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Response to Comments: MolDX: Biomarkers in Cardiovascular Risk Assessment

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Response to Comments: MolDX: Biomarkers in Cardiovascular Risk Assessment
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Response to Comments
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06/01/2016
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Noridian's Response to Provider Recommendations (for comment period ending 12/07/2015):

CV risk assessment biomarker panels, except the basic lipid panel, are non-covered per this policy. Under preventative services, Medicare Part B covers cardiovascular disease screening, consisting of tests for cholesterol, lipid and triglyceride levels, every 5 years when ordered by a doctor. NCD 190.23 covers basic lipid panel testing for evaluating atherosclerotic CV disease, to monitor the progress of patients on anti-lipid dietary management and pharmacologic therapy for various lipid disorders. “Routine screening and prophylactic testing for lipid disorders are not covered by Medicare. Lipid testing in asymptomatic individuals is considered to be screening regardless of the presence of other risk factors such as family history, tobacco use, etc.”

This policy denies coverage for all CV risk assessment panels, except the basic lipid panel. Additionally, the policy defines the medical necessity for individual lipid biomarkers for CV risk assessment, each of which must be specifically ordered and the reason for the test order documented in the patient’s medical record. The policy denies coverage (not reasonable and necessary) for non-lipid biomarkers including biochemical, hematologic, immunologic, and genetic biomarkers for CV risk assessment.

A lipid biomarker may be covered to characterize a given lipid abnormality or disease, to determine a treatment plan or to assist with intensification of therapy. These markers include hs-CRP, Lp(a), Lp-PLA2, LDL particles, and Apo B. For each of these biomarkers, professional association recommendations and evidence from the scientific literature guide the limited use of these biomarkers. Wholesale use for every patient at every patient visit is not supported in the literature and is not anticipated per this policy.

Response To Comments

Number Comment Response
1 Asymptomatic vs Pre-existing Risk Factor Patients Throughout the draft policy, the contractor fails to recognize a distinction between the use of these tests for asymptomatic patients and the use of these tests for patients with pre-existing risk factors. The contractor misapplies this evidence to disallow coverage for any cardiovascular risk assessment tool other than the lipid panel and hs-CRP. The commenters indicates the draft LCD denies coverage for asymptomatic patients but also denies coverage for patients with pre-existing risk disease such as pre-diabetes, smoking, hypertension, and hyperlipidemia. The draft policy is clear. NCD 190.23 covers the basic lipid panel for testing symptomatic individuals. Screening is only covered as a preventative service in asymptomatic patients every 5 years. This policy denies coverage of CV risk assessment panels, except the basic lipid panel, for all patients. The third sentence in the 2nd paragraph specifically states that “Medicare coverage is limited to the use of specific biomarkers that may be used to characterize a given lipid abnormality or disease, to determine a treatment plan, or to assist with intensification of therapy, not as part of a broad CV risk assessment panel.” Any of the specific lipid biomarkers listed, when included in a CV risk assessment panel, regardless of the size of the panel are non-covered”. Additionally, the policy denies coverage of biochemical, immunologic, hematologic or molecular biomarker testing for CV risk assessment either as part of a CV risk assessment panel or when ordered individually. The policy does not prohibit a physician from ordering a specific CV lipid (risk assessment test on a symptomatic patient) that characterizes a lipid abnormality, helps determine a treatment plan or assists with intensification of therapy. However, the policy sets forth the limited intended use for each CV lipid markers based on the available science. It also provides regulatory authorities with intended use recommendations from professional association and pertinent scientific literature to allow them to review medical documentation and assess inappropriate utilization and over-utilization of services.
