pitavastatin and Carotid-Stenosis

We determined time course of stabilization of echolucent carotid plaques by statin therapy in patients with acute coronary syndrome (ACS). Treatment with 4 mg/d pitavastatin (n = 33) or placebo (n = 32) was initiated within 3 days after onset of ACS in 65 patients with echolucent carotid plaque. Vulnerable carotid plaques were assessed by measuring plaque echolucency using carotid ultrasound with integrated backscatter (IBS) analysis before and 1 month after treatment in all patients. The calibrated IBS value (intima-media IBS value minus adventia IBS) of vulnerable carotid plaques favorably changed at 1 month after treatment in both groups, but the echolucency at 1 month improved more in the pitavastatin than in the placebo group (pitavastatin group: -18.7 +/- 3.3 dB at pretreatment versus -12.7 +/- 2.3 dB at 1 month *P < 0.001; placebo: -19.0 +/- 3.5 dB versus -16.9 +/- 3.2 dB, P < 0.05, *P < 0.01 versus the value at 1 month in placebo group). Levels of CRP, VEGF, and TNFalpha at 1 month were significantly lower in pitavastatin than placebo group. In conclusion, pitavastatin improved carotid plaque echolucency within 1 month of therapy in patients with ACS, in association with decrease in the inflammatory biomarkers related to vulnerable plaques.

Topics: Acute Coronary Syndrome; C-Reactive Protein; Carotid Stenosis; Cholesterol, HDL; Cholesterol, LDL; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Prospective Studies; Quinolines; Time Factors; Triglycerides; Tumor Necrosis Factor-alpha; Ultrasonography; Vascular Endothelial Growth Factor A

Periprocedural ischemic stroke is one problem associated with carotid artery stenting (CAS). This study was designed to assess whether preoperative statin therapy reduces the risk of periprocedural ischemic complications with CAS.. In this prospective study at 11 centers, patients with carotid artery stenosis (symptomatic ≥50%, asymptomatic ≥80%) and a high risk of carotid endarterectomy but without previous statin treatments were divided into two groups by low-density lipoprotein cholesterol (LDL-C) levels. With LDL-C ≥120 mg/dl, the pitavastatin-treated (PS) group received pitavastatin at 4 mg/day. With LDL-C <120 mg/dl, the non-PS group received no statin therapy. After 4 weeks, both groups underwent CAS. Frequencies of new ipsilateral ischemic lesions on diffusion-weighted imaging within 72 h after CAS and cerebrovascular events (transient ischemic attack, stroke, or death) within 30 days were assessed.. Among the 80 patients enrolled, 61 patients (PS group, n = 31; non-PS group, n = 30) fulfilled the inclusion criteria. New ipsilateral ischemic lesions were identified in 8 of 31 patients (25.8%) in the PS group and 16 of 30 patients (53.3%) in the non-PS group (P = 0.028). Cerebrovascular events occurred in 0 patients in the PS group and in 3 of 30 patients (10.0%) in the non-PS group (P = 0.071). Multivariate analyses demonstrated the pitavastatin treatment (β = 0.74, 95% confidence interval 0.070-1.48, P = 0.042) to be an independent factor for decreasing post-CAS ischemic lesions.. Pretreatment with pitavastatin significantly reduced the frequency of periprocedural ischemic complications with CAS.

Topics: Aged; Carotid Stenosis; Diffusion Magnetic Resonance Imaging; Endarterectomy, Carotid; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Ischemic Attack, Transient; Japan; Lipoproteins, LDL; Male; Prospective Studies; Quinolines; Risk Factors; Stents; Stroke; Treatment Outcome