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2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults.

The ACC and the American Heart Association (AHA), in collaboration with the National Heart, Lung, and Blood Institute (NHLBI) and other specialty societies, released four guidelines focused on the assessment of cardiovascular risk, lifestyle modifications to reduce cardiovascular risk and management of elevated blood cholesterol and body weight in adults.

These four prevention guidelines were among five initially commissioned by NHLBI starting in 2008 and transitioned to the ACC and AHA in June 2013 as part of a collaborative arrangement to facilitate their completion and publication. A fifth guideline addressing hypertension will be initiated in early 2014. Each provides important updated guidance for primary care providers, nurses, pharmacists and specialty medicine providers on how best to manage care of individuals at risk for cardiovascular-related diseases based on the latest scientific evidence.

NLA Statement on the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults

The American College of Cardiology and the American Heart Association released the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. The National Lipid Association (NLA) was invited to participate in this process and worked initially with the NHLBI and then eventually with the AHA and ACC as the guidelines were transitioned and finalized. We provided our comments but after multiple revisions, ultimately felt that the document presented - although important and constructive--does not go far enough to address gaps in clinical care and therefore decided not to endorse them as guidelines. We understand the constraints that the NHLBI panel had in limiting their review to only high quality randomized controlled trials but also believe that other important types of clinical evidence should not have been excluded. We also do not find evidence-based support for the Panel’s recommendation for removing LDL-C (and Non-HDL-C) treatment targets. We question the need to remove such important and well-known clinical performance metrics that have been so widely endorsed by the clinical community. Further we find there to be an absence of discussion regarding other therapeutic options for patients on high-dose statins but which still exhibit high residual risk and/or significantly elevated LDL-C levels. There also needs to be more discussion on managing special populations such as older patients above age 75, those with familial hypercholesterolemia, those who are statin-intolerant, and younger high risk patients under age 40.

The NLA understands and appreciates the considerable effort and professionalism that went into creating this document which should serve as an initial focal point for ongoing discussion. We have been invited and will participate fully in the next phase of guidelines development with the AHA and ACC, along with other stakeholder groups, to discuss further implementation options and considerations. Our goal is to contribute our vast expertise and experience to the next set of guidelines so that clinicians can better and more comprehensively manage their patients in both primary care and specialty practice. The NLA looks forward to a continued collaborative partnership with the ACC and the AHA to enhance these guidelines in the next phase.

Please login to provide your comments and thoughts on the Guidelines and the NLA statement below.


To read the entire Guidelines document, please click here.

Original Posting Date: 
Tuesday, November 12, 2013 - 11:30
Average: 4.5 (6 votes)


rlaforge's picture

Although I agree with the NLA's position stand on affirming the considerable constraints handed to the ATP IV and Lifestyle panels - I think the 2013 IAS more succinct dyslipidemia guidelines are more clear and to the point and perhaps most importantly easier to explain and enact for health care providers but also for organizations such as the NCQA and the IHS who ground themselves in achieving quality objective outcome measures.  The four major statin benefit group concept is very interesting but without more directed target lipid/lipoprotein goals seems to leave a lot to be explained particularly since lipidologists/lipid specialists have spent the last decade reinforcing target goal attainment as imperfect as they may be.  I did very much like and appreciate the recommendations on safety and managing statin therapy which will be very helpful.

I was very disappointed in some of the lifestyle recommendations - particularly the overemphasis of the DASH and underemphasis on the Mediterranean dietary approach to managing dyslipidemia.    That is my simplified take.

Regarding the Physical Activity (PA) and management of dyslipidemia (prinicpally LD-C, TG and nonHDL-C) recommendations - the panel elected to review only the studies that used physical activity alone (i.e., not in combination with other interventions, such as dietary interventions or weight loss) versus no physical activity or other type of intervention.  They fell back to the more conservative 2008 generalized PA recommendations which clearly were not focused on the guideline focus of PA and lipids: aerobic physical activity to reduce LDL–C and non-HDL–C:  3 to 4 sessions a week, lasting on average 40 minutes per session, and involving moderate-to- vigorous intensity physical activity.  This guideline is laudable for overall improvement in CV health but clearly short of the level and volume of PA required for managing LDL-C, TG, and nonHDL and is at odds with the IAS, ACSM, ACE, IHS, and the recent NLA Consensus Statement on Obesity, Adiposity, and Dyslipidemia - all of which state that Physical Activity recommendations for dyslipidemia - particularly LDL-C and nonHDL-C reduction are: aerobic physical activity, 40-75% of aerobic capacity, for 5-7 days a week, for 30-60 minutes per day.  This level is similar to the recommendation (ACSM, IAS, IHS, etc.) advised for weight loss.e.g., 250–300 min/week or >2000 kcal/week of leisure-time physical activity. The AHA/ACC's PA's recommendation serves no practical purpose from a patient recommendation and public health standpoint because virtually no clinician would advise using physical activity programming for managing dyslipidemia without some emphasis on fat weight loss and instituting dietary changes - certainly not in a lipid clinic.  This is a misleading recommendation regarding the advisement of PA ALONE and serves no one.  

