To keep it simple, bring the LDL down to the HDL level. Keep the triglycerides below 150 mg/dL. To prevent heart disease, an ideal strategy would be to get LDL to <100 mg/dL for everybody. Non-HDL and TG should be lowered below 150 mg/dL.

One reason for measuring hs-CRP would be when one is undecided whether to start statin therapy or not. CRP levels should also be preferably measured in the ageing Indian population (age 40+ for men and 50+ for women), regardless of other factors. In case of a slightly overweight Indian patient, hs-CRP should be measured to see if it is elevated and then statin therapy should be used. If a patient is pre-diabetic or hypertensive, then hs-CRP levels would be useful to decide treatment. If a patient with cardiovascular disease is to be treated, then measuring CRP would help to decide the strategies for maximum cholesterol reduction. Hence, hs-CRP should be checked and attempts be made to get it below 1.

The US National Health Association recommends performing liver function tests prior to initiation of statin therapy. However, it is not really necessary to monitor periodically, especially for lower doses like 5 and 10 mg, which do not increase risk of liver dysfunction vs. placebo. As per prescribing information of statins, liver function should be monitored at three or six months and thereafter once a year. However, liver enzymes might be elevated in people with diabetes and metabolic syndrome with fatty liver. In such cases, it may be erroneously thought that statins are responsible for the elevated liver enzymes. But in reality, statins help in reducing cardiovascular risk in these patients. Hence, one would recommend liver function testing at baseline and once subsequently during long term statin therapy.

Screening for Apo A alone will not be of much help. High risk patients should be screened for Apo B if the facility is available. It may be useful to measure Apo B/ Apo A ratio in India. Apo B is a good marker in patients with high TG (> 150 mg/dL). The ADA-ACC guideline recommends Apo B <80 for patients with diabetes and CVD and <90 for non-diabetics with CVD.

At least total cholesterol levels should be assessed before starting treatment with statins. If a patient has diabetes or CVD then statin therapy can be initiated without determining lipid levels. However, cholesterol levels should be preferably determined before initiation of statin therapy.

This strategy will not work because once LDL is brought down using a particular dose and then if that dose is lowered, then LDL levels would increase again. Hence, the dose has to be maintained at the dose at which LDL goal was achieved.

If there is a lifetime risk issue and lowering LDL in young adults will give substantial benefits, then statin therapy can be started. Thus, in case of a patient with very high LDL of above 190 mg/dL along with family history of hypercholesterolemia or presence of diabetes, the earlier statin therapy is started, the greater will be the long term benefits.

The 20 mg dose was chosen more for commercial reasons. The generic statin manufacturers in the United States do not have the 20 mg strength. The financial aspect is that, when 100 million dollars or more is being spent on a study, then a dose that cannot be matched by a generic drug will be preferred.

There was no relationship between reduction in LDL and CRP.

The starting dose should be 5 mg for Indian patients as people are smaller. A 10 mg starting dose can be used for larger people. If one compares the LDL lowering effect of rosuvastatin and atorvastatin, 10 mg of rosuvastatin is slightly better than 20 mg of atorvastatin and 20 mg of rosuvastatin is better than 40 mg of atorvastatin. Thus, rosuvastatin is better than double the atorvastatin dose.

Another important point is that HDL increase is better with rosuvastatin. The HDL increase is about 10% with rosuvastatin vs. 5% with atorvastatin. So, we get double LDL lowering and HDL raising effects along with better tolerability with rosuvastatin as compared to atorvastatin.

Reaching the LDL goal is very important in reducing risk. In ACS patients, atorvastatin may have drug interactions leading to adverse effects. Hence, it would be fine to use rosuvastatin in ACS patients because it is as effective as atorvastatin but with greater LDL reduction.

Type I diabetics with coronary disease have good survival rates with insulin therapy. There is no evidence with statins in type I diabetes but preferably young patients should be put on statin therapy. Since these patients are at high risk, the target LDL should be <70 mg/dL.

The CORONA study which included patients with ischemic cardiomyopathy showed a reduction in CV events with statin therapy but mortality was not reduced. The efficacy will depend on severity of disease. In case of severe, end stage heart failure patients, statin therapy will not work; in fact nothing but heart transplant would work in such patients. If a patient has moderate ischemic cardiomyopathy, then statins could be used. If doctors think that the myocardium can be salvaged, then they can use statins at their discretion.

