein graft restenosis (Fig. 1c). The anastomotic LIMA / LAD lesion had progressed to a 70% luminal narrowing.
2. Case two A 61 year old man underwent coronary artery bypass grafting. At surgery he received a LIMA to his left anterior descending artery and SVGs to his intermediate, diagonal and right coronary arteries. He presented 4 months later with classical recurrent,
class III angina. Repeat cardiac catheterisation revealed an occluded SVG to the diagonal, an ostial 90% stenosis in the SVG to the intermediate (Fig. 2a), a normal SVG to the right coronary artery and a functioning (LIMA) to the left anterior descending. Both native intermediate and anterior descending arteries were occluded proximally, and the proximal circumflex had developed an 80% stenosis. Also of note was the presence of a large side branch arising from the proximal LIMA. The patient underwent successful primary PTCA / stenting of the ostial SVG stenosis with a Palmaz Schatz biliary stent (PS154 Johnson and Johnson Cordis) with a final high pressure (16 atm) inflation
H.L. White et al. / International Journal of Cardiology 66 (1998) 11 – 15
13
Fig. 2. Serial angiograms – case two. (a) Ostial stenosis in the saphenous vein graft to intermediate artery. (b) Saphenous vein graft following angioplasty and stenting of ostial lesion. (c) Ostial in-stent restenosis within saphenous vein graft 6 months later. (d) Saphenous vein graft ostium following TEC atherectomy. (e) Saphenous vein graft ostium following adjunctive angioplasty.
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H.L. White et al. / International Journal of Cardiology 66 (1998) 11 – 15
using a 4.5 mm (Schneider Chubby) balloon (Fig. 2b). The final post-procedural stenosis measured 20%. At the same session he also underwent successful PTCA to the native circumflex resulting in a residual 10% stenosis. His medication on discharge was aspirin and warfarin in addition to his usual anti-anginal therapy. Six months later he again developed classical angina on minimal exertion, and was re-investigated. This revealed a 90% in-stent restenosis (Fig. 2c). A 10 Fr hockey stick TEC guiding catheter was introduced into the saphenous vein graft and a TEC wire advanced to the distal native vessel. TEC atherectomy was initially performed cautiously using a smaller 1.5 mm catheter involving several passes through the stent, then followed by a 2.5 mm TEC device, leaving only a 20% residual stenosis (Fig. 2d). Finally, PTCA was performed using a 4.5 mm Schneider Chubby balloon inflated to 16 atm. The post-procedural stenosis measured 10% (Fig. 2e). He was discharged on aspirin 300 mg daily and his previous anti-anginal medication. Further cardiac catheterisation was undertaken 5 months later which revealed no evidence of in-stent restenosis (Fig. 3). The side branch of the IMA appeared of large calibre and was felt to be accountable for his residual angina (‘steal’ effect).
Fig. 3. Serial angiograms – case two. Saphenous vein graft 5 months later showing no evidence of restenosis (all projections RAO).
3. Discussion Primary stenting is the treatment of choice for lesions in SVGs greater than 3 mm in diameter because of its favourable impact on restenosis compared to PTCA alone [1–4]. However, the event-free survival for stented aorto-ostial lesions is only approximately 50% [5]. The use of TEC for SVG stenoses has previously been described but adjunctive angioplasty is required in over 90% of cases to achieve a satisfactory luminal diameter [6]. Studies involving angiographic follow-up after TEC have demonstrated restenosis rates of 69%, but some of the patients included in this series had diffuse disease within degenerated SVGs and complex lesion morphology was frequently identified [6]. Our first case, however, demonstrates that for a discrete eccentric SVG lesion TEC atherectomy alone can produce a good immediate and long term result. Recently, the role of atherectomy devices has been extended to the treatment of in-stent restenosis in both native vessels and SVGs [7,8]. TEC relies on cutting and aspiration and is particularly suited for thrombus-containing lesions in stented SVGs. There was no suggestion of thrombus in our second case but TEC was chosen rather than directional atherectomy because of the slower rotating co-axial cutting mechanism which is less likely to damage the stent or SVG wall, especially if a small cutter is used initially. This risk can be reduced further by the prior use of IVUS (Intravascular Ultrasound) to exclude incomplete stent strut expansion, but this was unavailable in our laboratory at the time. Rotablation would be a difficult technique to use in this ostial location and also carries the risk of distal embolisation. Histological studies reveal that by 6 months following stent deployment smooth muscle cells and an extracellular matrix form the bulk of the re-stenotic material [9]. The TEC is able to extract this material and thus increase the luminal diameter. This is supported by the findings of MacDonald et al. suggesting that the luminal diameter achieved by PTCA within restenotic stents is predominantly the result of compression and extrusion of material rather than stent expansion [10]. Goods et al. successfully treated a restenotic stented segment in the native LAD with the TEC device followed by adjuvant PTCA [7]. Patel et al. have already reported the successful use of this
H.L. White et al. / International Journal of Cardiology 66 (1998) 11 – 15
combination in re-stenotic stented segments of SVGs [10]. We describe a further case, with follow-up angiography, supporting the theory that the debulking mechanism of TEC, followed by adjuvant PTCA, may be the best available treatment for the management of SVG in-stent re-stenosis.