feeman's picture

     I am a family physician who has worked in the fields of interventional lipidology and preventive cardiology for the last 40-odd years.  I have set up my practice of family medicine into an age-sex database and over the decades have accumulated a large database of atherothrombotic disease (ATD) risk factors.  Since many of my patients in the early years refused to take dyslipidemia medications, I rapidly accumulataed an ATD database.  Framingham taught us that the ATD population differs from the general population by certain risk factors, by the severity of those risk factors and the mix of those risk factors.  Comparison of the General Population and ATD databases permits the identification of the constellation of ATD risk factors that characterize the ATD.  This constellation of risk factors is also present to an extent in people in the General Population, presumably in those people in the process of developing clinical ATD.  Since the risk of ATD is determined by the degree of risk factor severity and the duration that that risk factor has been operative, those people in the General Population clinically free of ATD may not have had their risk factors long enough or the risk factors may not have been severe enough to produce clinical ATD.  The difference is secondary versus primaray prevention.  The constellation of risk factors leading to ATD is characterized by dyslipidemia (defined as an imbalance between LDL- and HDL-cholesterol, and I prefer the Cholesterol Retention Fraction, or CRF, defined as [LDL-HDL]/LDL), cigarette smoking, and hypertension, defined in terms of systolic blood pressure (SBP) of 140 mmHg or higher.  I have created a graph with the CRF on the ordinate and SBP on athe abcissa.  An ATD threshold line has been generated, above which lie the CRF-SBPplots of the vast majority (85%) of ATD patients.  (The line coordinates are [0.74,100] and [0.49,140] if the precipitation method of HDL measurement is used, but [0.62,100] and [0.40,140] if the enzymatic method of HDL measurement is used.)  Of the 15% of ATD patients whose CRF-SBP plots lie below the threshold line, most are cigarette smokers, current or past.  That leaves only 6% of all ATD patients who can not be predicted by CRF-SBP plot above the threshold line and/or cigarette smoking status.  And these patients do not develop their ATD evens till, on average, the late eighth decade of life, and do not die, on average, for an additional 10-15 years.  I have also created a table using 2821 CRF values from the General Population database and divided those CRF values into sextile and age groups.  For each CRF-age group cohort, I have listed the incidence of ATD in that cohort, thus giving an indication of when to initiate treatment in a primary prevention scenario.  The goal of treatment is to bring the CRF-SBP plot below the threshold line, but if HDL is very low, then to bring LDL levels down to 80 mg/dl if the precipitation method of HDL measurement is used or 70 mg/dl if the enzymatic method of HDL measurement is used. This approach is simple to use and in my hands works very well.  The last treated  male to suffer an AMI did so 2 1/2 years ago--and he had systemic sclerosis and pneumonia when his event occurred.  I did have a treated female patient with established PAD who sustained ACI last summer when a clot formed over an inactive plaque.  She did undergo a catheriterization, but the coronary arteries were open and nothing further was done, not even a stent.  1 1/2 years ago a treated female patient of mine also had an ACI event and had a stent placed.  I could not get her to lipid goals becasue she required other medication which interacted with her statin.

     I write this because the AHA/ACC guidelines in primary preention are way too complex for family physiians to use--and family physicians must be able to use those guidelines if we are ever going to win the war against ATD.  The AHA/ACC guidleines for those with ATD are straight forward and require a goal of 80 mg/dl if the precipitation method of HDL measurement is used but 70 mg/dl if the enzymatic  method of HDL measurement is used.  Diabetics are treated the same way in which the General Population is treated in a primary prevetnion scenario.  Assuming that patietns with Type II Hyperlipoproteinemia have had their disorder all of athaeir lives, such patients are treated in the same manner as ATD patients.  The real problem with the new guidelines is their use in the primary prevention scenario.  If one looks at the tables in the Circulation paper, as I have, one realizes how complex the family physician's decision must be to initiate treatment will be, and when guidelines are too cmplex, most physicians will not use them. 

