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Effective Date: 08/01/2013 Title: Lipid Risk Factors in Management of Cardiovascular Disease
Revision Date: 01/01/2017 Document: BI408:00
CPT Code(s): 83695, 83698, 83700, 83701, 83704
Public Statement

Effective Date:

a)    This policy will apply to all services performed on or after the above revision date which will become the new effective date.

b)    For all services referred to in this policy that were performed before the revision date, contact customer service for the rules that would apply.

  1. Many non-traditional lipid markers are considered investigational and are not covered. 
  2. These biomarkers have been proposed for screening, assessment, or management of cardiovascular disease. While these measurements may provide some risk prediction, such measurement has not been shown to improve health outcomes compared to standard risk assessment with measurement of traditional lipid levels such as LDL and HDL cholesterol.
  3. The American College of Cardiology (ACC) and the American Heart Association (AHA) jointly published the Guidelines on Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults (Circulation 11/12/2013).  These are the most current and updated practice guidelines.  Their emphasis of risk determination to guide treatment decisions does not include any of the non-traditional lipid markers.  Estimation of 10 year risk of atherosclerotic cardiovascular disease (ASCVD) should use the following calculator available online:  

Medical Statement

1)    Numerous lipid biomarkers have been proposed as potential risk markers for cardiovascular disease.  Traditional risk factors, such as total cholesterol, LDL-cholesterol, and HDL-cholesterol have established utility in predicting individuals at increased risk, and certain types of treatments of these risk factors has been demonstrated to improve clinical outcomes.  Many other lipid markers have been proposed as useful for screening or risk segregation.  In order for these markers to be clinically useful, they must be demonstrated to add to the utility of traditional risk factors. 


2)    QualChoice, the ACC and the AHA do not consider such biomarkers to meet this criterion, including but not limited to:

a)    Lipoprotein (a)

b)    Apolipoprotein B

c)     Apolipoprotein E

d)    LDL subclasses

e)    HDL subclasses

f)      Lipoprotein-associated phospholipase A2


3)     Estimation of 10 year risk for ASCVD risk (per the ACC/AHA guideline) should use the following calculator:

Codes Used in This Policy:


Lipoprotein (a)


Lipoprotein-associated phospholipase A2 (Lp-PLA2)


Lipoprotein, blood; electrophoretic separation and quantitation


Lipoprotein, blood; high resolution fractionation and quantitation of lipoproteins including lipoprotein subclasses when performed (eg, electrophoresis, ultracentrifugation)


Lipoprotein, blood; quantitation of lipoprotein particle numbers and lipoprotein particle subclasses (eg, by nuclear magnetic resonance spectroscopy)


1)    Lipoprotein (a):

a)    The apolipoprotein (a) molecule is structurally similar to plasminogen, suggesting that Lp (a) may contribute to the thrombotic and atherogenic basis of cardiovascular disease. Levels of Lp (a) are relatively stable in individuals over time, but vary up to 1000-fold between individuals, presumably on a genetic basis. The similarity between apolipoprotein (a) and fibrinogen has stimulated intense interest in Lp (a) as a link between atherosclerosis and thrombosis. In addition, approximately 20% of patients with coronary artery disease (CAD) have elevated levels of Lp (a). Therefore, it has been proposed that levels of Lp (a) may be an independent risk factor for coronary artery disease.

b)    The Lipid Research Clinics (LRC) Coronary Prevention Primary Trial, one of the first large-scale, randomized, controlled trials of cholesterol-lowering therapy, measured initial Lp (a) levels and reported that Lp (a) was an independent risk factor for coronary artery disease (CAD) when controlled for other lipid and non-lipid risk factors. (Schaefer, 1994) The Atherosclerosis Risk in Communities (ARIC) study evaluated the predictive ability of Lp(a) in 12,000 middle-aged individuals free of CAD at baseline who were followed up for 10 years, and Lp(a) levels were an independent predictor of CAD above traditional lipid measures. (Sharrett, 2001)

