Tips and Tricks for Rotational Atherectomy

Gianmarco Iannopollo, MD1*;  Francesco Gallo, MD2,3*;  Antonio Mangieri, MD2;  Alessandra Laricchia, MD2;  Andrea Erriquez, MD3;  Georgios Tzanis, MD, PhD4;  Antonio Colombo, MD2;  Francesco Giannini, MD

Gianmarco Iannopollo, MD1*;  Francesco Gallo, MD2,3*;  Antonio Mangieri, MD2;  Alessandra Laricchia, MD2;  Andrea Erriquez, MD3;  Georgios Tzanis, MD, PhD4;  Antonio Colombo, MD2;  Francesco Giannini, MD

Abstract: The use of debulking devices improved in the last few years, due to the expanding indications to percutaneous coronary angioplasty, involving an elevated number of coronary stenoses with heavy calcification. Rotational atherectomy has become one of the most used devices in this challenging scenario. The aim of this review is to analyze the components and the use of the Rotablator System (Boston Scientific) and to better understand helpful tips and tricks in order to face the most common complications occurring during the procedure.

J INVASIVE CARDIOL 2019;31(12):E376-E383.

Key words: calcified lesions, heavy calcifications, percutaneous coronary intervention, rotational atherectomy

Heavily calcified plaques represent a challenging scenario when treated with percutaneous coronary intervention (PCI); the result could be suboptimal due to stent malapposition and stent under-expansion, leading to potential clinical complications such as intrastent restenosis and stent thrombosis.1 To overcome these possibly negative results, optimal lesion preparation is fundamental. Several devices are currently available for this purpose. Noncompliant and cutting/scoring balloons allow acceptable lesion preparation, although balloon-lesion preparation is not always enough to adequately break the intimal calcium. 

Rotational atherectomy (RA) is a specific technique adopted for the treatment of complex lesions — especially those with heavy calcification that cannot be adequately dilated with conventional balloons or stents, leading to balloon rupture or stent under-expansion. RA induces lumen enlargement by physical removal of plaque and reduction of plaque rigidity, facilitating proper dilation. 

The combination of RA plus stent therapy has been associated with the highest target-lesion revascularization (TLR)-free survival rate as well as the highest event-free survival rate at 9 months (85.4% and 85.4%, respectively). The final minimal luminal diameter (MLD) of the treated lesion was the only significant independent predictor of an event-free survival.2 As demonstrated in a large, retrospective analysis, the use of RA is also safe, with a low rate of procedural complications such as dissection, perforation, and no-reflow. In-hospital, 30-day, and 12-month major adverse cardiovascular event (MACE), myocardial infarction (MI), and stroke rates were low and not significantly different when compared with a standard lesion preparation.3

The commercially available Rotablator System (Boston Scientific) ablates plaque using a diamond elliptical burr, rotating at 135,000 to 180,000 rpm by a helical driveshaft that advances gradually across a lesion over a dedicated guidewire (Rotawire). High rotational speeds facilitate longitudinal burr movement across calcific lesions by orthogonal displacement of the friction.4 The basic physical principle is differential cutting, which allows the advancing burr to selectively cut inelastic material while elastic tissue deflects away from the burr.5

The Rotablator System (Figure 1). The Rotablator System comprises the following different parts: (1) the console; (2) the pedal; (3) the advancer; (4) the burr; and (5) the Rotawires. The console regulates the flow of air to the advancer, controlling burr rotation speed. Burr rotation speed and RA procedural time are also monitored and displayed. The pedal can be powered by both nitrogen and compressed air. It initiates the flow of air through the system, activating the burr. The pedal also switches the system into and out of Dynaglide mode, which facilitates burr advancement or removal. The advancer features a proximal knob, helping advancement and retrieval of the burr, and a distal black button that helps to release the valve that blocks the Rotawire during ablation. Three connecting tubes emerge from the advancer: the pneumatic tube (connected to high pressure, enabling the movement of the turbine); the fiber optic tube; and the saline infusion tube (connected to a high-pressure washing system).The burr comprises an elliptical distal end with 2000-3000 ablating diamonds on the tip and a connecting proximal end with a helical driveshaft that is connected to the advancer’s driveshaft (Figure 2). The Rotawires are either floppy or stiff wires. They are both >300 cm with a 22 mm radiopaque tip, consisting of an .009˝ stainless-steel core, with tapered distal ends (the stiff wire has a shorter tapered part than the floppy wire) and an .014˝ distal platinum coil that prevents the burr from traveling beyond the tip of the wire.

