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Commentary

Rotational Atherectomy in the DES Era — Away Go Troubles Down the Drain?

James R. Wilentz, MD
January 2011
David Auth first described rotational ablation in 1986 as a technique for winding up coronary thrombus at low rotational speeds, thus capturing it on the rotating burr and shaft. In addition, he believed it decreased the force required to penetrate organized thrombus.1 The technique was fine-tuned, becoming high-speed rotational atherectomy, and was presented as a novel modality to create a uniform lumen with less barotrauma to the artery in the hope of reducing restenosis.2 Much has happened in interventional cardiology since Auth introduced the Rotablator® (Boston Scientific Corp., Natick, Massachusetts), and the report of Benezet and colleagues in this issue of the Journal is a testament to just how much time has gone by.3 This consecutive series of 102 patients with severely calcified coronary lesions treated at a single institution over a 4-year period with rotational atherectomy followed by drug-eluting stent (DES) implantation showed a 99% angiographic success rate, with a low dissection rate, no perforations and no procedural deaths. These patients had severe angiographic coronary artery disease: 46.1% had three-vessel disease, 68.6% had type C lesions and the average implanted stent length was 39.3 mm. 12.7% of patients had lesions treated in the left main coronary artery. The patients were clinically high-risk as well, with half the group over the age of 70, a 53% rate of diabetes and a 13% incidence of chronic renal failure. Despite the odds stacked against them, the outcomes were acceptable. The clinical success rate was 97.1%, with an in-hospital major adverse cardiac event (MACE) rate of 2.9%. The 30-day event rate was also as might be expected for this group, with 3 (2.9%) deaths and 5 (4.8%) stent thromboses (3 definite and 2 probable). Late outcomes were also commensurate with expectations. At a median follow up of 15 months, there were 2 more deaths for an overall mortality rate of 4.9%, no further stent thromboses, a 3.9% rate of myocardial infarction and an 8.8% target lesion revascularization rate. It should be noted that the authors used the smallest burr judged necessary to modify the plaque and facilitate stent delivery, with an average burr size of 1.5 mm and a burr/artery ratio of 0.56. This is in line with current concepts of plaque modification rather than maximal debulking. They also used intravascular ultrasound guidance for the stent post-dilatation if residual stenosis after initial stent deployment was ≥ 20%. High-pressure postdilatation was utilized in two-thirds of the patients and glycoprotein IIb-IIIa inhibitor in 30%. Pretreatment with 300 mg of clopidogrel and aspirin 100–300 mg was performed, and the dual antiplatelet agents were to be continued for 12 months. The authors review previous studies of rotastenting with bare-metal stents and DES, make the point that the results of their single-center study are in line with or better than previous results, and admit the limitations of any observational or post-hoc analysis. So what has happened since the introduction of rotational ablation? We began with great enthusiasm for a technique unlike Gruentzig’s balloon, but the initial hope for a lower restenosis rate due to lack of barotrauma and vessel dissection was not corroborated by the DART,4 the ERBAC,5 the STRATAS6 or CARAT trials7 or a meta-analysis of multiple trials published by Bittl.8 The initial tide of enthusiasm was then supplanted by a severe decrease in the rate of utilization of this procedure almost to the point where emerging fellows from interventional training programs are reluctant to use the Rotablator, since they have had minimal exposure to it. By 2003–2004, the rate of rotational atherectomy use in the U.S. as reported by the ACC-NCDR9 and in Europe10 was ≤ 5%. It is clear that complex calcification remains the bugaboo of intervention. Rotational atherectomy is one of the few techniques that can quickly and elegantly address the difficulty of traversing these heavily calcified arteries by metal stents, no matter how tightly they are affixed to their balloon catheters or how compliant and flexible the delivery system is rendered by their manufacturers. Since DES have become the mainstay of coronary intervention, the ability to easily deliver and optimally