Multiple and Recurrent Coronary Stent Fractures

ABSTRACT: Coronary stent fracture is an increasingly recognized complication mainly involving drug- eluting stents. Important clinical implications, including in-stent restenosis and stent thrombosis, have been associated with this phenomenon. Variable incidence rates and several predisposing factors have been reported, but no general agreement exists on the best treatment strategy. We report a case of recurrent multiple left anterior descending artery sirolimus-eluting stent fractures, with variable clinical presentations ranging from recurrent angina to acute myocardial infarction and ventricular fibrillation cardiac arrest, that were ultimately treated with coronary artery bypass surgery.

J INVASIVE CARDIOL 2014;26(1):E7-E12

Key words: drug-eluting stent, stent fractures, percutaneous transluminal coronary angioplasty, coronary artery bypass surgery

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Coronary stent fracture (SF) recently gained attention as a potential cause of in-stent restenosis (ISR) and stent thrombosis, especially after drug-eluting stent (DES) implantation. Reported SF rates after DES vary from less than 1% to 8% in clinical studies^1,2 and up to 29% in autopsy studies.³ Different predictors of SF include factors related to the vessel, stent, and technique.⁴ Few reports described multiple SF whether diagnosed simultaneously or as a recurrent complication after percutaneous coronary intervention (PCI). Moreover, the best management strategy for patients with isolated or multiple SF remains unclear.⁵ We report a case of recurrent multiple left anterior descending (LAD) artery sirolimus-eluting stent (SES) fractures with variable clinical presentations ranging from recurrent angina to acute myocardial infarction and ventricular fibrillation cardiac arrest.

Case Report. A 41-year-old female with multiple coronary artery disease risk factors, including hypertension, dyslipidemia, and cigarette smoking, was referred for elective coronary angiography after presenting with recurrent anginal chest pain. The patient had multiple previous PCIs, with a total of 5 SESs placed in her LAD artery. In September 2003, at age 31, she presented with chest pain, and electrocardiography (ECG) showed anterior ST-segment elevation in leads V2-V6. She was taken urgently to the catheterization laboratory, where coronary angiography showed 90% stenosis in the mid-LAD artery. She underwent PCI with deployment of two overlapping 2.5 x 28 mm and 2.5 x 18 mm Cypher SESs (Cordis Corporation), with good angiographic results (Figure 1). The patient was discharged on guideline-recommended medications, including dual-antiplatelet therapy. Eight months later, in May 2004, the patient presented to another hospital with chest pain; ECG again showed anterior ST-segment elevation. Given the lack of PCI facilities at the institution, she was treated with thrombolytic therapy. Two days later, she was transferred to our hospital and underwent coronary angiography, which revealed a 70% mid-LAD lesion and a complete stent fracture involving the more distal LAD stent. A third Cypher stent (2.75 x 8 mm) was deployed across the fractured stent. Unfortunately, the patient developed a proximal LAD catheter-induced dissection during the procedure, which was treated with another Cypher stent (3 x 13 mm) deployed in the proximal LAD artery, with a good angiographic result (Figure 2).

 In June 2006, the patient underwent coronary angiography after presenting with non-ST segment elevation myocardial infarction. Interestingly, she was found to have two complete SFs, resulting in focal 60% ISR at the corresponding SF site (Figure 3). Given that her symptoms improved with medical management, a decision was made not to perform PCI at that point.

Three years later, in 2009, she presented to the emergency department (ED) with an anterior ST-segment elevation myocardial infarction. In the ED, she developed ventricular fibrillation and responded quickly to resuscitation and electrical defibrillation. She underwent emergent coronary angiography, which revealed complete mid-LAD artery occlusion with evidence of stent thrombosis. The two previously known SFs were also identified with greater displacement when compared to the 2006 angiography (Figure 4). Intravascular ultrasound (IVUS) confirmed the absence of stent struts in the two SF sites corresponding to the two angiographically identified SF locations.  The more distal fracture was treated with deployment of a 2.5 x 8 mm Cypher stent, while the proximal fracture was treated by percutaneous transluminal coronary angioplasty (PTCA) with satisfactory results.

The patient remained stable from a cardiac standpoint until January 2013, when she experienced recurrent angina on exertion. Stress echocardiography showed anterior-wall ischemia suggestive of LAD artery stenosis. Coronary angiography revealed two SFs with complete separation of stent segments at the previous fracture sites (Figure 5), resulting in complete occlusion of the mid-LAD artery with right-to-left collaterals. A 50%-60% stenosis of the proximal left circumflex (LCX) artery was also noted. Given her recurrent SFs and LAD occlusion that was unlikely to resolve with additional PCI, the patient was referred for coronary artery bypass graft (CABG) surgery. A few days later, she underwent CABG surgery using the left internal mammary artery as a conduit to the LAD artery and a saphenous vein graft as a conduit to the LCX artery. Her CABG surgery was uneventful. At 3-month follow-up exam, the patient was asymptomatic from a cardiac standpoint, with good functional capacity. Of note, the patient has been on dual-antiplatelet therapy with aspirin and clopidogrel since her first PCI. 

Discussion. Stent fracture is a well-known complication following DES implantation. Although several predisposing factors for this phenomenon have been described, certain aspects, such as the true incidence, clinical impact, and treatment decisions for SF remain controversial. Recent reports suggested several risk factors for SF. Vessel-related factors include tortuosity, calcification, excessive artery movement during the cardiac cycle, and right coronary artery (RCA) or ostial location. Stent-related factors include longer stents and SES implantation (as opposed to other DES variations). Procedure-related factors include postdilatation with high-pressure balloons, overlapping stents, and longer implant duration.^1,3-7 In this patient, the implantation of long, overlapping SES could have contributed to recurrent SFs.