2 Hs-CRP Commenters note that although statins and LDL-C reduction reduce CV events, a significant residual risk for CV events remains in both primary and secondary prevention populations receiving statin therapy, and note that the residual risk is most evident in patients with metabolic syndrome and/or diabetes, and note that the prevalence of obesity has markedly shifted the risk profile towards metabolic syndrome. They also note that the use of generic statins has made the cost of treatment very low, and has enhanced the cost-effectiveness of biomarkers to identify additional patients at increased risk of CV events for whom more aggressive intervention may improve morbidity and mortality. The commenters note that CRP should be measured routinely in men >50 and women>60 with intermediate risk given its capacity to enhance risk prediction. The policy does cover hs-CRP testing for intermediate risk patients according to consensus guidelines.
3 Lipoprotein-Associated Phospholipase (Lp-PLA2) Commenter states that recent research has found vascular inflammation is the final common pathway for atherosclerotic heart disease. They note that hs-CRP levels of >10 mg/L has been shown to have clinical utility, noting that hs-CRP is associated with vulnerable plaque, suggesting it may represent plaque burden more than plaque activity. The commenter indicate that Lp-PLA2 is indicative of rupture-prone plaque and a strong independent predictor of CV risk; that it is elevated in response to macrophage activation in the intima/median of atherosclerotic plaque which is associated with vulnerable plaque formation. Increased levels of Lp-PLA2 and MPO mark a patient at near term risk (Penn). The commenters cite Lp-PLA2 has been cleared by the FDA as a marker for coronary heart disease and ischemic stroke. They also noted that there is a greater need to assess near-term CVD risk in order to determine which patients need therapy and which patients on therapy still have excessive risk, and suggest that by more accurately stratifying CVD risk, physicians can better manage patient outcomes. The commenters argue that Lp-PLA2 is useful in the following ways:
  • Identification and quantification of active rupture prone atherosclerotic plaques
  • Prediction of risk for primary and secondary CAD in addition to traditional risk factors
  • Prediction of risk for cerebrovascular disease events in addition to traditional risk factors
  • Prediction of risk of mortality in patient with known PAD
  • Assist physician in determining how to approach the treatment of risk factors for atherosclerosis
The commenter summarizes as follows: if Lp-PLA2 is elevated, the patient is at increased risk for an atherosclerotic complication – which indicates that known causative factors like dyslipidemia, insulin resistance, hypertension, smoking, etc., need to be more aggressively treated. 		Numerous large-scale systematic reviews and meta-analyses have examined whether Lp-PLA2 is an independent risk factor for CV disease. All are observational studies, most of which show a direct association of Lp-PLA2 with CV events. A study by Allison and colleagues (2007), and the Rotterdam study reported that the association was not significant after adjustment for established risk factors. The Emerging Risk Factors Collaboration (Di Angelantonio E, 2013) performed a patient-level meta-analysis of the association of novel lipid risk factors with CV risk. Records from 37 prospective cohort studies enrolling more than 165,000 individuals was combined to predict CV risk over a median follow-up of 10.4 yrs. The authors examined the independent association of markers with CV risk and the ability to reclassify risk into clinically relevant categories, for Lp-PLA2 there were 11 studies enrolling more than 32,000 individuals. The authors showed that Lp-PLA2 was an independent risk factor for CV events with a hazard ratio of 1.12 for each 1 SD increase in Lp-PLA2 activity. However, there was no significant improvement in risk reclassification following the addition of Lp-PLa2 to the reclassification model, with a net reclassification improvement of 0.21. The net reclassification improvement crossing 0.0 indicates that the addition of Lp-PLA2 to the model may result in either improvement or worsening of reclassification. Although Lp-PLA2 has been shown to be a significant predictor of risk for CHD events, stroke, and mortality in primary and secondary prevention studies, there are no randomized trials that demonstrate the benefits of lowering Lp-PLA2 with any specific