c)     Other studies, however, have failed to demonstrate such a relationship. The European Concerted Action on Thrombosis (ECAT) study, a trial of secondary prevention, evaluated Lp (a) as a risk factor for coronary events in 2,800 patients with known angina pectoris. (Bolibar, 2000) In this study, Lp (a) levels were not significantly different among patients who did and did not have subsequent events, suggesting that Lp (a) levels were not useful risk markers in this population.   In the Physicians’ Health Study, initial Lp (a) levels in the 296 participants who subsequently experienced a myocardial infarction were compared with Lp (a) levels in matched controls who remained free from CAD. (Ridker, 2003) The authors found that the distribution of Lp (a) levels between the 2 groups was identical.

d)    Subsequent studies have evaluated the predictive ability of Lp (a) for cardiovascular events. (Suk Danik, 2006; Ohira, 2006, Rigal, 2007)  A number of these studies focused on the predictive ability of Lp (a) for ischemic stroke, with mixed results. In the Atherosclerotic Risk in Communities (ARIC) prospective cohort study of 14,221 participants (Ohira, 2006), elevated Lp (a) was a significant independent predictor of stroke in women but not in men (African-American and white).  In another prospective cohort study of 100 consecutive patients with ischemic stroke, Rigal and co-workers (2007) reported that an elevated Lp (a) level was an independent predictor of ischemic stroke in men but not in women.

e)    Tools for linking Lp (a) to clinical decision making, both in risk assessment and treatment response, are currently not available. The Adult Treatment Panel III (ATP III) practice guidelines continue to tie clinical decision making to conventional lipid measures, such as total cholesterol, LDL-C, and HDL-C. There is a lack of recommendations from this body regarding how the additional information from Lp (a) levels might be used in clinical practice. As a result, there is considerable uncertainty regarding its clinical role, specifically how knowledge of Lp (a) levels can be used in clinical care of patients who are being evaluated for lipid disorders.

2)    Apolipoprotein B (Apo-B):

a)    The Emerging Risk Factors Collaboration published a patient-level meta-analysis of 37 prospective cohort studies enrolling 154,544 individuals (Di Angelantonio, 2012). Risk prediction was examined for a variety of traditional and non-traditional lipid markers. For apo B, evidence from 26 studies on 139,581 individuals reported that apo B was an independent risk factor for cardiovascular events, with an adjusted hazard ratio of 1.24 (95% confidence interval [CI] 1.19-1.29). On reclassification analysis, when apo-B and apo-AI were substituted for traditional lipids, there was not improvement in risk prediction. In fact, there was a slight worsening in the predictive ability, evidenced by a decrease in the C-statistic of -0.0028 (p<0.001), and a decrease in the net reclassification improvement of -1.08% (p<0.01).

3)    Apolipoprotein E (Apo-E):

a)    A meta-analysis published by Bennet and colleagues summarized the evidence from 147 studies on the association of apo E genotypes with lipid levels and cardiac risk (Bennet, 2007). Eighty-two studies included data on the association of apo E with lipid levels, and 121 studies reported the association with clinical outcomes. The authors estimated that patients with the apo e2 allele had LDL levels that were approximately 31% less compared to patients with the apo e4 allele. When compared to patients with the apo e3 allele, patients with apo e2 had an approximately 20% decreased risk for coronary events (OR: 0.80; 95% CI: 0.70–0.90). Patients with the apo e4 had an estimated 6% higher risk of coronary events that was of marginal statistical significance (OR: 1.06; 95% CI: 0.99–1.13).

b)    Chiodini et al. examined differential response to statin therapy according to apo E genotype, by reanalyzing data from the GISSI study according to apo E genotype (Chiodini, 2007). GISSI was an RCT comparing pravastatin with placebo in 3,304 Italian patients with previous myocardial infarction (MI). Patients with the apo e4 allele treated with statins had a greater response to treatment as evidenced by lower overall mortality (1.85% vs. 5.28%, respectively, p=0.023), while there was no difference in mortality for patients who were not treated with statins (2.81% vs. 3.67%, respectively, p=0.21). This study corroborates results reported in previous studies but does not provide evidence to suggest that changes in treatment should be made as a result of apo E genotype.

c)     Apo-E does not appear to add clinically relevant information for assessing cardiovascular risk compared to standard risk factor assessment.  While apo E genotype may predict the level of response to statins, there is no evidence to suggest that this genotype should lead a clinician to change therapy in an individual.

