mp-155 - Medical Policies - Alabama
Measurement of Lipoprotein-Associated Phospholipase A2 in the Assessment of Cardiovascular Risk
Policy Number: MP-155
Latest Review Date: December 2020
Policy Grade: B
Measurement of lipoprotein-associated phospholipase A2 (Lp-PLA2) is considered investigational and not medically necessary.
DESCRIPTION OF PROCEDURE OR SERVICE:
Lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet-activating factor acetylhydrolase, is an enzyme that hydrolyzes phospholipids and is primarily associated with low-density lipoproteins (LDLs). Accumulating evidence has suggested that Lp-PLA2 is a biomarker of coronary artery disease and may have a proinflammatory role in the progression of atherosclerosis.
Low-density lipoproteins (LDLs) have been identified as major atherogenic lipoproteins and have long been identified by the National Cholesterol Education Project (NCEP) as the primary target of cholesterol-lowering therapy. LDL particles consist of a surface coat composed of phospholipids, free cholesterol, and Apo lipoproteins, surrounding an inner lipid core composed of cholesterol ester and triglycerides. Traditional lipid risk factors such as LDL-C, while predictive on a population basis, are weaker markers of risk on an individual basis. Only a minority of subjects with elevated LDL and cholesterol levels will develop clinical disease, and up to 50% of cases of coronary artery disease occur in subjects with ‘normal’ levels of total and low-density lipoprotein cholesterol.
Although treatment for elevated coronary disease risk with statins targets cholesterol levels, selection for treatment involves estimation of future CAD risk using well validated prediction models that use additional variables.
Lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet-activating factor acetylhydrolase, is an enzyme that hydrolyzes phospholipids and is primarily associated with LDLs. Accumulating evidence has suggested that Lp-PLA2 is a biomarker of CAD and may have a proinflammatory role in the progression of atherosclerosis. The recognition that atherosclerosis represents, in part, an inflammatory process has created considerable interest in measurement of proinflammatory factors as part of cardiovascular disease risk assessment.
Interest in Lp-PLA2 as a possibly causal risk factor for CAD has generated development and testing of Lp-PLA2 inhibitors as a new class of drugs to reduce risk of CAD. However, clinical trials of Lp-PLA2 inhibitors have not shown significant reductions in CAD end points. Furthermore, assessment of Lp-PLA2 levels has not been used in the selection or management of subjects in the clinical trials.
The most recent literature review was updated through October 26, 2020.
Summary of Evidence
For individuals who have a risk of cardiovascular disease who receive Lp-PLA2 testing, the evidence includes studies of the association between Lp-PLA2 and various coronary artery disease outcomes. Relevant outcomes are overall survival, disease-specific survival, and test validity. The studies have demonstrated that Lp-PLA2 levels are an independent predictor of cardiovascular disease. Although Lp-PLA2 levels are associated with cardiovascular disease risk, changes in patient management that would occur as a result of obtaining Lp-PLA2 levels in practice are not well-defined. To demonstrate clinical utility, clinicians must have the tools to incorporate Lp-PLA2 test results into existing risk prediction models that improve classification into risk categories, alter treatment decisions, and lead to improved health outcomes. Direct evidence for such improved health outcomes with Lp-PLA2 testing in clinical practice is lacking. The evidence is insufficient to determine the effects of the technology on health outcomes.
Practice Guidelines and Position Statements
American College of Cardiology and American Heart Association
In 2019, The American College of Cardiology Foundation and American Heart Association published joint guidelines on the assessment of cardiovascular risk in asymptomatic patients in. Lipoprotein-associated phospholipase A2 (Lp-PLA2) testing was not mentioned in these guidelines, which was a change from 2010 guidelines. In their prior guideline, Lp-PLA2 was given an IIb recommendation for assessing cardiovascular risk in intermediate-risk asymptomatic adults.
American Association of Clinical Endocrinologists and American College of Endocrinology
In 2012, The American Association of Clinical Endocrinologists and the American College of Endocrinology published guidelines for the management of dyslipidemia and prevention of atherosclerosis. These guidelines made the following recommendations for Lp-PLA2 testing (see Table below)
Table. Guidelines on Dyslipidemia and Atherosclerosis
Assess markers of inflammation in patients where further stratification of risk is necessary. Highly sensitive CRP (hsCRP) and Lp-PLA2 provide useful information in these instances and appear to be synergistic in predicting risk of CVD and stroke
Measure Lp-PLA2, which in some studies has demonstrated more specificity than hsCRP, when it is necessary to further stratify a patient’s CVD risk, especially in the presence of systemic highly sensitive CRP elevations
CRP: C-reactive protein; CVD: cardiovascular disease; GOE: grade of evidence; hsCRP: high-sensitivity C-reactive protein; LOE: level of evidence; Lp-PLA2: lipoprotein-associated phospholipase A2.
