Recently, reports of stent fracture with focal restenosis have suggested that it is another mechanism of in-stent restenosis after implantation of sirolimus-eluting stents. However, the mechanism by which strut disruption occurs remains unknown. Current reports of in-stent restenosis suggest that fracture of drug-eluting stents is different from bare-metal stents, and can progress to restenosis and reocclusion. We report on a patient with a fractured stent in a patent coronary artery that progressed to diffuse neointimal hyperplasia presenting with acute myocardial infarction 2 years after stent placement. J INVASIVE CARDIOL 2007;19:E43–E45

Drug-eluting stents (DES) have, for the most part, replaced bare-metal stents (BMS) as a safe and effective therapeutic modality for treating coronary stenosis. Post-DES restenosis with sirolimus-eluting stents (SES) or paclitaxel-eluting stents (PES) has become a serious problem despite their proven efficacy and superiority.¹ Recently, stent fracture has been suggested as one of the causes of restenosis after DES placement.^2,3 This problem is usually identified at a routine follow-up coronary angiography in patients presenting with angina.^4,5 We report a case of stent fracture in a patent coronary artery that was diagnosed at a 6-month follow-up visit and led to acute coronary syndrome in the patient.

Figure 1

1. Coronary angiogram shows that the first obtuse marginal (OM) branch is totally occluded at the ostium (A, RAO caudal view). The OM branch was successfully recanalized and a sirolimus-eluting stent was implanted (Cypher 3.0 x 23 mm) (B). The stent was patent at 6-month follow-up angiography (C). Fluoroscopic images showed some discontinuity and misalignment in the middle of the stent (white lines in the box).

Case Report. A 63-year-old male was admitted with a history of chest pain for 20 minutes; the electrocardiogram (ECG) showed 1–2 mm ST-segment depression in leads V5–6 and I, aVL. The patient was diagnosed as having a non-ST-elevation myocardial infarction (NSTEMI) and underwent coronary angiography (CAG). A CAG performed immediately for primary coronary angioplasty revealed total occlusion of the first obtuse marginal branch (OM) (Figure 1A). We planned an angioplasty for the OM branch lesion, and the left coronary artery was engaged with a 7 Fr guide catheter (JL 4.0, Cordis Corp., Miami, Florida). A guidewire was used to cross the OM branch lesion; predilatation was performed with a balloon (Maverick^® 2.5 x 20 mm, Boston Scientific Corp., Natick, Massachusetts). A SES stent (Cypher™ 3.0 x 23 mm, Cordis) was deployed at 12 atm, with a good angiographic result (Figure 1B).

After the procedure, the patient remained asymptomatic treated with aspirin and clopidogrel. Six months after the procedure, a routine follow-up angiography was performed. The OM branch was patent with only minimal in-stent stenosis. However, the fluoroscopic images showed that the SES in the OM branch had a gap in the middle of the stent indicating a stent fracture (Figure 1C). Medical follow up without further intervention was planned, as the patient was asymptomatic.

One year later, the patient was admitted to our emergency department with a one-hour history of chest pain and was diagnosed with NSTEMI. We performed coronary angiography which revealed a total occlusion of the first OM branch at the proximal segment of the stent. On fluoroscopic imaging the fractured stent segments were displaced more proximally and distally, with a wide stent-free space in the middle where the stent was expected to be (Figure 2A). Crossing with a soft guidewire (Whisper, Guidant Corp., Indianapolis, Indiana) was difficult; the stent was crossed with a stiffer guidewire (Miracle3, Asahi Intecc Co. Ltd., Seto, Japan) with some difficulty. Intravascular ultrasonography (IVUS) (Galaxy™, Boston Scientific) with an automated pullback speed of 0.5 mm/second was performed after predilatation with a balloon (Aqua^® 2.0 x 15 mm, Cordis). The IVUS study revealed diffuse neointimal hyperplasia and an absence of the metallic stent struts in the middle of the stent, corresponding to the area of stent fracture (Figure 2B). The most significant neointimal hyperplasia was observed at the strut-free segment in the middle of the separated two stent segments. Only a moderate amount of neointimal hyperplasia was observed at the proximal and distal segments of the stent. A PES (Taxus^® 2.75 x 28 mm, Boston Scientific) was implanted at 16 atm, resulting in TIMI 3 distal flow demonstrated by angiography and IVUS and full expansion of the stent without protrusion of neointima. One month after recanalization, the patient was asymptomatic on medications.

Figure 2

Coronary angiographic images at 2 years after stent implantation. The stent was totally occluded and extended to the ostium (A). On fluoroscopy, the stent was completely separated into two segments (white line in the box). IVUS after predilatation with a small balloon revealed diffuse neointimal hyperplasia with the absence of the stent strut in the middle of the stent (B).

Discussion. The introduction of DES has dramatically improved early and late outcomes, such as restenosis and target vessel revascularization, in patients who require such coronary intervention. However, angiographic restenosis remains a problem; although its frequency is less than 10% and the restenosis patterns demonstrate a more focal type.⁶ Several reports on the mechanism of in-stent restenosis (ISR) suggest that inadequate delivery of sirolimus into the vessel wall is likely a common cause of SES restenosis.⁷ This inadequate delivery may be due to factors such as overexpansion or underexpansion of the stent, as well as uneven distribution of the stent struts at the site of DES deployment.⁸ Recently, stent fracture with focal restenosis has been reported as another mechanism of ISR after implantation of SES; Georgios et al described the first two cases of stent fracture.⁵ Stent fracture is a common problem and is associated with a higher rate of ISR after femoro-popliteal stenting.⁹ All reported DES fractures have occurred in long (33 mm) and postdilatated stents under high pressure or at a bifurcation lesion with high angulation.⁴ Although all of the factors causing strut disruption remain to be identified, shearing forces by repeated cardiac contraction are likely to be major contributors to disruption or fracture of an implanted stent.⁵

Compared to previous reports, our case demonstrated stent fracture in a short stent — 23 mm in length — that was implanted under normal pressure. We suggest that chronic stress caused by the repeated twisting forces of the heart facilitated the stent fracture. This possible mechanism is supported by the finding that the two stent segments had increased separation over time and that the stent was fractured in the middle. The neointimal hyperplasia observed in the middle area may have been accelerated by the mechanical stimulation caused by the two stent segments at the drug-free area.

Therefore, based on our findings, a patent stent with strut fracture has the potential to progress to restenosis or acute coronary syndrome despite the absence of symptoms. Most of the reported cases of DES fracture were accompanied with significant stenosis and were treated with implantation of another DES.^4,5 However, the data is insufficient to elucidate the prognosis of DES fracture in patients without symptoms and angiographic restenosis. Our case suggests that DES fracture in silent should be treated with another DES with greater strut strength. Further studies need to be performed to better understand the mechanisms and treatment options of stent fracture in the DES era.