The Rotapro System (Figure 3). The evolution of the Rotablator System is the new Rotapro System (Boston Scientific), in which the components have been simplified.

The most important difference is the absence of the pedal; the burr rotation is activated by pushing the knob on top of the advancer. It is possible to turn the knob 180° to hold the guidewire firmly during burr rotation to prevent the wire from spinning or moving. The Dyna mode button is located on the back of the advancer; it can toggle the system between full speed and Dynaglide, which  is confirmed by a green advancer LED and console indicator. The new console consists of a digital display that relays information about the burr speed and deceleration indicator. Three connecting tubes emerging from the advancer are connected to the console. 


The Technique

Step 1. Positioning the Rotawire at the distal segment of the target vessel. The correct maneuver for positioning the Rotawire is to advance the wire with the left hand (index and thumb) and torque using the Rotaclip with the right hand. This Rotawire maneuver reduces the chance of wire kinking and the consequential difficulty in advancing the burr. Additionally, the Rotawire is particularly stiff in its body and has little maneuverability at the tip. Therefore, advancing the wire distally could become challenging, especially through severely calcified and obstructive stenosis, with an additional increased risk of vessel dissection and perforation due to the Rotawire’s stiffness. An alternative approach to cross the lesion is the advancement of a workhorse coronary wire (eg, Balance or Universal [both Abbott Vascular]) or hydrophilic coronary wire (Sion Black or Fielder wire [both Asahi Intecc]) distal to the stenosis over an over-the-wire (OTW) balloon or microcatheter; once the target position has been achieved, the wire can be exchanged with the Rotawire.  

The following techniques are proposed for cases with highly stenotic lesions that are uncrossable by microcatheter or an OTW balloon:

(1) Advance a standard wire across the lesion and dilate the lesion with a 1.25 monorail balloon; subsequently advance the microcatheter and exchange the standard wire with the Rotawire. 

(2) Advance the OTW balloon or microcatheter proximal to the target lesion and then exchange the standard wire with the Rotawire, trying to cross the lesion directly. Consider dipping the Rotawire in a solution with propofol, which enhances the lubricity of the wire and facilitates lesion crossing. 

Step 2. Appropriate console settings.

(1) The three connecting tubes emerging from the advancer are connected to the console and to the high-pressure wash system.

(2) The rotation speed is set between 15,000-180,000 rpm.

(3) The proximal black knob is tightened and the distal black button is pushed in order to remove the valve that blocks the Rotawire from advancing.

Step 3. Advancement of the burr along the Rotawire using Dynaglide. The burr can be advanced along the Rotawire by activating the Dynaglide setting by pressing a button on foot pedal. The activation of this mode reduces the friction during burr advancement and its activation is confirmed by a characteristic noise and by a green signal on the console. The burr is advanced up to the tip of the guiding catheter. Before starting rotablation, normal mode has to be reactivated by pressing the Dynaglide button on the foot pedal again, and releasing the brake defeat on the advancer in order to activate the inner valve that keeps the Rotawire in position during rotablation.

Step 4. Rotablation. A pecking motion with the burr, ie, a quick back-and-forth movement, is advised. This type of motion avoids crossing the entire lesion during the initial passage and prevents “trenching” into the arterial wall causing vessel injury. It also helps minimize deceleration during rotablation, as does the short duration of the individual runs (no longer than 30 seconds). A gradual deceleration translates into effective debulking of the calcific plaque. A practical tip to verify that the rotablation has been performed adequately is the maintenance of a constant rotational speed during the crossing of the burr through the lesion.  

