Effects of statins on restenosis after carotid artery stenting

Abstract

Objective

Carotid artery stenting is a minimally invasive procedure often chosen to treat carotid artery stenosis. In-stent restenosis is a well-known complication of this procedure. Statins, primarily recognized for their role in lowering LDL cholesterol, have been demonstrated to reduce in-stent restenosis following coronary artery stenting. This effect is often attributed to their pleiotropic properties rather than solely their impact on LDL cholesterol. Given that neointimal hyperplasia is the mechanism underlying in-stent restenosis in both coronary and carotid artery stenting, this study aims to investigate the effects of statins on in-stent restenosis in patients undergoing carotid artery stenting, as well as to identify factors that contribute to restenosis.

Methods

The study included 51 patients who underwent carotid artery stenting. Data collected included the patients’ age, gender, presence of hypertension, diabetes mellitus, hyperlipidemia, smoking history, post-procedure smoking, statin use, plaque morphologies, and Doppler and NASCET stenosis rates. Follow-ups were performed at 3rd and 6th months post-procedure. Maximum LDL cholesterol levels and HbA1c levels were measured at the 6-month follow-up. Intima-media thickness within the stent lumen was assessed, and restenosis was evaluated based on spectral Doppler findings.

Results

In our study, according to the measurements obtained from the in-stent segment, restenosis was detected in 5 patients (9.8%) overall. After the procedure, 37 patients (72.5%) were on statins, while 14 (27.5%) were not. Restenosis occurred in 4 patients (28.6%) in the non-statin group and 1 patient (2.7%) in the statin group, with a statistically significant difference (p = .017). All patients in the non-statin group had maximum LDL cholesterol levels ≥100 mg/dl during the follow-up. In the statin group, 67.6% of patients had maximum LDL cholesterol levels ≥100 mg/dl, while 32.4% of patients had <100 mg/dl. The difference was found statistically significant (p = .022). All 5 patients who developed restenosis had left-sided stents, and the difference between the groups was found to be close to statistical significance (p = .051). No significant differences were found between groups concerning other factors influencing restenosis and neointimal hyperplasia (p > .05).

Conclusions

Our study is the first in the literature to demonstrate that statin use is effective in preventing the development of restenosis in patients who underwent carotid artery stenting. This effect appears to occur independently of LDL cholesterol levels and is attributed to the pleiotropic effects of statins. Based on the data obtained, we believe that statin use after the procedure may reduce restenosis rates, regardless of LDL cholesterol levels.