The Undilatable Lesion: A Striking Example of Plaque
Modification for Severe Calcification with Rotational
Atherectomy – Impet

The undilatable lesion requiring rotational atherectomy is an uncommon occurrence with the current availability of noncompliant balloons and other methods of “focused-force” angioplasty. The use of noncompliant balloons, or a “buddy” cutting wire, and finally, the use of nonablation devices such as the Cutting Balloon Ultra (Boston Scientific Corp., Natick, Massachusetts) or the FX miniRAIL^™ catheter (Abbott Laboratories Inc., Abbott Park, Illinois) have all been described in previous reports.^2,3 Each of these plaque modifying therapies has had reported success in tackling severely calcified lesions that may be undilatable with conventional balloons. Rotational atherectomy remains the ultimate ablation and plaque modification therapy for truly undilatable lesions that are resistant to the above devices. Heavily calcified lesions are associated with reduced procedural success and increased complications.¹ Underexpanded stents in segments of severe calcification are predisposed to increased rates of restenosis.¹ Rotational atherectomy has two functions with regard to calcified or resistant lesions.¹ Plaque ablation, or true plaque debulking, has been documented with intravascular ultrasound post-rotational atherectomy.⁴ Altering plaque, and therefore arterial wall compliance, is also presumed to be an important mechanism related to the efficacy of rotational atherectomy.¹ Because this is a functional rather than an anatomical property, it is more difficult to quantify. We document a striking example of this property of rotational atherectomy.

Case Report. A 55-year-old male with hypertension, hyperlipidemia and obesity had received rescue angioplasty for an inferior infarction 3 months prior. An 85% mid left anterior descending artery (LAD) stenosis with calcification was left untreated for intervention at a later date (Figure 1). The patient had Canadian Cardiovascular Society class II angina and was brought back for the LAD intervention.
The left main artery was engaged with a 6 Fr large lumen VL 3.5 guiding catheter. A Pilot 50^™ wire (Guidant Corp., Indianapolis, Indiana) was passed down the LAD. A 2.5 x 15 mm compliant balloon was dilated to 12 atm and finally 22 atm with severe “dog-boning” at the lesion site (Figure 2). Next, a “buddy” Extrasport^™ wire (Guidant) was introduced down the LAD to act as a “cutting wire” to implement focused-force angioplasty. Once again, compliant and noncompliant 2.5 x 15 mm and 3.0 x 9 mm noncompliant balloons were inflated to 22 atm alongside the cutting wire. The lesion was completely resistant to this attempt as well. The buddy wire was removed and a 3.0 x 10 mm cutting balloon was passed over the initial Pilot 50 wire to the lesion site with significant difficulty. Two inflations of this balloon to the maximum recommended pressure of 10 atm (for 2 minutes each) were performed with no evidence of yielding (Figure 3). At this point, there was no macrodissection or disruption of the vessel with good distal flow. Due to the high pressure and multiple balloon inflations utilized, the possibility of microdissection couldnot be ruled out angiographically. The possibility of creating a larger dissection with rotational atherectomy after high pressure balloon inflations discouraged us from performing the procedure the same day. In addition, the amount of contrast already used, the lengthy procedure time and patient fatigue were also factors in favor of opting for a separate procedure. Since the patient was stable and had class II symptoms, the decision was made to bring the patient back for rotational atherectomy in 3 to 4 weeks’ time to allow for plaque healing.
 
Three weeks later, repeat angiography demonstrated a stable LAD stenosis. A 7 Fr large-lumen VL 3.5 guiding catheter was engaged into the left main and an Extra Support 0.009 inch Rotawire was passed down the LAD. A 1.25 mm burr was prepared with the Rotaglide^™ (Boston Scientific Corp., Natick, Massachusetts) solution and three runs were made at 150,000 rpm for 15–20 seconds each (Figure 4). There were no decelerations during these runs. The vessel was pretreated with intracoronary verapamil and nitroglycerin before and after each run. A 1.5 mm burr was chosen next and three further runs were performed in a similar fashion. There was a small localized dissection flap within the calcified segment, and therefore no further burrs were used (Figure 5). Angiographically, the lumen did not appear significantly larger than before atherectomy. Next, a 2.5 x 15 mm compliant balloon was inflated to 9 atm at the lesion site with residual significant restriction at the lesion site. A 3.5 x 20 mm Liberté^™ (Boston Scientific) stent was inflated to 14 atm with very significant “dog-boning” of the stent (Figure 6A). The stent was further inflated to 16 and 18 atm and suddenly expanded remarkably well (Figure 6B).

