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Rotational atherectomy: re-emergence of an old technique
  1. Adam J de Belder
  1. Correspondence to Dr Adam J de Belder, Department of Cardiology, Brighton and Sussex University Hospitals NHS Trust, Eastern Road, Brighton, UK; adam.debelder{at}bsuh.nhs.uk

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Learning objectives

  • Understand the incidence, pathophysiology and treatment options for human coronary arterial calcification.

  • Understand the different imaging options for determining the extent of coronary vascular calcification and their role in planning treatment.

  • Understand the role and limitations of rotational atherectomy in the management of obstructive calcific coronary disease.

Introduction

The generation of mineralised matrix within arterial conduits is common (see Figure 1). About 10%–20% of atherosclerotic vessels contain architecturally complete trabecular bone with fully formed marrow cavities with haematopoietic cells and vascular sinusoids. Although it is recognised that bone formation and arterial vessel calcification have common biochemical pathways, this so-called vascular calcification is a complex and incompletely understood phenomenon, which has proved difficult to prevent and treat.1 The process of extraskeletal ossification is not unlike embryonic ossification pathways which can be triggered by a variety of metabolic, inflammatory and genetic factors. For example, it is likely that proteins that normally restrict biomineralisation to skeletal bone are diminished (eg, fetuin A, matrix GIa, among others), and raise the prospect of identifying targets for therapeutic intervention. The two types of calcification—atherosclerotic (intimal calcification) and medial artery calcification—have different mechanisms, but both affect arterial stiffness and physiology, and increase the risk of adverse cardiovascular events.2

Figure 1

Three-dimensional reconstruction showing extensive aortic and coronary calcification (image courtesy of Dr V Parish).

Vascular calcification: therapeutic targets

Vascular calcification is more common with ageing, patients with diabetes mellitus, hypertension, renal dysfunction, hypercalcaemia and hyperphosphataemia, but can occur in patients without any of these characteristics. Patients with a high calcium diet do not have an increased risk of coronary calcification, suggesting that the pathogenesis lies in dysfunctional regulatory pathways. There is a substantial literature on the potential genetic and acquired mechanisms for this process, but specific mechanisms leading to therapeutic prevention have proved elusive. For example, small studies using statins, calcium blockers, hormonal therapies, phosphate binding drugs and medicinal supplements have all suggested a possible role in limiting progression of calcification, but there are no prospective randomised studies with definitive positive outcomes, as yet.2

Coronary artery calcification: angiography and intravascular imaging

Coronary angiography is highly specific for the detection of coronary calcification but has low sensitivity. Severe coronary calcification (that seen without contrast injection) gives little information about effect on coronary flow.

Intravascular ultrasound (IVUS; resolution 150–200 μM) has high sensitivity and specificity and is more accurate in defining the anatomical distribution of calcific disease (figure 2). There are classifications of IVUS calcification defining number of quadrants involved, location (superficial and deep) and length. Ultrasound does not penetrate calcium and therefore calcific depth is not measurable.3

Figure 2

Intravascular ultrasound of a left main coronary artery showing a 270° arc of calcification (A) preatherectomy and (B) postatherectomy and stenting.

Optical coherence tomography gives a high-resolution (10–20 μM) characteristic appearance of a low signal space defined by sharp borders, and thus gives high sensitivity and specificity. In addition, light penetrates calcium giving an indication of calcium depth, volume and length (figure 3).4

Figure 3

Optical coherence tomography image identifying coronary artery medial calcific deposition.

Coronary artery calcification: CT scanning

Coronary artery calcification (CAC) is common—90% of men and 67% of women over 70 years have CAC. CT quantification of coronary calcium is in routine clinical use and there are some prognostic data on the correlation between adverse events and volumetric quantification of calcium (figure 4).5–7 In one study of 9715 asymptomatic patients undergoing CT scanning between 1996 and 1999, the mortality over a mean of 14.6-year follow-up was 3% for those with a zero score and 28% with a score greater than 1000, with incremental increases in mortality for scores in between.8 As the CAC score increases, it gains specificity but loses sensitivity for predicting coronary artery disease.

Figure 4

Extensive calcification of the left coronary artery and tributaries (image courtesy of Dr V Parish).

