Optical coherence tomographic analysis of in-stent neoatherosclerosis after drug-eluting stent implantation.

Background: We report findings from optical coherence tomography (OCT) of in-stent neoatherosclerosis as a cause of drug-eluting stent (DES) failure.

Methods And Results: Optical coherence tomography and grayscale and virtual histology intravascular ultrasound were performed in 50 patients (30 stable, 20 unstable angina) with 50 DES in-stent restenosis lesions and intimal hyperplasia >50% of stent area. Median follow-up time was 32.2 months. Overall, 26 lesions (52%) had at least 1 OCT-defined in-stent thin-cap fibroatheroma (TCFA)-containing neointima and 29 (58%) had at least 1 in-stent neointimal rupture. Patients presenting with unstable angina showed a thinner fibrous cap (55 μm [interquartile range 42 to 105 μm] versus 100 μm [interquartile range 60 to 205 μm], P=0.006) and higher incidence of OCT-defined TCFA-containing neointima (75% versus 37%, P=0.008), intimal rupture (75% versus 47%, P=0.044), thrombi (80% versus 43%, P=0.010), and red thrombi (30% versus 3%, P=0.012) than stable patients. Fibrous cap thickness negatively correlated with follow-up time (r=-0.318, P=0.024). Compared with DES <20 months after implantation (the best cut-off to predict TCFA-containing neointima), DES ≥20 months after implantation had a higher incidence of TCFA-containing neointima (69% versus 33%, P=0.012) and red thrombi (27% versus 0%, P=0.007). Patients with unstable (versus stable) angina had an increasing number of unstable OCT findings including TCFA-containing neointima, neointima rupture, and thrombus (P=0.027). The rate of agreement between grayscale intravascular ultrasound and OCT for detecting intimal rupture was 50% and for detecting thrombus was 44%. The agreement between virtual histology intravascular ultrasound and OCT for identifying TCFA-containing neointima was 78%.

Conclusions: In-stent neoatherosclerosis may be an important mechanism of DES failure, especially late after implantation.