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Risk of Stroke in Chronic Heart Failure Patients Without Atrial Fibrillation: Analysis of the Controlled Rosuvastatin in Multinational Trial Heart Failure (CORONA) and the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza Cardiaca-Heart Failure (GISSI-HF) Trials.
Abdul-Rahim, AH, Perez, AC, Fulton, RL, Jhund, PS, Latini, R, Tognoni, G, Wikstrand, J, Kjekshus, J, Lip, GY, Maggioni, AP, et al
Circulation. 2015;(17):1486-94; discussion 1494
Abstract
BACKGROUND Our aim was to describe the incidence and predictors of stroke in patients who have heart failure without atrial fibrillation (AF). METHODS AND RESULTS We pooled 2 contemporary heart failure trials, the Controlled Rosuvastatin in Multinational Trial Heart Failure (CORONA) and the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza cardiaca-Heart Failure trial (GISSI-HF). Of the 9585 total patients, 6054 did not have AF. Stroke occurred in 165 patients (4.7%) with AF and in 206 patients (3.4%) without AF (rates 16.8/1000 patient-years and 11.1/1000 patient-years, respectively). Using Cox proportional-hazards models, we identified the following independent predictors of stroke in patients without AF (ranked by χ(2) value): age (hazard ratio, 1.34; 95% confidence interval, 1.18-1.63 per 10 years), New York Heart Association class (1.60, 1.21-2.12 class III/IV versus II), diabetes mellitus treated with insulin (1.87, 1.22-2.88), body mass index (0.74, 0.60-0.91 per 5 kg/m(2) up to 30), and previous stroke (1.81, 1.19-2.74). N-terminal pro B-type natriuretic peptide (available in 2632 patients) was also an independent predictor of stroke (hazard ratio, 1.31; 1.11-1.57 per log unit) when added to this model. With the use of a risk score formulated from these predictors, we found that patients in the upper third of risk had a rate of stroke that approximated the risk in patients with AF. CONCLUSIONS A small number of demographic and clinical variables identified a subset of patients who have heart failure without AF at a high risk of stroke.
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Rosuvastatin Treatment for Preventing Contrast-Induced Acute Kidney Injury After Cardiac Catheterization: A Meta-Analysis of Randomized Controlled Trials.
Yang, Y, Wu, YX, Hu, YZ
Medicine. 2015;(30):e1226
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Abstract
We performed a meta-analysis of randomized controlled trials (RCTs) to evaluate the protective effects of rosuvastatin on contrast-induced acute kidney injury (CI-AKI) and major adverse cardiovascular events (MACEs) in patients undergoing cardiac catherization.PubMed, MEDLINE, Web of Science, EMBASE, ClinicalTrials.gov, and the Cochrane Central RCTs were searched for RCTs from inception to May 2015, to compare rosuvastatin for preventing CI-AKI with placebo treatment in patients undergoing cardiac catherization.Five RCTs with a total of 4045 patients involving 2020 patients pretreated with rosuvastatin and 2025 control patients were identified and analyzed. Patients treated with rosuvastatin had a 51% lower risk of CI-AKI compared with the control group based on a fixed-effect model (OR = 0.49, 95% CI = 0.37-0.66, P < 0.001), and showed a trend toward a reduced risk of MACEs (OR = 0.62, 95% CI = 0.36-1.07, P = 0.08). A subgroup analysis showed that studies with Jadad score ≥3 showed a significant reduction of CI-AKI (OR = 0.53, 95% CI, 0.38-0.73, P < 0.001). However, the risk of CI-AKI did not significantly differ in the studies with Jadad score <3 (OR = 0.54, 95% CI, 0.13-2.24, P = 0.40). In addition, the rosuvastatin treatment showed no effect for preventing CI-AKI in patients with chronic kidney disease (CKD) undergoing elective cardiac catherization (I = 0%, OR = 0.81, 95% CI = 0.41-1.61, P = 0.55).This updated meta-analysis demonstrated that preprocedural rosuvastatin treatment could significantly reduce the incidence of CI-AKI, with a trend toward a reduced risk of MACEs in patients undergoing cardiac catheterization. However, rosuvastatin treatment did not seem to be effective for preventing CI-AKI in CKD patients undergoing elective cardiac catheterization.
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[Impact on the carotid intima-medial thickness and safety of rosuvastatin in Chinese patients with carotid atherosclerosis: a meta-analysis].