When this process affects the coronary vascular tree, leading to angina syndromes, the obstructive nature of densely calcific coronary arteries requires specific tools to allow the safe passage of drug-eluting stent (DES) for therapeutic relief. The identification of coronary calcification can be done with plain radiographs, coronary angiography, IVUS and optical coherence tomography.

As our population ages and coronary calcification becomes more prevalent, we have turned to a tool from the past to help resolve this difficult dilemma.

Coronary intervention

In 1979, plain old balloon angioplasty (POBA) emerged as a percutaneous means of providing relief from angina for many patients. The problem of restenosis limited long-term success, so alternative technologies were considered. One such development, rotational atherectomy or rotablation (RA) was able to improve coronary flow by debulking atheromatous plaque, with the theoretical advantage that it would improve outcomes by leaving a larger residual lumen. The initial interest in this technology dwindled when early trials showed high restenosis rates. It was only when DES technology emerged to blunt the restenotic reaction that RA was reborn as the best option for modifying calcific plaques, that would otherwise obstruct the safe placement and expansion of these stents.

Rotational atherectomy

The concept of using a high-speed nickel-coated brass burr with diamond chips spinning at 150 000 rpm driven by compressed air to clear an artery that is 2–3 mm in diameter is a triumph of engineering ingenuity. Its initial use in human coronary arteries was by Bertrand (Lille, France) and Erbel (Essen, Germany).

Pathophysiology

RA ablates plaque—when properly used, it minimises wall stretch in all plaque morphologies, not only calcified disease, and the end result is a smooth lumen, which allows further vessel modification with balloon and stent placement (figure 5).

Figure 5

Porcine model (non-calcified vessel) (A) before and (B) after rotablation highlighting the smooth appearance (figure courtesy of Boston Scientific).

RA leads to pulverisation of tissue rather than fragmentation—the debris is similar in size to red blood cells (5 µm), which is taken up by the reticuloendothelial system (figure 6). In clinical use, it is important to use appropriate sizing and good technique to ensure pulverisation is the end result—for example, use of too big a burr size can lead to fragmentation and distal embolisation leading to myocardial infarction (MI).

Figure 6

Microparticles caused by rotablation, showing size similar to red blood cells (figure courtesy of Boston Scientific).

From debulking to plaque modification

The development of RA was an alternative to balloon angioplasty treating calcific pathology and softer plaque with a view to lumen enlargement and avoiding the complication of recoil that besets pre-stent percutaneous transluminal coronary angioplasty. There is a substantial literature comparing RA with POBA with a view to investigating this hypothesis, which is dominated by the use of large burrs at high speeds trying to optimise vessel ablation. These trials are littered with high rates of complications particularly no reflow, MI, rhythm abnormalities and perforation.9–11 The consequence of this aggressive approach lead to unacceptable procedural complications and concerning restenosis rates, and RA use substantially declined.

Interest in RA re-emerged with the advent of DES technology, where its role is an adjunct to stent placement when balloon technology was unable to adequately expand a lesion for stent deployment, particularly in the heavily calcified plaque. This concept of plaque modification, rather than debulking, has led to a rewriting of the rules of RA technique, with an emphasis on smaller guide catheter requirements, lower calibre burrs at lower speeds, which has led to a marked diminution in the complications traditionally associated with this technique.

Rotational atherectomy equipment

As with all procedures, familiarity with the equipment is essential to ensure its safe use.

RA equipment (figure 7) consists of:

Figure 7

Disposable and hardware equipment for rotablation (figure courtesy of Boston Scientific).

  • Hardware—a console that controls and monitors the rotational speed, monitors the procedural and ablation time periods, and has an advancer stall warning light.

  • Disposables—these include an advancer, which provides housing for the air turbine, brake assemblies and the burr control knob, a guide wire, and a torquer.

Guide wire

The stainless steel guide wires are 0.009’ in diameter and have an overall length of 325 cm. The spring tip is 0.014’ and is atraumatic, radiopaque and can be shaped to form a steerable system (figure 8).

Figure 8

Detailed view of the rotawire tip (figure courtesy of Boston Scientific).

The rotawire is smaller in diameter than the standard 0.014’ coronary wires and is prone to damage if not carefully handled. The rotablator system should not be used if there is a bend, kink or loop in the guide wire or if the spring tip is prolapsed.

Manipulating the rotawire is highly operator sensitive—it has different handling and its lubricity is inferior to modern coronary guide wires. Some operators choose to use a routine coronary guide wire to cross the lesion, and then use an over-the-wire balloon or exchange catheter to place the rotawire in the distal vessel.