expand the DES is key to successful treatment. We not infrequently see an operator confronted with a severely calcific complex artery trying to perform balloon angioplasty to “save the time and expense” of rotablation, only to realize, when switching to rotablation after considerable time and many (often ruptured) balloons, that an initial strategy of vessel preparation with rotational atherectomy would have resulted in an earlier and less expensive success. That said, it is frequent that a long segment of calcific disease may require rotablation proximal to the stent implantation target lesion. What should the approach then be? If the entire proximal segment is not in itself a cause for ischemia, the operator must make a calculation regarding the long-term risk of “full-metal-jacket” stenting versus the benefit of facilitating stent implantation. In these circumstances, it is potentially feasible to do “spot” rotablation of the proximal areas precluding stent passage as well as the target lesion itself. Most operators will then wish to stent all the rotablated areas to avoid potential “geographic miss,” where the drug-eluting therapy is unavailable to an area of endothelium that has been abraded by the burr. Abstract data with up to 6-month angiographic follow up of regions adjacent to rotablated segments suggest that this may not be as important as expected,11 but as with balloon preparation, one seeks to avoid inducing endothelial injury in a segment that will not be covered by the DES. Another possibility that has been recently advanced is the use of the phospholipid lubricant Rotaglide® (Boston Scientific) normally used during rotablation, but in this case, just topically applied to the stent and instilled in the stent wire lumen to facilitate stent advancement without rotablation!12 Specific anatomic considerations are worth mentioning in the use of rotational atherectomy with DES. Highly calcific lesions of the left main coronary,13 bifurcations,14,15 ostial side branches16 and chronic total occlusions17 have been proposed as potential uses for rotational ablation, but not enough data are available regarding these subsets to advocate routine use. In highly tortuous calcific arteries, the stakes are higher and the chance of eccentric passage of the burr and potential perforation increases. In these circumstances optical coherence tomography has visualized eccentric crater formation around the outside of the vessel curve in such a way as to preclude excellent DES apposition at the site of the crater.18 This raises the specter of stent thrombosis due to malapposition. Sometimes it is still reasonable to recommend coronary bypass, or even medical therapy! Finally a few comments about technique. It has been abundantly clear that this is a technique to modify plaque compliance and smooth passage for DES rather than a true debulking strategy, and in this regard, burr sizes should not exceed 0.6 of the luminal diameter.6,7 Rotational speed is a determinant of platelet activation and liberation of kinins, and should be kept within the range of 140,000–160,000 rpm, except in the rare case of highly resistant lesions where higher speeds may be necessary for short runs.19 Run time should be kept short (≤ 30 sec/run) to limit liberation of particulates and avoid hypotension and bradycardia. Special consideration should be given to rotablation of a long area proximal to a subtotal occlusion. In this case, a great deal of ablated particulate matter can be stored at the subtotal occlusion, and when this is opened, suddenly liberated into the distal bed with poor outcomes. Avoid this by a simple predilatation if possible with a tiny balloon. Clinically, the patient with severely diminished heart function and a last coronary artery standing to be treated remains a poor candidate for rotablation, even with the availability of cardiac support. Although an intra-aortic balloon or ventricular assist device may help in the short run, for the patient truly lacking in reserve, damage to the myocardium from liberated materials may be unsustainable in the long run, when the support device is to be withdrawn. The paper by Benezet adds to our understanding of rotational atherectomy in the DES era. Given proper respect, and a clear understanding of the adjunctive nature of this technique, it can make a whole world of troubles disappear and allow successful DES implantation in complex coronary anatomy.