Excessive deceleration (>5000 rpm) must be avoided because it results in improper ablation and increases the risk of vessel injury, the formation of large particles and ischemic complications related to excessive heat generation.6 A safe range of speed for rotablation is between 135,000 and 180,000 rpm. A speed <135,000 rpm might be associated with burr lodging, while a speed >180,000 rpm might increase platelet activation and thrombotic complications, heat generation, microcavitation, and particulate debris.7,8 During rotablation, it is mandatory to check the runs on the console, paying additional attention to the rotablation sound, which gives feedback on burr deceleration.  

What Do I Need to Consider?

Patient and lesion selection. Lesion and patient characteristics should be taken into account when considering RA. A severely calcified lesion, which carries a high risk of material embolization, in the context of high-risk PCI (eg, hemodynamically unstable patient, ejection fraction <35%, or PCI on a single remaining vessel)9,10 should force the operator to re-evaluate the procedure due to the risk of hemodynamic impairment, which is attributed to no-reflow phenomenon. In this clinical setting (and if RA is the treatment of choice), the procedure should be “protected” with a mechanical circulatory support device, such as intra-aortic balloon pulsation or Impella device (Abiomed).11 A recent study showed that the use of Impella CP in high-risk patients undergoing PCI with RA was associated with a better procedural outcome.12

Vessel tortuosity. The second aspect to consider when performing rotablation is vessel tortuosity. This complex anatomy condition enhances the difficulty of advancing the Rotawire distally and increases the risk of guidewire bias (a divergence from the central axis of the guidewires), a condition that might lead to vessel dissection or perforation. Ablation of “healthy” tissue can occur, in fact, if the tension on the wall exceeds the elasticity of the vessel as can occur in a “guidewire bias” condition.13 In addition, the performance of the Rotawire is notoriously “moody.” Therefore, a regular PCI guidewire can be advanced through the tortuous vessel and then switched to the Rotawire using an OTW balloon or a microcatheter.7 Significant vessel tortuosity, proximal to the lesion, might also prevent the delivery of the burr to the site of interest. In this situation, the operator should consider a GuideLiner (Teleflex), a rapid-exchange mother-and-child guide-extension catheter that allows deep intubation of the target vessel, allowing for improved support during delivery of burrs in highly tortuous vessels.14 Placing the GuideLiner beyond the tortuous site should allow the delivery of the burr and enable safe RA of the calcified lesion.15 Additionally, burr advancement can be facilitated by wetting the Rotawire in Rotaglide lubricant or propofol, which decreases friction and increases the tactile feedback. 

Support of the rotablation system. An important aspect to be considered is the adequate support of the RA system and proper guiding catheter selection. Most burrs (up to 1.75 mm diameter) can be accommodated in a 6 Fr guiding catheter, while 7 or 8 Fr guiding catheters (or transradial sheathless guiding catheters) might be necessary with the use of larger burrs (>1.75 mm diameter). In order to achieve good support, the guiding catheter should be placed in a coaxial position in order to avoid guidewire bias,13 which could affect the efficacy of the debulking. 

Support for the RA system should be maintained by distal positioning of the Rotawire. Particularly, the radiopaque tip of the Rotawire should be placed as distally as possible (from the target coronary segment) in order to prevent wire fracture or burr lodging. The inner lumen of the burr is loaded on the Rotawire shaft, and has a thickness of 0.009˝, while the radiopaque tip of the Rotawire has a thickness of 0.014˝ to prevent the burr from traveling beyond the tip. However, the contact of the guidewire tip and the burr could cause guidewire damage/fracture or even cause the burr to become stuck on the wire and/or in the lesion.7 

As mentioned before, the GuideLiner is a tool that increases support for the RA system, particularly in complex anatomies such as tortuous vessels.

