MEMOTHERM IN-STENT RESTENOSIS DUE TO INTIMAL HYPERPLASIA: AN INTRAVASCULAR ULTRASOUND STUDY

Trude C. Leertouwer¹, MD, Elma J. Gussenhoven¹, MD, PhD, Winnifred van Lankeren¹, MD, Hans van Overhagen², MD, PhD, Marc R.H.M. van Sambeek³, MD
Departments of Cardiology¹, Radiology² and Vascular Surgery³,
University Hospital Rotterdam Dijkygt, Erasmus University Rotterdam,
the Netherlands

This study was supported by grants from the Netherlands Heart Foundation (91.016), Sorbo Heart Foundation and the Interuniversity Cardiology Institute, the Netherlands. In a previous serial intravascular ultrasound study we established that lumen area reduction in Palmaz. stents placed in the superficial femoral artery was the result of both intimal hyperplasia and stent area reduction; a higher degree of restenosis was found at stent junctions. In the present study the changes seen on intravascular ultrasound immediately after placement of 2 Memotherm stents and at 11 months follow-up in a patient with a subtotal stenosis of the superficial femoral artery, were documented. Restenosis occurred at the stent junction and was the result of intimal hyperplasia. The degree of intimal hyperplasia at the stent junction (26.9 mm²) was larger than seen at the stent edges (21.2 mm²) and inside the stents (12.0 mm²), and resulted in a percentage area stenosis of 80%, 57% and 37%, respectively. Stent/vessel area enlargement was evidenced at the stent junction (9%), at the stent edges (16%), and in the adjacent reference segments proximally and distally (9%). This intravascular ultrasound study showed that restenosis in Memotherm stents occurred at the stent junction. Intimal hyperplasia was the sole factor contributing to restenosis.

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