SF may occur less frequently with bare-metal stents because of the protective effect of neointimal hyperplasia,^8,9 or potentially because the hyperplasia may mask the SF and make it difficult to visualize.⁴ The majority of SFs were reported with SES implantations. This was thought to be secondary to the closed-cell design of the SES, which can result in less flexibility and more vessel straightening.^4,6,7 Furthermore, the SES is more radiopaque because of thicker struts, which allow easier visualization of SF compared to other DES types,⁸ although SF has been reported in other DESs.⁷

Stent fracture has been associated with ISR and stent thrombosis, which has been linked to adverse clinical outcomes, such as target vessel revascularization.^2,5-7 Conceivably, this is related to mechanical irritation by fractured struts as well as decreased drug delivery in the fractured segment.^7,10 Stent fracture with total separation of struts was associated in a post mortem study with adverse pathologic findings, including stenosis and thrombosis in almost 70% of the lesions.³

Reports of patients with multiple SFs that occurred in the same coronary artery, whether all SFs were found simultaneously or presented in a recurrent fashion (Table 1), were consistent with studies that examined isolated SF. More SFs occurred in the RCA (10 of 14 cases), the overlapping stents technique was used in the majority of cases (13 of 14 cases), and SES was the predominant stent type complicated by a fracture (12 of 14 cases). Most of these patients were treated with another PCI with similar or different DES type.

Several interesting observations can be made in this case. Recurrent multiple SFs in the LAD artery are rare. Most of the isolated or multiple SFs have occurred in the RCA, which is probably related to more vessel angulation and movement during the cardiac cycle.^8,9 Our patient had a variable clinical presentation with her SF events (recurrent angina pain, non-ST segment and ST-segment elevation myocardial infarction, as well as ventricular fibrillation cardiac arrest), which illustrates the wide clinical spectrum for presentation of SF. Moreover, this case suggests that PCI may not be the ideal treatment for all patients with SF, especially those with recurrent fracture at the same location, because adding more stents in this situation probably will not prevent further SF. Hetterich et al reported a similar case in which the patient had recurrent SF in the same segment despite multiple PCIs with SES deployment.¹¹ Little is known about managing patients with recurrent SF to make any strong recommendations. We do not advocate CABG surgery for every patient with SF. However, CABG surgery should be considered, if feasible, in those uncommon patients with recurrent SF, given the probable high chance of SF recurrence, which can occasionally present in a life-threatening manner as experienced by our patient.

Conclusion. Stent fracture is a potential complication after DES implantation, with possible significant clinical sequelae. Recurrent or multiple SFs are uncommon. However, the management of SF is challenging and often requires multiple interventions, including CABG.

References

1. Chung WS, Park CS, Seung KB, et al. The incidence and clinical impact of stent strut fractures developed after drug-eluting stent implantation. Int J Cardiol. 2008;125(3):325-331.
2. Umeda H, Kawai T, Misumida N, et al. Impact of sirolimus-eluting stent fracture on 4-year clinical outcomes. Circ Cardiovasc Interv. 2011;4(4):349-354.
3. Nakazawa G, Finn AV, Vorpahl M, et al. Incidence and predictors of drug-eluting stent fracture in human coronary artery a pathologic analysis. J Am Coll Cardiol. 2009;54(21):1924-1931.
4. Chakravarty T, White AJ, Buch M, et al. Meta-analysis of incidence, clinical characteristics and implications of stent fracture. Am J Cardiol. 2010;106(8):1075-1080.
5. Aoki J, Nakazawa G, Tanabe K, et al. Incidence and clinical impact of coronary stent fracture after sirolimus-eluting stent implantation. Catheter Cardiovasc Interv. 2007;69(3):380-386.
6. Lee MS, Jurewitz D, Aragon J, Forrester J, Makkar RR, Kar S. Stent fracture associated with drug-eluting stents: clinical characteristics and implications. Catheter Cardiovasc Interv. 2007;69(3):387-394.
7. Kuramitsu S, Iwabuchi M, Haraguchi T, et al. Incidence and clinical impact of stent fracture after everolimus-eluting stent implantation. Circ Cardiovasc Interv. 2012;5(5):663-671.
8. Amico F, Geraci S, Tamburino C. Acute coronary syndrome due to early multiple and complete fractures in sirolimus-eluting stent: a case report and brief literature review. Catheter Cardiovasc Interv. 2013;81(1):52-56.
9. Kim EJ, Rha SW, Wani SP, et al. Coronary stent fracture and restenosis in the drug-eluting stent era: do we have clues of management? Int J Cardiol. 2007;120(3):417-419.
10. Lee SE, Jeong MH, Kim IS, et al. Clinical outcomes and optimal treatment for stent fracture after drug-eluting stent implantation. J Cardiol. 2009;53(3):422-428.
11. Hetterich H, Rieber J. Multiple stent fractures at the site of coronary artery bypass insertion. Catheter Cardiovasc Interv. 2009;73(1):84-87.

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From the ¹Department of Medicine, Division of Cardiology, Heart and Vascular Institute and ²Department of Medicine, 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 June 24, 2013, provisional acceptance given July 8, 2013, final version accepted August 6, 2013.

Address for correspondence: Mayra Guerrero, MD, Department of Medicine, Division of Cardiology, Heart and Vascular Institute, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202. Email: MGUERRE1@hfhs.org