The extra support rotawire provides a firmer line of forward RA propulsion, and some have proposed its use in ostial and tortuous lesions. The disadvantage is that the wire bias potentially increases the risk of perforation, and so the operator must decide the balance between operative necessity and risk of complication. The author has never used the extra support wire.

Burr size

Burr sizes vary and are available in 1.25, 1.5, 1.75 (6F typically compatible, but related to internal diameter of the guide wire), 2.0 and 2.15 mm (7F or above). The drive shaft is enclosed by a 4.3F sheath (figure 9).

Figure 9

Detailed view of the diamond-tipped burr (figure courtesy of Boston Scientific).

The drive shaft has a simple advance mechanism, with three ports:

  1. One for high flow solution (see below) that bathes the artery during the procedure, as the heat generation during RA is quite significant;

  2. One fibre optic cable to allow rotational speed measurement;

  3. One for transmission of compressed air.

The newer systems (Rotalink) allow for one advancer per case and multiple burr use using a simple exchange mechanism.

Air supply set-up

The compressed air cylinder can be a source of technical failure. Failure of compressed air equipment at a critical time can lead to unwanted complications. An adequate supply in tank and regulation to working pressures are fundamental.

Technique for plaque modification

Compressed air generates rotational speeds of 130 000–180 000 rpm—the ideal speed for ablation is debated but there is increasing consensus that lower speeds for shorter runs lead to less complications.

The debulking procedure is preferred as a ‘pecking’ motion rather than a continuous ‘push’ into the plaque. Generally, short engagements of RA, totalling no longer than 20 s per run, are recommended. Pausing adequately before the next run allows particle washout and vessel perfusion.

Practical tips

Preparation of the patient

Although good technique avoids many complications, the risk of heart block, impaired flow, possible dissection and the use of vasodilators in the flush can compromise the patients, particularly if they are hypotensive and dehydrated. To avoid this, all patients undergoing RA should be optimally hydrated (with intravenous fluid if necessary), and ventricular support (eg, intra-aortic balloon pump) considered in the setting of significantly impaired left ventricular (LV) dysfunction.

RA technique

Marked reductions in rotational speed (>5000 rpm) generate unnecessary heat in vessel wall, suggesting either the burr is too big, and it is recommended the size of burr be decreased, or the engagements of plaque are too vigorous or too long.

A stepwise approach to plaque modification is safer, with a 0.50 mm incremental increase in burr size—this does increase the cost though. Some operators use a single burr strategy, but it is recommended that the lesion be ‘tested’ with a balloon before stenting, or an IVUS done, because in some cases the ring of calcium has not been fully ablated to allow safe stenting.

There are a few things which can commonly happen to the inexperienced operator, which should be avoided:

  • Do not stop the burr distal to the lesion.

  • Avoid dottering the lesion.

  • Do not alter the rpm during RA.

  • Do not start RA with the burr in the lesion.

  • Avoid advancing the rotating burr to make contact with the guide wire spring tip.

  • Avoid RA in a forward motion within the guide catheter (difficult for ostial lesions).

Good technique involves the gentle advancement and retraction of an appropriately sized burr at high speed.

There has been wide variation in the technical aspects of RA among users, probably as a result of the traditional teaching for debulking continuing into the era of plaque modification. A recent publication has highlighted a consensus between experts emphasising a contemporary approach with increased use of radial artery access, single curve catheters with strong support and smaller burr sizes at lower speeds with a marked reduction in the incidence of complications associated with the more aggressive techniques (table 1).12

Table 1

Modern RA techniques reduce complications and improve outcomes

Coronary calcification: other useful tools

Coronary calcification leads to rigidity and is often accompanied by tortuosity. Despite the use of strong guide catheters and extra support wires, stent placement even after successful RA can prove challenging. This common clinical dilemma has been greatly helped with the use of ‘mother-and-child’ catheters to provide enough support for stent deployment. Occasionally, the ‘mother-and-child’ catheter can only be advanced with the support of a distally placed balloon.

Use of glycoprotein IIb/IIIa inhibitors

The pulverisation of heavily calcified tissue by RA would seem an ideal milieu for the use of these agents. There are surprisingly little data to support their use. The relative lack of complication in modern-day practice would appear to support the current view that these drugs are not mandated for RA cases. There may, of course, be individual situations where an operator feels its use might be helpful to the outcome.