Feng, X, Zhang, J, Liu, M, Li, X
Zhonghua xin xue guan bing za zhi. 2014;(3):247-53
Abstract
OBJECTIVE To evaluate the efficacy and safety of rosuvastatin in Chinese patients with carotid atherosclerosis. METHOD A systematic search of Pubmed, EMBase, CENTRAL, CBMdisc, CNKI and WANFANG databases up to January 2013 was performed to identify studies comparing rosuvastatin with a placebo or other statins on carotid intima-medial thickness (IMT) with a minimum follow-up of 6 months in Chinese patients. Meta-analysis was performed by using RevMan 5.0 software after the strict evaluation of the methodological quality of the included studies independently by two reviewers. RESULTS Twenty-eight studies involving 1 392 individuals were included in this review. The pooled weighted mean difference (WMD) between rosuvastatin and placebo or control on IMT was 0.28 mm (95%CI 0.14-0.42, P < 0.01), with 0.31 mm (95%CI 0.14-0.49, P < 0.01) on 6-8 months and 0.16 mm (95%CI 0.05-0.27, P = 0.005) on 12 months, respectively. Analysis on studies in core journals showed the WMD between rosuvastatin and placebo or control on IMT was 0.18 mm (95%CI 0.09-0.27, P < 0.01). The WMD between rosuvastatin and other statins on IMT was 0.06 mm (95%CI 0.04-0.08, P < 0.01). The WMD between rosuvastatin and placebo or control on plaque score was 0.89 (95%CI 0.78-0.99, P < 0.01). The WMD between rosuvastatin and placebo or control on plaque area was 1.46 (95%CI 0.67-2.25, P < 0.01).Reports of adverse effect were elevated liver enzyme (2.30%, 19/825), elevated muscle enzyme (0.73%, 6/825), muscle aches (0.61%, 5/825). CONCLUSIONS Rosuvastatin therapy is effective and safe to decrease IMT in Chinese patients with carotid atherosclerosis.
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A meta-analysis of randomized head-to-head trials for effects of rosuvastatin versus atorvastatin on apolipoprotein profiles.
Takagi, H, Umemoto, T, ,
The American journal of cardiology. 2014;(2):292-301
Abstract
To determine which statin will better improve the apolipoprotein (Apo) profiles (ApoA-I levels, ApoB levels, and ApoB/A-I ratios), we performed a meta-analysis of randomized head-to-head trials of rosuvastatin versus atorvastatin therapy. MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through December 2012 using Web-based search engines (PubMed and OVID). The search terms included "apolipoprotein," "rosuvastatin," "atorvastatin," "randomized," "randomly," and "randomization." Of 42 potentially relevant studies initially screened, 25 reports of randomized trials enrolling 14,283 patients were included. A pooled analysis for the percentage of changes in ApoA-I demonstrated a benefit of rosuvastatin versus atorvastatin in the comparison of all rosuvastatin/atorvastatin dose ratios (mean difference 2.97%, 3.39%, 5.77%, and 6.25%). For the percentage of changes in ApoB, a benefit was seen for rosuvastatin versus atorvastatin in the 1/1 (-6.06%) and 1/2 dose ratio (-1.80%). However, a benefit was seen for atorvastatin versus rosuvastatin in the 1/4 (2.38%) and 1/8 dose ratio (6.59%). The pooled analysis for the percentage of changes in the Apo B/A-I ratios demonstrated a benefit for rosuvastatin versus atorvastatin in the 1/1 (-7.22%) and 1/2 dose ratio (-3.51%), with no difference in the 1/4 dose ratio. In contrast, a benefit was seen for atorvastatin versus rosuvastatin in the 1/8 dose ratio (4.03%). In conclusion, rosuvastatin might increase Apo A-I levels at all dose ratios and decrease ApoB levels and ApoB/A-I ratios in the 1/1 and 1/2 dose ratio versus atorvastatin. Only higher dose atorvastatin appeared to be more effective for the reduction in ApoB levels (1/4 and 1/8 dose ratio) and Apo B/A-I ratios (1/8 dose ratio).
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Lipid-lowering efficacy of rosuvastatin.