     My approach differs from the Framingham Risk Score in that I use the risk factors as continuous dependent variables rather than as independent variables.  Peter Wilson tells me that the reson that the Framingham Studfy used the variables as independent risk factors is because their statisticians said that the latter approach would make the statistics stronger.  Also, I use LDL instead of total cholesterol, and I put in age after a risk factor has been identified, not as a primary risk factor.  However, the Framingham Risk Score mis-predicts younger patients with Type II HLP and women in general.  Since the risk calculator for the AHA/ACC guidelines has not been revealed, only time will tell as to how well their calculator will work--apparently not so well, if Ridker is to be believed.  This should not be surprising since the AHA/ACC guidelines rely solely on RCT's and RCT's by definition suffer from selection bias, making them difficult to be generalized to the population as a whole.  And why would anyone throw out the long-term results of the Framingham Study--they showed us the way, and the AHA/ACC ignores them???  Moreover, throwing out LDL goals and ignoring HDL goals entirely gives the practitioner not real idea of how far to treat.  If plaque stabilization/regression goals are not met, the plaque will progress--and that will lead to ATD events.

     I submit that my approach is simple and therefore useable.  When I have applied it to every RCT whose database I can examine, those RCT's validate my approach.  I invite NLA members to try in their own practices.  However,  I must note that most ATD events that occur in the USA are associated with lipid levels that will never make it to the lipidologist, so I invite any family physicians reading this blog to try it as well.  References are available at my website at www.bowlinggreenstudy.org, which is free and open to all.


schiavet's picture

Unfortunately the AHA/ACC guidelines left out the value of LDL-Particle concentration or Apolipoprotein B as a determinate of cardiovascular risk and target of therapy.  The data is clear to me that CV risk is directly proportional to the concentration of LDL particles as measured by NMR or by immunoassay of Apolipoprotein B. The LDL-cholesterol (LDL-C) may be misleading, particularly in patients with a family history of diabetes and in patients with metabolic syndrome or diabetes. In my own pratice I measure both the LDL-C and LDL particle concentration to see if they correlate, i.e.both are in the same percentile.  If they correlate then I feel comfortable in following the LDL-C. After statins or other drugs are started I repeat both of the tests to determine if they still correlate. If they do not, then the LDL-particle concentration or Apolipoprotein B values are followed to the appropriate target of therapy.

It is the LDL particles that form the plaque in the vessel wall. Cholesterol is dumped into the plaque after the particle enters the wall. The greater the number of particles in the plasma, the greater is the risk. The concentration of LDL-C does not necessarily correlate with the paticle concentration. The amount of LDL-C in the particle is proprotionaly to the size of the LDL particle. The amount of residual risk in patients who are treated to established  LDL-C goal is significant.  We cannot ignore the value of determining the concentration of LDL-particles as measured by NMR or apolipoprotein B.

drbobgleeson's picture

We can argue about the new guidelnes, but at some time we, as lipid experts, have to start to implement these in our institutions and our practices.  

Lab reference ranges are an acute problem for me.

Lab normal reference ranges: 

  • I've told my lab to add the calculator to their report page.  (They weren't keen on this, but agreed.)
  • I'm thinking the only reference range left on the "cholesterol" side of  lipids is LDL > 190.  So what do we put as a normal reference range for other cholesterol values?  Is "blank" the right answer?
  • Trigs?  Since the guidelines are silent on trigs, should I tell the lab to use the Endocrinology reference values?  
  • low HDL.  Does an HDL of 27 only direct us to the calculator and nothing more?   
  • non-HDL   Do I even need this on the lipid report any longer?  I certainly think so (since it is free and a close approximation for the risk associated with high LDL-P).  

I am getting more comfortable with the calculator and actually find it quite workable.  But what about the outliers, those with Lp(a) > 80 or HDL < 25 , etc.  Where is the guidance or my latitude as the local clinic expert?  

I look forward to your answers.  

R. Gleeson

by Dr. Radut.