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.