Sirs: Stent fracture (SF) is no longer a ‘‘zebra’’ in interventional cardiology. Although, initially unrecognized even in large randomized trials involving drug-eluting stents (DES), the clinical occurrence of SF has been noted to be up to 7.7% [1]. Furthermore, a recent pathologic analysis revealed a higher incidence of 29% [2]. Sirolimus-eluting stents (SES) were the main culprit with 63–100% of SF occurring in these stents [2, 3]. The timing of clinically detected SF has ranged from acute fractures to events up to 3 years [3, 4]. However, no report so far has been able to determine the interval between fracture and clinical event. Accordingly, we report a case of stent thrombosis due to SF of a Cypher SES implanted 3 years earlier. Incidentally, there was a documented although not recognized fracture 2 and a half years before on a study protocol follow-up angiogram. A 53-year-old man presented with acute anterior STsegment myocardial infarction (STEMI). Coronary risk factors included hyperlipidemia, previous smoker and significant family history. Regular medications were acetylsalicylic acid (ASA) 100 mg and simvastatin 40 mg daily. He had temporarily discontinued ASA a week before due to a dental extraction. Three years prior, he underwent elective percutaneous coronary intervention (PCI) of a symptomatic subtotal stenosis of the left anterior descending artery (LAD) and first diagonal (D1) bifurcation (Fig. 1). He received a Sideguard self-expanding nitinol sidebranch bare metal stent in the D1 and a 3.5 mm by 33 mm Cypher in the LAD. The Cypher was longer than initially planned because of inadvertent dissection after pre-dilatation. Moreover, a segment of myocardial bridging in the mid LAD was noted and the distal Cypher stent edge was within this bridge. There was also a moderate degree of angulation in the mid LAD that was partially straightened after stenting. He subsequently received 1 year of dual antiplatelet therapy with ASA and clopidogrel followed by lifelong ASA. A routine angiogram was performed 6 months after the index procedure according to the Sideguard II trial protocol. At this point, there was no evidence of significant instent restenosis but a small aneurysm was noted in the mid segment of the Cypher (Fig. 2). Retrospectively, the stent had evidence of a fracture but this was not recognized initially. In the current presentation, primary PCI was performed. The LAD stent was totally occluded by thrombus at the level of D1 and complete SF was now recognized (Fig. 2). The occlusion and SF were successfully crossed with a hydrophilic wire supported by a micro-catheter and a bare metal stent was implanted within the previous Cypher with the aim of restoring flow followed by eventual coronary bypass surgery which he subsequently underwent uneventfully. To the best of our knowledge, we report the first case of a delayed very late stent thrombosis due to a definite SF already present more than 2 years before the event. The importance of this is twofold. First, it raises the possibility of an unrecognized cohort of asymptomatic patients with undiagnosed complete SF but carrying the risk of lifethreatening cardiac events. In the pathologic study above, up to 5.1% of patients have complete SF and these were the only ones who developed clinical events [2]. Although, the clinical significance of SF has been an area of discussion previously, the evidence shows that it is unlikely benign. Reported rates of in-stent restenosis in SF ranged from 37.5 S. H. Ong (&) R. Mueller P. Boekstegers Department of Cardiology/Angiology, HELIOS Klinikum Siegburg, Medizinische Klinik-Kardiologie, Ringstrasse 49, 53721 Siegburg, Germany e-mail: seahing@gmail.com