A Case of Early Drug-Eluting Stent Fracture

ABSTRACT: Although stent fracture following femoro-popliteal intervention is well recognized, coronary stent fracture represents an underrecognized entity. Its incidence is low but it represents an important clinical entity as it may complicate with stent thrombosis causing acute coronary syndromes, or may predispose to instent restenosis. Although coronary stent fracture may involve both bare metal stents (BMS) and drug-eluting stents (DES), a recent analysis of the literature indicates that reports of stent fracture have increased since DES was introduced. Furthermore, chronic stretch at specific vessel sites as bends may lead to late occurrence of fracture. We present the case of a patient with a non-ST-segment elevation acute coronary syndrome caused by the early fracture of an everolimus-eluting stent (Xience^®) implanted only three days before. J INVASIVE CARDIOL 2010;22:E186–E188 ——————————————————————————— Stent fractures have been commonly detected after periferic interventions, especially in cases of long reconstructions of superficial femoral artery. However, in the last few years, the attention has been paid to coronary stent fractures, especially after long reconstructions of chronic total occlusion (CTO) vessels. Interestingly, a recent pathological study showed that stent fractures are more common than clinically reported, and often associated with restenosis and thrombosis. The occurrence of stent fracture is usually detected in the late follow-up of stenting, especially at sites of chronic stretch as bends, and is increasingly reported with DES. However cases of very early stent fracture are lacking. We describe a case of stent fracture after 3 days of coronary stenting of a diffusely diseased first diagonal (D1). Case report. A 59-year old male was admitted to our emergency room for chest pain at rest three days after coronary stenting. He was hypertensive, hypercholesterolemic, Type-2 diabetic and past smoker. In 1997 he had undergone coronary artery bypass graft surgery with left internal mammary artery (LIMA) to the proximal segment of the left anterior descending artery (LAD) of the left coronary artery and two saphenous vein grafts to the first diagonal branch of the LAD (D1) and to the right coronary artery (RCA), respectively. In June 2009, he received coronary angiography because of recurrence of severe effort angina with non-invasive (at exercise ECG) demonstration of inducible ischemia. The angiogram demonstrated patency of LIMA, non-obstructive degeneration of the venous graft to RCA, proximal occlusion of the venous graft to D1 with a long critical stenosis of the native vessel involving the left main coronary artery (LMCA) and D1 (Figure 1A) which was treated with angioplasty. After cannulation of the LMCA with an extra backup catheter 3.5 GF by radial approach, two BMW wires were inserted in D1. Predilatation with a Falcon Bravo^® (Invatec, Italy) (2 x 20 mm at 10 atm) and Sprinter NC^® (Medtronic, USA) (2.5 x 12 mm at 12 atm) was performed. Two overlapping Xience^® (Abbott, Abbott Park, Illinois) stents (2.25 x 28 mm and 2.25 x 28 at 14 atm) were deployed in the proximal part of D1. Post dilatation was performed with a Sprinter NC^® (2.75 x 12 mm at 18 atm) at the level of overlap (Figure 1B). The troponin T peak level after PCI was 0.18 ng /ml. The patient was discharged on aspirin, clopidogrel, beta-blocker, ACE-inhibitor, diuretic and statin therapy. After three days, the patient developed chest pain at rest and ST segment downsloping in lateral precordial leads with abnormal cardiac troponins. Because of the persistence of chest pain and electrocardiographic abnormalities despite maximal medical therapy (aspirin, clopidogrel, ACE-inhibitors, beta-blockers, iv. nitrates) he underwent coronary angiography. The selective left coronary angiography showed the presence of a fracture localized at the body of the distal one of the two previously implanted stents on D1 associated with intermittent kinking of the vessel, causing a transient sub-occlusion of the vessel (Figure 2). IVUS was not performed due to the angiographic evidence of stent fracture. We decided to implant another drug-eluting stent with different features from that previously implanted. Due to the low thrombogenicity and the flexibility with good radial strength, we chose an Endeavor^® (Medtronic, Santa Rosa, California) 2.75 x 18 mm. Briefly, after left main cannulation with a guiding catheter XB^® 3.5, two wires were positioned aiming at a “buddy wire” technique (BMW + BHW). The Endeavour^® stent was deployed at 16 atm and subsequent postdilation with a Sprinter NC^® balloon (2.75 x 15 mm at 18 atm) was performed. The final angiographic result was good (Figure 3). The troponin T peak level after PCI was 2.73 ng/ml. The post-procedural course was uneventful and he was discharged after six days. At 3-month follow-up, the patient was asymptomatic and the treadmill exercise ECG revealed no signs of ischemia. Discussion. Although stent fracture following femoro-popliteal intervention is well recognized, coronary stent fracture represents an underrecognized entity. Its incidence is low but it represents an important clinical entity as it may combine with stent thrombosis causing acute coronary syndromes, or may predispose to instent restenosis.¹ Of note, a recent pathological study showed that the incidence of stent fracture is much higher than clinically reported and that grade V stent fractures (transection causing gap in the stent segment) are associated with restenosis and thrombosis.² Although coronary stent fracture may involve both bare metal stents (BMS) and drug-eluting stents (DES), a recent analysis of the literature indicates that reports of stent fracture have increased since DES was introduced.³ Multiple risk factors that predispose to this complication have been identified. The site of implantation plays an important role in determining the risk of fracture; indeed, the majority of cases occur in the RCA and in the vein graft to this artery since they are subject to the forceful and exaggerated motion in the atrioventricular groove and at the acute margin. Fractures have also been reported in ostial lesions and at the point of maximal curvature in tortuous vessels.⁴ Other important risk factors are the stent length, likely because longer stents are subject to higher radial forces and stent overexpansion as it may weaken stent struts. Stent overlapping represents another risk factor, whereas stent diameter seems to be protective.⁵ Interestingly, in a recent study, the ACROSS/TOSCA 4 Study, stent fracture was particularly frequent in the complex lesion subset of chronic total occlusion.⁶ Most reported cases of stent fracture have involved Cypher^® stents. The apparently higher rate of fracture with this type of stent has been attributed to the closed-cell design of Cypher that may decrease its flexibility and contribute to fracture.⁷ Moreover, it is typically considered a delayed complication of coronary angioplasty and it has been generally reported within months to years after stent implantation.⁴ In the present case, our patient suffered from an acute coronary syndrome caused by transient mechanical occlusion of the vessel during systole caused by a fractured stent with no angiographic evidence of thrombus apposition. Interestingly, the stent fracture occurred within a few days after stent implantation probably since a long stent was implanted on a high mobile segment of the vessel which determined a high mechanical stress. This case highlights the possibility that stent fracture may occur also early after stenting when mechanical factors forcefully stretch the stent, and may be complicated by acute coronary syndromes.

References

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————————————————————————— From the Institute of Cardiology, Catholic University of the Sacred Heart – Rome, Italy. The authors report no conflicts of interest regarding the content herein. Manuscript submitted January 25, 2010, provisional acceptance given February 8, 2010, 2009, final version accepted February 19, 2010. Address for correspondence: Giampaolo Niccoli, MD, PhD, Institute of Cardiology, Catholic University, Rome, Italy. E-mail: gniccoli73@hotmail.it