General description of procedure, equipment, technique
Following the introduction of balloon angioplasty as treatment for obstructive coronary artery disease, it became quickly evident that this procedure was associated with two major problems—acute closure of the vessel and chronic restenosis. While the former was related mostly to dissection, the latter was felt to be related to unfavorable vessel healing either due to negative remodeling (“elastic recoil”) or reaction to deep tissue injury resulting in an inflammatory response and neointimal formation.
The basis of all of these was felt to be due to uncontrollable and unpredictable response to balloon inflations. Therefore an angioplasty technique that would not involve subjecting the vessel to high pressure inflation, but indeed widen the lumen by removal of atheromatous material, could possibly overcome this drawback, and “debulking” devices were introduced.
Directional coronary atherectomy, laser ablation, and rotational atherectomy were techniques that were tried and tested as the next generation of angioplasty devices. Disappointingly, the goals of reduction in procedural complications and lower chronic restenosis rates were not fulfilled and these techniques fell out of favor, particularly with the advent of stent technology. However, rotational atherectomy and to a much lesser degree, laser atherectomy continue to have significant niche roles in current management of obstructive coronary artery disease.
Indications and patient selection
Indications for rotational atherectomy
Calcified and "undilatable" lesions
Heavily calcified lesions may not respond well to predilation and hence stents placed may be underexpanded in these lesion subsets. These would be good cases for rotational atherectomy prior to stent placement.
Undilatable lesions may be suspected in the following scenarios:
Coronary calcification visible on fluoroscopy, computed tomography (CT) scan, or intravascular ultrasound (IVUS)
Previous balloon angioplasty that failed to dilate the lesion adequately (i.e., persistence of a “waist” on the dilated balloon)
In-stent restenosis is sometimes due to an incompletely expanded stent from a resistant lesion. This can be suspected on angiography and confirmed by IVUS or optical coherence tomography (OCT).
Often the lesions will not respond to high pressure balloon inflation. Rotational atherectomy can be used in such situations to shave off stent struts and the underlying resistant plaque, and enable placement and appropriate expansion of the original lesion and/or a second stent. Usually larger burr sizes (2.0 mm and above) are needed to perform such cases successfully.
Aorto-ostial lesions and bifurcation lesions exhibit elastic recoil after predilation, inhibiting stent crossing and appropriate stent expansion. Since these lesions often jeopardize large amounts of myocardium (e.g., left main coronary artery), where quick stent placement, avoidance of multiple balloon dilatations, and appropriate stent expansion are all important, a strategy of rotational atherectomy prior to stent placement may be prudent to reduce both short- and long-term complications. In other ostial locations, such as bifurcation lesions, debulking a lesion may avoid plaque shift and the need for a two-stent strategy.
This procedure may be sometimes used in treating chronic total occlusions or resistant lesions when the stenosis cannot be crossed with a balloon after successful wire passage. Caveats include ensuring that the wire is in the true lumen, that there is reasonable flow in the distal coronary bed, and that a small diameter burr (1.25 to 1.5 mm) is used.
Another rare indication is the treatment of graft anastomotic lesions where the presence of a suture is the nidus for the lesion and the suture itself prevents adequate vessel expansion. In both these situations the rates of perforation are likely to be higher.
Rotational atherectomy will most likely result in embolization into the distal bed. Moreover, thrombi usually overlie unstable or ruptured plaques and these may be prone to dissection or perforation. Thrombi may not be visible but are suspected in patients with an acute myocardial infarction (MI) or acute coronary syndrome (ACS), and generally these clinical scenarios are relative contraindications.
Dissection in the lesion
Dissections may have been caused by previous attempts at angioplasty or spontaneously due to plaque disruption . Rotational atherectomy may further propagate these or even cause a perforation. However, if dissection is really due to inability to dilate a resistant lesion and is localized, rotational atherectomy may offer a solution to the problem.
The presence of severe tortuosity proximal to the lesion may make it difficult to get close to the lesion and spinning the burr in tortuous segments may increase the chance of complications. For the same reason, lesions in tortuous segments or in acute bends should be avoided.
Poor flow in the distal bed
Poor flow in the coronary branches distal to the bed either due to the severity of the lesion, diffuse disease, or embolization are relative contraindications since wash out of debulked debris would be limited resulting in a further decrease in coronary flow.
Severe left ventricular dysfunction
Patients with severe left ventricular dysfunction may be unable to tolerate somewhat prolonged ischemia that may result from this procedure. The 10% to 15% incidence of postprocedural enzyme and troponin elevation may result in further left ventricular dysfunction and worsen prognosis.
Sole remaining vessel or large amount of myocardium in jeopardy
This is a relative contraindication since prolonged ischemia in this situation may be associated with deterioration in clinical condition. Left ventricular support devices such as an intraaortic balloon pump (IABP), impella device, or tandem heart may be helpful in such situations to tide over consequences of left ventricular dysfunction.
