Rotational Atherectomy is Useful to Treat Restenosis Lesions due to Crushing of a Sirolimus-Eluting Stent (Full title below)

From the Division of Cardiology, Sakurabashi Watanabe Hospital, Osaka, Japan. The authors report no conflicts of interest regarding the content herein. Manuscript submitted February 17, 2009, provisional acceptance given June 9, 2009, and final version accepted June 12, 2009. Address for correspondence: Hiroshi Ito, MD, Division of Cardiology, Sakurabashi Watanabe Hospital, 2-4-32 Umeda, Kita-ku, Osaka 530-0001, Japan. E-mail: itomd@osk4.3web.ne.jp

_______________________________________________ ABSTRACT: We have occasionally encountered restenosis due to the crushing of drug-eluting stents (DES) implanted in severely calcified lesions. We aimed to establish the role of rotational atherectomy (RA) in its treatment. At first, we conducted an experimental study and found that the size of the metallic particles generated during RA of stent struts was 5.6 ± 3.6 µm. We performed RA on the restenosis of the sirolimus-eluting stents implanted in the severely calcified lesions of a 66-year-old male who had received hemodialysis for 13 years. He had restenosis in the proximal and mid-segments of the right coronary artery, and intravascular ultrasound images documented that these stents were crushed by calcified plaque behind them. RA ablated both crushed stent struts and the calcified lesions behind them, and there was no hemodynamic derangement during the procedure. Maximum dilatation of the lesions was achieved with balloon angioplasty, followed by stent implantation. RA is an effective strategy to treat restenotic lesions resulting from the crushing of DES in severely calcified lesions.

_______________________________________________

J INVASIVE CARDIOL 2009;21e191–E196 Drug-eluting stents (DES) inhibit neointimal hyperplasia and reduce the rates of restenosis and target vessel revascularization.^1,2 There is increasing interest in the technical and mechanical reasons for restenosis after DES implantation including balloon injury at the stent edges,³ stent underexpansion, stent fracture,^4,5 and so forth. We often experience restenosis caused by the crushing of DES implanted in severely calcified lesions. In such cases, it is difficult to prevent recurrent restenosis with additional balloon angioplasty or implantation of another DES because the severely calcified lesion will crush the stent again. We first studied the number and size of the particles generated during rotational atherectomy (RA) for stent struts in the experimental model. We applied RA to ablate crushed stent struts and the calcified plaques behind them for recurrent restenosis in a patient. Experimental Circuit System. We used an experimental circuit system (Hybrid Model, Abbott Vascular, Santa Clara, California) made of 3.5 mm internal diameter silicon tubing with a 15 mm long severely stenosed lesion corresponding to the right coronary artery (RCA), which has a gentle curve proximal to the mid-RCA. We filled the system with water and created constant flow with an electric motor. Next, a 3.5 x 23 mm Cypher sirolimus-eluting stent (SES) (Cordis Corp., Miami Lakes, Florida) was deployed at 20 atmospheres (atm) and the middle of the stent was manually crushed by up to 2 mm in internal diameter from the outside of the tube, which mimicked the restenosis caused by a hard, calcified plaque. A RotaWire Extra-Support guidewire (Boston Scientific Corp., Natick, Massachusetts) was passed through the stenosis, and a 2.25 mm burr was used, set at a rotational speed of 180,000 revolutions per minute (rpm) (Figure 1A). The burr was advanced without reducing the rotational speed by more than 5,000 rpm (Figure 1B). The total ablation time was 180 seconds, and the burr successfully passed the site of stenosis. Finally, the stenotic site was dilated using a 3.5 mm balloon at 20 atm. We sampled the water that was collected distal to the ablation site to analyze the number and size of particles generated from the stent struts. RA ablated the stent struts over a length of 16 mm mainly along the inner curvature (Figure 1C). At first, we checked the presence or absence of the particles > 200 µm in diameter with a microscope of low magnifying power (2.5 x and 5 x). No particles in this size range were found. Then, a FPIA-3000 flow particle analyzer (Sysmex, Kobe, Japan) was used,6 which can measure particle size and circularity. The FPIA-3000 can measure the particle size with an effective range of 0.5–200 µm and calculates circularity as the circle circumference/perimeter length, ranging between 0 (line) and 1 (perfect circle). The number of particles was 644; they were 5.6 ± 3.6 µm in diameter (Figure 2A), and their circularity was 0.831 (Figure 2B). We considered that the particles of this size range are not likely to produce complications in clinical settings. Background Case. In January 2005, a 60-year-old male presented to our hospital with exertional angina pectoris. He had a history of hemodialysis over the past 4 years due to chronic renal failure. Coronary angiography (CAG) showed a total occlusion in the mid-RCA, which was a severely calcified lesion (Figure 3A). A 3.0 x 12 mm high-pressure balloon was used to dilate these lesions at 20 atm, and a 3.0 x 23 mm SES was implanted. Adequate dilatation was confirmed by CAG (Figure 3B) and intravascular ultrasound (IVUS) (Figure 3A). In August 2005, the patient was admitted for recurrent angina pectoris and underwent catheterization. A total occlusion in the mid-RCA (Figure 3C) was found. After predilatation at 6 atm with a 2.0 x 15 mm balloon, IVUS imaging showed that the SES was crushed by the calcified plaques behind them (Figure 3B). A high-pressure balloon measuring 3.0 x 10 mm was used to dilate these lesions at 20 atm, and another 3.0 x 28 mm SES was implanted in the mid-RCA. Sufficient dilatation was confirmed by CAG (Figure 3D). However, in January 2006, the patient was admitted for recurrent angina pectoris and underwent catheterization. We found recurrent restenosis in this lesion (Figure 3E) and coronary artery bypass grafting was required to control his exertional angina. Case Report. In November 2007, a 66-year-old male presented to our hospital with unstable angina pectoris. He had a history of hemodialysis over the past 13 years due to chronic renal failure. CAG showed a long, severely calcified lesion with 62% stenosis in the proximal and 99% stenosis in the mid-RCA (Figure 4A). A 3.5 x 15 mm high-pressure balloon was used to dilate these lesions at 20 atm, and two 3.5 x 18 mm SES were implanted in the proximal and mid lesions. A 3.5 x 15 mm high-pressure balloon was used for postdilatation of these 2 stents at 22 atm. Sufficient dilatation was confirmed by CAG (Figure 4B) and IVUS (Figure 4A). In June 2008, the patient was admitted for recurrent angina pectoris and underwent emergent catheterization. Restenosis of the stented lesions, i.e., a 99% stenosis in the proximal and a total occlusion in the mid-RCA (Figure 5A) were found. An 8 French (Fr) JR4 guide catheter (Medtronic, Inc., Minneapolis,, Minnesota) was inserted into the RCA and an intermediate guidewire was used predilate the lesion with a balloon measuring 2.0 x 15 mm at 6 atm (Figure 5B). On IVUS imaging, the minimum luminal diameter (MLD) of these lesions was 3.5 mm in diameter. We carefully and gently advanced the burr without decreasing the rotational speed by more than 5,000 rpm. Neither a transient reduction in coronary flow nor an elevation of creatinine kinase was observed. In the experimental study, we confirmed that the size of the metallic particles generated during RA of the stent struts was 5.6 ± 3.6 µm. In rabbit atherosclerotic lesions, 98% of the particles produced by RA were