In 2017, an update to guidelines published jointly by the American Association of Clinical Endocrinologists and American College of Endocrinology recommended the measurement of Lp-PLA2 as an additional indication of cardiovascular risk. Citing several studies in which Lp-PLA2 was comparable with high-sensitivity C-reactive protein as a risk predictor, the guidelines accordingly recommended the use of Lp-PLA2 data in situations requiring a more specific evaluation of risk of atherosclerotic cardiovascular disease that is provided by high-sensitivity C-reactive protein.
European Society of Cardiology et al
In 2016, the European Society of Cardiology and other cardiovascular disease societies issued clinical practice guidelines on cardiovascular disease prevention. These guidelines include the following statements:
- Routine assessment of circulating or urinary biomarkers is not recommended for refinement of CVD risk stratification (Class IIIB recommendation)
The guideline also noted that "there is evidence of publication bias in the field of novel biomarkers of CV risk, leading to inflated estimates of strength of association and potential added value.
U.S. Preventive Services Task Force Recommendations
No U.S. Preventive Services Task Force recommendations on the use of Lp-PLA2 in the assessment of cardiovascular risk have been identified.
Lipoprotein-associated phospholipase A2, Lp-PLA2, PLAC test, coronary risk assessment, high-sensitivity C-reactive protein, hs-CRP, low density cholesterol, LDL
APPROVED BY GOVERNING BODIES:
In December 2014, the PLAC® Test (diaDexus, San Francisco, CA), a quantitative enzyme assay, was cleared for marketing by the U.S. Food and Drug Administration through the 510(k) process for Lp-PLA2 activity. It was considered substantially equivalent to a previous version of the PLAC® Test (diaDexus), which was cleared for marketing by the Food and Drug Administration in July 2003. Food and Drug Administration product code: NOE.
Coverage is subject to member’s specific benefits. Group specific policy will supersede this policy when applicable.
ITS: Home Policy provisions apply
FEP contracts: FEP does not consider investigational if FDA approved and will be reviewed for medical necessity.
Lipoprotein, blood, high resolution fractionation and quantitation of lipoproteins, including all five major lipoprotein classes and subclasses of HDL, LDL, and VLDL by vertical auto profile ultracentrifugation. (VAP Cholesterol Test)
Secretory type II phospholipase A2 (sPLA2-IIA)
Lipoprotein-associated phospholipase A2 (Lp-PLA2)
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- Johnston N, Jernberg T, et al. Improved identification of patients with coronary artery disease by the use of new lipid and lipoprotein biomarkers. American Journal of Cardiology, March 2006, Vol. 97, Issue 5.
- Kardys I, Oei HH, et al. Lipoprotein-associated phospholipase A2 and measures of extracoronary atherosclerosis: The Rotterdam Study. Arteriosclerosis, Thrombosis, and Vascular Biology, March 2006; 26(3): 631-636.
- Kardys I, Oei HH, Hofman A, Oudkerk M and Witteman JC. Lipoprotein-associated phospholipase A2 and coronary calcification. The Rotterdam Coronary Calcification Study. Atherosclerosis, April 2007; 191(2): 377-383.
- Koenig W, et al. Lipoprotein-Associated phospholipase A2 adds to risk prediction of incident coronary events by C-reactive protein in apparently healthy middle-aged men from the general population. Results from the 14-year follow-up of a large cohort from southern Germany. Circulation 2004; 110(4): 1903-1908.
- Koenig W, et al. Lipoprotein-associated phospholipase A2 predicts future cardiovascular events in patients with coronary heart disease independently of traditional risk factors, markers of inflammation, renal function, and hemodynamic stress. Arteriosclerosis, Thrombosis and Vascular Biology, July 2006; 26(7): 1586-1593.
- Kolodgie FD, et al. Lipoprotein-associated phospholipase A2 protein expression in the natural progression of human coronary atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology 2006; 26: 2523-2529.
- Kuvin JT, Dave DM, et al. Effects of extended-release niacin on lipoprotein particle size, distribution, and inflammatory markers in patients with coronary artery disease. American Journal of Cardiology, September 2006, Vol. 98, Issue 6.
- Lanman RB, et al. Lipoprotein-associated phospholipase A2: Review and Recommendation of a clinical cut point for adults. Preventive Cardiology, Summer 2006, pp. 138-143.
- Lind L, Simon T, Johansson L et al. Circulating levels of secretory- and lipoprotein-associated phospholipase A2 activities: relation to atherosclerotic plaques and future all-cause mortality. Eur Heart J 2012; 33(23):2946-54.
- Liu CF, Qin L, Ren JY et al. Elevated plasma lipoprotein-associated phospholipase A (2) activity is associated with plaque rupture in patients with coronary artery disease. Chin Med J (Engl) 2011; 124(16):2469-73.