4)    LDL subclasses:

a)    A nested case-control study from the Physician’s Health Study, a prospective cohort study of approximately 15,000 men, investigated whether LDL particle size was an independent predictor of CAD risk, particularly in comparison to triglyceride levels (Stampfer, 1996). This study concluded that while LDL particle diameter was associated with risk of MI, this association was not present after adjustment for triglyceride level. Only triglyceride level was significant independently.

b)    Mora et al (Mora, 2009) evaluated the predictive ability of LDL particle size and number measured by NMR in participants of the Women’s Health Study, a prospective cohort study of 27,673 women followed over an 11-year period. After controlling for no lipid factors, LDL particle number was a significant predictor of incident cardiovascular disease, with a hazard ratio of 2.51 (95% CI: 1.91-3.30) for the highest, compared to the lowest quintile. LDL particle size was similarly predictive of cardiovascular risk, with a hazard ratio of 0.64 (95% CI: 0.52–0.79). When compared to standard lipid measures and apolipoproteins, LDL particle size and number showed similar predictive ability but were not superior in predicting cardiovascular events.

5)    HDL subclasses:

a)    In the Kuopio Ischemic Heart Disease Risk Factor Study, both total HDL-C and levels of HDL-2 had significant independent associations with risk of acute MI (Salonen, 1991). The Quebec Cardiovascular Study investigated the association of HDL-2 and HDL-3 subclasses with ischemic heart disease in a subsample of 944 French-Canadian men participating in the larger trial (Lamarche, 1996). During the 10-year follow-up, levels of HDL-2 were statistically significant as independent predictors of CAD events, but the difference in predictive value with and without HDL subclasses was not considered clinically significant. The ARIC study, a large prospective cohort study, followed 12,000 middle-aged individuals free of CAD at baseline for 10 years (Sharrett, 2001). In this study, prediction of CAD was not improved by the addition of either apo A-I levels or HDL density. Similarly, in the Physicians’ Health Study (Stampfer, 1991) and the Caerphilly and Speedwell Collaborative Heart Disease Studies, (Sweetnam, 1994) both of which were studies of middle-aged men, risk prediction based on HDL-C was also not improved by HDL sub classification.


2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults available for download at:


Bennet AM, Di Angelantonio E, Ye Z et al. (2007) Association of apolipoprotein E genotypes with lipid levels and coronary risk. JAMA 2007; 298(11):1300-11.


Bolibar I, von Eckardstein A, Assmann G et al. (2000) Short term prognostic value of lipid measurements in patients with angina pectoris. The ECAT Angina Pectoris Study Group: European Concerted Action on Thrombosis and Disabilities. Thromb Haemost 2000; 84(6):955-60.

Chiodini BD, Franzosi MG, Barlera S et al. (2007) Apolipoprotein E polymorphisms influence effect of pravastatin on survival after myocardial infarction in a Mediterranean population: the GISSI-Prevenzione study. Eur Heart J 2007; 28(16):1977-83.


Di Angelantonio E GP, Pennells L, et al. (2012) Lipid-Related Markers and Cardiovascular Disease Prevention. JAMA 2012; 307(23):2499-506.


Lamarche B, Moorjani S, Lupien PJ et al.(1996) Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Quebec cardiovascular study. Circulation 1996; 94(3):273-8.