Adams, SP, Sekhon, SS, Wright, JM
The Cochrane database of systematic reviews. 2014;(11):CD010254
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Abstract
BACKGROUND Rosuvastatin is one of the most potent statins and is currently widely prescribed. It is therefore important to know the dose-related magnitude of effect of rosuvastatin on blood lipids. OBJECTIVES Primary objective To quantify the effects of various doses of rosuvastatin on serum total cholesterol, low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, non-HDL-cholesterol and triglycerides in participants with and without evidence of cardiovascular disease. Secondary objectives To quantify the variability of the effect of various doses of rosuvastatin.To quantify withdrawals due to adverse effects (WDAEs) in the randomized placebo-controlled trials. SEARCH METHODS We searched the Cochrane Central Register of Controlled Trials (CENTRAL) Issue 10 of 12, 2014 in The Cochrane Library, MEDLINE (1946 to October week 5 2014), EMBASE (1980 to 2014 week 44), Web of Science Core Collection (1970 to 5 November 2014) and BIOSIS Citation Index (1969 to 31 October 2014). No language restrictions were applied. SELECTION CRITERIA Randomized controlled and uncontrolled before-and-after trials evaluating the dose response of different fixed doses of rosuvastatin on blood lipids over a duration of three to 12 weeks. DATA COLLECTION AND ANALYSIS Two review authors independently assessed eligibility criteria for studies to be included and extracted data. WDAEs information was collected from the placebo-controlled trials. MAIN RESULTS One-hundred and eight trials (18 placebo-controlled and 90 before-and-after) evaluated the dose-related efficacy of rosuvastatin in 19,596 participants. Rosuvastatin 10 to 40 mg/day caused LDL-cholesterol decreases of 46% to 55%, when all the trials were combined using the generic inverse variance method. The quality of evidence for these effects is high. Log dose-response data over doses of 1 to 80 mg, revealed strong linear dose-related effects on blood total cholesterol, LDL-cholesterol and non-HDL-cholesterol. When compared to atorvastatin, rosuvastatin was about three-fold more potent at reducing LDL-cholesterol. There was no dose-related effect of rosuvastatin on blood HDL-cholesterol, but overall, rosuvastatin increased HDL by 7%. There is a high risk of bias for the trials in this review, which would affect WDAEs, but unlikely to affect the lipid measurements. WDAEs were not statistically different between rosuvastatin and placebo in 10 of 18 of these short-term trials (risk ratio 0.84; 95% confidence interval 0.48 to 1.47). AUTHORS' CONCLUSIONS The total blood total cholesterol, LDL-cholesterol and non-HDL-cholesterol-lowering effect of rosuvastatin was linearly dependent on dose. Rosuvastatin log dose-response data were linear over the commonly prescribed dose range. Based on an informal comparison with atorvastatin, this represents a three-fold greater potency. This review did not provide a good estimate of the incidence of harms associated with rosuvastatin because of the short duration of the trials and the lack of reporting of adverse effects in 44% of the placebo-controlled trials.
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Achievement of 2011 European low-density lipoprotein cholesterol (LDL-C) goals of either <70 mg/dl or ≥ 50% reduction in high-risk patients: results from VOYAGER.
Karlson, BW, Nicholls, SJ, Lundman, P, Palmer, MK, Barter, PJ
Atherosclerosis. 2013;(1):265-9
Abstract
OBJECTIVE Guidelines published in 2011 by the European Atherosclerosis Society and the European Society of Cardiology recommend a goal of either low-density lipoprotein cholesterol (LDL-C) <70 mg/dl (~1.8 mmol/l) or ≥ 50% reduction in LDL-C for patients at very high cardiovascular risk. The aim of this study was to determine the percentage of high-risk patients from the VOYAGER individual patient data meta-analysis treated with rosuvastatin 10-40 mg, atorvastatin 10-80 mg or simvastatin 10-80 mg who achieved this goal. METHODS We analysed 25,075 patient exposures from high-risk patients. Paired comparisons were made between each rosuvastatin dose and an equal or higher dose of either atorvastatin or simvastatin, with a series of meta-analyses that included only randomised studies that directly compared rosuvastatin and its comparator treatments. RESULTS As statin dose increased, higher percentages of patients achieved LDL-C <70 mg/dl or ≥ 50% LDL-C reduction. A greater percentage achieved this goal with rosuvastatin 10-40 mg (43.8-79.0%) than with equal or double milligram doses of atorvastatin (16.1-65.2%) or simvastatin (0-39.7%). Paired comparisons showed statistically significant differences for: rosuvastatin 10 mg vs. atorvastatin 10-20 mg and simvastatin 10-20 mg; rosuvastatin 20 mg vs. atorvastatin 20-40 mg and simvastatin 20-80 mg; and rosuvastatin 40 mg vs. atorvastatin 40-80 mg and simvastatin 40-80 mg (all p < 0.001). CONCLUSION These data from VOYAGER highlight the importance of an effective statin at an appropriate dose to achieve treatment goals for LDL-C in patients with very high cardiovascular risk.
