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      Effect of Withdrawal of Statin on C-Reactive Protein

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          Background: C-reactive protein is considered a risk factor for coronary artery disease. In addition to its lipid-lowering properties, statin decreases the level of C-reactive protein. Abrupt cessation of statin therapy during treatment could increase the incidence of cardiac events in patients with atherosclerotic heart disease. The changes of C-reactive protein after withdrawal of statin therapy are still unknown. Methods: Twenty patients with hyperlipidemia received statin (atorvastatin, 10 mg/day) therapy for 3 months. The levels of lipid profiles and C-reactive protein were assessed before receiving the statin therapy, immediately after 3 months of therapy, and on the 3 consecutive days after withdrawal of statin treatment. Results: After 3 months of statin therapy, the total cholesterol, low-density lipoprotein cholesterol (LDL-chol), and C-reactive protein were significantly reduced (264.94 ± 16.23 vs. 183.44 ± 16.34 mg/dl, 183.17 ± 34.56 vs. 122.00 ± 17.66 mg/dl, and 2,309.00 ± 437.85 vs. 1,257.95 ± 207.99 ng/ml, respectively). The level of C-reactive protein increased on the second day after withdrawal of statin therapy (2,590.14 ± 1,045.05 vs. 1,257.95 ± 207.99 ng/ml); however, the total cholesterol and LDL-chol did not increase during the 3-day period after withdrawal of statin therapy. Conclusions: The increase in the level of C-reactive protein after withdrawal of statin therapy may be a contributing factor to the increased incidence of cardiac events in patients who have abruptly stopped statin therapy.

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          Most cited references 19

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          The acute phase response.

          Adult mammals respond to tissue damage by implementing the acute phase response, which comprises a series of specific physiological reactions. This review outlines the principal cellular and molecular mechanisms that control initiation of the tissue response at the site of injury, the recruitment of the systemic defense mechanisms, the acute phase response of the liver and the resolution of the acute phase response.
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            Pleiotropic effects of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitors.

            The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors or statins are potent inhibitors of cholesterol biosynthesis. Several large clinical trials have demonstrated the beneficial effects of statins in the primary and secondary prevention of coronary heart disease. However, the overall clinical benefits observed with statin therapy appear to be greater than what might be expected from changes in lipid profile alone, suggesting that the beneficial effects of statins may extend beyond their effects on serum cholesterol levels. Indeed, recent experimental and clinical evidence indicates that some of the cholesterol-independent or "pleiotropic" effects of statins involve improving or restoring endothelial function, enhancing the stability of atherosclerotic plaques, and decreasing oxidative stress and vascular inflammation. Many of these pleiotropic effects of statins are mediated by their ability to block the synthesis of important isoprenoid intermediates, which serve as lipid attachments for a variety of intracellular signaling molecules. In particular, the inhibition of small GTP-binding proteins, Rho, Ras, and Rac, whose proper membrane localization and function are dependent on isoprenylation, may play an important role in mediating the direct cellular effects of statins on the vascular wall.
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              Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study.

              The role of C-reactive protein (CRP) as a novel plasma marker of atherothrombotic disease is currently under investigation. Previous studies have mostly related CRP to coronary heart disease, were often restricted to a case-control design, and failed to include pertinent risk factors to evaluate the joint and net effect of CRP on the outcome. We related plasma CRP levels to incidence of first ischemic stroke or transient ischemic attack (TIA) in the Framingham Study original cohort. There were 591 men and 871 women free of stroke/TIA during their 1980 to 1982 clinic examinations, when their mean age was 69.7 years. CRP levels were measured by using an enzyme immunoassay on previously frozen serum samples. Analyses were based on sex-specific CRP quartiles. Risk ratios (RRs) were derived, and series of trend analyses were performed. During 12 to 14 years of follow-up, 196 ischemic strokes and TIAs occurred. Independent of age, men in the highest CRP quartile had 2 times the risk of ischemic stroke/TIA (RR=2.0, P=0.027), and women had almost 3 times the risk (RR=2.7, P=0.0003) compared with those in the lowest quartile. Assessment of the trend in risk across quartiles showed unadjusted risk increase for men (RR=1.347, P=0.0025) and women (RR=1.441, P=0.0001). After adjustment for smoking, total/HDL cholesterol, systolic blood pressure, and diabetes, the increase in risk across CRP quartiles remained statistically significant for both men (P=0.0365) and women (P=0.0084). Independent of other cardiovascular risk factors, elevated plasma CRP levels significantly predict the risk of future ischemic stroke and TIA in the elderly.

                Author and article information

                S. Karger AG
                September 2004
                29 September 2004
                : 102
                : 3
                : 166-170
                aSection of Cardiology, Department of Internal Medicine and bDepartment of Clinical Chemistry, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
                80486 Cardiology 2004;102:166–170
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 1, References: 30, Pages: 5
                Clinical Cardiology


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