References

1. Ritchie JL, Hansen DD, Vracko R, Auth DC. Mechanical thrombolysis: A new rotational catheter approach for acute thrombi. Circulation 1986;73:1006–1012. 2. Fourrier JL, Bertrand ME, Auth DC, et al. Percutaneous coronary rotational angioplasty in humans: Preliminary report. J Am Coll Cardiol 1989;14:1278–1282. 3. Benezet J, Díaz de la Llera LS, Cubero JM, et al. Drug-eluting stents following rotational atherectomy for heavily calcified coronary lesions: Long-term clinical outcomes. J Invasive Cardiol 2011;23:28–32. 4. Mauri L, Reisman M, Buchbinder M, et al. Comparison of rotational atherectomy with conventional balloon angioplasty in the prevention of restenosis of small coronary arteries: Results of the dilatation vs ablation revascularization trial targeting restenosis (DART). Am Heart J 2003;145:847–854.
5. Reifart N, Vandormael M, Krajcar M, et al. Randomized comparison of angioplasty of complex coronary lesions at a single center. excimer laser, rotational atherectomy, and balloon angioplasty comparison (ERBAC) study. Circulation 1997;96:91–98. 6. Whitlow PL, Bass TA, Kipperman RM, et al. Results of the study to determine rotablator and transluminal angioplasty strategy (STRATAS). Am J Cardiol 2001;15;87:699–705. 7. Safian RD, Feldman T, Muller DW, et al. Coronary angioplasty and rotablator atherectomy trial (CARAT): Immediate and late results of a prospective multicenter randomized trial. Catheter Cardiovasc Interv 2001;53:213–220. 8. Bittl JA, Chew DP, Topol EJ, et al. Meta-analysis of randomized trials of percutaneous transluminal coronary angioplasty versus atherectomy, cutting balloon atherotomy, or laser angioplasty. J Am Coll Cardiol 2004;43:936–942. 9. Anderson HV, Shaw RE, Brindis RG, et al. A contemporary overview of percutaneous coronary interventions. The American College of Cardiology – National Cardiovascular Data Registry (ACC-NCDR). J Am Coll Cardiol 2002;39:1096–1103. 10. Rubartelli P, Niccoli L, Alberti A, et al. Coronary rotational atherectomy in current practice: Acute and mid-term results in high- and low-volume centers. Catheter Cardiovasc Interv 2004;61:463–471. 11. Cowley M, Buchbinder M, Warth D, et. al. Effects of coronary rotational atherectomy abrasion on vessel segments adjacent to treated lesions. J Am Coll Cardiol 1992;19:333A. 12. Singh A, Awar M, Ahmed A, et al. Facilitated stent delivery using applied topical lubrication. Catheter Cardiovasc Interv 2007;1;69:218–222. 13. Tanaka N, Terashima M, Kinoshita Y, et al. Unprotected left main coronary artery bifurcation stenosis: Impact of plaque debulking prior to single sirolimus-eluting stent implantation. J Invasive Cardiol 2008;20:505–510. 14. Nageh T, Kulkarni NM, Thomas MR. High-speed rotational atherectomy in the treatment of bifurcation-type coronary lesions. Cardiology 2001;95:198–205. 15. Rihal CS, Garratt KN, Holmes DR Jr. Rotational atherectomy for bifurcation lesions of the coronary circulation: Technique and initial experience. Int J Cardiol 1998;1;65:1–9. 16. Ito H, Piel S, Das P, et al. Long-term outcomes of plaque debulking with rotational atherectomy in side-branch ostial lesions to treat bifurcation coronary disease. J Invasive Cardiol 2009;21:598–601. 17. Pagnotta P, Briguori C, Mango R, et al. Rotational atherectomy in resistant chronic total occlusions. Catheter Cardiovasc Interv 2010;76:366–371. 18. Tanigawa J, Barlis P, Di Mario C. Heavily calcified coronary lesions preclude strut apposition despite high pressure balloon dilatation and rotational atherectomy: In-vivo demonstration with optical coherence tomography. Circ J 2008 ;72:157–160. 19. Reisman M, Shuman BJ, Dillard D, et al. Analysis of low-speed rotational atherectomy for the reduction of platelet aggregation. Cathet Cardiovasc Diagn 1998;45:208–214.
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From the Lenox Hill Heart and Vascular Institute, New York, New York. The author reports no conflicts of interest regarding the content herein. Address for correspondence: J. R. Wilentz, MD, FACC, Lenox Hill Heart and Vascular Institute, 130 E. 77th Street 9th Floor, New York, NY 10075. E-mail: wilentz@gmail.com

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