ABSTRACT
Serial IVUS studies were fundamental to understanding the restenosis process. Previously, histologic studies or analysis of retrieved atherectomy specimens focused on plaque elements and postulated that restenosis in non-stented lesions was the result of intimal hyperplasia.1,2 (Of note, subsequent histologic studies confirmed that a late decrease in arterial dimensions was an important component of the restenosis process in non-stented lesions and that this process also impacted adjacent reference segments.3-14)
Angiographic studies are only able to analyze changes in lumen dimensions. For example, early studies comparing angiograms at stent implantation (in which full balloon inflation was erroneously equated with complete stent expansion) with follow-up IVUS studies (which showed stent underexpansion) suggested that chronic stent recoil was an important component of restenosis in stented lesions. Serial IVUS studies showed that instent restenosis was almost exclusively from intimal hyperplasia and only rarely from stent recoil.