Mora S, Glynn RJ, Boekholdt SM et al.(2012) On-treatment non-high-density lipoprotein cholesterol, apolipoprotein B, triglycerides, and lipid ratios in relation to residual vascular risk after treatment with potent statin therapy: JUPITER (justification for the use of statins in prevention: an intervention trial evaluating rosuvastatin). J Am Coll Cardiol 2012; 59(17):1521-8.

Mora S, Otvos JD, Rifai N et al. (2009) Lipoprotein particle profiles by nuclear magnetic resonance compared with standard lipids and apolipoproteins in predicting incident cardiovascular disease in women. Circulation 2009; 119(7):931-9.

Mora S, Wenger NK, Demicco DA et al. (2012) Determinants of residual risk in secondary prevention patients treated with high- versus low-dose statin therapy: the Treating to New Targets (TNT) study. Circulation 2012; 125(16):1979-87.

Ohira T, Schreiner PJ, Morrisett JD et al.(2006) Lipoprotein(a) and incident ischemic stroke: the Atherosclerosis Risk in Communities (ARIC) study. Stroke 2006; 37(6):1407-12.


Ridker PM, Hennekens CH, Stampfer MJ. (1993) A prospective study of lipoprotein (a) and the risk of myocardial infarction. JAMA 1993; 270(18):2195-9.


Rigal M, Ruidavets JB, Viguier A et al.(2007) Lipoprotein (a) and risk of ischemic stroke in young adults. J Neurol Sci 2007; 252(1):39-44.


Salonen JT, Salonen R, Seppanen K et al.(1991) HDL, HDL-2 and HDL-3 sub fractions and the risk of acute myocardial infarction. A prospective study in eastern Finnish men. Circulation 1991; 84(1):129-39.


Schaefer EJ, Lamon-Fava S, Jenner JL et al.(1994) Lipoprotein (a) levels and risk of coronary heart disease in men. The Lipid Research Clinics Coronary Primary Prevention Trial. JAMA 1994; 271(13):999-1003.


Sharrett AR, Ballantyne CM, Coady SA et al. (2001) Coronary heart disease prediction from lipoprotein cholesterol levels, triglycerides, lipoprotein (a), apolipoproteins A-I and B, and HDL sub fractions: the Atherosclerosis Risk in Communities (ARIC) study. Circulation 2001; 104(10):1108-13.

Stampfer MJ, Krauss RM, Ma J, et al. (1996) A prospective study of triglyceride level, low density lipoprotein particle diameter, and risk of myocardial infarction. JAMA 1996; 276:882-88.


Stampfer MJ, Sacks FM, Salvini S et al. (1991) A prospective study of cholesterol apolipoproteins, and the risk of myocardial infarction. N Engl J Med 1991; 325(6):373-81.


Suk Danik J, Rifai N, Buring JE et al.(2006) Lipoprotein(a), measured with an assay independent of apolipoprotein(a) isoform size, and risk of future cardiovascular events among initially healthy women. JAMA, 2006; 296(11):1363-70.


Sweetnam PM, Bolton CH, Yarnell JW et al. (1994) Associations of the HDL-2 and HDL-3 cholesterol sub fractions with the development of ischemic heart disease in British men. The Caerphilly and Speedwell Collaborative Heart Disease Studies. Circulation 1994; 90(2):769-74.


1)    Effective 01/01/2017: Information added regarding latest treatment guideline from ACC/AHA.

Application to Products
This policy applies to all health plans administered by QualChoice, both those insured by QualChoice and those that are self-funded by the sponsoring employer, unless there is indication in this policy otherwise or a stated exclusion in your medical plan booklet. Consult the individual plan sponsor Summary Plan Description (SPD) for self-insured plans or the specific Evidence of Coverage (EOC) for those plans insured by QualChoice. In the event of a discrepancy between this policy and a self-insured customer’s SPD or the specific QualChoice EOC, the SPD or EOC, as applicable, will prevail. State and federal mandates will be followed as they apply.
Changes: QualChoice reserves the right to alter, amend, change or supplement benefit interpretations as needed.
This policy has recently been updated. Please use the index above or enter policy title in search bar for the latest version.