4. Conclusion This case illustrates the value of TEC atherectomy in the primary treatment of eccentric filling defects in saphenous vein grafts, and demonstrates that adjuvant PTCA is not always required to attain an adequate post-procedure luminal diameter and a satisfactory long term angiographic result. This debulking technique also appears safe and effective in the management of in-stent restenosis within SVGs.
References [1] de Feyter PJ, van Suylen RJ, de Jaegure PPT, Topol EJ, Serruys PW. Balloon angioplasty for the treatment of lesions in Saphenous Vein Grafts. J Am Coll Cardiol 1993;21:1539–49. [2] Hirshfield JW, Schwartz JS, Jugo R, McDonald RG, Goldberg S, Savage MT, Bass T, Vetrovel G, Cowley M, Taussig AS, Whitworth HB, Margolis JR, Hill JA, Pepine C., the M-HEART investigators. Restenosis after coronary angioplasty: a multivariate statistical model to relate lesion and procedure variables to restenosis. J Am Coll Cardiol 1991;18:647–56.
15
[3] Urban P, Sigwart U, Golf S, Kaufman U, Sadeghi H, Kappenberger L. Intravascular stenting for stenosis of aortocoronary bypass grafts. J Am Coll Cardiol 1989;13:1085–91. [4] Strauss BH, Serruys PW, Bertrand ME, Peul J, Meier B, Goy JJ, Kappenberger L, Rickards AF, Sigwart U. Quantitative angiographic follow-up of the coronary wallstent in native vessels and bypass grafts (European experience – March 1986 to March 1990). Am J Cardiol 1992;69:475–81. [5] Chui Wong S, Popma J, Hong MK, Satler LF, Pichard AD, Kent KM, Chein Chuang Y, Bucher TA, Donovan K, Leon MB. Procedural results and long term clinical outcomes in aorto-ostial saphenous graft lesions after new device angioplasty. J Am Coll Cardiol 1995;25:394A. [6] Safian D, Grines CL, May MA, Lichtenberg A, Juran N, Schrieber TL, Pavlides G, Meany TB, Savas V, O’Neill WW. Clinical and angiographic results of transluminal extraction coronary atherectomy in Saphenous Vein Bypass Grafts. Circulation 1994;89:302–12. [7] Goods CM, Jain SP, Liu MW, Babu RB, Roubin GS. Intravascular ultrasound-guided transluminal extraction atherectomy for restenosis after Gianurco–Roubin coronary stent implantation. Catheter Cardiovasc Diagn 1996;37:317–9. [8] Patel JJ, Meadaa R, Cohen M, Adiraju R, Kussmaul III WG. Transluminal extraction atherectomy for aortosaphenous vein graft stenosis. Catheter Cardiovasc Diagn 1996;38:320–4. [9] Strauss BH, Umans VA, van Suylen RJ, de Feyter PJ, Marco J, Robertson GC, Renkin J, Heydrickx G, Vuzevski VD, Bosman FT, Serruys PW. Directional atherectomy for treatment of restenosis within coronary stents: clinical, angiographic and histological results. J Am Coll Cardiol 1992;20:1465–73. [10] MacDonald RG, O’Neill BJ, Creighton JE, Brown RIG, Slivocka JE, Penn IM. Is coronary stent expansion the mechanism for successful dilatation of stent restenosis? A quantitative angiographic study. Circulation 1991;II-84:196.