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 Table of Contents  
Year : 2016  |  Volume : 5  |  Issue : 2  |  Page : 51-61

Lipid Association of India Expert Consensus Statement on Management of Dyslipidemia in Indians 2016: Part 1 - Executive summary

1 Department of Cardiology, Manipal Hospital, Bengaluru, Karnataka, India
2 Department of Cardiology, Indraprastha Apollo Hospitals, New Delhi, India
3 SNN Specialties Clinic, Chennai, Tamil Nadu, India

Date of Web Publication18-Jul-2016

Correspondence Address:
Raman Puri
Lipid Association of India, A -26, 2nd Floor, South Extension Part-2, New Delhi - 110 049
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2250-3528.186492

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How to cite this article:
Iyengar SS, Puri R, Narasingan S N. Lipid Association of India Expert Consensus Statement on Management of Dyslipidemia in Indians 2016: Part 1 - Executive summary. J Clin Prev Cardiol 2016;5:51-61

How to cite this URL:
Iyengar SS, Puri R, Narasingan S N. Lipid Association of India Expert Consensus Statement on Management of Dyslipidemia in Indians 2016: Part 1 - Executive summary. J Clin Prev Cardiol [serial online] 2016 [cited 2023 Mar 29];5:51-61. Available from: https://www.jcpconline.org/text.asp?2016/5/2/51/186492

The burden of atherosclerotic cardiovascular disease (ASCVD) in India is alarmingly high and is a cause of concern. Indians are not only at high risk of developing ASCVD but also get the disease at an early age, have a more severe form of the disease, and have poorer outcomes compared with Western populations. Access to health care is also not optimal in India, and the treatment of ASCVD remains expensive. For all these reasons, prevention of ASCVD should take priority, not only from the perspective of governmental agencies and health care providers but also from the perspective of all Indians.

There are many modifiable risk factors for ASCVD. Of these, dyslipidemia has the highest population attributable risk for myocardial infarction (MI), [1] both because of its high prevalence and because of its direct pathogenic association with atherosclerosis. Accordingly, effective management of dyslipidemia remains one of the most important healthcare targets for prevention of ASCVD.

Management of dyslipidemia presents unique challenges in Indians. Not only the prevalence of dyslipidemia is constantly increasing in Indians, particularly at a younger age, but also the pattern of dyslipidemia is distinct compared with Western populations. The distribution and interplay of concomitant ASCVD risk factors and genetic susceptibility are also different. Furthermore, the population awareness about prevention of ASCVD, cultural beliefs, socioeconomic conditions, etc., is also quite different. For these reasons, it is important to formulate policies and guidelines that accommodate these differences and propose recommendations that are best suited for our conditions. To meet this objective, the Lipid Association of India (LAI) has undertaken the task to develop a consensus document on management of dyslipidemia in Indians. This consensus document is divided into two parts: Part 1 deals with all common issues related to lipid management encountered during routine clinical practice and Part 2 deals with management of dyslipidemia in special patient populations such as those with acute coronary syndrome, familial dyslipidemias, and chronic kidney disease. Part 1 of the consensus document has already been published in the March supplement issue of the Journal of the Association of Physicians of India. [2] Part 2 of the consensus document is currently under development and will be released shortly. The present report provides an execute summary of Part 1 of the consensus document. The readers interested in detailed discussion about various aspects of lipid management in Indians are encouraged to refer the full-length document published in the Journal of the Association of Physicians of India. [2]

  Methodology Top

LAI initiated the process of developing this consensus document during the early part of 2014. Leading experts from various specialties including Internal Medicine, Cardiology, Endocrinology, Nephrology, Neurology, Pharmacology, and Vascular Surgery were invited to participate in this process. A series of regional meetings were held with these experts in different parts of the country. The first meeting was held in Delhi on April 12, 2014, and subsequent meetings were held at Bengaluru (April 2014), Delhi (April 2014 and July 2015), Mumbai (May 2015), Kolkata (May 2015), Chennai (June 2015), and finally at Lucknow (Aug 2015). In all, there were eight meetings with 153 experts from 18 states and thirty cities of India. Each of these meetings followed a standard format. First, the key issues related to lipid management in Indians were presented to the entire group in the form of lectures, which were then followed by extensive discussion among experts on these topics. At the end of the discussion, a questionnaire covering all relevant topics was administered to all the participating experts to collect their responses about each specific aspect of lipid management in Indians. The proceedings of these meetings were video recorded for future reference.

