Atherosclerotic plaque behind the stent changes after bare-metal and drug-eluting stent implantation in humans: Implications for late stent failure?

- Atherosclerotic plaque behind the stent (PBS) changes after stent implantation.
- PBS decreases after bare-metal (BMS) implantation, whereas it increases after first-generation drug-eluting stent (DES).
- PBS area decrease is associated with an increase in neointimal area.
- PBS plays a role in neointimal formation after stent implantation.
- PBS may be implicated in stent restenosis and thrombosis.

Background and aimsThe natural history and the role of atherosclerotic plaque located behind the stent (PBS) are still poorly understood. We evaluated the serial changes in PBS following bare-metal (BMS) compared to first-generation drug-eluting stent (DES) implantation and the impact of these changes on in-stent neointimal hyperplasia (NIH).MethodsThree-dimensional coronary reconstruction by angiography and intravascular ultrasound was performed after intervention and at 6-10-month follow-up in 157 patients with 188 lesions treated with BMS (n = 89) and DES (n = 99).ResultsThere was a significant decrease in PBS area (−7.2%; p < 0.001) and vessel area (−1.7%; p < 0.001) after BMS and a respective increase in both areas after DES implantation (6.1%; p < 0.001 and 4.1%; p < 0.001, respectively). The decrease in PBS area significantly predicted neointimal area at follow-up after BMS (β: 0.15; 95% confidence interval [CI]: 0.10-0.20, p < 0.001) and DES (β: 0.09; 95% CI: 0.07-0.11; p < 0.001) implantation. The decrease in PBS area was the most powerful predictor of significant NIH after BMS implantation (odds ratio: 1.13; 95% CI: 1.02-1.26; p = 0.02).ConclusionsThe decrease in PBS area after stent implantation is significantly associated with the magnitude of NIH development at follow-up. This finding raises the possibility of a communication between the lesion within the stent and the underlying native atherosclerotic plaque, and may have important implications regarding the pathobiology of in-stent restenosis and late/very late stent thrombosis.