- Liu YS, Hu XB, Li HZ et al. Association of lipoprotein-associated phospholipase A (2) with characteristics of vulnerable coronary atherosclerotic plaques. Yonsei Med J 2011; 52(6):914-22.
- Mahler ER, 3rd, Ballantyne CM, Davidson MH, et al. The effect of darapladib on plasma lipoprotein-associated phospholipase A2 activity and cardiovascular biomarkers in patients with stable coronary heart disease or coronary heart disease risk equivalent: The results of a multicenter, randomized, double-blind, placebo-controlled study. JACC, April 2008; 51(17): 1632-1641.
- Muhlestein JB, May HT, et al. The reduction of inflammatory biomarkers by statin, fibrate, and combination therapy among diabetic patients with mixed dyslipidemia: the DIACOR (Diabetes and Combined Lipid Therapy Regimen) study. JACC, July 2006; 48(2): 396-401.
- Muller O, Ntalianis A, Wijns W et al. Association of biomarkers of lipid modification with functional and morphological indices of coronary stenosis severity in stable coronary artery disease. Journal of cardiovascular translational research 2013; 6(4):536-44.
- National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Available at www.nhlbi.nih.gov/guidelines/cholesterol/atp3xsum.pdf.
- National Institutes of Health, National Heart Lung and Blood Institute. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) (NIH Publication No. 01-3670). 2001; http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3xsum.pdf Accessed November 3, 2020
- Nicholls SJ, Kastelein JJ, Schwartz GG, et al. Varespladib and cardiovascular events in patients with an acute coronary syndrome: the VISTA-16 randomized clinical trial. JAMA. Jan 15 2014; 311(3):252-262.
- O'Donoghue M, Morrow DA, Sabatine MS et al. Lipoprotein-associated phospholipase A2 and its association with cardiovascular outcomes in patients with acute coronary syndromes in the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial. Circulation 2006; 113(14):1745-52.
- O'Donoghue ML, Braunwald E, White HD, et al. Effect of darapladib on major coronary events after an acute coronary syndrome: the SOLID-TIMI 52 randomized clinical trial. JAMA. Sep 10 2014; 312(10):1006-1015.
- Oei H, et al. Lipoprotein-associated phospholipase A2 activity is associated with risk of coronary heart disease and ischemic stroke, the Rotterdam Study. Circulation 2005, Vol. III, pp. 570-575.
- Oldgren J, James SK, et al. Lipoprotein-associated phospholipase A2 does not predict mortality or new ischemic events in acute coronary syndrome patients. European Heart Journal, March 2007; 28(6): 699-704.
- Packard Chris J, et al. Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. The New England Journal of Medicine, October 2000, Vol. 343, No. 16, pp. 1148-1155.
- Piepoli MF, Hoes AW, Agewall S, et al. 2016 European Guidelines on cardiovascular disease prevention in clinical practice: The Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of 10 societies and by invited experts) Developed with the special contribution of the European Association for Cardiovascular Prevention Rehabilitation (EACPR). Eur Heart J. Aug 01 2016; 37(29): 2315-2381.
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- Perrson M, et al. Elevated Lp-PLA2 levels add prognostic information to the metabolic syndrome on incidence of cardiovascular events among middle-aged nondiabetic subjects. Arterioscler Thromb Vasc Biol 2007; 27(6): 1411-1416.
- Ridker PM, Macfadyen JG, Wolfert RL et al. Relationship of lipoprotein-associated phospholipase A2 mass and activity with incident vascular events among primary prevention patients allocated to placebo or to statin therapy: an analysis from the JUPITER trial. Clin Chem 2012; 58(5):877-86.
- Rosenson RS. Fenofibrate reduces lipoprotein associated phospholipase A2 mass and oxidative lipids in hypertriglyceridemic subjects with the metabolic syndrome. Am Heart Journal, March 2008; 155(3): 499.e9-16.
- Ryu SK, Mallat Z, Benessiano J et al. Phospholipase A2 enzymes, high-dose atorvastatin, and prediction of ischemic events after acute coronary syndromes. Circulation 2012; 125(6):757-66.
- Sabatine MS, et al. Prognostic utility of lipoprotein-associated phospholipase A2 for cardiovascular outcomes in patients with stable coronary artery disease. Arterioscler Thromb Vasc Biol 2007; 27(11): 2463-2469.
- Saougos VG, Tambaki AP, Kalogirou M, et al. Differential effect of hypolipidemic drugs on lipoprotein-associated phospholipase A 2. Arteriosclerosis, Thrombosis, and Vascular Biology 2007; 27: 2236-2243.
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- Wallentin L, Held C, Armstrong PW, et al. Lipoprotein-associated phospholipase A2 activity is a marker of risk but not a useful target for treatment in patients with stable coronary heart disease. J Am Heart Assoc. Jun 21 2016; 5(6).