Apart from these meetings, a questionnaire was also sent to experts who could not attend the meetings.

The information thus collected through the questionnaires was collated and summarized, and the key findings were then further discussed among the members of the core expert group. After this final round of discussion, the expert panel prepared the final document, considering the following main objectives:

  • To ensure that the document remained simple yet scientifically robust
  • To be more informative rather than prescriptive
  • To maximally utilize the available Indian data
  • To make all the efforts to ensure practical applicability of the recommendations to the Indian population.
However, while every effort has been made to ensure that the recommendations presented in this document are based on the most update scientific evidence, it is important to remember that "Medicine is a constantly evolving field, and we often have to deal with moving targets. The recommendations made in the consensus statement are not a mandate to the medical community. Keeping patient's well-being uppermost in mind, clinicians should use their judgment and experience in applying these recommendations to their patients."

  Key Messages and Summary of Recommendations Top

Epidemiology of dyslipidemia in India

  • Although data are sparse, the available evidence suggests that the cholesterol levels are steadily rising among Indians, a trend which is opposite to what is observed in the Western populations
  • Compared with the Western populations, Indians tend to have higher triglyceride (TG) levels and lower high-density lipoprotein cholesterol (HDL-C) levels but the total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels are generally lower
  • Among various lipid markers, the ratio of apolipoprotein B to apolipoprotein A-I appears to be the best indicator of ASCVD risk.
Atherosclerotic cardiovascular disease risk stratification in Indians

The recommended approach to ASCVD risk assessment in Indians is outlined in [Figure 1] and the different ASCVD risk categories are summarized in [Table 1].
Figure 1: Recommended approach to atherosclerotic cardiovascular disease risk stratification in Indians. ASCVD: Atherosclerotic cardiovascular disease; CKD: Chronic kidney disease; HDL-C: High-density lipoprotein cholesterol; IMT: Intima-media thickness

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Table 1: Atherosclerotic cardiovascular disease risk categories

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Preexisting ASCVD may be in the form of any of the following:

  • History of MI or documented coronary artery disease (CAD)
  • History of ischemic stroke or transient ischemic attack or hemodynamically significant carotid plaque
  • Atherosclerotic peripheral arterial disease (includes ankle-brachial index <0.9)
  • Atherosclerotic aortic aneurysms
  • Atherosclerotic renal artery stenosis.
Lifetime ASCVD risk should be estimated in all individuals who are considered to have low 10-year ASCVD risk. [3] If the absolute lifetime risk is 30-44%, it is considered moderately high, and if it is >45%, it is considered high. [4] The individuals who have moderately high or high lifetime ASCVD risk should be treated on par with those who have moderate 10-year ASCVD risk. A number of different risk algorithms are available for estimation of lifetime ASCVD risk. These include the Joint British Societies' 3 rd Iteration (JBS3) risk calculator (which is based on QRISK lifetime risk model, http://www.qrisk.org/lifetime/), the recently proposed American College of Cardiology/American Heart Association Pooled Cohort Equations, [3] and the Lloyd-Jones/Framingham risk algorithm. [5] Although none of these has been validated in Indians, JBS3 risk calculator appears to be the most suitable and should be preferred for this purpose. The risk calculator can be accessed at www.jbs3risk.com.

Nonconventional cardiovascular risk factors

  • There is robust evidence to support prognostic value of coronary artery calcium (CAC) for ASCVD risk assessment. However, its cost, relatively limited availability, and radiation exposure are major limitations to its wider use. It is, therefore, recommended as an optional tool for ASCVD risk assessment in individuals at low- to moderate-risk. A CAC score >300 Agatston units indicates high ASCVD risk
  • Compared with CAC, carotid intima media thickness is simpler to perform, more widely available, and completely safe, but its accuracy for ASCVD risk prediction is inferior to that of CAC
  • Aortic pulse wave velocity (PWV) is a measure of arterial stiffness which is primarily a marker of arteriosclerosis. Measurement of aortic PWV is most useful in hypertensive subjects
  • Although there is enough evidence to support value of high sensitivity C-reactive protein as an ASCVD risk marker, its routine use in Indians is not recommended due to issues related to standardization of assays and the high prevalence of infectious diseases in our country
  • Lipoprotein (a) [Lp(a)] appears to be an important marker for ASCVD risk in Indians, particularly in those with family history of premature CAD. Lp(a) value of >20 mg/dL indicates increased ASCVD risk in Indians. Only those assays that are not influenced by Lp(a) isoform size should be used for its estimation
  • Homocysteine estimation is not recommended in asymptomatic individuals
  • Obesity and metabolic syndrome are associated with significantly increased risk of diabetes in the short-term and increased risk of ASCVD in the long-term.
The approach to integration of these nonconventional risk factors in the overall ASCVD risk stratification is discussed in the preceding section on "ASCVD risk stratification."