Burr selection. A single 1.5 mm-diameter burr can be used in a wide variety of lesions, achieving good plaque modification (burr-to-artery ratio of 0.6). Smaller burrs (1.25 mm) could be considered for very tight stenoses, very tortuous anatomies, or long lesions, whereas larger burrs (≥1.75 mm) could be considered for aorto-ostial lesions or for large vessels with larger MLD (where smaller burrs would hardly affect the plaque). A general rule is to down-size the burr if the lesion cannot be crossed after several attempts. A sample case demonstrating this principle is provided in Figure 4. If the smallest burr (1.25 mm) will not pass, the operator should consider changing to a larger or different guiding catheter to have more support.7 Burr sizes are pictured in Figure 5. 

Prevention of Complications

Dissection/perforation. Coronary perforation during PCI has an estimated incidence of 0.5%16,17 and is associated with a 13-fold increase in in-hospital major adverse events and a 5-fold increase in 30-day mortality.16 To prevent coronary dissection or perforation, the Rotawire should be placed in the distal part of the vessel, avoiding engagement of small side branches, which might increase the risk of wire fracture or vessel perforation. A practical tip to avoid loops or deep positioning in small side distal branches is to bend the Rotawire tip smoothly and to monitor its position throughout the procedure, since it may be displaced during the exchange of burrs and balloons. Vessel injury by rotablation could be operator dependent (mainly attributed to inappropriate technique such as over-sizing of burr, or “pushing” of the burr rather than pecking) or vessel dependent (for example, extreme tortuosity or small vessel size). 

Burr entrapment. Burr entrapment is the inability to rotate or retrieve the burr from within a coronary lesion. It is a relatively uncommon (but serious) complication during RA and surgical retrieval is usually necessary. This complication can be prevented by conscientiously performing the rotablation protocol (ie, pecking motion, short duration of ablation, short segment ablated during the runs, avoiding extreme angulation). Operators should not exert excessive forward force during burr advancement and should avoid significant decelerations of rotational speed (>5000 rpm) in order to avoid entrapment.7 

No-reflow. Another not so rare complication— and possibly the most feared adverse event of RA — is the no-reflow/slow-flow phenomenon, consisting of a failure to reperfuse myocardium after balloon inflation, stent deployment, or RA. No-reflow phenomenon is somewhat common during standard PCI, where it could be related to the following: (1) ischemia-reperfusion injury and its alteration of the vascular-regulation pathways; (2) microvascular obstruction from distal embolization; (3) dysfunction in vascular autoregulation; and (4) activation of the extrinsic coagulation pathway due to inflammation. These effects can induce coronary microvascular injury and cardiomyocyte death, manifesting as a slowing of the contrast media through the epicardial artery.18-20

Up to 6.7% of patients undergoing RA fail to achieve a complete myocardial reperfusion, as evidenced by failure of ST-segment resolution or poor myocardial blush grade.21 In the RA setting, no-reflow phenomenon could be related to improper RA technique or burr size choice. A general rule to reduce the incidence of rotablation-induced flow impairment is to use a smaller burr and to advance the burr at a lower speed and for shorter runs.7 This type of RA protocol might be particularly useful in high-risk PCI on highly calcified lesions where the hemodynamic tolerability of the no-reflow phenomenon is poor. In addition, in order to prevent thrombus formation, vascular spasm, and no-reflow phenomenon, a rotablation flushing cocktail with 500 mL of heparinized (5000 U) normal saline solution with 5 mg verapamil and 1000 µg nitroglycerin can be administered through a side-port of the Rotablator advancer.20 

Bradycardia. Another possible complication during RA of a calcified lesion in the right coronary artery or a dominant left circumflex artery is the occurrence of advanced atrioventricular block. In this case, a “protected” RA by carefully positioning a temporary pacemaker before vessel debulking is advised. However, it should be noted that a few cases of pericardial tamponade by small and undetected right ventricular perforation clinically manifesting after pacemaker removal have been described.23 A valid alternative is pretreatment with aminophilline, an adenosine antagonist, which can prevent adenosine-mediated bradyarrhythmias. In a small, retrospective study, aminophylline (250-300 mg intravenously over 10 minutes) was administered before RA of the right coronary artery and prevented bradyarrhythmias or atrioventricular block in all cases.24

