Desperate Times, Desperate Measures: Rotablating Dissections in Acute Myocardial Infarction

ABSTRACT: The concomitant existence of an acute ST elevation myocardial infarction (STEMI) and a truly undilatable lesion is not a common occurrence, although STEMI lesions can be calcified and sometimes difficult to fracture.

The manufacturer lists the presence of a dissection as a contraindication to use for rotational atherectomy. There are no previously reported cases in the literature of rotablation of significant macro dissections in the setting of acute myocardial infarction (MI). Noncompliant balloons, the Cutting Balloon Ultra (Boston Scientific), the Fx miniRAIL^™ (Abbott Vascular), and the “cutting wire” technique have all been previously described for calcific lesion modification.¹ Heavily calcific lesions especially in the setting of a thrombotic infarction may predispose to under expansion, restenosis, and stent thrombosis. Rotational atherectomy (RA) through plaque ablation and altering arterial wall compliance may be helpful in negotiating heavily calcific lesions.²

Previously, a single case report of the use of RA in the setting of a STEMI has been reported.³ Two previous RA reports have been described in the setting of acute and delayed healing of dissections; however neither were in the setting of acute STEMI.^4,5 We describe the first report to our knowledge of RA for a truly undilatable lesion with accompanying NHLBI type C iatrogenic dissection post balloon dilation during an acute STEMI to allow lesion fracture and subsequent stent deployment.

J INVASIVE CARDIOL 2011;23:E226–E228

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Case Report. A 73-year-old female with an acute anterior STEMI presented to our center for primary angioplasty. The patient was given 160 mg aspirin, 600 mg clopidogrel, and intravenous heparin bolus in the emergency room and subsequently brought forth for percutaneous intervention.

The LAD demonstrated 99% mid-body stenosis with TIMI II flow (Figure 1). The right coronary artery had another 85% distal stenosis, which was planned for staged intervention.

The left main was engaged with a 6 Fr VL 3.0 guiding catheter LAD lesion was traversed with a hydrophilic wire and balloon angioplasty was performed sequentially with a semi-compliant 2.0 x 15 mm balloon and subsequently with 2.25 x 15 mm noncompliant balloons. These demonstrated complete “dogboning” with no plaque fracture (Figure 2). Larger balloons would not cross the lesion site. A cutting wire strategy also did not yield the stenosis and a cutting balloon would not cross. At this point, there was a type B dissection just beyond the lesion site and a glycoprotein IIb/IIIa inihibitor (GPIIb/IIIa) was already administered. The patient still had chest discomfort with improved ST segments, however, and TIMI 2–3 flow. A rotawire would not cross the lesion. An over-the-wire balloon was not available at the time, therefore, a Twin-Pass^® catheter (Vascular Solutions Inc.) was utilized, but also would not cross the lesion to allow for wire exchange. Bypass grafting was contemplated, but given the ongoing chest pain and the presence of GPIIb/IIIa inhibitor on board, we pursued a high-risk PCI strategy. More aggressive dilation was performed with 2 separate 2.25 x 15 mm noncompliant balloons to allow passage of a rotawire. Inflations were performed with noncompliant balloons at pressures of 20–24 atm. This resulted in a NHLBI type C dissection with severe balloon “dogboning” (Figure 3). Given the limited revascularization options, we decided to proceed with careful rotational atherectomy. A Rotablator Floppy wire was tried again and did cross the lesion at this point. Gentle and extremely careful “pecking” with < 15 second runs and avoiding of > 5,000 rpm decelerations at 150,000 rpm was performed with frequent monitoring of contrast for perforation and dissection propagation (Figure 4). Four passes were performed without worsening dissection or perforation. Subsequently, noncompliant 2.25 mm balloon inflations did appear to yield the lesion and a 2.25 x 23 mm drug-eluting stent was implanted with excellent angiographic results and infarct resolution (Figure 5). Further postdilation was performed with a 2.75 mm noncompliant balloon to ensure excellent stent expansion (Figure 6). The patient was brought back for staged PCI to the right coronary artery, which demonstrated complete patency. There was no angiographic restenosis of the LAD stent at 3 months.

