Case Report

Two Patients with Extremely Late (8 and 12 Years) Bare-Metal Stent Thrombosis: The Risk Never Completely Disappears!

Roberto Martin-Reyes, MD, David Dobarro, MD, Raul Moreno, MD
Roberto Martin-Reyes, MD, David Dobarro, MD, Raul Moreno, MD
Author Affiliations: From the Division of Interventional Cardiology. University Hospital La Paz, Madrid, Spain. The authors report no conflicts of interest regarding the content herein. Manuscript submitted April 30, 2008, provisional acceptance given May 28, 2008 and final version accepted June 3, 2008. Address for correspondence: Raul Moreno, MD, FESC, Director of Interventional Cardiology. University Hospital La Paz, Paseo de la Castellana 261. 28046. Madrid. Spain. E-mail: raulmorenog@terra.es

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J INVASIVE CARDIOL 2008;20:E324-E326 Currently, stent thrombosis (ST) is one of the main limitations of percutaneous coronary interventions and occurs in 1–2% of cases. In the era of bare-metal stents (BMS), most episodes of ST occurred within 1 month after stent implantation, although some cases might also occur > 1 month after stenting (late ST).1 Very late ST (ST that occurs > 1 year after stent implantation) has only received more attention in the era of drug-eluting stents (DES),2 but some cases of very late ST were also described after BMS implantation.3 Two patients with ST-segment elevation acute myocardial infarction (MI) secondary to definitive ST 8 and 12 years after BMS implantation were recently admitted to our institution. To the best of our knowledge, no epidodes of ST > 10 years after stent implantation have been previously published. Case 1: A 50 year-old male ex-smoker was admitted for an acute anterior MI in November 2007. Clinical history highlighted stable angina pectoris in 1995 treated with a 3.0 x 15 mm Palmaz-Schatz coronary BMS (Cordis Corp., Miami Lakes, Florida) in the proximal left anterior descending artery (LAD). The patient was currently on aspirin 100 mg/day and beta-blockers. Emergency coronary angiography showed a complete occlusion of the proximal LAD due to BMS thrombosis (Figure 1A). Aspirin 500 mg, clopidogrel 600 mg, heparin 6000 IU and abciximab were administered. Manual thrombus aspiration was performed using an Export aspiration catheter (Medtronic Inc., Minneapolis, Minnesota) and, after adjunctive balloon dilatation using a 3.0 x 20 mm Maverick balloon (Boston Scientific Corp., Natick, Massachusetts), successful reperfusion of the LAD was achieved (Figures 1B and C). Finally, a 23 x 3.5 mm Chrono BMS was deployed intrastent (Sorin Group, Milan, Italy) with good angiographic results (thrombolysis in myocardial infarction [TIMI] 3 flow) (Figure 1D). The patient’s in-hospital clinical course was uneventful. Case 2: A 54-year-old male came to the emergency room because acute onset of chest pain. He had a history of dyslipidemia, hypertension and smoking. Eight years previously, a 28 x 3.0 mm Multi-Link BMS (Guidant Corp., Indianapolis, Indiana) was implanted in the proximal LAD to treat an anterior MI. The patient was currently on aspirin. Electrocardiography showed ST-segment elevation in the precordial leads. Emergent coronary angiography showed a complete thrombotic occlusion of the proximal LAD at the level of the stent (Figure 2A). Treatment with aspirin 500 mg, clopidogrel 600 mg, abciximab and 5000 UI of heparin was initiated. After crossing the coronary occlusion with a PT2 guidewire (Boston Scientific), manual thrombus aspiration with an Export aspiration catheter was perfomed, obtaining macroscopic thrombotic material and vessel recanalization (Figure 2B). Adjunctive balloon dilatation was performed using 3.0 x 20 mm and 3.5 x 20 mm Maverick balloons, yielding a good angiographic result (TIMI 3 flow), and a new stent implantation was not considered necessary (Figures 2C and D). One week later, the patient was discharged without clinical events. Discussion. Restenosis has been classically the most important limitation of percutaneous coronary intervention procedures. DES have revolutionized interventional cardiology, because they dramatically decrease the risk of angiographic restenosis and the need for subsequent revascularization procedures in comparison with BMS.4 A slight increase in the incidence of ST > 1 year after stenting has been identified as a limitation of DES compared to BMS,2 probably — at least in part — due to delayed stent endothelialization with DES. This is important, because ST is often clinically presented as acute MI and/or death, and because of that the clinical benefit of DES needs to be confirmed with long-term follow-up studies. However, cardiologists must keep in mind that very late (> 1 month) and even very late (> 1 year) ST can also occur after BMS implantation, and the risk of ST never completely dissappears, even after BMS implantation.3 This has been clearly illustrated by the 2 patients described here. Both suffered a ST-segment elevation MI secondary to very late (8 and 12 years after stent implantation) BMS thrombosis. To the best of our knowledge, we have described the most delayed (12 years) incidence of ST in the literature. Figure 1. A. Coronary angiography showing complete occlusion of the proximal left anterior descending artery due to stent thrombosis. (B and D) Normal coronary flow that showed succesful reperfusion after manual thrombus aspiration and stent implantation. (C) Macroscopical thrombotic material obtained after thrombus aspiration. Figure 2. (A) Complete occlusion of the proximal left anterior descending artery due to stent thrombosis. (B) Image showing TIMI flow 2 after manual thrombus aspiration. (C) Balloon dilatation. (D) Normal coronary flow after stent implantation.

References

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