RESUMEN
Percutaneous coronary intervention (PCI) is a frequently performed treatment option for recanalization in patients with chronic total occlusion (CTO). As CTO-PCIs are often complicated and challenging for interventionalists, the stressful and damaging nature of the procedure can be remarkable, thus platelets can be easily activated. Our aim was to investigate the effect of CTO-PCI on platelet activation and the expression of selected circulating microRNAs (miR) of platelet and endothelium origin after CTO-PCI. In this study, 50 subjects after CTO-PCI were enrolled. Blood samples were obtained before PCI, at 2 days and 3-6 months after the procedure to measure the degree of platelet activation and the level of plasma miR-223, miR-181b, and miR-126. Patients were divided based on the characteristics of the intervention. Patients with higher Japanese CTO scores and longer duration of PCI showed significantly elevated platelet P-selectin positivity (p = 0.004 and p = 0.013, respectively) 2 days after the procedure compared to pre-PCI and increased concentration of soluble P-selectin 3-6 months after the intervention (higher Japanese CTO score: p = 0.028 and longer duration of PCI: p = 0.023) compared to baseline values. Shorter total stent length caused a significantly lower miR-181b expression at 3-6 months after the intervention (p = 0.031), while no difference was observed in miR-223 and miR-126. One stent thrombosis occurred during the follow-up period. Although these technically challenging CTO-PCIs may cause enhanced platelet activation right after the intervention and long-term endothelial cell dysfunction, these interventions are not associated with more adverse clinical events.
RESUMEN
BACKGROUND: Percutaneous coronary intervention (PCI) is commonly used treatment for chronic total occlusion (CTO). PCI can be performed in two different ways using wire escalation (WE) or subintimal dissection and reentry (DR) technique. During both procedures patients are treated with anticoagulants, however a substantial activation of coagulation cascade is expected, which may affect clinical outcome. OBJECTIVES: Our aim was to compare the impact of WE and DR techniques regarding endothelial cell activation and thrombin formation. METHODS: Fifty patients after CTO-PCI were enrolled into this study. Blood samples were obtained before PCI, at 48 h and 3-6 months after the intervention to measure soluble endothelium-specific markers and to investigate thrombin generation. RESULTS: Twenty-nine patients were treated with WE, 21 received DR. In the DR group, soluble VCAM-1 (vascular cell adhesion molecule-1) and ICAM-1 (intercellular cell adhesion molecule-1) concentrations were gradually elevated and remained significantly increased at 3-6 months (p = 0.006 and p = 0.037, respectively) compared to pre-PCI. Furthermore, significant decrease in lagtime (p = 0.004) and time to peak (p = 0.002) with a substantial increment in peak thrombin (p = 0.001) were observed in these patients. In contrast, no significant alteration was found in the WE cohort. Clinical complications (myocardial infarction, stroke, thrombosis, revascularization) did not occur in the first 9 months of follow-up period in either group. CONCLUSION: Although DR intervention induces more thrombin generation with a larger degree of endothelium activation compared to WE, this technique does not cause more clinical complications.