The stent was further inflated to 20 atm to ensure adequat e expansi on. Next , intravascular ultrasound (IVUS) was performed with an Atlantis Pro^™ 40 MHz (Boston Scientific) catheter to ensure adequate stent deployment. The IVUS images demonstrated a 360 degree arc of calcium with almost complete dropout beyond the calcium (Figure 7). The minimum luminal area was quite large at 10.3 mm² (Figure 7). The superior portion of the post-stent IVUS images demonstrated dissection and disruption in the wall of the calcified vessel, further confirming the mechanism of action provided by the rotational atherectomy. Further inflations were performed with a 3.75 x 12 mm noncompliant balloon at 20 atm within the stent. An optimal final angiographic result was obtained with excellent TIMI 3 flow (Figure 8). One month later, the patient remains angina-free and demonstrates good exercise tolerance.

Discussion. Calcified and undilatable lesions carry risks of stent underexpansion and subsequent restenosis.¹ Plaque modification with the blades of a cutting balloon or a buddy cutting wire may create controlled dissection into resistant plaques, thereby enabling adequate expansion with routine balloon angioplasty and stenting.⁵ The Cutting Balloon is purported to focus 157,000 times as much pressure on the plaque as a conventional balloon.⁵ Rotational atherectomy, however, is the device of choice for resistant or heavily calcified lesions. Based on the CARAT and STRATAS trials, a lesion modification strategy with a burr/artery ratio of 0.6–0.7 is preferred compared to more aggressive ablation with a burr/artery ratio of > 0.7.1 A higher risk of periprocedural infarction and increased angiographic complications were demonstrated with an aggressive ablation strategy.¹ Lower platform speeds (150,000–160,000 rpm vs. 170,000–190,000 rpm) for ablation have been demonstrated to decrease platelet activation, decrease vascular wall injury and perhaps also reduce restenosis.⁶
The rota-stent approach (rotational atherectomy followed by stent implantation) to complex and calcified lesions was demonstrated to have a high procedural success rate, an acceptable complication rate and a relatively low restenosis rate.⁷ IVUS has been utilized to characterize the mechanism of plaque ablation and plaque modification with rotational atherectomy.⁴ Rotational atherectomy is associated with an increased lumen area, decreased plaque area and reduction of calcium arc at the target lesion.⁴ The pattern of dissection post-rotational atherectomy was within the calcified plaque.⁴
In this case, high-pressure inflations, noncompliant balloons, a cutting wire and a Cutting Balloon were all attempted unsuccessfully prior to atherectomy. The stent inflation was noted to have significant under expansion at moderate pressure, demonstrating that only minimal plaque was ablated, whereas at higher pressure, complete and optimal stent expansion was achieved, providing a striking visual example of modification of plaque and vessel wall compliance. This same lesion could not be dilated with higher-pressure balloon inflations or with maximal pressure with a Cutting Balloon with its highly focused effect. The degree and severity of calcium in the vessel post-ablation was clearly demonstrated on IVUS, which confirms that the volume of ablation may not be as critical as the change in arterial compliance. One limitation with our report is that there were no preatherectomy IVUS images, however, given the complete and heavy circumferential arc of calcium seen in the postprocedure images, significant calcium ablation was clearly not the mechanism for success in our case, but was rather due to a change in arterial wall compliance. More importantly, the final IVUS images demonstrated localized dissection and disruption in the calcified arterial wall, definitively documenting the mechanism of action of rotational atherectomy in this case (Figure 7). The LAD was 3.5–4 mm in diameter and the largest burr utilized was 1.5 mm, giving a burr/artery ratio of approximately 0.4. One hypothesis that may be derived from this case is that the more important function of rotational atherectomy may be plaque modification as opposed to plaque ablation. The impact of the degree of calcium arc as determined by IVUS (> 180 degrees versus < 180 degrees) does not seem to affect stent expansion or luminal area post-rotational atherectomy.⁸ This supports the hypothesis that ablation of superficial calcium and creation of localized dissection planes may largely account for change in vessel wall compliance as opposed to the debulking effect (Figure 7). Perhaps smaller burr/artery (< 0.5) ratios could be considered in appropriate vessels to avoid complications such as dissection and no-reflow, while preserving the efficacy of this technique. To achieve higher stent minimum luminal area, adjunctive high-pressure balloon inflation may be sufficient to reduce later restenosis. A formal randomized study of small-burr atherectomy (burr/artery ratio < 0.5) versus current standards (burr/artery ratio of 0.6–0.7) may be reasonable for future consideration of calcified lesions.

References

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