Treatment goals and thresholds for initiation of statin therapy according to the estimated atherosclerotic cardiovascular disease risk

[Table 2] outlines the recommended treatment goals and thresholds for initiation of statin therapy in various risk categories. It should be noted that therapeutic lifestyle change is recommended in all individuals who have LDL-C or non-HDL-C values above the desired goals, and preferably in everyone regardless of their cholesterol levels.
Table 2: Treatment goals and statin initiation thresholds according to atherosclerotic cardiovascular disease risk categories

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Low-density lipoprotein cholesterol as the therapeutic target: Is lower the better?

  • Given the epidemiological association of LDL-C levels with ASCVD risk and the evidence showing reduction in such risk with LDL-C lowering, LDL-C remains the primary target for lipid-lowering therapy
  • LDL-C lowering to a low level is essential to achieve the desired reduction in the risk of vascular disease. In those with elevated levels of ASCVD risk, lower LDL-C levels are associated with better outcomes
  • Various imaging trials and meta-analysis have shown that more aggressive lowering of LDL-C level to 50 mg/dL or less results in significant reduction in atheroma volume and ASCVD events
  • The available evidence also shows that LDL-C level <50 mg/dL is safe.
Nonhigh-density lipoprotein cholesterol: Should it be the primary target for lipid-lowering therapy?

  • Non-HDL-C, which is equal to total cholesterol - HDL-C, includes all atherogenic lipoproteins in blood [Figure 2] and is, therefore, a more accurate predictor of ASCVD risk, particularly in patients who have elevated TG levels (e.g., diabetics, obese persons, those with metabolic syndrome) and those already on statin therapy
    Figure 2: Various plasma lipoproteins. Apo A: Apolipoprotein A; Apo B: Apolipoprotein B; HDL: High-density lipoprotein; HDL-C: High-density lipoprotein cholesterol; IDL: Intermediate-density lipoprotein; LDL: Low-density lipoprotein; LDL-C: Low-density lipoprotein cholesterol; Lp (a): Lipoprotein (a); TG: Triglyceride; VLDL: Very low-density lipoprotein

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  • LAI recommends non-HDL-C as a co-primary target, as important as LDL-C, for lipid-lowering therapy
  • Monitoring of non-HDL-C will provide a simple, practical tool for treatment decisions relating to lipid-lowering therapy since it does not require a fasting blood sample and takes care of both LDL-C and TG targets
  • Non-HDL-C also covers, to some extent, the excess ASCVD risk imparted by the small, dense form of LDL, which is significantly more atherogenic than the normal large buoyant particles. Unfortunately, LDL-C levels do not provide any information about the LDL particle size but an elevated non-HDL-C, being a surrogate for elevated TG, indirectly suggests greater proportion of the small, dense variety of LDL particles
  • In all individuals, the non-HDL-C level should be kept within 30 mg/dL of LDL-C levels
  • Statins remain the first-line agent for lipid-lowering, regardless of whether LDL-C is the target for therapy or non-HDL-C
  • Increasing the dosage of statin or switching to a more potent statin and intensifying lifestyle measures should be the first step to achieve further non-HDL-C lowering when LDL-C target has already been reached. Correction of secondary causes of hypertriglyceridemia and adding a nonstatin drug such as ezetimibe, fibrate, etc., should be considered when above measures prove inadequate.
Relevance of high triglyceride levels

  • Elevated TG is associated with increased risk of ASCVD, independent of LDL-C levels. A combination of high TG and LDL-C imparts even greater risk
  • High TG is often accompanied by low HDL-C levels and increased proportion of small, dense LDL-C, a pattern known as atherogenic dyslipidemia
  • It is advisable to maintain TG level <150 mg/dL and preferably <100 mg/dL
  • In all patients with hypertriglyceridemia, intensification of lifestyle modification should be the first step, which can reduce TG by as much as 50%
  • It is also important to rule out secondary causes of hypertriglyceridemia and correct them. Common secondary causes of hypertriglyceridemia include:

