Interventional Rounds Current Status of Rotational …

1 Interventional RoundsCurrent Status of Rotational AtherectomyErdal Cavusoglu,1,2MD,Annapoorna S. Kini,1MD,Jonathan D. Marmur,2MD, andSamin K. Sharma,1*MDDespite the increasing use of percutaneous transluminal coronary angioplasty and in-tracoronary stent placement for the treatment of obstructive coronary artery disease, alarge subset of coronary lesions cannot be adequately treated with balloon angioplastyand/or intracoronary stenting alone. Such lesions are often heavily calcified or fibroticand undilatable with the present balloon technology and attempts to treat them withballoon angioplasty or intracoronary stent placement often lead to vessel dissection orincomplete stent deployment with resultant adverse outcomes. Rotational atherectomyremains a useful niche device for the percutaneous treatment of such complex lesions,usually as an adjunct to subsequent balloon angioplasty and/or intracoronary stentplacement.

2 In contrast to balloon angioplasty or stent placement that widen the coronarylumen by displacing atherosclerotic plaque, Rotational atherectomy removes plaque byablating the atherosclerotic material, which is dispersed into the distal coronary circu-lation. Other lesion subtypes amenable to treatment with this modality include ostial andbranch-ostial lesions, chronic total occlusions, and in-stent restenosis. This reviewdiscusses the technique and principles of Rotational atherectomy , the various treatmentstrategies for its use (including adjunctive pharmacotherapy), the lesion-specific appli-cations for this device, and the complications unique to this modality. Recommendationsare also made for its use in the Current Interventional Cardiovasc Interv2004;62:485 498.

3 2004 Wiley-Liss, words: Rotational atherectomy ; calcification; complex lesionsINTRODUCTIONS ince its introduction in 1977, percutaneous translu-minal coronary angioplasty (PTCA) has become a widelyaccepted form of treatment for obstructive coronary dis-ease [1]. While the procedure was initially reserved forthe treatment of discrete noncalcified proximal lesions,increased operator experience and improved technologyexpanded its application to more complex lesions. Inaddition, the introduction of stents has improved theprocedural success and the high restenosis rate seen withballoon angioplasty [2]. A major limitation of balloonangioplasty (and for that matter intracoronary stentplacement) remains the inability to dilate certain types oflesions. This is particularly the case with heavily calci-fied lesions, where even high-pressure inflations may failto dilate fully a very rigid lesion.

4 This could lead tovessel dissection or, in the case of attempted stent place-ment, incomplete deployment of the stent, with the at-tendant risks of stent thrombosis and restenosis. Atherec-tomy devices were developed to remove the obstructiveatherosclerotic plaque physically. Unlike balloon angio-plasty or stent placement, which widens the coronarylumen by merely displacing atherosclerotic plaque, atherectomy techniques widen the lumen by actuallyremoving tissue from the vessel wall. Several atherec-tomy devices have been developed, including directional,transluminal excisional, Rotational , and laser atherec-tomy. High-speed Rotational atherectomy (RA) removesplaque by ablating the atherosclerotic material, produc-1 Cardiac Catheterization Laboratory of the Cardiovascular Insti-tute, Mount Sinai Medical Center, New York, New York2 Department of Medicine, Division of Cardiology, State Univer-sity of New York Health Science Center at Brooklyn,Brooklyn, New York*Correspondence to: Dr.

5 Samin K. Sharma, Mount Sinai Hospital, Box1030, One Gustave Levy Place, New York, NY : 25 July 2003; Revision accepted 22 February 2004 DOI online in Wiley InterScience ( ).Catheterization and Cardiovascular Interventions 62:485 498 (2004) 2004 Wiley-Liss, small particles (5 10 m) that are dispersed into thedistal coronary circulation. David Auth first investigatedthe possibility of using a Rotational device to debulkatherosclerotic plaque in the early 1980s [3]. Subse-quently, after several experimental studies in animals,Fourier et al. [4] performed the first case of RA in humancoronary arteries in this review, we discuss the RA technique with theRotablator (Scimed, Boston Scientific, Boston, MA) de-vice (Fig. 1), the mechanisms and principles of rotaryablation, the various treatment strategies using this de-vice, the impact of lesion characteristics on results, andthe complications of this treatment modality.

6 We con-clude by making recommendations for the use of thisdevice in the Current OF ROTABLATIONHigh-speed mechanical RA relies on plaque ablationand pulverization by the abrasive diamond-coated Rotablator is able to ablate inelastic tissue selec-tively ( , plaque) while maintaining the integrity ofFig. 1. The components of the Rotablator (Scimed, Boston Scientific Corporation, Boston, MA) Cavusoglu et tissue ( , the normal vessel wall) due to theprinciple of differential cutting. Differential cutting isdefined as the ability to ablate one material selectivelywhile sparing and maintaining the integrity of another,based on differences in substrate composition, resultingin a polished smooth lumen (Fig. 2) [5] compared tomultiple intimal tears/dissections with balloon angio-plasty.

7 The other physical principle, which governs theeffectiveness of RA, is that of orthogonal displacementof friction. At Rotational speeds 60,000 rpm, the fric-tion, which occurs when sliding surfaces are in contact, isvirtually eliminated. As a result, there is reduced surfacedrag and unimpeded advancement and withdrawal of theburr, allowing the rotating burr to pass through tortuousand diseased segments of the coronary tree. The abradedplaque is pulverized into microparticles, which are 5 10 m in diameter. These particles are small enough to passthrough the coronary microcirculation and ultimately un-dergo phagocytosis in the liver, spleen, and lung [3].However, these particles may have a detrimental effecton the myocardial microcirculation that can be preventedby glycoprotein (GP) IIb/IIIa inhibitors, suggesting a rolefor the interaction of the atherosclerotic plaque withplatelets resulting in reduction in distal microperfusion[6].

8 Rotablator is most effective in hard inelastic lesions,while it will not be effective in soft and thrombus-containing lesions as present in acute myocardial infarc-tion or saphenous vein graft lesions, where its use THERAPIESP atients undergoing RA are treated in a similar phar-macological manner to patients undergoing balloon an-gioplasty. However, there are several important differ-ences, which relate to the prevention of complicationsthat are unique to the use of this technology. As with allcoronary interventions, aspirin in a dose of 325 mg/day isadministered to the patient prior to the procedure. Hep-arin is administered to maintain the activated clottingtime 300 sec or 250 sec if a GP IIb/IIIa inhibitor isused. Because the GP IIb/IIIa inhibitors have been asso-Fig.

9 2. Differential cutting by Rotational atherectomy resulting in a smooth, concentric lumenin comparison with multiple intimal dissections after balloon angioplasty [5]. Rotational atherectomy 487ciated with a 50% reduction in cardiac enzymes elevationduring the procedure, as well as a reduction in burr-induced platelet aggregation [6,7], they are often usedroutinely in many Interventional laboratories. This ben-eficial effect of the GP IIb/IIIa inhibitors underscores theimportance of the activation of platelets and their inter-action with atheromatous debris in causing slow flow andother adverse procedural events during RA. Abciximab isthe most commonly used GP IIb/IIIa inhibitor and wasshown to reduce both procedural morbidity and creatinekinase-MB (CK-MB) elevation by approximately 50% ina small randomized trial of 100 patients [8].

10 However,caution is advised in the upfront use of the GP IIb/IIIainhibitors in angulated, heavily calcified lesions under-going RA, where the risk of coronary perforation isincreased. In such cases, the GP IIb/IIIa inhibitor shouldbe administered after the completion of RA. One of thepotentially disastrous complications of RA is the devel-opment of coronary slow flow/no-reflow [9]. Coronaryslow flow/no-reflow is defined as a decrease or cessationof blood flow in the absence of an apparent occlusivedissection or spasm and is believed to occur as a result ofdistal microparticle embolization. Contrary to epicardialvessel spasm, it is usually treated with vasodilators, suchas calcium channel blockers (verapamil, diltiazem, ornicardipine), adenosine or nitroprusside, which havetheir effect at the microcirculation.