Discussion. The first utilization of RA in the setting of STEMI was described by Ho in 2005.³ Generally, the presence of thrombus is considered a contraindication as per the package insert for Rotablator^® (Boston Scientific, Natick, Massachusetts). Given the thrombotic environment of a STEMI and the potential for platelet activation by the Rotablator, a thrombotic STEMI is generally not considered ideal for rotational atherectomy. To modify entry into a complex LAD bifurcating lesion, Ho safely and successfully performed RA in this setting.³ Pedersen et al first described the use of rotational atherectomy post acute dissection in a patient with postinfarction angina and undilatable lesion with a type D post-inflation dissection, which was “tacked up” with repeat balloon inflation and subsequently treated with multiple stents successfully.⁴ More recently, Ho et al describe a delayed rotational atherectomy procedure performed 3 weeks post acute dissection due to occlusion at the previous dissection site with a successful outcome.⁵

Rotational atherectomy in the presence of dissection is contraindicated. Concerns include perforation and more commonly propagation of spiral dissection through potential entrapment of dissection flap in the rotational motion of the burr.

On this occasion we describe the use of RA in the combined setting of acute thrombotic STEMI with an undilatable lesion and post-ballooning type C dissection. Although early rotational atherectomy was contemplated and attempted, the rotawire would not traverse the lesion. Finally, careful RA was performed in the presence of a type C dissection with subsequent stenting. Techniques to avoid complications in this perilous setting may include small burr size (1.25 mm in this case), gentle “pecking” advancement and frequent angiographic monitoring between ablations to ensure absence of complications. The small caliber burr (1.25 mm) is likely quite important in this type of a situation and may prevent further complications such as dissection propagation or perforation in an already tenuous scenario. Most often dissections in calcified lesions may flank the most stenotic/calcific site and not actually be located at the calcified segment; in such a case, it may be advised to perform very localized rotablation and avoid multiple long “smoothing runs” to “polish” the lesion segment in order to avoid dissection flap entrapment and subsequent dissection propagation or perforation. Although operators may be somewhat reticent to initiate GPIIb/IIIa inhibition until late in rotablation to avoid catastrophic bleeding from perforations or in case of surgery requirement for dissection. In this case, further thrombus burden may have been prevented from early initiation of GPIIb/IIIa inhibitor.

Conclusion. We do not recommend this as a routine bailout procedure, and still believe that it should be relatively contraindicated. We describe the first use of rotablation with a small caliber burr (1.25 mm) in the setting of simultaneous acute STEMI and type C dissection. In our scenario of limited option availability, after careful consideration of surgical options, careful rotational atherectomy may be possible to accomplish safely. Our final recommendation is that operator experience and comfort with rotational atherectomy is paramount. The ability to negotiate propagating dissections or perforations as complications of this high-risk procedure should be planned for and surgical backup as well as covered stents should be readily available to the operator.

References

1. Moses JW, Carlier S, Moussa I. Lesion preparation prior to stenting. Rev Cardiovasc Med 2004;5 Suppl 2:S16–S21.
2. Safian RD, Feldman T, Muller DW, et al. Coronary angioplasty and Rotablator atherectomy trial (CARAT): Immediate and late results of a prospective multicenter randomized trial. Catheter Cardiovasc Interv 2001;53(2):213–220.
3. Ho PC. Rotational coronary atherectomy in acute ST-segment elevation myocardial infarction. J Interv Cardiol 2005;18(4):315–318.
4. Pedersen WR, Goldenberg IF, Johnson RK, Mooney MR. Successful rotational atherectomy in the setting of extensive coronary dissection: A case of failed balloon angioplasty in a nondilatable calcified lesion complicated by balloon rupture and extensive dissection. Catheter Cardiovasc Interv 2003;59(3):329–332.
5. Ho PC. Rotational atherectomy in coronary dissection. J Invasive Cardiol 2010;22(10):E204-207.

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From the ¹Department of Cardiac Sciences and ²Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted January 26, 2011, provisional acceptance given February 24, 2011, final version accepted February 28, 2011.
Address for correspondence: Farrukh Hussain, MD, FRCP, Assistant Professor of Medicine, Interventional Cardiology, Y-3012, Department of Cardiology, St. Boniface General Hospital, 409 Tache Avenue, Winnipeg, Manitoba, Canada. Email: fhussain@sbgh.mb.ca