therapies. Lipid-altering medications, including statins, fenofibrate, ezetimibe, and prescription omega-3 fatty acids, as well as weight loss, have been shown to reduce inflammatory markers, including Lp-PLA2. Notably, the degree of inflammatory marker reduction typically correlates with the extent of lipid lowering. While the NLA Biomarkers Expert Panel recommended LP-PLA2 testing be considered in intermediate-risk patients, as well as certain greater-risk subgroups (i.e., patients with CHD or a CHD risk equivalent, patients with family history of premature CHD, and patient with recent CHD events) to identify patients who might benefit from more intensive lipid therapy, no studies address whether testing strategies that use Lp-PLA2 levels lead to changes in patient management or improved patient outcomes. Whether Lp-PLA2 per se has a direct benefit on CVD events and mortality has been answered by the STABILITY trial. In this study, nearly 16,000 patients with stable coronary heart disease received either darapladib or placebo, and darapladib did not significantly reduce the risk of the primary composite end point of CV death, MI or stroke. These findings show that the measurement of Lp-PLA2 levels after institution of lipid-altering therapy is not warranted to help guide therapy. In the VISTA-16 randomized, phase III trial, a second phopholipase A inhibitor, varespladib in addition to atorvastatin was compared to atorvastatin alone in patients with acute coronary syndrome. This study was terminated after enrollment of 5189 subject for possible harm. While inhibitors of Lp-PLA2 have been developed, at least two phase III clinical trials with two medications failed to demonstrate improved health outcomes. In summary, there is a large body of literature evaluating Lp-PLA2 as an independent predictor of CV risk. To incorporate Lp-PLA2 into existing risk prediction models, the models must demonstrate improved classification into risk categories that will lead to more appropriate treatment. However, direct evidence that Lp-PLA2 improves health outcomes is lacking. Studies that directly evaluate patient management changes and/or improved patient outcomes are needed to determine if Lp-PLA2 has clinical value in CV diseases.
4 Lipoprotein Subclasses Over the past two decades, evidence has revealed that standard lipoprotein measurements of triglycerides, total cholesterol, LDL-C and HDL-C fail to identify many lipoprotein abnormalities that contribute to CHD and FAD risk. The commenters indicate that advanced lipoprotein tests (ALTs):
  • Enhance the accuracy of atherosclerosis risk prediction
  • Enhance the accuracy of outcome prediction
  • Assist in treatment selection and dose adjustment
  • Allow counsel of first-degree relatives of patients with atherosclerosis
Small, Dense Low-Density Lipoprotein (sd-LDL) – In patients with comparable LDL-C levels, higher sd-LDL concentrations carry a significantly greater risk (3 fold) of CAD and require more aggressive therapy. High Density Lipoprotein (HDL2b) – HDL2b is the key measure of efficacy of reverse cholesterol transport (RCT) and thus the most protective of the HDL subclasses. This comment is supported by articles from the early to the mid-1990s. The commenters note that HDL particles are not homogenous but rather consist of multiple subclasses that differ by density, migration characteristics, apoprotein content and relationships to disease. They note that increased HDL2b will aid in reversing or slowing down the progression of heart disease. The PROCAM study showed that risk prediction for MI using HDL subfractionation is independent of HDL cholesterol, and that several studies suggest that HDL2b is more strongly linked to risk of coronary artery disease than HDL cholesterol (1978-2004). 		The commenters support for lipoprotein subclasses is largely based on nearly 20 year old or older articles. Aside from a greater risk of CAD, no prospective studies on patient management or outcomes were provided, and none were found by this responder. In addition, HR Superko (2009) notes that not all studies have revealed an association of HDL subclass with CHD. In the Caerphilly and Speedwell Collaborative Heart Disease Studies involving nearly 5000 middle-aged men followed for 3-5 years, both HDL2 and HDL3 were inversely associated with CHD, and concluded that the risk for CHD based on HDL-C could not be improved on the determination of HDL2 or HDL3. The atherosclerosis Risk in Communities study also reported no large differences between HDL2-C in subjects with and without known CHD.