- White HD, Held C, Stewart R, et al. Darapladib for preventing ischemic events in stable coronary heart disease. N Engl J Med. May 01 2014; 370(18): 1702-11.
- Winkler K, Hoffmann, NM, et al. Lipoprotein-associated phospholipase A2 predicts 5-year cardiac mortality independently of established risk factors and adds prognostic information in patients with low and medium high sensitivity C-reactive protein (The Ludwigshafen Risk and Cardiovascular Health Study). Clinical Chemistry, June 2007; 53(8): 1440-7.
Medical Policy Group, April 2004
Medical Policy Administration Committee, April 2004
Available for comment May 17-June 30, 2004
Medical Policy Group, April 2006 (1)
Medical Policy Group, August 2006 (1)
Medical Policy Group, June 2007 (3)
Medical Policy Group, June 2009 (1)
Medical Policy Group, June 2010 (1): Description updated, Key Points updated, References added, no coverage change
Medical Policy Group, June 2011 (1): Update to Key Points and References
Medical Policy Group, June 2012 (1): 2012 Update to Title, Key Points and References related to MPP update; no change in policy statement
Medical Policy Panel, June 2013
Medical Policy Group, September 2013 (1): Update to Key Points and References; no change to policy statement
Medical Policy Panel, June 2014
Medical Policy Group, June 2014 (1): Update to Key Points and References; no change to policy statement
Medical Policy Panel, June 2015
Medical Policy Group, June 2015 (3): 2015 Update to Key Points & References; no change in policy statement
Medical Policy Panel, December 2015
Medical Policy Group, January 2016 (3): Updates to Description, Key Points & References; no change in policy statement
Medical Policy Panel, December 2016
Medical Policy Group, December 2016 (3): 2016 Updates to Title, Key Points, Approved by Governing Bodies & References; removed Previous Coding section (for DOS prior to 01/01/07); no change in policy statement.
Medical Policy Panel, December 2017
Medical Policy Group, January 2018 (3): 2017 Updates to Description, Key Points & References; no change in policy statement.
Medical Policy Panel, December 2018
Medical Policy Group, January 2019 (9): 2018 Updates to Description and Key Points; no change to policy statement. Added new PLA code 0052U (effective 7/1/18), added CPT code 0423T.
Medical Policy Panel, December 2019
Medical Policy Group, December 2019 (9): 2019 Updates to Description, Key Points. No change to policy statement.
Medical Policy Panel, December 2020
Medical Policy Group, December 2020 (9): 2020 Updates to Description, Key Points, References. No change to policy statement.
This medical policy is not an authorization, certification, explanation of benefits, or a contract. Eligibility and benefits are determined on a case-by-case basis according to the terms of the member’s plan in effect as of the date services are rendered. All medical policies are based on (i) research of current medical literature and (ii) review of common medical practices in the treatment and diagnosis of disease as of the date hereof. Physicians and other providers are solely responsible for all aspects of medical care and treatment, including the type, quality, and levels of care and treatment.
This policy is intended to be used for adjudication of claims (including pre-admission certification, pre-determinations, and pre-procedure review) in Blue Cross and Blue Shield’s administration of plan contracts.
The plan does not approve or deny procedures, services, testing, or equipment for our members. Our decisions concern coverage only. The decision of whether or not to have a certain test, treatment or procedure is one made between the physician and his/her patient. The plan administers benefits based on the member’s contract and corporate medical policies. Physicians should always exercise their best medical judgment in providing the care they feel is most appropriate for their patients. Needed care should not be delayed or refused because of a coverage determination.
As a general rule, benefits are payable under health plans only in cases of medical necessity and only if services or supplies are not investigational, provided the customer group contracts have such coverage.
The following Association Technology Evaluation Criteria must be met for a service/supply to be considered for coverage:
1. The technology must have final approval from the appropriate government regulatory bodies;
2. The scientific evidence must permit conclusions concerning the effect of the technology on health outcomes;
3. The technology must improve the net health outcome;
4. The technology must be as beneficial as any established alternatives;
5. The improvement must be attainable outside the investigational setting.
Medical Necessity means that health care services (e.g., procedures, treatments, supplies, devices, equipment, facilities or drugs) that a physician, exercising prudent clinical judgment, would provide to a patient for the purpose of preventing, evaluating, diagnosing or treating an illness, injury or disease or its symptoms, and that are:
1. In accordance with generally accepted standards of medical practice; and
2. Clinically appropriate in terms of type, frequency, extent, site and duration and considered effective for the patient’s illness, injury or disease; and
3. Not primarily for the convenience of the patient, physician or other health care provider; and
4. Not more costly than an alternative service or sequence of services at least as likely to produce equivalent therapeutic or diagnostic results as to the diagnosis or treatment of that patient’s illness, injury or disease.