Comparison of High-Dose Rosuvastatin Versus Low-Dose Rosuvastatin Plus Ezetimibe on Carotid Atherosclerotic Plaque Inflammation in Patients with Acute Coronary Syndrome

A comparison of the effects of monotherapy with rosuvastatin, atorvastatin or ezetimibe versus combination treatment with rosuvastatin-ezetimibe and atorvastatin-ezetimibe on the integrity of vascular endothelial cells damaged by oxidized cholesterol

“…Indeed, 90-day administration of atorvastatin combined with ezetimibe (40 + 10 mg/day) was associated with a significant reduction in serum levels of ICAM-1 and hsCRP in patients with hypercholesterolemia, but no such effect was observed for ezetimibe monotherapy (10 mg/day) [ 32 ]. Similarly, a low dose of rosuvastatin combined with ezetimibe (5 mg + 10 mg/day) can exert similar anti-inflammatory effects on carotid plaque observed in the 18FDG PET/CT study of patients with acute coronary syndrome, as high dose rosuvastatin treatment (20 mg/day) [ 33 ].…”

Carotid Artery Temperature Reduction with Statin Therapy in Patients with Familial Hyperlipidemia Syndromes

“…In specific, the combination of ezetimibe with statin, compared to statin monotherapy, exerts a similar anti-inflammatory effect on carotid atherosclerotic plaque [ 14 , 15 ]. It is noteworthy that in a recent study the combination of ezetimibe with low-dose rosuvastatin showed inferior carotid wall anti-inflammatory effect compared to high-dose rosuvastatin [ 19 ]. Nevertheless, all the above studies did not investigate the incremental anti-inflammatory impact of ezetimibe, but rather compared the combination of ezetimibe/statin to a statin dose with a similar LDL-lowering effect.…”

A new approach of statin therapy in carotid atherosclerosis: Targeting indices of plaque vulnerability on the top of lipid-lowering. A narrative review

“…Twenty-four prospective clinical trials have assessed the influence of statins on carotid plaque vulnerability concomitantly with the modulation of circulating inflammatory biomarkers. Based on imaging indices of plaque vulnerability, such as PET scans [47,[48][49][50]52] and carotid plaque echogenicity [53,54], most of those studies suggested an improvement in plaque stability after statin administration, accompanied by a significant reduction in inflammatory biomarkers. Those studies used the most known inflammatory biomarkers, like CRP [47][48][49][53][54][55][56][57][58][59], interleukin (IL)-6 [53,[55][56][57]59], tumor necrosis factor (TNF)-a [49,54,56,59], and monocyte chemoattractant protein-1 [49].…”