Rotational Atherectomy of Three Overlapping Stent Layers
Abstract: A patient was referred to us for Canadian Cardiovascular Society class III refractory angina. He was found to have in-stent restenosis within three layers of underexpanded stents implanted in 2004, 2011, and 2014. Rotational atherectomy safely yielded stent strut ablation (reduced to one layer), lesion expansion, and very good angiographic and physiologic results.
J INVASIVE CARDIOL 2016;28(9):E77-E79
Key words: rotational atherectomy, in-stent restenosis, refractory angina
Case Presentation
In fibrocalcific coronary lesions, high-pressure balloon inflation is sometimes insufficient to obtain luminal expansion. Rotational atherectomy preferentially cuts hard plaque, increasing plaque compliance and rendering the lesion more amenable to balloon dilation. While intimal hyperplasia is the preeminent etiology of in-stent restenosis, its occurrence predominantly due to stent underexpansion is also commonly observed, particularly in calcified lesions.1 Although most commonly used in native calcific disease, rotational atherectomy has also been utilized to ablate the metal struts of a stent.2,3 Intravascular imaging demonstrating successful atherectomy of three stent layers has not been reported.
A patient was referred to us for Canadian Cardiovascular Society class III refractory angina; he had three layers of mid left anterior descending (LAD) coronary artery stents (unknown size/type placed in 2004; 2.5 mm everolimus-eluting stent placed in 2011; and 2.75 mm everolimus-eluting stent placed in 2014). In 2015, for stent thrombosis, he had sequential non-compliant balloon dilations with 3.0 mm, 4.0 mm, and 4.5 mm balloons, with reportedly minimal lesion expansion.
On the day of intervention, angiography and intravascular ultrasound revealed a severe focal 1.5 mm-diameter lesion in the mid LAD stent (Figure 1). We performed rotational atherectomy with gentle but constant forward pressure with a 1.75 mm burr at ~160,000 rotations/minute, with vigorous intracoronary dye and saline injections to mitigate thermal injury and facilitate debris washout, for 12 runs and for a total atherectomy time of 6 minutes and 20 seconds. This was followed by a second set of runs with 2.0 mm burr for a total atherectomy time of 48 seconds. Four different injections of 300 µg intracoronary nicardipine administered in between various atherectomy runs were effective in treating slow-flow.
Angiography (Figure 2) and intravascular ultrasound (Figure 3) revealed luminal expansion post atherectomy. The lesion was dilated with a 3.5 mm non-compliant balloon. A 2.75 mm drug-eluting stent was deployed for native vessel disease just distal to the mid LAD stent; no stent was placed in the ablated lesion itself. Fractional flow reserve with intracoronary adenosine in the distal LAD post intervention was 0.95 (Figure 4). Intravascular ultrasound post atherectomy revealed ablation of the stent layers (Figure 5). There were no complications. Excimer laser ablation was not chosen because it is not as effective as rotational atherectomy for ablating calcified plaque or pruning stent struts.
In this patient with in-stent restenosis within three layers of underexpanded stents, rotational atherectomy safely yielded stent strut ablation (reduced to one layer), lesion expansion, and very good angiographic and physiologic (FFR) results. The patient endorsed significant symptomatic benefit at follow-up visits.
References
1. Mintz GS, Popma JJ, Hong MK, et al. Intravascular ultrasound to discern device-specific effects and mechanisms of restenosis. Am J Cardiol. 1996;78(Suppl 3A):18-22.
2. Kobayashi Y, Teirstein PS, Linnemeier TJ, Stone GW, Leon MB, Moses JW. Rotational atherectomy (stent ablation) in a lesion with stent underexpansion due to heavily calcified plaque. Catheter Cardiovasc Interv. 2001;52:208-211.
3. Vales L, Coppola J, Kwan T. Successful expansion of an underexpanded stent by rotational atherectomy. Int J Angiol. 2013;22:63-68.
From the 1Heart and Vascular Institute, Henry Ford Hospital, Detroit, Michigan; 2Department of Cardiology, Beaumont Health System, Royal Oak, Michigan; and 3Center for Structural Heart Disease, Heart and Vascular Institute, Henry Ford Hospital, Detroit, Michigan.
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 April 26, 2016, provisional acceptance given May 2, 2016, final version accepted May 9, 2016.
Address for correspondence: Tiberio M. Frisoli, MD, Heart and Vascular Institute, Henry Ford Hospital, 2799 W. Grand Blvd, Detroit, MI 48202. Email: Tfrisol1@hfhs.org
