Rotational Atherectomy is Useful to Treat Restenosis Lesions due to Crushing of a Sirolimus-Eluting Stent (Full title below)
- Volume 21 - Issue 10 - October, 2009
- Posted on: 10/13/09
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Rotational Atherectomy is Useful to Treat Restenosis Lesions due to Crushing of a Sirolimus-Eluting Stent Implanted in Severely Calcified Lesions: Experimental Study and Initial Clinical Experience
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: email@example.com
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 < 2 mm, and the 2 SES were crushed by the calcified plaques behind them (Figure 5A). In such cases, it is desirable to remove the calcified plaques behind the stent struts to prevent recurrent restenosis. Therefore, RA was performed to ablate the crushed stent struts and the calcified plaques behind them. The extra-support RotaWire was passed through the lesions using a 2.25 mm burr at a rotational speed of 180,000 rpm. The burr was gently advanced without reducing the rotational speed by more than 5,000 rpm. The total ablation time was 200 seconds. Angiographically, about 90% of the length of the proximal in-stent restenosis lesion was ablated. The remaining 10% of the length of the proximal lesion could not be ablated using this gentle procedure. We dilated this lesion with a 3.5 x 18 mm balloon at 20 atm. Then, the distal stented lesion was ablated using a 2.25 mm burr, with a total ablation time of 60 seconds (Figure 5C). During RA, the was no evidence of the no-reflow/slow-flow phenomenon or hemodynamic derangement (Figure 5D). After the procedure, IVUS confirmed that the stent struts and the calcified plaques behind them were ablated over a 14 mm length in the proximally stented lesion and over a 12 mm length in the distally stented lesion (Figure 5B). The proximally stented lesion was fully dilated using a 3.5 x 18 mm balloon, with no stent deployment. The distally stented lesion was dilated using a 3.5 x 18 mm balloon and a 3.5 x 23 mm SES was deployed at 20 atm because the stent’s proximal edge restenosis was involved in this restenotic lesion. CAG showed good final results, with thrombolysis in myocardial infarction (TIMI) grade 3 flow (Figure 5E) and IVUS showed a symmetrical maximum expansion of the stent (Figure 5C). There was no evidence of elevated creatinine-kinase levels the day after the procedure and the patient was asymptomatic at follow up 7 months later.
Discussion. As shown in the background case, we have occasionally experienced restenosis mainly due to the crushing of DES implanted in severely calcified lesions. The additional DES implanted in these lesions are often crushed again, and no coronary interventional solutions have been found for this type of restenosis. We therefore conducted an experimental study, and report here our initial case to demonstrate that RA can ablate calcified plaques behind the stent struts.
It is well recognized that stent fracture can be a mechanical reason for DES restenosis.4,5 However, this case report shows that stent crushing can be a cause of restenosis. The mechanisms differ between stent fracture and stent crushing. The definition of stent fracture is the separation of stent segments or stent struts.7 Stent crushing involves recoil of the stent struts caused by the external pressure derived from the vessel’s elasticity or a calcified plaque. In the present case, stent fracture was not observed on CAG or IVUS. It should be taken into consideration that IVUS does not necessarily differentiate between stent struts and calcified plaque because both are hyperechoic. Therefore, it is possible that calcified plaque caused the stent fracture and protruded from the surface of the vessel. Optical coherence tomography may differentiate stent struts from calcified plaque, which would allow clearer differentiation between stent crushing and stent fracture.