Abstract 4611: Circulating Endothelial Progenitor Cells in Patients Who Have Undergone Late Coronary Stent Thrombosis
Background: An important factor that may contribute to the development of late stent thrombosis (ST) after drug eluting stent (DES) implantation is delayed arterial healing and poor endothelialization. Endothelial progenitor cells (EPCs) have been shown to play an important role in repair and re-endothelialization following vascular injury, such as balloon angioplasty. We, therefore, hypothesized that patients who develop late ST may have reduced levels or function of EPCs as a factor contributing to their risk of ST. Accordingly, we aimed to compare EPC level and function in patients who underwent late ST versus matched controls.
Methods: Patients who developed late (>4 weeks following stenting) ST, within the past 3 years, were compared to a matched group of patients who underwent stenting and did not develop complications [matching according to gender, age, diabetes status, type of stent (DES vs. BMS), and current treatment with aspirin, clopidogrel and statins]. All patients had blood samples taken at least 3 months after the ST or index procedure. The percentage of peripheral mononuclear cells expressing VEGFR-2, CD133 and CD34 was evaluated by flow cytometry. EPC colony forming units (CFUs) were grown from peripheral blood mononuclear cells, characterized and counted following 7 days of culture (of non-adherent cells) on fibronectin-coated wells.
Results: The two groups (n=25 each) were well matched (92% men, mean age 60–63 years, 32% diabetes, 80% DES). The proportion of cells co-expressing VEGFR-2 and CD133 or VEGFR-2 and CD34 tended to be lower in the ST group. Furthermore, the mean number of CFUs was lower among the patients who underwent late ST (Table⇓).
Conclusions: Our study suggests that patients who have undergone late coronary ST have reduced levels of circulating EPC and reduced EPC CFUs, which reflect impaired functional properties. These findings require validation by larger studies, but may contribute to understanding the pathogenesis of late ST.