Stent thrombosis (ST) is classified by Academic Research Consortium into four types based on the time of event as; Acute: within 24 hours, Subacute: 24 hours to 30 days, Late: after 30 days, and very late: after 12 months. The consequences of ST could be catastrophic with a mortality rate of 45%, with the majority of others suffering nonfatal myocardial infarction [6
]. Angioscopic and optical coherence tomography studies have shown that lack of complete endothelialization of DES to be the most important predictor of LST [8
]. Virmani et al have confirmed the same mechanism using human pathological data [10
]. Risk factors for LST include patient and lesion characteristics, non-compliance of anti-platelet drugs and procedural factors like incomplete stent apposition, number and the length of stents, coronary dissection, etc. [11
]. It has been reported that the risk of stent thrombosis up to 4 years is significantly higher if the DES was placed during ACS [12
]. In the setting of myocardial infarction, underlying plaque morphology may affect the rate of healing, when stent struts penetrate deeply into a necrotic core and are not in contact with cellular areas, which impairs stent endothelialization [13
]. A large thrombus burden in the setting of ST-segment elevation myocardial infarction is a risk factor for future stent thrombosis [14
]. Hypercholesterolemia has recently been shown to cause endothelial progenitor cell dysfunction, thus contributing to the delay in endothelial healing, adding to the significance of statin therapy after PCI [15
]. There is consensus among cardiologists that stent endothelialization starts from the edges towards the center of the stent, leaving the middle portion of the stent to be the last to be covered by endothelium and usually the most likely site for LST [10
]. The same authors reported LST to be associated with diffuse in stent re-stenosis. The following factors could have contributed to the development of in-stent thrombosis in our patient: long stent [33 mm in length], history of hypercholesterolemia, implantation of DES emergently during ST-segment myocardial infarction with high thrombus burden necessitating rheolytic thrombectomy and the presence of in-stent re-stenosis.
The 2007 ACC/AHA/SCAI focused update of the 2005 guidelines on PCI recommended dual antiplatelet therapy with aspirin and a theinopyridine for at least 12 months after DES implantation. Recent reports of very late in-stent thrombosis of DES long years after implantation represent a growing evidence to continue dual antiplatelet therapy for a longer period of time, perhaps indefinitely given the devastating consequences of in-stent thrombosis. A retrospective observational trial has suggested that triple antiplatelet therapy using aspirin, clopidogrel and cilostazol may further reduce the risk of stent thrombosis especially in patients or lesions at increased risk with no difference in the rate of major bleeding [16
]. The advent of prasugrel as a more potent platelet inhibitor compared to clopidrogrel may decrease the long term adverse cardiovascular events [17
]. Finally, this case highlights the need of further long-term studies on the occurrence of very late in-stent restenosis in patients treated with DES, both as an independent factor, and as predisposing to very late stent thrombosis.