Complications and their management

Even in the most competent of hands, RA is associated with more complications than routine angioplasty and stenting. The management of these circumstances is central to good outcomes, although complications are minimised by meticulous attention to technique (table 2).

Table 2

Complication management—avoid with meticulous technique

Wire fracture

The distal spring coil portion of the rotawire has a slightly wider diameter (0.014) than the slender main shaft, which makes it vulnerable to fracture, particularly at the hinge point. It is more likely in patients with tortuous coronary segments and in the presence of burr bias along the rotawire in combination with poor technique (eg, persistent advancement of the burr in place of a gentle pecking). Should a distal wire fracture occur, various snare and twisted wire techniques are described for removal. Occasionally excluding the wire fragment by stent placement can avoid any consequences of leaving it in the circulation.

Heart block

Pulverisation with RA of calcified plaque within dominant right or circumflex arteries inevitably leads to temporary heart block. With traditional techniques using large burr to artery ratios, this complication was offset by the placement of a temporary pacing wire which in itself was the cause of unwelcome complications. Contemporary techniques with smaller burrs and shorter runs at lower speeds have reduced the incidence of heart block, which if prolonged is usually resolved by the prompt administration of intravenous atropine, which should be drawn up ready for administration prior to engaging the burr.

Vasospasm

RA procedures are performed with a constant heparinised saline flush (5000 U heparin in 500 mL normal saline) continually bathing the coronary vessel. Traditionally, 5 mg verapamil and 5 mg isosorbide dinitrate can be added to the 500 mL bag to potentially deal with vasospasm.13

Despite this, vasospasm does occur, but as long as good technique is used this complication is minimised and nearly always resolves with the passage of time and the delivery of intracoronary nitrate.

Dissection

This is uncommon and the occurrence of vessel obstruction unusual. The most important thing is to recognise it, and avoid further RA. Regular visualisation of burr progress is advised, but one of the limitations of using 6F catheters is that injecting dye past the burr to check progress is limited—it is the main reason why many RA operators choose 7Fr or 8Fr catheters from the outset of a procedure. Ultimately, stenting the vessel will deal with any dissection, as long as the RA has resolved the obstructive calcium. If obstructive calcium remains which prevents safe stent deployment, stopping the case and allowing the dissection to heal over a period of 2–3 weeks before embarking on further RA is advised.

Slow flow/no flow phenomenon

RA leads to showers of pulverised tissue passing through the microvasculature, and as long as the appropriate decisions have been made about size of burr and good technique applied, it nearly always resolves with the passage of time and intracoronary nitrates. If it occurs, adequate perfusion pressure is essential and adequate hydration of the patient is recommended in all cases.

There are users of other vasodilators to treat this phenomenon, such as verapamil, nitroprusside or adenosine and can be delivered directly to the microvasculature via an over-the-wire balloon or microcatheter. Occasionally, a balloon pump will encourage the perfusion pressure required to restore flow. This complication often reflects poor technique.

Abrupt closure

This is managed in the usual way to any other form of abrupt closure. The most important thing is to understand what the cause is—the management of dissection, vasospasm and no-flow phenomenon is quite different.

Perforation

This is uncommon and is usually due to poor technique (oversizing of burr, ‘pushing’ of burr rather than pecking) or poor choice of vessel (extreme angulation).

Its management depends on the degree of perforation and cardiac compromise. It can range from a catastrophic emergency (figure 10A,B) to a localised coronary injury. The use of covered stents can be lifesaving, as can sacrificing the disrupted vessel. Sometimes the perforated segment cannot be treated percutaneously—in which case, a balloon inflated proximal to the perforated segment to staunch flow while arrangements are made to undergo urgent coronary bypass surgery.

Figure 10

(A) Catastrophic perforation after rotablation with a 1.5 mm burr (B) perforation sealed with the insertion of stents .

Burr stalling in lesion

This is a very unusual occurrence and is often a reflection of poor technique, for example, burr size too large, the increase in burr size too great and using a ‘pushing’ rather than a ‘pecking’ technique. Attempts to continue spinning should be avoided as it can lead to a torsion dissection. Pulling the burr back while asking the patient to cough or taking a very large breath in. The help of a ‘mother-and-child’ catheter can provide extra support for removal (figure 11A-C).