How to Treat RA Complications

Burr entrapment. A sample case of burr entrapment is provided in Figure 6. When burr entrapment occurs, the following possible strategies might help to free the burr:

Pull back the burr with or without all systems. In some cases, the stuck burr can be withdrawal successfully by manual traction with or without Dynaglide rotation.25 However, while doing this maneuver, the operator must be cautious because vessel perforation may occur, the burr shaft may fracture, and the proximal segment may be injured by uncontrolled deep intubation of the guiding catheter. 

Deep intubation. A controlled deep intubation with subsequent pullback of all devices can be useful to focus the force on the burr and to protect the rest of the coronary artery.

Balloon dilation at entrapped site. The operator can position a second wire just beside the entrapped burr and inflate a balloon catheter in order to make a crack between the burr and vessel wall. This maneuver might help to relieve the burr.10,26 Both hydrophilic-coated wires and stiffer wires, such as the Conquest wire (Asahi Intecc), may be needed to pass the adjacent hard plaque.27 The profile of the rotablation drive shaft sheath is 4.3 Fr, which may prohibit the introduction of a balloon catheter (mostly 3 Fr in diameter) into the guiding catheter (if it is 6 Fr or 7 Fr).28 When there is no space to advance guidewires or balloons through the 6 Fr or 7 Fr guiding catheter, there are two balloon-dilation options for bail-out rotablation burr entrapment: the dual-catheter technique and the single-catheter technique. The dual-catheter technique consists of introducing another guiding catheter via another vascular access for the second guidewire and balloon advancement. The single-catheter technique consists of cutting off the RA system distal to the advancer and removing the drive sheath, leaving only the slim driveshaft surrounding the Rotawire in the catheter lumen.29 By doing so, further devices can be advanced along the Rotablator remnants through the same guiding catheter (the balloon catheter can be inserted even in a 6 Fr guiding catheter). 

Mother-and-child technique. An alternative technique that might be considered after the removal of the drive shaft sheath is the advancement of a child catheter (4 Fr or 5 Fr or GuideLiner)30,31 over the slim driveshaft up to the burr. Then, with simultaneous traction on the burr shaft and counter-traction on the child catheter, the catheter tip might change the axis or angulation of the burr and act as a wedge between the burr and the surrounding plaque. This could exert a larger and more direct pulling force to retrieve the burr.

Snaring. After cutting the RA system, as described above, a snare can be advanced over the shaft just proximal to the entrapped burr, and the burr could be successfully withdrawn by simultaneously retracting the snare and the guiding catheter.32

Surgery. If the above-mentioned bailout techniques are unsuccessful in removing the entrapped burr, the last resort is open surgery.33 However, surgical removal is much more invasive and is usually not immediately available; therefore, all previously discussed interventional techniques should be considered first. 

Coronary perforation. An important cause of perforation during RA is the inadvertent migration of the Rotawire into a small branch or a distal vessel, resulting in a tip-related perforation. Many of these perforations are small and self-limiting, and can be managed with a prolonged balloon occlusion proximal to the site of injury (or at the site of perforation). However, when extravasation persists despite these measures, definitive sealing of the perforation site can be achieved with the delivery of subcutaneous fat, or the use of thrombin, occlusive coils, or beads.34-37 These materials can be selectively injected into the distal target with a microcatheter, accepting a likely resultant localized MI with associated biomarker increase.38 If these interventions are unsuccessful, the vessel can be excluded with a covered stent placed across the origin toward another vessel. Cardiac surgery may be considered if the above measures are unsuccessful.