    • Diabetes
    • Hypothyroidism
    • Nephrotic syndrome
    • Chronic renal failure
    • Obstructive liver disease
    • Drugs such as steroids, beta-blockers, protease inhibitors for treatment of human immune deficiency virus infections.
  • Unless TG is very high (>500 mg/dL), statin should be the first drug to be prescribed in all patients requiring lipid-lowering therapy. Routine addition of a fibrate or another nonstatin drug must be avoided
  • Only when TG is not sufficiently lowered with above measures, a nonstatin drug should be added
  • Currently, fibrates are recommended for use in the treatment of severe hypertriglyceridemia (TG >500 mg/dL) and as an add-on to statin in combined dyslipidemia (when not corrected with statins alone)
  • In diabetic subjects, saroglitazar, which is a dual peroxisome proliferator-activated receptor-α/g agonist, is another option. It has been approved by the Drug Controller General of India for the treatment of diabetic dyslipidemia, not corrected with statin therapy alone. However, large-scale CV outcomes studies are needed to clearly establish the role of saroglitazar in the management of dyslipidemia.

High-density lipoprotein cholesterol as a therapeutic target

  • Low HDL-C is an independent risk factor for ASCVD. It becomes even more relevant when LDL-C is not elevated
  • Lifestyle modification plays an important role in raising HDL-C
  • Among pharmacological agents, statins remain mainstay in the treatment of low HDL-C also. Although several other agents have been tried specifically for raising HDL-C, none of them has been shown to result in clinical benefit.
Overall approach to primary prevention of atherosclerotic cardiovascular disease

  • Primary prevention of ASCVD should occupy the prime place in clinical practice
  • Screen for ASCVD - all adults at 20 years of age/college entry
  • Primary prevention should focus on controlling modifiable risk factors for ASCVD. While there are many conventional and nonconventional modifiable risk factors for ASCVD, the most robust are diabetes, tobacco use, high blood pressure (BP), lipid abnormalities, and obesity. Less often and in selected situations, one may look for the novel risk factors or markers of subclinical atherosclerosis for ASCVD risk assessment and management. In addition, one must also be aware of the disease conditions and drugs that may cause secondary dyslipidemia [Table 3]
    Table 3: Drugs and disease conditions that may cause secondary dyslipidemia

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  • Assess ASCVD risk and discuss the health program with the individual
  • Follow the "magnificent seven:"

    • No tobacco
    • Physical activity: ≥150 min moderate-intensity or equivalent exercise per week
    • Body mass index <23 kg/m 2
    • Healthy diet: Achieving at least four of the five important dietary components, focusing on fruits and vegetables, fish, fiber, and sodium intake and sweetened beverage intake
    • LDL-C level should be below 100 mg/dL
    • BP: <120/80 mmHg
    • Fasting plasma glucose level: <100 mg/dL.
  • Stains are safe and effective in both primary and secondary prevention of ASCVD. Their use for primary prevention of ASCVD should be guided by the estimated ASCVD risk in a given individual.
Therapeutic lifestyle changes

Physical activity for adults

  • All adults should avoid inactivity
  • For substantial health benefits, adults should do at least 150 min (2 h and 30 min) a week of moderate-intensity, or 75 min (1 h and 15 min) a week of vigorous-intensity aerobic physical activity, or an equivalent combination of moderate- and vigorous-intensity aerobic activity. Aerobic activity should be performed in episodes of at least 10 min, and preferably, it should be spread throughout the week
  • For additional and more extensive health benefits, adults should increase their aerobic physical activity to 300 min (5 h) a week of moderate-intensity, or 150 min (2 h 30 min) a week of vigorous-intensity aerobic physical activity, or an equivalent combination of moderate- and vigorous-intensity activity. Additional health benefits are gained by engaging in physical activity beyond this amount
  • Adults should also do muscle-strengthening activities that are moderate- or high-intensity and involve all major muscle groups on 2 or more days a week. However, time spent in muscle-strengthening activities does not count toward the aerobic activity guidelines.


  • Dietary patterns are more significant rather than individual dietary components. Thus, we recommend the adoption of a dietary pattern that emphasizes intake of vegetables, fruits, and whole grains, low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, nuts, etc.
  • Limit intake of sweets, sugar-sweetened beverages, and red meat
  • This above can be achieved by adopting a diet pattern such as Mediterranean or Indo-Mediterranean diet.