Figure 11

(A) Two heavily calcified segments seen either side of an acute bend in a right coronary artery. (B) 1.5 mm burr stuck in distal segment. (C) Removal facilitated by a deep-throated mother-and-child catheter to provide support.

Failing that, a small balloon inflated to 1 atm placed alongside may help dislodge the burr. A last resort is to seek the help of a cardiothoracic surgeon.

Clinical use

The debulking properties of RA meant it was used quite widely in the belief that it would complement the use of balloon strategies with greater lumen gain. The COBRA trial compared the use of RA with POBA for treating complex lesions and showed little clinical benefit for using RA routinely (in terms of adverse outcomes and relief of angina), but the use of RA did allow more complex cases to be successfully treated when compared with the POBA arm.14 The STRATAS trial found no advantage to a more aggressive RA technique, and the CARAT trial showed that aggressive debulking with a higher burr:artery ratio led to higher complication rates and worse clinical outcomes.15 16

A meta-analysis of randomised trials of POBA versus different forms of atherectomy (directional atherectomy, cutting balloon atherotomy, RA or laser angioplasty) concluded that ‘… the combined experience from randomised trials suggests that ablative devices failed to achieve predefined clinical and angiographic outcomes. This meta-analysis does not support the hypothesis that routine ablation or sectioning of atheromatous tissue is beneficial during percutaneous coronary interventions.’9

There were niche areas where RA might have a theoretical advantage—it appeared logical that RA would have a role in the management of the diffuse intimal hyperplasia that characterises in-stent restenosis. The ARTIST trial showed a significantly worse outcome for RA when compared with POBA, but the ROSTER trial suggested that MACE at 1 year was significantly better for the patients undergoing RA.17 18 Overall, the current situation did not advocate the routine use of RA for in-stent restenosis.

Routine bare-metal stenting post-RA gave superior results to POBA alone, but the results at 6 months were still disappointing.19 20 The advent of DES to inhibit the restenotic process has led to the re-emergence of this technology—interventional cardiologists feel more confident in dealing with the challenges of coronary calcification, knowing that the potential for restenosis has been blunted with the availability of DES. The prospective randomised Rotational Atherectomy Prior to Taxus Stent Treatment for Complex Native Coronary Artery Disease trial determined that routine pretreatment of calcific lesions with RA did not improve angiographic and clinical outcomes despite an early acute luminal advantage gained over the non-RA group. There is no role for RA as a routine if balloon expansion post-stent placement is considered feasible.21

This is now reflected in the European Society of Cardiology guidelines—recommendation for rotablation of fibrotic or heavily calcified lesions that cannot be crossed by a balloon or adequately dilated before planned stenting: intra-coronary.22

Other techniques for plaque modification

There are other techniques described for plaque modification in calcific coronary disease:

  • Laser atherectomy has little evidence to support its use in heavily calcified arteries where it appears to have little impact at the expense of increasing complications. Occasionally, laser modification of non-calcified plaque has allowed full-stent expansion in rare cases when full-stent expansion has not been achieved.9

  • Cutting and scoring balloons do not ablate calcium but may improve vessel compliance by creating splits within the atherosclerotic plaque. Their use as a primary tool is limited by their high profile, but in specific cases this technology may help final stent expansion, particularly if RA preparation has not fully cracked a concentric ring of calcium.

  • Orbital atherectomy is not dissimilar to RA in that it ablates hard material producing particulate matter <2 μm. The ablative element is a diamond-coated crown which rotates at speeds ranging from 60 000 to 120 000 rpm, with the faster speeds giving an increased depth of ablation. Early trials have shown some promise for this technique.23

Higher complications associated with RA: is it the device or is it the patient?

The contemporary use of RA to modify calcified plaque to facilitate DES implantation has led to a significant decrease in the ‘traditional’ complications associated with RA. Cockburn et al 24 compared DES procedures with (n=2152) and without (n=221 496) RA over a 4-year period in the UK, and found that the increased complication rate associated with the RA group was associated with the patient (older, increased rates of diabetes, hypertension, peripheral vascular disease, stroke, impaired LV function, impaired renal function, concomitant valve disease) rather than the technique itself.24

Specific indications for RA

Ostial lesions

The coronary aorto-ostia are a common site for calcification, frequently from aortic plaque extension. Aggressive balloon dilatation can lead to retrograde aortic dissection, which can be avoided by the judicious debulking of the calcific burden with RA, which then allows adequate stent expansion and apposition. There are specific RA techniques to avoid burr stalling—a good coaxial position to avoid angulated engagement, a larger guide catheter so that rotation can start within the catheter without causing catheter ablation, and releasing the tension within the system before RA to avoid jumping of the burr into the calcium.