Details of how the procedure is performed
The procedure is performed by using a Rotablator catheter (Boston Scientific), which consists of a spring coil shaft with a burr at the tip. The front edge of the burr is the ablating portion, oval shaped (like an American football), and covered with fine diamond crystals. The shaft is encased in a plastic sheath and both are connected to an advancer, which has a hand-controlled knob with which the burr can be moved to and fro.
The advancer in turn is connected to a console that houses a turbine run by pressurized nitrogen. The burr can rotate up to speeds of 250,000 rpm ( we typically use 140,000 rpm to 165,000 in the lesion). The revolution speed can be set by using controls on the console. In addition, the console also gives a readout of duration of burring through a fiberoptic cable connection to the end of the advancer.
In order to reduce friction between the shaft and the sheath and to reduce the heat generated, saline is run through the sheath as well as the central lumen of the burr, through a connection again from the advancer. Typically, a bag of heparinized saline in a pressure bag with nitroglycerine and verapamil added to it, is used.
Rotaglide solution (Boston Scientific) can also be added to this mixture to further reduce friction of the burr in the sheath. The addition of vasodilators theoretically can reduce vessel spasm and dilate the distal coronary bed to reduce the incidence of slow-flow phenomenon.
The rotational atherectomy catheter is introduced into the coronary artery over a dedicated long rotational atherectomy wire, which consists of a monofilament stainless steel 0.09-inch wire with a floppy, curveable spring coil tip, which is 0.11 inch. The tip cannot be pulled through the central lumen of the shaft, and therefore the burr can only be loaded over the back end of the wire, which also prevents the burr from inadvertently traveling into the vessel without being guided over the wire, causing it to whip with possible disastrous consequences.
There are two kinds wires that can be used—a floppy and an extra-support rota wire. The floppy wire is used in most cases and the extra support wire can be used in tortuous vessels or in situations when one suspects wire bias as a reason for the burr not crossing the lesion. The latter wire straightens out proximal tortuosity to allow the burr to get to the lesion but often this results in proximal vessel spasm and “pseudo-stenosis.”
The device is connected to a console that houses the turbine that rotates the burr with pressurized nitrogen gas, which flows from a tank connected to the console. The console has a window that reads out the rpm, which can be controlled. Typically the rpm is set at 150,000 to 180,000 rpm.
This adjustment is set with the burr outside the body but on the wire, and the lesion is crossed with the burr spinning at slightly lower speeds. Higher speeds will generate more heat and lower speeds could theoretically produce reduced plaque shaving. Both can result in reduced coronary flow and hence appropriate judgment based on lesion length, distal vessel size and burr size should be made in regards to choosing burr speed.
After the lesion is crossed with the wire, the burr is brought close to the lesion, ensuring flow around the burr before spinning. The lesion is crossed with multiple to and fro “pecking” movements, with each run lasting not more than 20 seconds. The burr is parked well proximal to the lesion after each run.
Multiple runs are made until the lesion is completely crossed. After each run it is advisable to check for reduced coronary runoff with a small volume contrast injection. In the presence of slow flow or contrast extravasation, the rotational atherectomy procedure is terminated.
After successful rotational atherectomy with one or more burrs, the procedure is completed with balloon angioplasty and stent placement. This can be achieved by exchanging the rota wire with a workhorse wire and using standard equipment. IVUS is recommended to ensure adequate stent expansion.
Other options for nondilatable lesions
Calcified and fibrotic lesions may be dilated with high pressure balloon dilations or with “cutting” or “scoring” balloons prior to stent placement to ensure adequate stent expansion.
The downside of these approaches is the occurrence of a dissection without adequate vessel dilatation, which will prevent adequate stent deployment due to residual resistant lesion. Rotational atherectomy at this stage is relatively contraindicated due to the high incidence of vessel perforation and dissection propagation. Hence, if a nondilatable lesion is suspected, strong consideration for rotational atherectomy should be given at the very outset.
Excimer laser atherectomy is an alternate technique that can sometimes be used. Very few centers have this device on hand and this a limitation. In addition, calcified lesions do not yield well to this treatment.
A good niche for this device is in the treatment of in-stent restenosis due to incomplete stent expansion due to resistant plaque. Laser energy can theoretically extend beyond the stent border to soften this resistant plaque and enable adequate stent expansion with high pressure balloon dilation or the placement of another stent.
Complications and their management
Complications and management
Hypotension and bradycardia
These are very common complications, particularly while treating the right coronary artery. Although temporary pacemakers were advocated in the past, these are rarely used prophylactically anymore due to modifications in technique. Bradycardia is most often due to sinus node slowing, but transient A-V blocks can also occur.
The mechanism is thought to be the release of adenosine, and treating patients with boluses of aminophylline during burr runs will often correct or prevent these from happening. Occasionally intravenous (IV) pressors, such as dobutamine or epinephrine as bolus doses or even as a drip, will be needed to correct hemodynamic instability.
