Incomplete stent apposition may cause late stent thrombosis
MedWire News: Incomplete stent apposition (ISA) without neointimal hyperplasia is associated with thrombus development and may be a substrate for late stent thrombosis, indicate optical coherence tomography (OCT) findings.
“Our findings suggest that the primary mechanism responsible for persistent acute ISA, identified at follow-up in previous studies as late ISA, is likely to be inhibition of neointimal hyperplasia,” say the authors.
Yukio Ozaki (Fujita Health University Hospital, Toyoake, Japan) and colleagues assessed stent deployment using quantitative coronary angiography, intravascular ultrasound (IVUS), and OCT analyses pre- and post-procedure and at a 10-month follow-up in 32 patients undergoing IVUS-guided percutaneous coronary intervention (PCI) and coronary stenting with sirolimus-eluting stents (SES).
They report in the European Heart Journal that 309 (7.15%) stent struts analyzed were malapposed immediately after intervention. Only a small proportion of initially well apposed struts were malapposed at 10-month follow-up owing to vascular remodeling and/or dissolution of jailed thrombus, “suggesting this is a quantitatively less important mechanism of late ISA than preservation of acute ISA,” Ozaki and team note.
The researchers found that 4.67% of struts with ISA failed to heal and 7.59% that were well apposed did not develop neointimal hyperplasia at 10 months.
Late ISA due to lesion remodeling occurred in only 0.37% of struts, while failure of adequate neointimal hyperplasia was the most important mechanism responsible for persistent acute ISA.
Thrombus was visualized in 20.6% of struts with ISA at follow-up compared with just 2.0% of struts with good apposition (p<0.001). Of the small number of well-apposed struts that developed thrombosis, only two had no neointimal coverage.
The researchers conclude: “Failure of struts to heal with time occurs in a substantial number of stent struts in patients with SES. The presence of late ISA was significantly associated with the development of OCT-detected thrombus at follow-up, which was also seen to a lesser extent with complete stent apposition.
“The presence of late ISA and the absence of neointimal hyperplasia could constitute a potent thrombogenic substrate for late-stent thrombosis and warrants further study.”
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By Caroline Price