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Published on: September 14, 2009
Self-Apposing Stents in Coronary Chronic Total Occlusions: A Pilot Study
Ahmed Elborae1, Mohamed Hassan2, Mohammed Abdel Meguid2
1Department of Cardiovascular Medicine, Faculty of Medicine, Cairo University, Giza, Egypt; Department of Cardiology, Aswan Heart Centre, Magdi Yacoub Global Heart Foundation, Aswan, Egypt.
Objectives:
This pilot study assessed the 12-month angiographic and clinical outcomes of self-apposing (SA) stents in patients undergoing chronic total occlusion (CTO) percutaneous coronary intervention (PCI).
Background:
Self-apposing (SA) stents may decrease incomplete strut apposition and stent strut coverage that are common after CTO PCI.
Methods:
We compared 20 patients who underwent CTO PCI using SA drug-eluting stents (DESs) with 20 matched control patients who underwent CTO PCI using balloon-expandable (BE)-DESs. All patients were followed up clinically for 12 months and had coronary angiography with optical coherence tomography at the end of the follow-up period. The primary end points were stent strut malapposition and strut coverage. The secondary end point was composite major adverse cardiovascular events (MACEs) at 12 months.
Results:
Both groups had high prevalence of diabetes mellitus, and most of the treated lesions were complex, with 62% having a J-CTO score of ≥3. All CTO PCI techniques were allowed for recanalisation, and 75% of the procedures were guided by intravascular ultrasound. At 12 months, the SA-DES group had fewer malapposed struts (0% [interquartile range (IQR) 0%-0%] vs 4.5% [IQR 0%-20%]; p<0.001) and uncovered struts (0.08% [IQR 0%-1.6%] vs 8.2% [IQR 0%-16%]; p<0.001). However, they showed significantly higher rates of MACEs due to clinically-driven target lesion revascularisation (45% vs 15%; p=0.038).
Conclusions:
In this pilot study, compared with conventional BE-DESs, SA-DESs used in CTO PCI were associated with fewer malapposed and uncovered stent struts but also with significantly higher rates of in-stent restenosis and MACEs, mainly caused by clinically driven target lesion revascularisation.
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