FROM ANNALS OF INTERNAL MEDICINE
A new clinical practice guideline for managing dyslipidemia to reduce adults’ CVD risk will likely draw criticism for the simple reason that it calls for change, according to the co-chairs of the panel that compiled the guideline’s 26 recommendations.
Like the existing American College of Cardiology/American Heart Association guideline, this guideline issued jointly by the U.S. Department of Veterans Affairs and the U.S. Department of Defense in January 2015 calls for eliminating the use of cholesterol levels as treatment targets. But the VA/DOD guideline differs in its more conservative approach: It recommends against the routine use of extensive testing to estimate CVD risk, calls for a more nuanced and “shared” approach to weighing the risks and benefits of statin therapy, advocates initiating such therapy at a lower dose, and recommends against routine laboratory monitoring using liver function panels and lipid testing.
These new recommendations are based on strong and recent evidence, but they challenge previous, firmly embedded beliefs and so “will undoubtedly provoke criticism,” said panel co-chairs Dr. John R. Downs of South Texas Veterans Health Care System, San Antonio, and Dr. Patrick G. O’Malley of the Uniformed Services University of the Health Sciences, Bethesda, Md.
“We hope we have brought some order to the chaos of clinical guidelines by providing a rigorous, simple, transparent, and high-quality guideline that providers can use to efficiently care for their patients,” they noted (Ann. Intern. Med. 2015 June 22 [doi:10.736/M15-0840]).
The recommendations include:
• No longer using LDL or non-HDL cholesterol levels as treatment targets, because the only data to suggest that this is beneficial are both indirect and questionable.
• No routine use of new genetic, serologic, physiologic, anatomical, or psychosocial risk markers to improve CVD risk prediction. In particular, high-sensitivity C-reactive protein testing and coronary artery calcium testing add only a little information to conventional risk calculations, do not improve CVD outcomes, and are costly; the latter test also exposes patients to potentially harmful radiation.
There is no evidence that primary prevention benefits low-risk patients (those with less than a 6% 10-year risk of CVD events) and only limited evidence that it benefits intermediate-risk patients (those at 6%-12% 10-year risk), so any decision to initiate statin therapy in this patient population must be “nuanced” and must include patient input.
For secondary prevention, statins should be initiated at a moderate dose and titrated to a higher dose only when medically indicated, such as when acute coronary syndrome or recurrent CVD events develop. Higher doses are not consistently beneficial and are associated with side effects that may lead to decreased adherence.
Patients no longer need to fast before lipid testing because fasting makes only a small difference in test results that is unlikely to affect risk classification or therapeutic decisions. Moreover, fasting is a burden for patients, who may avoid lipid testing altogether if they have to fast for 9-12 hours, and a burden for laboratories because of the large number of patients who present for testing early in the morning.
Routine lipid testing to monitor treatment effect is now unnecessary because lipid levels are no longer to be used as treatment targets.
Routine liver-function tests are unnecessary because evidence doesn’t show this improves detection of statin-associated liver damage (except at the highest doses), and serious liver damage is extremely rare. Moreover, frequent testing is a burden for both the patient and the clinician.
The full guideline is available at www.healthquality.va.gov/guidelines/CD/lipids