Hypotension is deleterious since it will result in reduced coronary perfusion pressure, decreasing the rate of debris clearance from the distal coronary bed resulting in the “slow reflow” or “no reflow” phenomena, which will potentiate myocardial ischemia.
Steps to prevent and treat include:
Ensure adequate filling pressure to counteract hypotension from vasodilatation by IV fluid administration prior to the procedure
Slow, short burr runs with minimal forward pressure on the burr to avoid >5,000 rpm decelerations
Choosing smaller sized burrs with very severe stenosis and long lesions
Aminophylline boluses or infusion during burr runs
Correcting hypotension promptly with vasopressors
Coronary dissections and perforations
These occur more frequently than with routine balloon/stent procedures because of the inherent mechanism of rotational atherectomy. Though the burr is most often the culprit, perforation after stent placement or after high pressure balloon inflation done after stent placement, can also occur. Dissections with wire passage are known, and perforations that occur are due to distal wire positioning into small branches.
Once these are suspected, the procedure is terminated and steps to correct the situation are to be initiated. These include prompt stenting of the vessel for dissections to ward off acute closure. Perforations are to be treated in the usual manner with steps including reversing anticoagulation, sealing off the perforation with prolonged balloon inflation and possibly the use of a covered stent.
An echocardiogram should be done promptly to look for a pericardial effusion followed by pericardial tap and drain placement for any evidence of cardiac tamponade. Emergent surgery will be sometimes required for persistent coronary leak and early surgical consultation is advisable once a perforation is detected. If these steps are successful and the patient is stable, patients should be observed in the intensive care unit and frequent echocardiograms are indicated.
"Slow and no reflow" phenomena
The terminology is self-explanatory and is defined as less than the TIMI III flow in the coronary artery. Mechanisms include microembolization of the distal coronary bed from plaque debris, macroembolization of friable plaque material or clots from an unstable plaque, platelet activation and aggregation, and activation of vasoactive mediators and consequent small vessel spasm.
Further burring will only aggravate the situation and the procedure will have to be terminated before the endpoint is realized and hence prevention is key. Steps to do this have been listed under hypotension and bradycardia.
The use of glycoprotein (GP) IIb-IIIa inhibitors is of some benefit but is hazardous should a perforation occur and hence is not advisable as prophylactic treatment. Use of bivalirudin instead of unfractionated heparin has been described, though immediate reversal is not possible should a perforation occur.
Intracoronary nitroglycerin, adenosine, verapamil, and nitroprusside boluses are used to improve flow. Other methods to correct ensuing ischemia and its consequences should be employed and may include the placement of an IABP.
The lesion should be adequately treated with stent placement to ensure adequate distal flow and to treat any underlying dissection, which may sometimes explain this slow flow. This phenomenon is associated with a high incidence of a postprocedural cardiac enzyme and troponin elevation, and patients should be managed as ACS patients.
What’s the evidence?
Kini, A, Marmur, JD, Duvvuri, S. “Rotational atherectomy: improved procedural outcome with evolution of technique and equipment. Single center results of first 1,000 patients”. Catheter Cardiovasc Interv. vol. 46. 1999. pp. 305-11. (This paper describes techniques that reduce complications based on newer methods that were tested in a large number of patients. This is the basis for current practice.)
Bittl, JA, Chew, DP, Topol, EJ. “Meta-analysis of randomized trials of percutaneous transluminal coronary angioplasty versus atherectomy, cutting balloon atherectomy, or laser angioplasty”. J Am Coll Cardiol. vol. 43. 2004. pp. 936-42. (This meta-analysis discusses the available techniques of plaque modification and their role in contemperory percutaneous coronary interventions.)
Sharma, SK, Kini, A, Mehran, R. “Randomized trial of Rotational Atherectomy Versus Balloon Angioplasty for Diffuse In-stent Restenosis (ROSTER))”. Am Heart J. vol. 147. 2004. pp. 16-22. (Results from this trial suggests improved procedural outcome with debulking using rotational atherectomy for diffuse in-stent restenosis.)
Rubartelli, P, Niccoli, L, Alberti, A. “Coronary rotational atherectomy in current practice: Acute and mid-term results in high- and low-volume centers”. Catheter Cardiovasc Interv. vol. 61. 2004. pp. 463-71. (As the practice of coronary interventions have evolved and the techniques of rotational atherectomy have been refined, the complication rates and early success rates are very favorable as compared to the early days of this technique.)
Tran, T, Brown, M, Lasala, J. “An evidence-based approach to the use of rotational and directional coronary atherectomy in the era of drug-eluting stents: when does it make sense?”. Catheter Cardiovasc Interv. vol. 72. 2008. pp. 650-62. (This paper describes the role of plaque debulking in the current era and the niche role of this technique when drug-eluting stents are used.)
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.
- General description of procedure, equipment, technique
- Indications and patient selection
- Details of how the procedure is performed
- Complications and their management
- What’s the evidence?