No-reflow/slow-flow. As in standard PCI, the operator should primarily ensure the restoration of blood flow through the epicardial artery. If hemodynamic stability is preserved, coronary injection with various vasodilator drugs should be initiated. In order to treat this phenomenon, vasodilators like adenosine,39 nitroprusside,40 nicardipine,41 nicorandil,42 and verapamil43 can be considered as a pharmacological treatment and can be administered via an OTW balloon or a microcatheter. If the first injection is unable to restore blood flow, it is possible to repeat drug injection until the maximum dose is reached (adenosine, 200 mg; nicardipine, 400 mg; nitroprusside, 300 mg).43 In cases of hemodynamic instability, intracoronary administration of adrenaline can be performed.21,44 An alternative strategy to pharmacological treatment of no-reflow is mechanical support with intra-aortic balloon pump or Impella device. As demonstrated by Alqarqaz et al,45 the mechanism of action of Impella device in this setting may be due to the improvement in the effective coronary perfusion pressure, the increase of mean and diastolic blood pressures, and the concomitant reduction in left ventricle diastolic pressure. In the PROTECT II study,12 Impella 2.5 showed a superior hemodynamic support in comparison with intra-aortic balloon pump in high-risk PCIs. The choice of device is done on a case-by-case basis and according to the availability of the device. Sometimes, it is also possible to combine intra-aortic balloon pump with Impella in order to optimize the hemodynamic support.45

RA Versus Orbital Atherectomy (OA)

The Diamondback 360 Coronary Orbital Atherectomy System (Cardiovascular Systems, Inc) is the currently available OA technology utilized for treatment of calcified lesions. A diamond-coated crown eccentrically mounted in a drive shaft provides proximal and distal sanding to remove or reduce occlusive material and restore luminal patency. The crown’s orbital diameter expands radially via centrifugal force and differential sanding is achieved; softer tissue flexes away from the crown while fibrotic tissue or arterial calcium is engaged and treated, facilitating stent delivery. The elliptical orbit allows blood and microparticles to flow away from the crown, thus continually dispersing the particulate, cooling the crown, and reducing the risk of thermal injury of the target vessel.

ORBIT I46 was the first-in-human OA trial, with 50 patients enrolled; <20% residual stenosis after stent placement was achieved in 94% of patients, 12% of patients had coronary dissections (types A-C) without clinical sequelae, 1 had a perforation, and there were no reported incidences of slow-flow or distal embolization.

ORBIT II47 was a prospective, multicenter, non-blinded clinical trial that enrolled 443 consecutive patients with severely calcified coronary at 49 sites in the United States. Low rates of in-hospital Q-wave MI (0.7%), cardiac death (0.2%), and TVR (0.7%) were reported. 

Comparative studies for RA versus OA are not available in the literature; nevertheless, some authors suggest that OA provides some favorable aspects, such as the bidirectional property that allows continuous blood flow during treatment, minimizing heat damage, slow-flow, and subsequent need for revascularization. Indeed, low TVR rates are reported, and these results have been shown to be durable out to 3 years.48 Further studies are needed to understand which type of calcified coronary lesions are best treated by OA versus other atherectomy devices.


Good lesion preparation before stent implantation improves outcomes after PCI. RA offers a safe and useful tool that an operator should consider for treating heavily calcified coronary lesions. Complications occurring during RA are rare, but potentially life-threatening; knowledge of some tips and tricks is essential to prevent and treat these complications.


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*Joint first authors.

From the 1Division of Cardiology, Laboratory of Interventional Cardiology, Maggiore Hospital, Bologna, Italy; 2 Interventional Cardiology Unit, GVM Care & Research Maria Cecilia Hospital, Cotignola, Italy; 3Cardiology Unit, Azienda Ospedaliera Universitaria di Ferrara, Cona, Italy; and 43rd Department of Cardiology/Interventional Cardiology & Valvulopathy, Henry Dunant Hospital Center, Athens, Greece.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted May 11, 2019, provisional acceptance given May 21, 2019, final version accepted June 12, 2019.

Address for correspondence: Dr Francesco Giannini, Cardiology Unit, GVM Care & Research, Maria Cecilia Hospital, Via Corriera, 1, 48010, Cotignola, Ravenna, Italy. Email: