Eleven male patients with primary hyperlipidemia received 20 mg atorvastatin daily for 4 weeks. Blood was collected at baseline, 12 h, 36 h, 1 and 4 weeks after the start of treatment.
Clopidogrel decreased MCP-1 expression in the carotid artery at 4 weeks after irradiation. Expression of VCAM-1, ICAM-1, thrombomodulin, tissue factor and eNOS was unchanged in atorvastatin and clopidogrel-treated mice. Neither drug inhibited either age-related or radiation-induced atherosclerosis. Furthermore, loss of the inflammatory mediator CD40L did not influence the development of age-related and radiation-induced atherosclerosis.
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All four patients repeatedly distinguished blinded statin therapy from placebo. Strength testing confirmed weakness during statin therapy that reversed during placebo use. Muscle biopsies showed evidence of mitochondrial dysfunction, including abnormally increased lipid stores, fibers that did not stain for cytochrome oxidase activity, and ragged red fibers. These findings reversed in the three patients who had repeated biopsy when they were not receiving statins. Creatine kinase levels were normal in all four patients despite the presence of significant myopathy.
In this triple-blind controlled randomized clinical trial, 190 candidates for elective PCI, who were already using statins and/or other lipid lowering agents such as fibrates, were randomly assigned to two equal groups to receive either atorvastatin (80 mg) or placebo within 24 hours before the procedure. Serum levels of creatinine kinase myocardial isoenzyme (CK-MB), cardiac troponin I (cTNI) and high-sensitive C-reactive protein (hs-CRP) were measured at baseline and then 6 and 12 hours following PCI. Post-procedural MI was defined as troponin elevation>5-fold in patients with normal baseline or >20% in those with elevated baseline measurements with or without chest pain or ST segment or T wave abnormalities.
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This multicenter, randomized, double-blind study compared the effects of atorvastatin 40 mg/day versus placebo over 12 weeks on endothelial function (the primary endpoint) measured by peripheral arterial tone (PAT). Secondary endpoints included office blood pressure (BP), early carotid atherosclerosis, arterial stiffness measured by pulse wave velocity (PWV), and metabolic parameters.
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In clinical trials which have which have included over 40,000 patients there was no difference in all cause mortality for patients randomised to a fibrate compared to placebo. Treatment with a fibrate was associated with a small reduction in the risk of non-fatal cardiovascular events.
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This review shows that there is clear evidence in favor of calcium channel blockers and iloprost (oral and IV) to treat secondary RP. For all other interventions, only limited, conflicting, or no evidence was found. More high-quality, well-designed RCTs are needed in this field, especially for new interventions based on recent knowledge about the pathophysiology of secondary RP.
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Total cholesterol was reduced by 40.6+/-11.2% (p<0.001), low density lipoproteins cholesterol by 55.4+/-14% (p<0.001), triglycerides by 29.6% (p<0.05) and high density lipoproteins cholesterol was increased by 24.7% (p<0.05) in atorvastatin group after 6 months of therapy. No significant lipid changes were observed in the control group. Sixteen target segments in the treatment group and 12 segments in the control group were selected for primary efficacy parameter. The vasoconstrictor reaction to acetylcholine was similar at baseline in both groups: -16.8%+/-11.6% of diameter in atorvastatin group and -14.2%+/-13.7% in control group (p=0.58) at dose 10(-6) mol/l, -43.5%+/-21.2% in atorvastatin group and -41.2%+/-22.4% in control group (p=0.79) at dose 3.3x10(-6) mol/l, -64.5%+/-12.4% in atorvastatin group and -57.4%+/-15.6% in control group (p=0.35) at dose 10(-5) mol/l. Treatment with high doses of atorvastatin markedly decreased acetylcholine - induced vasoconstriction: -6.5%+/-14.5% of diameter in atorvastatin group versus -18.3%+/-14.0% in control group (p=0.04) at dose 10(-6) mol/l, -19.7%+/-22.8% in atorvastatin group versus -40.0%+/-25.0% in control group (p=0.034) at dose 3.3x10(-6) mol/l, -29.9%+/-21.3% in atorvastatin group (6 segments) versus -48.7%+/-19.0% in control group (3 segments, p=0.24) at dose 10(-5) mol/l.
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The Sanjiao theory is useful in guiding the treatment of hyperlipidemia.
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In patients with recent stroke or TIA and without known coronary heart disease, 80 mg of atorvastatin per day reduced the overall incidence of strokes and of cardiovascular events, despite a small increase in the incidence of hemorrhagic stroke. (ClinicalTrials.gov number, NCT00147602 [ClinicalTrials.gov].).