Bifurcation lesions

The geometrical alterations (plaque and carinal shift) induced by intervention to a bifurcation can prompt side vessel closure, particularly if the ostial side branch segment is heavily calcified. Side branch occlusion can be reduced by using RA at the origin of the side branch, which reduces the chance of occlusion after main vessel stent deployment. RA of a side branch does preclude passage of a wire into the main branch, and there is a theoretical risk of vessel closure without wire protection, but in reality the nature of the device mechanism makes this extremely unusual.

Unprotected left main lesions

It is increasingly common in the ageing population to have elderly patients with severe calcific left main lesions who due to comorbidities are unsuitable for surgical revascularisation. The use of RA in such a setting needs to be performed in experienced hands. As the area of ischaemic territory is very substantial, errors in technique with too aggressive a strategy can lead to profound ischaemia and hypotension, and therefore a cautious approach with smaller burrs having shorter runs will reduce the impact, with a view to stepping up in burr size if needed. Occasionally, if myocardial function is already compromised, these procedures can be supported with a balloon pump or LV assist devices.

Chronic total occlusions

The rapid advances made in recent years at improving the success rates of chronic total occlusion angioplasty have been mainly down to the improvement in guide wire technology, microcatheters and specifically designed tools to aid plaque cap penetration and re-entry. Not infrequently, after long periods of effort to achieve a suitable wire position, balloons will not pass due to calcific plaque. Conversion to RA to facilitate this requires the placement of the fragile rotawire, but the use of microcatheters has allowed this to happen in most cases. A single pass of the smallest 1.25 mm burr is usually sufficient to allow subsequent balloon and stent placement. Concerns about increased risk of perforation with RA within subintimal spaces have not been realised in experienced hands.

Unexpanded stents

There are odd anecdotal cases of using RA within a deployed stent that has not been fully expanded due to poor lesion preparation of a heavily calcified lesion. The author’s experience would be to use laser in this situation, as the clinical risk of RA use in this setting is potentially hazardous. These cases highlight the need for thorough lesion preparation before stent deployment.

When should RA not be done?

Complications are more likely in cases that are on the edge of the device’s capability. Extreme angulation and tortuosity increase the risk of perforation and burr stalling, and it might be sensible to discuss with experienced operators before proceeding.

Who should do RA and where?

On-site surgical cover

Complications of RA are uncommon in experienced hands. The nature of the device does mean occasional life-threatening complications can occur, and under these circumstances the availability of immediate bypass facilities can be lifesaving. However, the vast majority of cases performed do not require surgery, and it would seem restrictive to compel every case to be done in a surgical facility.

Many of these cases would have been discussed at a multidisciplinary forum to decide whether RA is the appropriate strategy.

As with all cases with percutaneous coronary intervention cases, thorough documentation of procedures should be kept, and a forum for audit be available for scrutiny of individual and unit results.

Training and certification

In some countries, physicians intending to perform RA must:

  • attend an RA certification course

  • complete some RA cases with a recognised RA proctor

  • be signed off by the RA training directorate.

This is not a universal arrangement but represents a model of introducing a technique that requires new skills for all members of the multidisciplinary team in a safe and appropriate manner.

Whatever system of governance is in place, RA is a procedure that requires regular use to ensure optimal outcomes.

Conclusions

Societal and medical advances have led to patients surviving long enough to present with clinical consequences of vascular calcification.

The pathogenesis of vascular calcification is poorly understood and therapeutic options for prevention are currently limited.

Modern imaging techniques are able to quantify the extent and nature of calcific coronary disease.

Resolving obstructive calcific coronary stenoses is feasible with rotational atherectomy to allow implantation of coronary stents.

The concept of debulking atherosclerotic disease with rotational atherectomy has been replaced by plaque modification, employing techniques that have far fewer complications traditionally associated with this technique.

Outcomes of coronary revascularisation procedures using contemporary RA techniques are in line with non-RA procedures.

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References

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Footnotes

  • Contributors None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

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