Rotational atherectomy was developed as a secondgeneration vascular interventional device specifically to address lesions known to be difficult to manage with balloon angioplasty. Commercialized as the Rotablator, this device utilizes a high-speed rotating elliptical burr coated with a fine diamond abrasive to achieve plaque ablation [1]. The very fine diamond abrasive and flexible drive shaft were incorporated into the design to allow normal soft elastic components of the vessel wall to deflect away from the device so that tissue ablation occurs preferentially against the relatively hard and inelastic components of atheromatous plaque [2][3][4][5][6]. This unique property of differential plaque ablation makes the rotational atherectomy ideally suited for treatment of lesions that are unfavorable for balloon angioplasty, especially calcified lesions, bifurcation lesions, ostial stenoses, chronic total occlusions, and diffuse disease [7][8][9][10][11][12][13][14]. Since its introduction in 1990, the Rotablator has undergone a number of design modifications and changes in recommended technique. The device has been used for both lesion modification and plaque debulking on virtually all types of lesions. Its role in the stent era has also been evaluated. The present article summarizes what we have learned over the past decade about the use of the device to treat obstructive atherosclerosis in the coronary circulation.
Patient SelectionAlthough much emphasis is placed on lesion selection in the application of rotational atherectomy, patient selection and clinical characteristics require special emphasis. The diamond abrasive of the Rotablator ablates atheromatous plaque into microparticles, which are not retrieved but rather washed out through the distal coronary circulation. Most ablated microparticles are Յ 10 m in diameter, but larger particles are also produced, which can obstruct microcirculation and cause ischemic complications or patchy microinfarctions [4,15]. Highspeed rotation of the burr also produces microcavitations as a result of the Bernoulli effect. The microcavitations are in a size range of 60 -90 m, which can also temporarily obstruct the microcirculation for 20 -30 sec [16]. Microparticulate embolization and microcavitation contribute to the slow flow and no-reflow, which occurs more frequently with this device than with others [16 -19]. Transient ischemic complications thus may be more frequent than with other devices, even though the incidence of non-Q-wave and Q-wave myocardial infarction are not necessarily increased [20]. Patients with compromised ventricular function, poor distal run-off, multivessel disease with contralateral coronary occlusions, and large plaque burdens (lesion lengths Ն 25 mm) are at greater risk for ischemic complications [21]. Use of this device in these settings, and in the last remaining conduit and with severely compromised LV function, is discouraged unless appropriate measures are taken to protect the patient from ischemic complications, including placement of an in...