CRESTOR (Rosuvastatin) belongs to a group of drugs called HMG-CoA reductase inhibitors (also known as statins). HMG-CoA reductase is an enzyme involved in the regulation of lipids in the body. CRESTOR (Rosuvastatin) is usually used along with changes to diet and exercise to reduce the levels of lipids in the blood. If high lipid levels are left untreated, they can build up in the walls of the vessels carrying blood around the body which, over time, can lead to narrowing of these vessels. This disease is called atherosclerosis and is one of the most common causes of heart disease. CRESTOR (Rosuvastatin) belongs to a group of drugs called HMG-CoA reductase inhibitors (also known as statins).
Crestor side effects rarely can occur. Contact your doctor right away if you have any of the following Crestor side effects:
CRESTOR, a once-daily oral tablet, works by inhibiting HMG-CoA reductase: an enzyme that is crucial for cholesterol synthesis. By inhibiting this enzyme less cholesterol is synthesised in the liver - which is where most of the body’s cholesterol is produced. This in turn leads to a reduction in the amount of cholesterol in the blood. Although the structures of all statins are broadly similar and they all act at the same enzyme, CRESTOR offers important advantages over other currently available statins: Clinical studies show that CRESTOR is significantly more effective at reducing LDL-cholesterol than the same and even some higher doeses of atorvastatin, simvastatin or pravastatin. CRESTOR 10mg gets significantly more patients to their European LDL-cholesterol goal than Lipitor (atorvastatin) 10mg (88% vs 76% respectively). CRESTOR 10mg gets significantly more patients to their US NCEP ATP III LDL-cholesterol goal than both atorvastatin 10mg (80% vs 63% respectively) and Lipitor (atorvastatin) 20mg. CRESTOR produces a significant increase in HDL-cholesterol which is maintained across the dose range. Risk factors for the development and progression of cardiovascular disease include abnormal plasma lipid levels (high levels of low density lipoprotein cholesterol [LDL-C] or triglycerides [TG], and low levels of high density lipoprotein cholesterol [HDL-C]) , obesity, hypertension, impaired glucose tolerance and smoking. These modifiable risk factors often exist together and may also be associated with non-modifiable risk factors such as family history, age, gender and ethnic group. Epidemiological studies have established that elevated LDL-C is the major lipid risk factor associated with the development and progression of cardiovascular disease, and as a consequence it is now considered to be the principal target of therapeutic intervention. In addition to LDL-C, HDL-C and triglycerides, the role of other lipid parameters in cardiovascular disease is also attracting interest. For example, assessment of the apolipoprotein ApoB/ApoA-I ratio and non HDL-C levels provide further indications of total atherogenic risk.
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