2. Schofer J, Schlüter M, Gershlick AH, et al; E-SIRIUS Investigators. Sirolimus-eluting stents for treatment of patients with long atherosclerotic lesions in small coronary arteries: double-blind, randomised controlled trial (E-SIRIUS). Lancet 2003;362:1093–1099.

3. Lemos PA, Saia F, Ligthart JM, et al. Coronary restenosis after sirolimus-eluting stent implantation: morphological description and mechanistic analysis from a consecutive series of cases. Circulation 2003;108:257–260.

4. Sianos G, Hofma S, Ligthart JM, et al. Stent fracture and restenosis in the drug-eluting stent era. Catheter Cardiovasc Interv 2004;61:111–116.

5. Lee MS, Jurewitz D, Aragon J, et al. Stent fracture associated with drug-eluting stents: Clinical characteristics and implications. Catheter Cardiovasc Interv 2007;69:387–394.

6. Komabayashi T, Spångberg LS. Comparative analysis of the particle size and shape of commercially available mineral trioxide aggregates and Portland cement: a study with a flow particle image analyzer. J Endod 2008;34:94–98.

7. Aoki J, Nakazawa G, Tanabe K, et al. Incidence and clinical impact of coronary stent fracture after sirolimus-eluting stent implantation. Catheter Cardiovasc Interv 2007;69:380–386.

8. Abdelmeguid AE. New technique for stent jail: another niche for the rotablator. Cathet Cardiovasc Diagn 1997;42:321–324.

9. Kobayashi Y, Teirstein P, Linnemeier T, et al. Rotational atherectomy (stentablation) in a lesion with stent underexpansion due to heavily calcified plaque. Catheter Cardiovasc Interv 2001;52:208–211.

10. Medina A, de Lezo JS, Melián F, et al. Successful stent ablation with rotational atherectomy. Catheter Cardiovasc Interv 2003;60:501–504.

11. Hansen DD, Auth DC, Vracko R, Ritchie JL. Rotational atherectomy in atherosclerotic rabbit iliac arteries. Am Heart J 1988;115:160–165.

12. Hansen DD, Auth DC, Hall M, Ritchie JL. Rotational endarterectomy in normal canine coronary arteries: preliminary report. J Am Coll Cardiol 1988;11:1073–1077.