Rosuvastatin versus atorvastatin to prevent contrast induced nephropathy in patients undergoing primary percutaneous coronary intervention (ROSA-cIN trial).
ABSTRACT We aimed to compare the incidence of contrast-induced nephropathy (CIN) between atorvastatin versus rosuvastatin in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary coronary angioplasty.
One hundred ninety-two consecutive patients, who underwent primary percutaneous intervention (p-PCI) with the diagnosis of STEMI, were included in the study. The patients were randomized to take atorvastatin 80 mg (n=98) or rosuvastatin 40 mg (n= 94) before the procedure. Biochemical and complete blood count measurements were done at baseline and at 48 hours following admission.
The incidence of CIN was 8.9% (n= 17) in the entire groups. The analysis performed between the statin groups revealed no statistical difference in any of the renal dysfunction indicators [baseline creatinine, baseline estimated glomerular filtration rate (eGFR), creatinine at 48 h, eGFR at 48 h, difference between baseline and 48 h creatinine, the per cent increase in the creatinine at 48 hours relative to basal creatinine]. In STEMI patients undergoing primary PCI, only the amount of the contrast agent administered was determined to be an independent predictor for CIN (OR and 95% CI: 1.08 (1.03- 1.13), P< or = 0.001). Left ventricular ejection fraction exhibited borderline statistical significance (OR and 95% CI: 0.88 (0.77-1.01), P= 0.07).
Atorvastatin and rosuvastatin had similar efficacy in preventing CIN in patients with STEMI undergoing P-PCI.
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ABSTRACT: Contrast-induced nephropathy is a common complication of iodinated contrast administration. Statins may reduce the risk of contrast-induced nephropathy, but data remain inconclusive. We summarized the evidence based on statins for the prevention of contrast-induced nephropathy with a network meta-analysis. Randomized trials focusing on statins were searched and pooled with random-effect odds ratios. A total of 14 trials (6,160 patients) were included, focusing on atorvastatin (high/low dose), rosuvastatin (high dose), simvastatin (high/low dose), and placebo or no statin therapy before contrast administration. The risk of contrast-induced nephropathy was reduced by atorvastatin high dose and rosuvastatin high dose, with no difference between these two agents. Results for atorvastatin low dose and simvastatin (high/low dose) in comparison to placebo were inconclusive. Atorvastatin and rosuvastatin administered at high doses and before iodinated contrast administration have a consistent and beneficial preventive effect on contrast-induced nephropathy and may actually halve its incidence.BioMed Research International 09/2014; 2014:213239. DOI:10.1155/2014/213239 · 2.71 Impact Factor
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ABSTRACT: Rosuvastatin has been marketed for approximately a decade. In this review we critically discuss available evidence on the benefits and risks from its use. In clinical trials using rosuvastatin, 'lowest is best' was relevant for on-treatment low-density lipoprotein cholesterol levels. Targeting levels <50 mg/dl was associated with the greatest decrease in vascular morbidity/mortality in the primary prevention setting. Also, such reduction can induce atherosclerosis regression without increasing the risk of adverse effects. Pooled data suggest that the safety profile of rosuvastatin is not different from that of other statins. It was estimated that rosuvastatin-associated absolute hazards of muscle-, liver- and renal-related adverse effects are lower than the corresponding vascular benefits in moderate vascular risk individuals. However, these data are subject to biases and need confirmation on a prospective basis. Significant liver enzyme elevations are rare. These often imply underlying non-alcoholic fatty liver disease (NAFLD), which is associated with increased vascular risk. Rosuvastatin can improve biochemical biomarkers and histological score of NAFLD. Whether this benefit is associated with vascular risk reduction should be assessed by prospective studies. Both chronic kidney disease and albuminuria independently predict vascular morbidity and mortality. Rosuvastatin improved the estimated glomerular filtration rate and decreased albuminuria in patients with moderately impaired kidney function. Also, vascular morbidity and mortality might be reduced in these patients. The same was not relevant in end-stage renal disease. Rosuvastatin-induced proteinuria appears to be of tubular origin, not relating to kidney injury. Rosuvastatin increases the risk of new-onset diabetes by dose-dependently impairing insulin sensitivity. Obese individuals with prediabetes appear to be predominantly affected. However, absolute vascular benefits of rosuvastatin may counterbalance this risk. Rosuvastatin is effective for the prevention and management of atherosclerotic vascular disease. Individualization of its use can maximize benefits and reduce the risk of adverse effects.Drug Safety 05/2014; 37(7). DOI:10.1007/s40264-014-0169-4 · 2.62 Impact Factor
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ABSTRACT: Preprocedural statin administration may reduce contrast-induced acute kidney injury (CI-AKI), but current evidence is controversial. Randomized controlled trials (RCTs) comparing preprocedural statin administration before coronary catheterization with standard strategies were searched in MEDLINE/PubMed, EMBASE, Scopus, Cochrane Library, Web of Science, and ScienceDirect databases. The outcome of interest was the incidence of postprocedural CI-AKI. Prespecified subgroup analyses were performed according to baseline glomerular filtration rate (GFR), statin type, and N-acetylcysteine use. Eight RCTs were included for a total of 4,984 patients. The incidence of CI-AKI was 3.91% in the statin group (n = 2,480) and 6.98% in the control group (n = 2,504). In the pooled analysis using a random-effects model, patients receiving statins had 46% lower relative risk (RR) of CI-AKI compared with the control group (RR 0.54, 95% confidence interval [CI] 0.38 to 0.78, p = 0.001). A moderate degree of non-significant heterogeneity was present (I(2) = 41.9%, chi-square = 12.500, p = 0.099, τ² = 0.100). In the subanalysis based on GFR, the pooled RR indicated a persistent benefit with statins in patients with GFR <60 ml/min (RR 0.67, 95% CI 0.45 to 1.00, p = 0.050) and a highly significant benefit in patients with GFR ≥60 ml/min (RR 0.40, 95% CI 0.27 to 0.61, p <0.0001). Statin type and N-acetylcysteine or hydration did not significantly influence the results. In conclusion, preprocedural statin use leads to a significant reduction in the pooled RR of CI-AKI.The American Journal of Cardiology 06/2014; 114(4). DOI:10.1016/j.amjcard.2014.05.036 · 3.43 Impact Factor