Recent evidence indicates that rosuvastatin 40 mg may exert a beneficial effect in both carotid and coronary atherosclerosis progression. In particular, 2-year rosuvastatin treatment reduced the progression of carotid intima-media thickness (cIMT) in patients with low cardiovascular risk. However, despite the fact that in clinical practice lower doses of rosuvastatin are usually administered at this time, there are no clear data about its effect on cIMT. Thus, the aim of this study was to evaluate the effect of rosuvastatin 10 mg/day on cIMT over a 2-year follow-up.
Forty-five patients with hypercholesterolemia and asymptomatic carotid atherosclerosis on baseline carotid ultrasound investigation were treated with rosuvastatin 10 mg/day for 24 months. cIMT and lipid profile were assessed after 12 months and at the end of the study (24 months).
After 24 months, the treatment showed a 35.67% reduction in low-density lipoprotein cholesterol concentration (171 vs 110 mg/dl; p < 0.001), a 32.27% reduction in total cholesterol (251 vs 170 mg/dl; p < 0.001), a 19.67% increase in high-density lipoprotein cholesterol concentration (49 vs 61 mg/dl; p < 0.001), and a 10% reduction in triglycerides (120 vs 108 mg/dl; p < 0.01). Rosuvastatin treatment was associated with a 26.6% reduction in left cIMT (1.20 vs 0.90 mm; p < 0.001) and a 22.2% reduction in right cIMT (1.22 vs 0.95 mm; p < 0.001).
Two-year treatment with rosuvastatin 10 mg/day in hypercholesterolemic adults with evidence of subclinical atherosclerosis establishes a significant reduction in cIMT and improves lipid and lipoprotein levels, with a good tolerability profile.
"However, lower doses of rosuvastatin are usually administered in asymptomatic patients with hypercholesterolemia in clinical practice. Riccioni et al performed an open-label, noncontrolled study to evaluate the effect of rosuvastatin 10 mg daily for 2 years on CIMT in 45 patients with hypercholesterolemia and asymptomatic carotid atherosclerosis (CIMT ≥ 0.8 mm at baseline).48 Rosuvastatin treatment was significantly associated with a 26.6% reduction in left CIMT (1.20 vs 0.90 mm, P < 0.001) and a 22.2% reduction in right CIMT (1.22 vs 0.95 mm, P < 0.001).48 "
[Show abstract][Hide abstract] ABSTRACT: Rosuvastatin is one of the most potent statins available for reducing circulating low-density lipoprotein cholesterol (LDL-C) levels, which enables more high-risk patients to achieve their lipid goals. Its favorable balance of effects on atherogenic and protective lipoproteins and its pleiotropic effects, including anti-inflammatory and antioxidant effects and improvement in endothelial dysfunction, are associated with slowing of progression of atherosclerosis within the artery wall and have been translated into clinical benefits for cardiovascular outcomes. This review provides an update on the safety and the efficacy of rosuvastatin in recent large clinical trials. It appears that rosuvastatin has a beneficial effect on the progression of atherosclerosis across the clinical dosage range of 2.5-40 mg. It reduced cardiovascular events in relatively low-risk subjects with elevated high-sensitivity C-reactive protein and normal low-density lipoprotein cholesterol. As with other statins, rosuvastatin did not show overall benefit in terms of survival in patients with heart failure, but certain clinical or biochemical markers reflecting underlying disease characteristics may help to identify subgroups of patients that benefit from statin therapy. In patients with end-stage renal disease undergoing chronic hemodialysis, rosuvastatin had no effect on reducing cardiovascular events. Although there is a slightly increased risk of incident diabetes with this class of agents, the absolute benefits of statin therapy on cardiovascular events overweigh the risk in patients with moderate or high cardiovascular risk or with documented cardiovascular disease. As with other statins, rosuvastatin is an appropriate therapy in addition to antihypertensive treatment to reduce cardiovascular risk in hypertensive patients.