  • Alcohol intake, even in moderation should preferably be avoided by Indians
  • Patients with ASCVD who do not consume alcohol should not be encouraged to start regular drinking
  • However, for patients who drink, alcohol should not exceed 1 drink per day for women or up to 2 drinks per day for men (1 drink = 12 oz beer, 5 oz wine, or 1.5 oz distilled spirits).
Tobacco products

  • Complete abstinence from tobacco products is recommended. Avoid passive smoking as well.
Stress management

  • Although no clear, large-scale studies are available with different forms of practice, we recommend that all Indians should be encouraged to incorporate yogasana and meditation in daily life.
Usage of statins for lipid management

Of all the lipid-lowering drugs currently available, statins are the drugs of choice because of because of their profound ability to reduced ASCVD risk in wide variety of patient populations. [6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16] The net effect of statins on lipid profile is roughly 25-55% reduction in LDL-C, 15-51% reduction in non-HDL-C, 7-30% reduction in TG, and approximately 5-15% increase in HDL-C. Apart from these lipid-modifying actions, statins also have numerous pleiotropic effects that help minimize risk of vascular events.

Initiation of statin therapy

• The clinical benefit of statins depends primarily on the extent of LDL-C reduction and not on the type of statin used

• The type of statin and dose to be used should be based on the degree of LDL-C reduction that is required to reach the target LDL-C in a given patient

• The expected magnitude of LDL-C reduction with the different dosages of commonly used statins is provided below:

o >50% reduction from baseline (i.e., high-intensity therapy)

§ Rosuvastatin 20-40 mg/day

§ Atorvastatin 40-80 mg/day.

o 30 to <50% reduction from baseline (i.e., moderate-intensity therapy)

§ Rosuvastatin 5-10 mg/day

§ Atorvastatin 10-20 mg/day

§ Simvastatin 20-40 mg/day

§ Pitavastatin 2-4 mg/day

§ Pravastatin 40-80 mg/day

§§ Lovastatin 40 mg/day.

· At least moderate- or high-intensity statin therapy is required to bring about a clinically meaningful reduction in LDL-C in most patients.

Statin intolerance

Statin and muscle-related side effects

  • Its true frequency is unknown; however, reported incidence is around 10%
  • Routine monitoring is not needed
  • When patients present with symptoms, check serum creatine kinase level and rule out drug-drug interactions, Vitamin D deficiency, hypothyroidism, and other potential causes of statin-induced myopathy. Treatment options include using statin treatment in lower doses, reduced frequency or use of alternative statins.
Statin and liver

  • An asymptomatic rise in hepatic enzyme activity is one of the most common adverse effects of statin therapy but the incidence of elevated aminotransferase activity >3 times upper limit of normal is still no >3%. Hepatitis, cholestasis, and acute liver failure are extremely rare
  • In patients with nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH), statin treatment is safe and substantially reduces ASCVD risk by a greater margin than in those with normal liver function. In fact, statins may even contribute to the resolution of NAFLD/NASH.
Statin and new onset diabetes

  • Although statins are associated with an increase in the risk of new-onset diabetes, this risk is significantly outweighed by the benefits
  • The risk is greater with intensive statin therapy and in patients already predisposed to develop diabetes
  • Patients with risk factors for diabetes mellitus should be screened with fasting blood glucose or glycosylated hemoglobin, ideally before starting statin therapy. Thereafter, monitoring should be repeated within 1 year of initiation and at intervals no longer than 3 years
  • Aggressive lifestyle management is very important in preventing development of diabetes in patients receiving statin therapy.
Statin and neurological side effects

  • A very small relationship exists between statin therapy and hemorrhagic stroke, mainly in patients who have had a previous hemorrhagic stroke and who have poorly controlled BP. However, this risk is generally outweighed by the reduction in ischemic stroke with statins
  • There is no definitive evidence to suggest that statins lead to cognitive impairment or peripheral neuropathy
  • If a patient presents with symptoms suggestive of cognitive impairment or peripheral neuropathy and no alternate etiology is found, statins may have to be withdrawn temporarily.
Statin and cancers

  • Statin therapy had no effect on the incidence of, or mortality from, any type of cancer (or the aggregate of all cancers).
Approach to management of suspected statin intolerance

A practical approach to management of statin intolerance is provided below:

1. Look for reversible causes:

• Drug interaction

• Hypothyroidism

• Hypovitaminosis D.

2. Reduce the dose of statin or stop it depending on the severity of symptoms:

• With mild symptoms, reduce the dose

• With severe symptoms, stop the statin.

3. Once symptoms disappear, restart statin:

• Reduced dose of same or different statin

• Use statin twice or thrice a week

• Alternatively, use statin with ezetimibe or bile acid sequestrants.

