1.
Rosuvastatin reduces ischemia-reperfusion injury in patients with acute coronary syndrome treated with percutaneous coronary intervention.
Jiang, F, Yang, J, Zhang, L, Li, R, Zhuo, L, Sun, L, Zhao, Q
Clinical cardiology. 2014;(9):530-5
Abstract
BACKGROUND Statins reduce the incidence of cardiovascular events after percutaneous coronary intervention (PCI), but no clinical studies have investigated the role of statins in ischemia-reperfusion injury after PCI. HYPOTHESIS Rosuvastatin could reduce ischemia-reperfusion injury in patients with acute coronary syndrome treated with PCI. OBJECTIVES We investigated the effects of rosuvastatin on ischemia-reperfusion injury in patients with acute coronary syndrome after PCI and evaluated short-term prognosis. METHODS Patients scheduled for emergent PCI were given either rosuvastatin for ≥6 months (10 mg/d, every night; n = 55) or no statins (control group; n = 65). Serum superoxide dismutase activity, malondialdehyde, brain natriuretic peptide (BNP), and high-sensitivity C-reactive protein (hs-CRP) were determined before and after PCI, as well as left ventricular ejection fraction and left ventricular end-diastolic volume. Major adverse cardiac events were observed at follow-ups for 6 months. RESULTS Superoxide dismutase activity in the rosuvastatin-treated group was higher than that of the control group; serum levels of malondialdehyde were lower. BNP and hs-CRP levels in the rosuvastatin-treated group were lower than that of the control group. Four weeks after PCI, the left ventricular ejection fraction in the treatment group was higher than that of the control group, and the left ventricular end-diastolic volume was lower. At the 6-month follow-up, there was no difference in major adverse cardiac events between the 2 groups. CONCLUSIONS Rosuvastatin before PCI reduced ischemia-reperfusion injury in patients with acute coronary syndrome, which suggests the importance of application of rosuvastatin before PCI for early intervention.
2.
Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis.
Moura, LM, Ramos, SF, Zamorano, JL, Barros, IM, Azevedo, LF, Rocha-Gonçalves, F, Rajamannan, NM
Journal of the American College of Cardiology. 2007;(5):554-61
Abstract
OBJECTIVES The objective of this study was to test the effect of a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor on the progression of moderate to severe aortic stenosis as measured by echocardiography. BACKGROUND Recent retrospective studies support the hypothesis that statins slow the progression of aortic stenosis. METHODS We performed an open-label, prospective study evaluating 121 consecutive patients with asymptomatic moderate to severe aortic stenosis (aortic valve area > or = 1.0 cm2; mean age 73.7 +/- 8.9 years; 57 men and 64 women), treated with and without rosuvastatin according to the National Cholesterol Education Program Adult Treatment Panel III guidelines. Echocardiographic, serum lipid, and inflammatory markers were measured at baseline and every 6 months for 18 months. RESULTS Sixty-one patients (50.4%) with elevated LDL (159.7 +/- 33.4 mg/dl), aortic valve velocity (3.65 +/- 0.64 m/s), and aortic valve area (1.23 +/- 0.42 cm2) received rosuvastatin (20 mg/day), and 60 (49.6%) with a normal LDL (118.6 +/- 37.4 mg/dl), aortic valve velocity (3.62 +/- 0.61 m/s), and aortic valve area (1.20 +/- 0.35 cm2) received no statin. During a mean follow-up of 73 +/- 24 weeks, the change in aortic valve area in the control group was -0.10 +/- 0.09 cm2/year versus -0.05 +/- 0.12 cm2/year in the rosuvastatin group (p = 0.041). The increase in aortic valve velocity was 0.24 +/- 0.30 m/s/year in the control group and 0.04 +/- 0.38 m/s/year in the rosuvastatin group (p = 0.007). There was significant improvement in serum lipid and echocardiographic measures of aortic stenosis in the statin group. CONCLUSIONS Prospective treatment of aortic stenosis with rosuvastatin by targeting serum LDL slowed the hemodynamic progression of aortic stenosis. This is the first prospective study that shows a positive effect of statin therapy for this disease process. (Rosuvastatin Affecting Aortic Valve Endothelium; http://www.clinicaltrials.gov/ct/show/NCT00114491?order = 1; NCT0014491).
3.
Lipid and apolipoprotein ratios: association with coronary artery disease and effects of rosuvastatin compared with atorvastatin, pravastatin, and simvastatin.
Rader, DJ, Davidson, MH, Caplan, RJ, Pears, JS
The American journal of cardiology. 2003;(5A):20C-23C; discussion 23C-24C
Abstract
Plasma lipid and apolipoprotein ratios that include both an atherogenic and an antiatherogenic lipid component (eg, total cholesterol/high-density lipoprotein [HDL] cholesterol ratio, low-density lipoprotein [LDL] cholesterol/HDL cholesterol ratio, non-HDL cholesterol/HDL cholesterol ratio, and apolipoprotein [apo] B/apo A-I ratio) have been found to be strong predictors of coronary artery disease (CAD) risk. Three trials that compared the effects of rosuvastatin 10 mg versus atorvastatin 10 mg and 2 trials that compared the effects of rosuvastatin 10 mg versus simvastatin 20 mg and pravastatin 20 mg on lipid ratios in patients with hypercholesterolemia were prospectively designed for pooled analysis. At 12 weeks, in the 3-trial pooled analysis, rosuvastatin 10 mg (n = 389) showed significantly greater reductions in all 4 lipid ratios compared with atorvastatin 10 mg (n = 393) (p <0.001). The mean percent reduction from baseline in the LDL cholesterol/HDL cholesterol ratio was 51% in patients treated with rosuvastatin 10 mg versus 39% in patients treated with atorvastatin 10 mg. In the 2-trial pooled analysis, treatment with rosuvastatin 10 mg (n = 226) also resulted in significantly greater reductions in all 4 lipid ratios compared with both simvastatin 20 mg (n = 249) and pravastatin 20 mg (n = 252) (p <0.001). Mean percent reductions from baseline in the LDL cholesterol/HDL cholesterol ratio were 52%, 39%, and 30% for rosuvastatin 10 mg, simvastatin 20 mg, and pravastatin 20 mg, respectively, in these 2 trials.