Rosuvastatin is not officially approved for aortic stenosis. The clinical benefits of statins in aortic stenosis are due to their pleiotropic effects viz. endothelial function and anti-inflammatory effects. A prospective study (Rosuvastatin Affecting Aortic Valve Endothelium [RAAVE]) treating hypercholesteremic patients with rosuvastatin, found a significantly slower rate of progression of calcified aortic stenosis as compared to patients with normal cholesterol levels who were not treated with rosuvastatin. Another study showed that treatment of aortic stenosis with rosuvastatin by targeting serum LDL levels slowed the hemodynamic progression of aortic stenosis.

The JUPITER trial did suggest a favorable effect on the microcirculation with rosuvastatin.

The CORONA study which was done on patients with heart failure showed that, in late stage heart failure, rosuvastatin showed no benefits in reducing mortality unless patients had ischemia.

One should use lower doses of statins in elderly. One of the benefits of rosuvastatin is that it is highly potent. 10 mg of rosuvastatin is equal to 80 mg of simvastatin and 40 mg of atorvastatin. The beauty of this molecule is that even with low doses you get good efficacy as well as safety in elderly patients with severe heart failure. A low dose of rosuvastatin may reduce cardiovascular events in such patients. However, for someone who has a bad prognosis and poor life expectancy, the drug won't help in prolonging life. On the other hand, if we have a healthy 90 year old patient who is at high risk of stroke and death, then therapy should not be withheld. Age is a relative parameter and the decision to prescribe a statin should be based on the patient's overall health. Appropriate clinical judgment has to be used

Statins are contraindicated in pregnant women or women who may become pregnant. This is because HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol and hence cause fetal harm when administered to pregnant women. If the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus and the lack of known clinical benefit with continued use during pregnancy.

In case of low HDL, LDL should be brought down to very low levels. The approach could be to get the LDL level equal to HDL i.e., if HDL is 30 then LDL should be brought down to 30. Niacin may be administered to increase HDL and fenofibrate to lower TG but LDL should be lowered to as low a level as possible. Rosuvastatin is a great option since it can lower LDL by about 50% at the starting dose. Ezetimibe too may be co-administered to raise HDL levels. People with low HDL levels have been seen to be at reduced risk of developing CVD if they also have very low LDL levels.

Due to the long half life of rosuvastatin (18-19 hours) vs. other statins, it can be administered at any time of day, with or without food.

Rosuvastatin exposure is not influenced by mild to moderate renal impairment (CL _cr >/= 30 mL/min/1.73 m ²); however, exposure to rosuvastatin is increased to a clinically significant extent in patients with severe renal impairment who are not receiving hemodialysis. Rosuvastatin dosing should be adjusted in patients with severe renal impairment (CL _cr < 30 mL/min/1.73 m ²) not requiring hemodialysis.

This is actually a class effect. There is a strong belief that statins have pleiotropic benefits. However, it is important to remember that it is primarily reduction in LDL levels that determine the benefits of statins. The right way is to target statin therapy to reach a specific LDL goal.

These benefits should not take us away from the most important objective of getting the LDL as low as possible, to reduce risk in patients.

There is no dose-related phenomenon; it is primarily the LDL lowering effect. The most important point is to lower LDL, other risk factors and achieve lipid targets in patients.

Cardiovascular disease is common in patients with COPD and COPD has an adverse effect on survival in patients with coronary artery disease. Statins have been shown to be beneficial in reducing cardiovascular morbidity and mortality. These benefits are mediated by their pleiotropic benefits. Due to an inflammatory component being present in COPD, anti-inflammatory effects of statins may play a significant role in reducing cardiovascular events in these patients. A retrospective analysis of 854 patients with COPD exacerbations (118 statin users vs. 736 non-statin users) revealed that statin use was associated with a significant 43% reduction in mortality. These benefits with statins were significant irrespective of the presence or absence of heart disease. Another retrospective analysis done in COPD patients showed that statins significantly reduced the risk of COPD hospitalization, total mortality and composite of MI or death in steroid users as well as non steroid users.

There are better drugs that can be used in DVT, especially in hospitalized patients. However, if patients have a history of DVT or Pulmonary embolism or genetic factors like factor V, then use of statins can be considered.

