Journal of Invasive Cardiology

In a meta-analysis involving 10 DES trials, Moreno et al found that longer stent lengths completely accounted for the increased risk of LAST in the DES-treated patients.²⁷ In their 3-year follow-up analysis of RAVEL, Fajadet and others reported only 1 possible SAT in 120 patients. Freedom from target lesion revascularization (TLR) and overall MACE rates was significantly improved at 93.7% versus 87.9% and 16.7% versus 34.5%, for SES versus BMS, respectively. Additionally, no differences were seen for rates of death or MI.²⁸

A meta-analysis of all 4 randomized SES trials (RAVEL, SIRIUS, C-SIRIUS and E-SIRIUS) revealed no significant differences in thrombosis for any time interval or cumulatively. Similarly, no increased thrombosis was seen for the premarket zotarolimus-eluting stents (ZES, Endeavor, Medtronic, Inc.).²⁵ In a 2-year follow up of the RESEARCH study, overall MACE was 15.4% versus 22.0% (p = 0.01) for SES versus BMS, respectively. No cases of LAST and no differences in mortality or cumulative death and MI rates were observed.²⁹ Weisz and co-authors likewise reported no increased ET, SAT or LAST associated with SES over control BMS at 2- year follow up of the SIRIUS trial patients.³⁰

Pathophysiology of LAST. The 3 major determinants of thrombosis are endothelial injury, alterations in blood flow and hypercoagulability, collectively known as Virchow’s triad. Endothelial damage can occur from trauma, inflammation, infection or hypertension-induced sheer stress. Furthermore, static or turbulent flow can promote platelet-endothelial contact and aggregation, as occurs in areas of atherosclerotic plaques or aneurysmal dilatation. Disturbances in the coagulation cascade such as antithrombin III or protein C/S deficiency, as well as decreased activity of the endogeous fibrinolytic system, are yet another less common cause of pathologic thrombosis.³¹

Intracoronary stent implantation satisfies two, and potentially all three, of the above criteria. By definition, stent deployment is direct mechanical intimal trauma. Plaque disruption thus created, subsequently releases prothrombotic cytokines and promotes platelet adhesion and aggregation. Lastly, while successful stent deployment certainly increases overall coronary flow, it is possible that small, local pockets of turbulence or even stasis can form around the struts.