Abstract
We report a case of very late stent thrombosis of a bare metal stent with a concurrent drug eluting stent’s patency in the same coronary vessel, in a patient undergoing primary angioplasty who discontinued his clopidogrel regimen a few weeks after successful deployment of the stents.
BACKGROUND
Coronary stent thrombosis remains a dramatic event responsible for high mortality and morbidity rates.1 The risk of very late stent thrombosis (VLST) has been reported with both drug eluting stents (DES) and bare metal stents (BMS).2 Discontinuation of dual antiplatelet regimen has been identified as a strong predictor of VLST, notably in DES patients.3 We report a particular case of VLST advancing the possible causes involved in this type of stent thrombosis.
CASE PRESENTATION
A 79-year-old man with clinical evidence of acute myocardial infarction (AMI) was referred for emergency coronary angiography. He had suffered an ST elevation myocardial infarction (STEMI) 1 year before. At that time coronary angiography demonstrated significant stenosis in the proximal tract of the right coronary artery (RCA), with total thrombotic occlusion in the distal segment of the same vessel. He underwent percutaneous coronary intervention (PCI) with implantation of a 3.5×23 mm DES (Cypher, Cordis, Johnson & Johnson, Warren, USA) and a 3.0×20 mm BMS (Leader, Dynamic Medical BV, Netherlands) respectively in the proximal and distal segment of the vessel. He self-discontinued his daily clopidogrel regimen 3 months after the procedure, continuing only with aspirin. At admission a 12 lead electrocardiogram showed ST segment elevation in the inferior leads. The patient was transferred to our catheterisation laboratory and the angiogram documented distal RCA BMS thrombotic occlusion and concomitant proximal RCA DES patency (fig 1). PCI was performed using a 3.0×20 mm Voyager Rx balloon (Abbott Vascular California, USA) with a good angiographic result (fig 2). An intracoronary bolus of abciximab, followed by a 12 h infusion, was administered. Heparin was administered at the start of the intervention at a dose of 70 IU/kg. A postprocedural clopidogrel loading dose of 300 mg was given. The patient remained stable, and he was discharged with a daily antiplatelet regimen of clopidogrel 75 mg for at least 1 year and aspirin 100 mg life long.
Figure 1.
Coronary angiogram showing distal right coronary artery (RCA) bare metal stent thrombotic occlusion and concomitant proximal RCA drug eluting stent patency.
Figure 2.
Final angiographic result: complete opacification of the right coronary artery.
DISCUSSION
Recent evidence has proven that: (1) the incidence of VLST is comparable in BMS and DES patients2–4; (2) premature clopidogrel withdrawal in the acute coronary syndrome setting is significantly associated with higher mortality risk among patients receiving BMS or DES1,2; (3) the risk of late thrombosis persists long after cessation of dual antiplatelet therapy.2,3
Nevertheless, a stent specific aetiology in stent thrombosis cannot be denied considering that in patients with multistent placement and concomitant DES and BMS in different arteries, stent thromboses occurs at DES sites while BMS are patent.4 Our patient contradicts this current opinion and raises some hypotheses and answers about VLST.
The first hypothesis is that de novo atherosclerotic plaque occurred within the boundaries of the BMS and then underwent rupture, leading to a sudden thrombotic vessel occlusion. This suggests that these plaques can have a natural history comparable with the history of plaques occurring in native untreated coronary arteries.5
Apart from the well recognised risk factors for VLST, we suggest, as a second hypothesis, that DES per se could have fostered a milieu prone to thrombosis in the distal segment of the RCA. Previous experimental studies reported that vessel segments distal to sirolimus eluting stents (SES) are subject to a significant reduction of diameter compared with proximal and near proximal segments.6 In addition, clinical studies have shown an endothelium vasomotor dysfunction of the distal portion of the treated vessel which persists months after SES implantation but not after BMS apposition.7 These results suggest that coronary vessels in the area proximal and far from SES are subjected to the late activity of sirolimus. If so, in our case the antiproliferative activity of sirolimus may have caused a delayed healing with incomplete endothelium coverage of the BMS’s struts. Moreover, the BMS was placed in a thrombotic lesion (the one causing the first “spontaneous” STEMI), while the DES was placed in a probably “stable” pre-existing lesion; so, stenting of a highly necrotic plaque for acute myocardial infarction and early discontinuation of clopidogrel therapy could have been the co-factors affecting the occurrence of acute BMS thrombosis in our patient.
Thrombus aspiration was not performed in our case because the operators (GT, AA) judged the anatomy of the target artery to be of concern in regard to permitting the passage of the aspiration device through it. Certainly, mechanical removal of the thrombus would have provided valuable insights into the composition and the age of the aspirated material. Probably intravascular ultrasound (IVUS) would have been detrimental in this case; however, at angiography the stent appeared correctly expanded without fracture of struts nor balloon notch during dilation, thus suggesting a causative role of stent thrombosis in this patient.
LEARNING POINTS
Our case is “hypothesis generating” on the coronary pathobiology in the late phase after SES implantation. Stent releasing sirolimus may have caused the delayed healing of the BMS in the distal coronary vessel.
Our recommendation is to prolong dual antiplatelet therapy for more than 1 year in patients undergoing PCI in a prothrombotic milieu.
Physicians should be aware of this condition, when examining patients, especially when both SES and BMS are implanted in the same vessel.
Footnotes
Competing interests: none.
Patient consent: Patient/guardian consent was obtained for publication
REFERENCES
- 1.Wernick MH, Jeremias A, Carrozza JP. Drug-eluting stents and stent thrombosis: a cause for concern? Coron Artery Dis 2006; 17: 661–5 [DOI] [PubMed] [Google Scholar]
- 2.Garg P, Mauri L. The conundrum of late and very late stent thrombosis following drug eluting stent implantation. Curr Opin Cardiol 2007; 22: 565–71 [DOI] [PubMed] [Google Scholar]
- 3.Karvouni E, Korovesis S, Katritsis DG. Vary late thrombosis after implantation of Sirolimus eluting stent. Heart 2005; 91: e45. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Rodriguez AE, Mieres J, Fernandez-Pereira C, et al. Coronary stent thrombosis in the current drug-eluting stent era: insights from the ERACI III trial. J Am Coll Cardiol 2006; 47: 205–7 [DOI] [PubMed] [Google Scholar]
- 5.Agostoni P, Vermeersch P, Knaapen M, et al. Stent thrombosis is not always stent thrombosis: De novo atherosclerosis in a stented coronary segment. Int J Cardiol 2009; doi:10.1016/j.ijcard.2008.12.078 [DOI] [PubMed] [Google Scholar]
- 6.Shin DI, Kim PJ, Seung KB, et al. Drug–eluting stent implantation could be associated with long–term coronary endothelial dysfunction. Int Heart J 2007; 48: 553–67 [DOI] [PubMed] [Google Scholar]
- 7.Hofma SH, van der Giessen WJ, van Dalen BM, et al. Indication of long-term endothelial dysfunction after sirolimus-eluting stent implantation. Eur Heart J 2006; 27: 166–70 [DOI] [PubMed] [Google Scholar]