4. If symptoms recur, use nonstatin drugs such as ezetimibe or bile acid sequestrant (e.g., colesevelam)

5. Encourage therapeutic life change to all.

Role of nonstatin drugs in lipid management

  • As already emphasized, LDL-C remains the primary target for lipid-lowering therapy and statins remain the first choice for LDL-C lowering
  • Nonstatin drugs may be used in the following settings:

    • As alternative to statins when the patient is completely statin intolerant
    • In combination with statins when the desired dose of statin cannot be used due to intolerance
    • In combination with statins when serum TG levels remain persistently elevated despite optimum dose of statins, adequate lifestyle modifications, and correction of other treatable causes of hypertriglyceridemia (e.g., uncontrolled diabetes), and
    • As first-line of treatment, before adding a statin, when serum TG levels are very high (>500 mg/dL)
  • Fibrates are the most commonly used nonstatin lipid-lowering agents. Ezetimibe, omega-3 fatty acids, and bile acid sequestrants are other options. Saroglitazar is another new molecule, being used as an add-on to statin therapy for management of diabetic dyslipidemia. Alirocumab and evolocumab are monoclonal antibodies against the enzyme proprotein convertase subtilisin/kexin type 9 and result in profound LDL-C reduction. They are currently approved for the use in patients with heterozygous familial hypercholesterolemia and also in nonfamilial dyslipidemia when LDL-C goal is not achieved with statin alone or if the patient is intolerant to statin.

  References Top

Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet 2004;364:937-52.  Back to cited text no. 1
Iyengar SS, Puri R, Narasingan SN, Wangnoo SK, Mohan V, Mohan JC, et al. Lipid association of India expert consensus statement on management of dyslipidemia in Indians 2016: Part 1. J Assoc Physicians India 2016;64:S7-52.  Back to cited text no. 2
Goff DC Jr., Lloyd-Jones DM, Bennett G, Coady S, D'Agostino RB, Gibbons R, et al. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;129 25 Suppl 2:S49-73.  Back to cited text no. 3
International Atherosclerotic Society Position Paper: Global Recommendations for the Management of Dyslipidemia; 2013. Available from: http://www.Athero.Org/iaspositionpaper.Asp. [Last accessed on 2015 Mar 21].  Back to cited text no. 4
Lloyd-Jones DM, Leip EP, Larson MG, D'Agostino RB, Beiser A, Wilson PW, et al. Prediction of lifetime risk for cardiovascular disease by risk factor burden at 50 years of age. Circulation 2006;113:791-8.  Back to cited text no. 5
Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: The scandinavian simvastatin survival study (4S). Lancet 1994;344:1383-9.  Back to cited text no. 6
Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, MacFarlane PW, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med 1995;333:1301-7.  Back to cited text no. 7
Downs JR, Clearfield M, Weis S, Whitney E, Shapiro DR, Beere PA, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: Results of AFCAPS/TexCAPS. Air Force/Texas Coronary Atherosclerosis Prevention Study. JAMA 1998;279:1615-22.  Back to cited text no. 8
Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial Investigators. N Engl J Med 1996;335:1001-9.  Back to cited text no. 9
Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. N Engl J Med 1998;339:1349-57.  Back to cited text no. 10
Heart Protection Study Collaborative Group. MRC/BHF heart protection study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: A randomised placebo-controlled trial. Lancet 2002;360:7-22.  Back to cited text no. 11
Shepherd J, Blauw GJ, Murphy MB, Bollen EL, Buckley BM, Cobbe SM, et al. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): A randomised controlled trial. Lancet 2002;360:1623-30.  Back to cited text no. 12
Sever PS, Dahlöf B, Poulter NR, Wedel H, Beevers G, Caulfield M, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial - Lipid Lowering Arm (ASCOT-LLA): A multicentre randomised controlled trial. Lancet 2003;361:1149-58.  Back to cited text no. 13
Cannon CP, Braunwald E, McCabe CH, Rader DJ, Rouleau JL, Belder R, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med 2004;350:1495-504.  Back to cited text no. 14
Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr., Kastelein JJ, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359:2195-207.  Back to cited text no. 15
Shepherd J, Barter P, Carmena R, Deedwania P, Fruchart JC, Haffner S, et al. Effect of lowering LDL cholesterol substantially below currently recommended levels in patients with coronary heart disease and diabetes: The treating to new targets (TNT) study. Diabetes Care 2006;29:1220-6.Core Committee  Back to cited text no. 16


  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3]

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