Clinical Efficacy and Safety of Statins in Managing Cardiovascular Risk

Division of Cardiology, Tufts University, New England Medical Center, Boston, MA 02111, USA.
Vascular Health and Risk Management 02/2008; 4(2):341-53.
Source: PubMed


Since their introduction in the 1980s, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have emerged as the one of the best-selling medication classes to date, with numerous trials demonstrating powerful efficacy in preventing cardiovascular outcomes. As our understanding of low-density lipoprotein cholesterol (LDL-C) and atherosclerosis continues to grow, the concept of 'lower is better' has corresponded with a more is better' approach to statin-based therapy. This review provides a detailed understanding of the clinical efficacy and safety of statins with a particular emphasis on the third generation drug, rosuvastatin.

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    • "The most recent drugs developed for this purpose are statins or 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitors which used for prevention and treatment of CHD; they lower cholesterol levels by 20% -30%, and even more at higher doses, and this has been clinically proven to produce an equivalent decrease in the risk of myocardial infarction and death [4]. Statins have become one of the best-selling medication classes to date since their introduction into the marketplace in 1986, and include the following drugs commercially available in the US: atorvastatin, lovastatin, pravastatin, fluvastatin, simvastatin and rosuvastatin [5]. Statins are highly effective in reducing cardiovascular mortality and are widely prescribed with best selling. "
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    ABSTRACT: Statins, which are inhibitors of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, are consi-dered as one of the most important drugs and the drug of choice for reducing an abnormal choles-terol level. Statins are normally used to decrease the risk of coronary heart disease (CHD), but they tend to be associated with liver adverse effects. The objective of this prospective study was to investigate the effect of atorvastatin therapy on the liver function in patients with CHD. Study comprised of 66 newly diagnosed CHD patients who were selected from UNRWA clinics in the Gaza Strip. The patients were clinically examined and treated with atorvastatin (10 -40 mg/day). A questionnaire was used to collect the data concerning patient's characteristics. Total cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), liver enzymes tests such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and total and direct blood bilirubin were measured before starting treatment and after 3 and 6 months of treatment. The results showed a significant increase in the mean values of ALT, AST, total bilirubin and direct bilirubin levels after 3 months then decreased after the next 3 months, but they were higher than the baseline with insignificant association.
    Pharmacology & Pharmacy 07/2014; 05(08). DOI:10.4236/pp.2014.58088
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    • "Several clinical trials have shown a positive correlation between greater levels of LDL-C lowering and greater reductions in coronary heart disease risk.83,84 Statins, currently the most powerful class of lipid-lowering drugs, can help decrease LDL-C levels by 20%–55%, depending on the statin molecule and dosage.85 In addition, combination of statins with ezetimibe, bile-acid sequestrants, or niacin produces an additional 10%–20% decrease in LDL-C.86 "
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    ABSTRACT: Proprotein convertase subtilisin/kexin type 9 (PCSK9) directly binds to the epidermal growth factor-like repeat A domain of low-density lipoprotein receptor and induces its degradation, thereby controlling circulating low-density lipoprotein cholesterol (LDL-C) concentration. Heterozygous loss-of-function mutations in PCSK9 can decrease the incidence of coronary heart disease by up to 88%, owing to lifelong reduction of LDL-C. Moreover, two subjects with PCSK9 loss-of-function mutations on both alleles, resulting in a total absence of functional PCSK9, were found to have extremely low circulating LDL-C levels without other apparent abnormalities. Accordingly, PCSK9 could represent a safe and effective pharmacological target to increase clearance of LDL-C and to reduce the risk of coronary heart disease. Recent clinical trials using anti-PCSK9 monoclonal antibodies that block the PCSK9:low-density lipoprotein receptor interaction were shown to considerably reduce LDL-C levels by up to 65% when given alone and by up to 72% in patients already receiving statin therapy. In this review, we will discuss how major scientific breakthroughs in PCSK9 cell biology have led to the development of new and forthcoming LDL-C-lowering pharmacological agents.
    Drug Design, Development and Therapy 10/2013; 7:1135-1148. DOI:10.2147/DDDT.S36984 · 3.03 Impact Factor
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    • "For individuals on lipid-lowering therapy, the LDL-C value was multiplied by 1.42 to model a 30% reduction in LDL-C on therapy. This represents the average expected reduction in LDL-C with a first-generation statin, the most commonly used lipid-lowering medication during the study periods of most of the cohorts [9]. TG values were log(10)-transformed. "
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    ABSTRACT: Whereas it is well established that plasma lipid levels have substantial heritability within populations, it remains unclear how many of the genetic determinants reported in previous studies (largely performed in European American cohorts) are relevant in different ethnicities. We tested a set of ∼50,000 polymorphisms from ∼2,000 candidate genes and genetic loci from genome-wide association studies (GWAS) for association with low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) in 25,000 European Americans and 9,000 African Americans in the National Heart, Lung, and Blood Institute (NHLBI) Candidate Gene Association Resource (CARe). We replicated associations for a number of genes in one or both ethnicities and identified a novel lipid-associated variant in a locus harboring ICAM1. We compared the architecture of genetic loci associated with lipids in both African Americans and European Americans and found that the same genes were relevant across ethnic groups but the specific associated variants at each gene often differed. We identify or provide further evidence for a number of genetic determinants of plasma lipid levels through population association studies. In many loci the determinants appear to differ substantially between African Americans and European Americans.
    PLoS ONE 05/2012; 7(5):e36473. DOI:10.1371/journal.pone.0036473 · 3.23 Impact Factor
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