The efficacy of statins for plaque stabilization is mainly due to their lipid lowering effects. Rosuvastatin is the most potent statin in improving lipid levels. However, there are no studies involving direct comparison of statins for plaque stabilization. The ASTEROID and METEOR trial showed that rosuvastatin 40 mg/day for 2 years significantly reduces the progression of atherosclerosis.

Rosuvastatin is a better statin than atorvastatin. Hence, if cost is not an issue, then rosuvastatin is the best option. However, if a patient taking atorvastatin is doing well then he should be continued on the same therapy.

Omega-3-fatty acid is superior to rosuvastatin in reduction of triglyceride levels, but it causes excessive elevation of LDL-C and may also increase non-HDL-C. Hence, it is only indicated to reduce triglyceride (TG) levels in adult patients with very high (>500 mg/dL) triglyceride levels.

If the LDL is at goal, then there is no reason to switch. But, if HDL is low, LDL is higher than target levels or if CRP is still high then patients may be switched to rosuvastatin. If the lipid goals are not met with atorvastatin, then the patient should be switched to rosuvastatin.

In case of fatty liver, lower doses should be administered. Rosuvastatin is a preferable drug for fatty liver as lower doses with good safety can be used. If liver enzymes increase to double the baseline level, then statin therapy should be reduced or stopped.

A couple of cases of kidney failure were observed with rosuvastatin 80 mg during the pre- approval stages. No data was available regarding other concomitant therapies in those patients. Now we have six years of clinical experience with rosuvastatin and thousands of patients have participated in rosuvastatin trials. In these trials, the rate of kidney failure was lower than placebo. Thus, good safety data is available with respect to kidney function and rosuvastatin.

The AURORA study done in patients with renal failure showed that rosuvastatin did not have any adverse effects on muscle toxicity in this population. This implies that rosuvastatin is a safe drug to use, in appropriate doses, in patients with renal insufficiency. Preferably, therapy should be started with 5 mg and then up-titrated to 10 mg or 20 mg depending on goal attainment.

One study suggested a very small increased risk of developing diabetes with statins but there is a belief that it is not related to statin therapy. The most important point is that statins profoundly decrease death in diabetes patients due to reduction in cardiovascular events. The ADA recommends all diabetic patients to be on statin therapy. Hence all diabetics should be on statins and any slight increased risk of diabetes would be offset by the overall benefits that statins provide to this patient population.

Dose lowering of rosuvastatin to alternate day dosing or even once-a-week dosing is very effective. Ezetimibe can be administered on alternate days. The data on Coenzyme Q10 to manage statin intolerance is not very compelling.

Statin therapy should be considered in such a case. If liver enzymes increase to double the baseline level, statins should be stopped. These patients are at a high risk of cardiovascular events. Hence, it is important to attain the LDL target in this patient. Low dose rosuvastatin would be appropriate for the same.

If the patient has hyperthyroidism then her LDL levels should be checked, because LDL levels go down in such cases. After 6 months, LDL levels should be checked again. If LDL levels are still high, then statin therapy may be started.

Both, statins and ACE inhibitors are cardiovascular risk modifying therapies. So, in case of diabetes, ACE inhibitors and statins can together provide renal and cardiovascular event prevention.

Rosuvastatin is not extensively metabolized; approximately 10% of radio-labeled dose is recovered as metabolite. Drugs like verapamil, amiodarone, diltiazem and erythromycin are microsomal enzyme inhibitors and drugs like phenytoin, rifampicin and efavirenz are microsomal enzyme inducers. No clinically significant interactions have been found with rosuvastatin and these drugs.

Firstly, statin therapy should be maximized. If LDL is still high, then ezetimibe should be added. If TG is high, fenofibrate should be added and if HDL is low, then niacin should be added. Ezetimibe in conjunction with statins is useful for LDL reduction. There are tolerability issues with niacin and glucose levels need to be monitored. Fenofibrate can also be given with statins but it may raise homocysteine and creatinine. Hence, all these factors have to be considered when using combination therapy in risk management.

The risk of skeletal muscle effects may be enhanced when rosuvastatin is used in combination with niacin. Hence, a reduction in dose should be considered.

Yes, Ezetimibe and fenofibrate reduce levels of hs-CRP.