Managing Dyslipidemia in Adults

Guideline Watch |
July 7, 2015

Managing Dyslipidemia in Adults

  1. Jamaluddin Moloo, MD, MPH and
  2. Allan S. Brett, MD

A new guideline joins the 2013 ACC/AHA guideline in abandoning treatment to targets, but the two guidelines differ in several important ways.

  1. Jamaluddin Moloo, MD, MPH and
  2. Allan S. Brett, MD

Sponsoring Organizations: U.S. Department of Veterans Affairs, U.S. Department of Defense

Target Audience: Primary care providers, cardiologists

Background and Objective

In 2014, a panel from the U.S. Department of Veterans Affairs (VA) and the U.S. Department of Defense (DoD) approved a joint clinical practice guideline for managing dyslipidemia. In this synopsis, the authors summarize the guideline's key elements.

Key Recommendations

  • Eliminate LDL cholesterol and non–HDL cholesterol levels as specific treatment targets. Evidence supports use of moderate, fixed-dose statin therapy to lower risk for early all-cause death and adverse cardiovascular (CV) events.

  • Routine use of additional testing to refine risk prediction is not recommended. Among various markers that have been evaluated, only high-sensitivity C-reactive protein (hsCRP) and coronary artery calcium (CAC) scores add significantly to existing risk-prediction models. HsCRP levels improve net classification marginally (by 1.5%); CAC scores improve net reclassification by 5% to 16%, but this effect is considered to be small. Studies have not shown whether these tests improve outcomes; hence, neither is recommended routinely.

  • Tailor primary prevention for each patient. The benefit of statin therapy depends on risk level. In patients whose 10-year risk for CV disease is <6%, no benefit has been shown; in those whose risk is 6% to 12%, limited evidence suggests that statins lower risk by about 8%; and in patients whose risk is >12%, trials indicate that statins lower risk by 20% to 30%. Treatment with moderate statin doses should be offered to those whose risk is >12%; for those at intermediate risk, the net benefit of statins is uncertain, and the decision to initiate therapy should be shared with the patient.

  • For secondary prevention, moderate-dose statin therapy should be initiated. The additive benefit of high-dose statin therapy is relatively small (approximately 6.5 fewer adverse CV events per 1000 patients treated with high-dose vs. moderate-dose statins for 5 years), so clinicians should consider its use primarily in patients at greatest risk for CV disease.

  • Fasting lipid measurement and routine monitoring are not required. Nonfasting total and HDL cholesterol levels differ little from fasting measurements. Compared with nonfasting levels, fasting LDL cholesterol levels might be 10% lower and triglyceride levels might be ≤20% higher, but these differences are unlikely to affect treatment decisions. Baseline creatine kinase levels and tests of liver function should be obtained before initiating statin therapy, but routine monitoring of lipids, creatine kinase, or liver function during follow-up is not recommended.


This new guideline agrees with the American College of Cardiology and American Heart Association (ACC/AHA) guideline in abandoning treatment to specific lipid targets (NEJM JW Gen Med Dec 15 2013 and J Am Coll Cardiol 2014; 63:2889). However, important differences exist. First, the new guideline acknowledges limitations of various risk calculators (including that of the ACC/AHA) and does not endorse any particular one. Second, for primary prevention, the guideline designates a fairly broad intermediate-risk group (6% to 12% 10-year risk) for which evidence of benefit from statin therapy is considered to be limited; this contrasts with the ACC/AHA's fairly narrow 5% to 7.5% treatment threshold. Third, the new guideline suggests initiation of moderate-dose statin therapy for most patients, with titration to higher doses for highest-risk patients. Fourth, the new guideline allows for nonfasting lipid determinations and discourages monitoring of lipid levels.

We find this guideline to have many attractive features. Although it is intended for clinicians and patients in the U.S. VA and DoD systems, clinicians who practice in civilian settings might find it to be a viable alternative to the ACC/AHA guideline.

Editor Disclosures at Time of Publication

  • Disclosures for Jamaluddin Moloo, MD, MPH at time of publication Nothing to disclose

  • Disclosures for Allan S. Brett, MD at time of publication Grant / Research support Colorado Health Foundation


Reader Comments (6)

Jamaluddin Moloo, MD, MPH Physician, Internal Medicine, University of Colorado

A number of readers have added thoughtful comments to our piece. Here are a few additional thoughts:

1. We would agree that the new guidelines, use indirect assumptions from observational data and then assume that RCT intervention data can be superimposed on patients selected by observational risk. The ACC/AHA authors do make an attempt to address this criticism but leaves a great deal of room for disagreement.
2. Use of CRP: Given data from Jupiter one could certainly argue it should be utilized to select individuals for primary prevention howver, it should not be the only criterion giventhat several other primary prevention studies did not select enrollees by CRP.
3. The ACC/AHA risk equation was developed from Framingham plus 3 other databases and one can argue that it is more representative of the US population.

Dr. Richard Hochman Physician, Internal Medicine, Beth Israel Deaconess

I'm commenting on the statement in the article that the other markers for risk only add little to the equation and that there are no studies showing outcome benefits in their use.

In fact, the ONLY method to recommend patients for statins with support for changing outcomes is CRP! None of the guidelines have PROSPECTIVE data to support their efficacy in changing outcomes; They just calculate Framingham risk and then assume that treatment would be helpful to those with higher risk!

The Jupiter Study (respected enough to be included in a recent book from UCLA , "The Fifty Studies All doctors Should Know") did show statistically significant differences in significant clinical outcomes in treating patients with CRP greater than 2 and normal LDL's who were then randomized and followed prospectively. The only criticism methodologically, was the fact that many centers were used and many patients were screened to come up with the normal ldl and elevated crp group. Obviously, CRP has to be used carefully because of false positive with inflammatory illnesses etc, But, it is wrong for the article you reviewed to state that there are no outcomes data re its use to identify patients for whom statins would be helpful!

I don't understand how the only documented method to predict who will benefit clinically from statins is totally ignored in our latest two guidelines (VA and ACP) in favor of Framingham risk assessment without intervention data!


As other people have stated, these new guidelines give a better look at how to treat real patients. From now one, the Framingham coronary heart disease risk score should be used routinely for better contextualization of the need of statin treatment in a particular patient.

GAURANGA DHAR Physician, Family Medicine/General Practice, Dhaka, Bangladesh

Very much practical review. Many physicians and even cardiologists still in hesitation, start statin or not? If started how long to continue? Who are the specific candidates for statin? When I need to stop statin if LDL at goal? Is it possible to go for lipid profile random?
Do we use statin only as a lipid lowering agent? No. This group of drug offers other beneficial effects e.g. protection of vasculature and so on.
Statin induced hepatotoxicity, myotoxicity are extremely low. We need to take care to start statin in patients with hypothyroidism.
This is the excellent review for physician who are still in hesitation in starting and continuing statin.

alderisio william Physician, Cardiology, amc

excellent review

Sheldon Ball, PhD,MD Physician, Geriatrics, Humana

These guidelines seem to ignore the benefits of diet and exercise in primary cardiovascular event prevention and propose an open-ended "Evidence supports use of moderate, fixed-dose statin therapy to lower risk for early all-cause death and adverse cardiovascular (CV) events" for every one? There is no discussion of the number need to treat vs the number needed to harm nor a consideration of the effects of statins on cognition. (PMID: 26054031). What ever happened to do no harm? The last time I attended wards on the VAMC in Sacramento, I had 2 patients on my service in the ICU on dialysis for rhabdomyolysis due to statins.

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