Very Late Sirolimus-Eluting Stent Displaced Fracture in the<br />
Mid-Left Anterior Descending Artery

Case Report. A 66-year-old female was admitted in March 2005 with non-ST-segment elevation myocardial infarction (NSTEMI). She had a prior history of hypertension, dyslipidemia and paroxysmal supraventricular tachycardia (SVT). Her coronary angiogram showed severe disease at the mid-left anterior descending artery (LAD) (Figure 1) and first obtuse marginal artery (OM1). The LAD lesion was predilated with 2.5 x 20 mm mercury (Abbott Vascular, Abbott Park, Illinois) balloon. A 3.0 x 33 mm Cypher (Cordis Corp., Miami Lakes, Florida) stent was deployed at the mid-LAD at 14 atm (Figure 2). The OM1 was predilated with a 2.5 x 20 mm Mercury balloon and a 3.0 x 15 mm Driver (Medtronic, Inc., Minneapolis, Minnesota) stent was deployed at 12 atm.
After the procedure, the patient experienced two episodes of SVT for which she was advised to undergo an electrophysiological (EP) study. She remained asymptomatic on medical treatment until September 2006 (approximately 18 months later), but then began having palpitations and chest discomfort again. A myocardial perfusion scan performed in December 2006 was normal.
In February 2007, due to recurrent palpitations, she finally decided to undergo an EP study. The study confirmed atrioventricular node reentrant tachycardia (AVNRT) which was successfully ablated. At the end of the procedure, after removal of the femoral venous sheaths, the patient became hypotensive and bradycardic. She was given intravenous atropine and fluids for a presumed vasovagal reaction. Her bradycardia and blood pressure improved, but she then complained of chest pain with significant ST depressions in the anterior precordial leads. An immediate coronary angiogram revealed a fracture at the center of the LAD stent with severe in-stent restenosis at the site of the fracture (Figure 3). Also noted were positive remodeling with in-stent restenosis in the stent area and ectasia at the distal edge (Figure 4). Diffuse proliferative in-stent restenosis was also noted in the OM1. Immediately after angiography, the patient was free of chest pain and hemodynamically stable. The risks and benefits of percutaneous coronary intervention versus coronary artery bypass graft surgery (CABG) were discussed with the family, and the patient opted for the latter, which was successfully performed with a LIMA to the LAD and a SVG to the OM. Postoperatively, the patient had an uneventful recovery and was discharged 5 days later.

Discussion. Percutaneous coronary stent implantation frequently results in significant three-dimensional changes in the geometry of native coronary arteries.¹ Coronary artery stent fracture is a very rare condition. There are a few case reports in the literature.^2,3 In a large study of 256 patients, stent fractures were present in only 8 out of 307 lesions, with only 1 out of 8 occurring in the LAD.⁴
In a study by Michael et al, stent fracture was shown to occur most frequently at sites that serve as hinges or at the site of 2 overlapping stents. The mean duration of stent fracture was 226 days, with the longest duration being 620 days.⁵ Strut fractures have also been reported with aggressive postdilatation after stent deployment.⁶ Thus far, the drugeluting stent fracture cases reported in the literature have been associated only with sirolimus-eluting stents, suggesting a possible role of the medication or the polymer coating.
This is an unusual case with a very late presentation — in fact the longest duration reported in the literature — i.e., 699 days. It was a “displaced” fracture, a term adopted from bone fractures and at a non-hinge site in the LAD. Since no postdilatation was done after the initial deployment of the stent, the stent fracture cannot be attributed to overdilatation. Interesting to note was the positive remodeling of the vessel in the stented area, which has been associated with late stent malapposition. An ectatic segment was also noted at the distal edge of the stent.
Conclusion. Stent fracture is rarely associated with restenosis, and sirolimus-eluting stents, in particular, appear to be more frequent culprits in this phenomenon. Questions remain to be answered about whether this phenomenon has a definite association with drug-eluting stents, and what the best approach to the problem is.