Integrated Blood Pressure Control 04/2013; 6:15-25. DOI:10.2147/IBPC.S34814
"large) VLDL particles. This is consistent with previous research demonstrating that statin therapy can promote regression of atherosclerotic plaques (24) and CIMT (25). Improvements in internal CIMT were also associated with decreasing trends in VCAM-1 and MCP-1 and an increasing trend in PAI-1 activity, consistent with decreased inflammation and atherogenesis. "
[Show abstract][Hide abstract] ABSTRACT: OBJECTIVE
Determine the impact of islet transplantation on carotid intima-media thickness (CIMT), a marker for atherosclerosis, in type 1 diabetes without kidney disease.RESEARCH DESIGN AND METHODS
Consecutive case series of 15 adults (mean age [SD], 49 years [10 years]; 87% female) with type 1 diabetes for ≥5 years (mean duration [SD], 30 years [12 years]; mean HbA(1c) [SD], 7.2% [0.9%]), without kidney disease, presenting with severe hypoglycemic unawareness to undergo allogeneic pancreatic islet transplant(s) (one to three each) in a phase 1/2 and 3 clinical trial. Current follow-up ranges from 1 to 5 years (2005-2011). CIMT of the common and internal carotid arteries was measured before and every 12-16 months after the first transplant (two to six CIMTs each) by one ultrasonographer and one blinded reader. CIMT was analyzed as change from baseline to 12- and 50-month follow-up; a combined CIMT score was calculated as the sum of the standardized IMT scores (SD units [SDs]) of both arteries.RESULTSAll patients achieved insulin independence after one to three transplants. CIMT decreased at 12 months (n = 15) for the common carotid (-0.058 mm; P = 0.006) and combined score (-1.28 SDs; P = 0.004). In those with 50-month follow-up (n = 7), the decrease in the combined score continued from 12 (-1.59 SDs; P = 0.04) to 50 months (-0.77 SDs; P = 0.04). During follow-up, the decreasing slope of change in CIMT was associated with decreasing slopes of change in HbA(1c), lipoproteins, and cardiovascular/inflammatory markers.CONCLUSIONS
Islet transplantation may ameliorate diabetes-related atherosclerosis through improved glycemic control consequent to restoring endogenous insulin secretion, and optimal lipid management posttransplant also contributes.
Diabetes care 11/2012; 36(2). DOI:10.2337/dc12-0679 · 8.42 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: High-dose rosuvastatin induces regression of coronary atherosclerosis, but it remains uncertain whether usual-dose statin has similar effects. We compared the effects of atorvastatin 20 mg/day versus rosuvastatin 10 mg/day on mild coronary atherosclerotic plaques (20% to 50% luminal narrowing and lesion length >10 mm) using intravascular ultrasound (IVUS). Three hundred fifty statin-naive patients with mild coronary atherosclerotic plaques were randomized to receive atorvastatin 20 mg/day or rosuvastatin 10 mg/day. IVUS examinations were performed at baseline and 6-month follow-up. Primary end point was percent change in total atheroma volume (TAV) defined as (TAV at 6 months - TAV at baseline)/(TAV at baseline) × 100. Evaluable IVUS was obtained for 271 patients (atorvastatin in 143, rosuvastatin in 128). Clinical characteristics, lipid levels, and IVUS measurements at baseline were similar between the 2 groups. At 6-month follow-up, percent change in TAV was significantly less in the atorvastatin group than in the rosuvastatin group (-3.9 ± 11.9% vs -7.4 ± 10.6%, respectively, p = 0.018). In contrast, change in percent atheroma volume was not different between the 2 groups (-0.3 ± 4.2 vs -1.1 ± 3.5, respectively, p = 0.157). Compared to baseline, TAV and TAV at the most diseased 10-mm subsegment were significantly decreased in the 2 groups (p <0.001). Changes in lipid profiles at 6-month follow-up were similar between the 2 groups. In conclusion, usual doses of atorvastatin and rosuvastatin induced significant regression of coronary atherosclerosis in statin-naive patients, with a greater decrease in favor of rosuvastatin.
The American journal of cardiology 03/2012; 109(12):1700-4. DOI:10.1016/j.amjcard.2012.01.399 · 3.28 Impact Factor
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