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Preventive effects of rosuvastatin on atrial fibrillation: a meta-analysis of randomized controlled trials.
Liu, T, Korantzopoulos, P, Li, L, Li, G
International journal of cardiology. 2013;(6):3058-60
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Renal safety of intensive cholesterol-lowering treatment with rosuvastatin: a retrospective analysis of renal adverse events among 40,600 participants in the rosuvastatin clinical development program.
Stein, EA, Vidt, DG, Shepherd, J, Cain, VA, Anzalone, D, Cressman, MD
Atherosclerosis. 2012;(2):471-7
Abstract
OBJECTIVE Intensive lowering of low-density lipoprotein cholesterol (LDL-C) with statins reduces cardiovascular risk but can cause liver-, muscle-, and possibly renal-related adverse events (AEs). We assessed the effects of rosuvastatin on the risk of developing renal impairment or renal failure among participants in the rosuvastatin clinical development program. METHODS The analysis was based on AE data reported by investigators from 36 studies that included 40,600 participants who did not have advanced, pre-existing renal disease. Rates of renal AEs were determined based on time to first occurrence of renal impairment or renal failure. RESULTS Renal impairment or renal failure was reported in 536 study participants during 72,488 patient-years of follow-up. Renal event rates were higher in patients with history of heart failure (n = 5011), hypertension (n = 21,864), diabetes (n = 5165), or estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m(2) (n = 9507) at baseline but did not differ with rosuvastatin compared with placebo or with rosuvastatin 40 mg compared with rosuvastatin 10mg. Relative risk (RR) estimates obtained from pooled analysis of placebo-controlled trials were RR: 1.03 (95% CI: 0.86-1.23, p = 0.777) for any reported renal impairment or renal failure event, RR: 1.02 (95% CI: 0.76-1.37, p = 0.894) for serious renal AEs, and RR: 0.70 (95% CI: 0.36-1.35, p = 0.282) for renal AEs leading to death. CONCLUSION These findings suggest that intensive LDL-C-lowering treatment with rosuvastatin does not affect the risk of developing renal insufficiency or renal failure in patients who do not have advanced, pre-existing renal disease.
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Atorvastatin, not rosuvastatin, improves cardiac function in heart failure: a meta-analysis of randomized trials.
Takagi, H, Umemoto, T
International journal of cardiology. 2012;(2):296-9
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Meta-analysis of comparative efficacy of increasing dose of Atorvastatin versus Rosuvastatin versus Simvastatin on lowering levels of atherogenic lipids (from VOYAGER).
Nicholls, SJ, Brandrup-Wognsen, G, Palmer, M, Barter, PJ
The American journal of cardiology. 2010;(1):69-76
Abstract
Statins are the most commonly prescribed agents for lowering levels of low-density lipoprotein (LDL) cholesterol. Although dose-dependent reductions in levels of atherogenic lipids are observed with all statins, the impact of increasing dose has not been fully elucidated. An individual patient data pooled analysis was performed of 32,258 patients in studies comparing the efficacy of rosuvastatin with that of atorvastatin or simvastatin. The impact of increasing dose on lowering LDL cholesterol, triglycerides, non-high-density lipoprotein (HDL) cholesterol, and apolipoprotein B was investigated. Doubling the dose of each statin was accompanied by a 4% to 7% greater degree of lowering of all atherogenic lipids. A stronger correlation was observed between changes in LDL cholesterol and non-HDL cholesterol (r = 0.92, p <0.001) or apolipoprotein B (r = 0.76, p <0.001) than triglycerides (r = 0.14, p <0.001). On multivariate analysis, baseline lipid level (p <0.0001) and increasing statin dose (p <0.0001) were strong predictors of achieving treatment goals in high-risk patients. Increasing age was a strong independent predictor of achieving goal for all atherogenic lipids (p <0.0001). Achieving LDL cholesterol goals was also more likely in women (p <0.0001), patients with diabetes (p <0.0001), and patients without atherosclerotic disease (p = 0.0002). In contrast, normal triglyceride levels were more often observed in men (p <0.0001) and patients without diabetes mellitus (p = 0.03). In conclusion, doubling statin dose was associated with greater lowering of LDL cholesterol by 4% to 6% and non-HDL cholesterol by 3% to 6%. Greater lipid goal achievement with increasing dose supports the use of high-dose statin therapy for more effective cardiovascular prevention.