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Published on: December 6, 2024
Effect of statins on coronary bifurcation atherosclerosis: an intravascular ultrasound virtual histology study
Eun-Seok Shin1, Hector M Garcia-Garcia, Takayuki Okamura
1Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands. ses@uuh.ulsan.kr
Insights
Statins reduced overall plaque volume in coronary arteries. Rosuvastatin halted necrotic core progression, unlike simvastatin, suggesting differential effects on vulnerable plaque components.
Area of Science:
- Cardiology
- Vascular Biology
- Pharmacology
Background:
- Coronary bifurcation atherosclerosis affects non-culprit vessels.
- Intravascular ultrasound virtual histology (VH-IVUS) assesses plaque composition.
- Statins are used to manage atherosclerosis.
Purpose of the Study:
- To assess the effect of simvastatin versus rosuvastatin on coronary bifurcation atherosclerosis in non-culprit vessels using VH-IVUS.
- To evaluate changes in plaque volume and composition after 12 months of statin therapy.
Main Methods:
- Non-randomized study of 48 patients with 51 bifurcation sites.
- Baseline and 12-month follow-up VH-IVUS analysis.
- Treatment with simvastatin (20 mg) or rosuvastatin (10 mg) daily.
Main Results:
- Overall plaque and external elastic membrane volume decreased.
- Dense calcium volume increased, while fibrous and fibrofatty volumes decreased.
- Necrotic core volume did not change significantly overall, but increased with simvastatin and remained stable with rosuvastatin.
Conclusions:
- Statin therapy leads to favorable plaque remodeling and compositional changes in non-culprit coronary artery bifurcations.
- Rosuvastatin demonstrated a potential benefit in halting necrotic core progression compared to simvastatin.
- Changes in HDL-cholesterol and hsCRP levels predicted reduction in necrotic core volume.
Abstract:
This study is aimed at assessing by intravascular ultrasound virtual histology (VH-IVUS) the effect of statins on coronary bifurcation atherosclerosis in non-culprit vessels. In this non-randomized study, in 48 patients, 51 bifurcation atherosclerotic sites in non-culprit vessels without significant angiographic stenosis, underwent baseline and 12 months follow-up VH-IVUS. Patients received treatment with either simvastatin (20 mg daily, n = 24) or rosuvastatin (10 mg daily, n = 24) for the same period. VH-IVUS analysis of bifurcation lesions included the 5-mm proximal, bifurcation only (side-branch point) and 5-mm distal subsegments. Overall plaque and external elastic membrane volume decreased after 1 year (115.7 ± 35.5 to 106.1 ± 29.3 mm³, P < 0.001; and 241.0 ± 57.0 to 232.4 ± 54.2 mm³, P = 0.005, respectively). Similarly, overall dense calcium volume significantly increased (7.1 ± 5.3 to 11.0 ± 8.5 mm³, P < 0.010), while fibrous and fibrofatty volumes significantly decreased (36.9 ± 19.2 to 24.1 ± 11.7 mm³, P < 0.001; and 5.1 ± 3.8 to 2.3 ± 2.0 mm³, P < 0.001, respectively), and necrotic core volume did not change significantly (17.0 ± 11.1 to 19.8 ± 13.5 mm³, P = 0.053). There were no significant differences in compositional analysis between the simvastatin and rosuvastatin treatment groups. However, within groups, necrotic core volume significantly increased in the simvastatin treatment group (19.7 ± 13.9 to 24.3 ± 16.1 mm³, P = 0.029) but not in the rosuvastatin treatment group. (14.3 ± 6.7 to 15.6 ± 8.7 mm³, P = 0.423). The independent clinical predictors for reduction of necrotic core volume by multiple stepwise logistic regression analysis were the percent change of HDL-cholesterol level (P = 0.041, odds ratio: 1.052, 95% confidence interval (CI): 1.002 to 1.104) and the percent change of hsCRP level (P = 0.021, odds ratio: 0.989, 95% CI: 0.980 to 0.998). After 1 year, overall dense calcium volume significantly increased whilst fibrous and fibrofatty volumes significantly decreased; no significant change in the content of necrotic core was observed. Although changes in the volumes of all plaque components were not significantly different between the simvastatin and rosuvastatin treatment groups, halting of necrotic core progression was apparent in the rosuvastatin group.
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