Comparative evaluation of the effect of statin drugs--论文代写范文精选

他汀类药物(或β-还原酶抑制剂)是一种用于降低胆固醇的药物，通过抑制酶HMGCoA,在生产的过程中扮演着重要的角色，由于胆固醇水平与心血管疾病(CVD)有关,因此和他汀类药物可以用于预防这些疾病。随机对照试验表明,对于已经患有心血管疾病的人来说，他们是最有效的。

Abstract
Statins clearly confer substantial benefit in people with established cardiovascular (CV) disease (secondary prevention). The effectiveness of various statin drugs in hyperlipidaemic patients is evaluated in the present study. This work was undertaken to assess the effective role of statin in hyperlipidaemic patients with cardiovascular disease and comparison was made between various classes of statin drugs. The study population contained 50 subjects with hyperlipidaemia and they were administered with statin class of drugs. The administration of Rosuvastatin and Atrovastatin was found to be more effective in the treatment of hyperlipidaemic patients than that of Simvastatin and Pravastatin. Although flavostatin also had a profound effect, the dosage was high compared to other statins. Hence its effectiveness compared to Rosuvastatin and Atrovastatin need to be further investigated. Rosuvastatin and Atrovastatin can be more effective in reducing hyperlipidemia compared to other classes of statin drugs and thus further reduce the risk of cardiovascular disease in such patients.In addition to that,Rosuvasatin had less side effects in patients as compared to atrovastatin and can be defined as the most effective among the statin class of drugs.

Introduction
Statins (or HMG-CoA reductase inhibitors) are a class of drug used to lower cholesterol levels by inhibiting the enzyme HMGCoA reductase, which plays a central role in the production of cholesterol in the liver. Increased cholesterol levels have been associated with cardiovascular diseases (CVD), and statins are therefore used in the prevention of these diseases [1,2,3]. Randomized controlled trials have shown that they are most effective in those already suffering from cardiovascular disease (secondary prevention), but they are also advocated and used extensively in those without previous CVD but with elevated cholesterol levels and other risk factors (such as diabetes and high blood pressure) that increase a person's risk.A number of statins are on the market: atorvastatin (Lipitor and Torvast), fluvastatin (Lescol), lovastatin (Mevacor, Altocor, Altoprev), pitavastatin (Livalo, Pitava), pravastatin (Pravachol, Selektine, Lipostat), rosuvastatin (Crestor) and simvastatin (Zocor, Lipex) [4,5]. On average, statins can lower LDL cholesterol (so-called "bad cholesterol") by 1.8 mmol/l (70 mg/dl), which translates into a 60% decrease in the number of cardiac events (heart attack, sudden cardiac death) and a 17% reduced risk of stroke after longterm treatment [6]. They have less effect than the fibrates or niacin in reducing triglycerides and raising HDL-cholesterol ("good cholesterol"). Clinical practice guidelines generally recommend that the patient has tried "lifestyle modification", including a cholesterol-lowering diet and physical exercise, before statin use is considered; statins or other pharmacologic agents may then be recommended for patients who do not meet their lipid-lowering goals through diet and lifestyle approaches [7,8].

Mechanism of action
Statins act by competitively inhibiting HMG-CoA reductase,the first committed enzyme of the HMG-CoA reductase pathway. HMG-CoA reductase inhibitors are a group of prescription drugs used to lower cholesterol, a white waxy substance that can stick to the inside of blood vessels, resulting in clogged arteries, heart disease, and strokes [5]. These medicines work by slowing down the body's ability to make cholesterol. Because statins are similar to HMG-CoA on a molecular level they take the place of HMG-CoA in the enzyme and reduce the rate by which it is able to produce mevalonate [11], the next molecule in the cascade that eventually produces cholesterol, as well as a number of other compounds. This ultimately reduces cholesterol via several mechanisms.

Discussion
Cholesterol has been singled out as the primary factor in the development of atherosclerosis. HDL is regarded as one of the most important protective factors against arteriosclerosis. HDL's protective function has been attributed to its active participation in the reverse transport of cholesterol. Numerous cohort studies and clinical trials have confirmed the association between a low HDL and an increased risk of coronary heart disease [20,21]. The concentration of LDL correlates positively whereas HDL correlates inversely to the development of coronary heart disease. Smokers have significantly higher serum cholesterol, triglyceride, and LDL levels, but HDL is lower in smokers than in non-smokers. Evidence suggests that oxidatively modified LDL contribute to the pathogenesis of atherosclerosis. Increased oxidative stress and the generation of the free oxygen radicals can result in modification of LDL to oxidized LDL that could lead to atherosclerotic lesions[20].

CK and more particularly its isoenzyme CK-MB still have a formal place in defining myocardial infarction. These enzymes normally exist in cellular compartment and leak out into the plasma during myocardial injury due to disintegration of contractile elements and sarcoplasmic reticulum . An elevated apolipoprotein B–apolipoprotein A-I (apo B–apo A-I) ratio is a risk factor for future coronary artery disease (CAD). 

It is not known whether this ratio is better than traditional lipid values for risk assessment and prediction and whether it adds predictive value to the Framingham risk score. Several mechanisms have been proposed to explain the relationship between Lp(a) and heart disease. Apo(a) has a sticky adhesive nature, making it easy to attach LDL, calcium and other components into an a atherosclerotic plaque on the blood vessel wall (endothelium). Lp(a) has been associated with endothelial dysfunction as well. Due to its structural similarity with plasminogen, Lp(a) competes for binding with fibrin, thereby inhibiting the breakdown of fibrin. This action could promote blood clot formation. Finally, Lp(a) activates immune cells including monocytes and macrophages, and could induce inflammation. All of these effects help to induce plaque formation, and to promote clot formation after the plaque is ruptured. Apparently, Lp(a) is attracted to the artery wall by means of Lysine Binding Sites that become exposed when the endothelial wall is damaged[21].

Conclusion
Rosuvastatin and Atrovastatin can be more effective in reducing hyperlipidemia compared to other classes of statin drugs and thus further reduce the risk of cardiovascular disease in such patients.In addition to that,Rosuvasatin had less side effects in patients as compared to atrovastatin and can be defined as the most effective among the statin class of drugs.(paper代写)

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