5 Lipoprotein (a) (Lp(a)) The commenter offers a number of publications ranging from 1987 to 2006 to refute the draft policy statement that “there are no clinical trials that have adequately tested the hypothesis that Lp(a) reduction reduces the incidence of first or recurrent CVD events”. The commenters noted that the gene is inherited in a dominant fashion which may explain why some patients with relatively normal blood LDL-C and HDL-C values suffer from atherosclerosis. They present the biological interactions, and note that typical lipid-reducing drugs, diet, and exercise have little to no effect in lowering Lp(a) levels. Another commenter notes that the development of recent guidelines has become highly regulated and sometimes narrowly focused in the type of information that is reviewed and summarized, and the aim of committee members is to give a heavily weighted focus on large populations and well-controlled outcome studies in creating a document for the health care professional to best manage patient care. However, the commenter states that guidelines should not supersede the individual physician’s responsibility of make appropriate medical decisions in the best interest of their patient. The commenter notes that by using novel biomarkers, like Lp(a), clinicians may use this in a cost effective manner to identify patients that may need additional therapy to prevent a CV event. The Emerging Risk Factors Collaboration published a patient-level meta-analysis of 37 prospective cohort studies enrolling nearly 155,000 individual. For Lp(a), evidence from 24 studies on roughly 133,000 subjects reported that Lp(a) was an independent risk factor for reduced CV risk, with an adjusted HR for CV events of 1.13. The authors noted that the addition of Lp(a) to traditional risk factors resulted in a small improvement in risk prediction, and a reclassification analysis found no significant improvement in the net reclassification index. Also a systematic review by Genser et al included 67 prospective studies on nearly 182,000 subjects, with pooled analysis on 37 studies that reported the end points of CV events. The relative risk for these studies, comparing the uppermost and lowest strata of Lp(a) ranged from 1.64 to 2.37. The risk ratio for CV events was higher in patients with previous CVD compared with patients without previous disease, but there was no significant associations found between Lp9A) levels, overall mortality, or stroke. Multiple randomized controlled trials and studies , including the Lipid Research Clinics Coronary Primary Prevention Trial, the Framingham Offspring Study, The ARIC study, The JUPITER study, The LIPID RCT, the AIM-HIGH, the Copenhagen City heart Study The Edinburgh Artery Study, the Cardiovascular Health Study , the Physicians’ Health Study, the European Concerted Action on Thrombosis and Disabilities (ECAT) study, and several meta-analyses have examined the relationship between Lp9a) and CV risk. The independent association of Lp(a) with vascular disease is consistent across studies but modest in size. Genetic studies have examined the association of various genetic loci with Lp(a) levels, and Mendelian randomization studies have examined whether Lp(a) is likely causative for CAD. Three separate loci appear to be associated with increased Lp(a) levels, and 2 of these loci are independently associated with coronary disease. This finding does imply that elevated Lp(a) levels are causative of coronary disease, not simply associated with coronary disease. At the current time, while there is considerable evidence that Lp(a) is an independent risk factor for CV disease, there is a lack of evidence to determine whether Lp(a) can be used as a target of treatment. Although studies have shown that Lp(a) is reduced in patients on statin therapy, there is little data to suggest how this test should be incorporated into management algorithms to improve patient outcomes.
6 Apolipoprotein B The commenters state that numerous recent (ranging from 1986 to 2009)studies demonstrate the value of apolipoprotein B in risk assessment, and comment that others have suggested that apolipoprotein measurements replace the standard LDL-C and HDL-C because they are more accurate, more reproducible, and reflect CHD risk better than standard lipoprotein cholesterol measurements. They note that with increasing prevalence of diabetes and metabolic syndrome, which tend to be associated with larger numbers of small, dense LDL but normal LDL-C, the direct measurement of apo B is favored over the Friedewald calculation to accurately account for risk and deliver proper treatment. The clinical importance of determining apo B values lies not only in the identification of hyperapobetalipoproteinemia, but in the association of elevated apo B with other CV risk predictors that results in identification of a group of patients at extremely high risk for CV events. They note that in the Quebec CV Study, small LDL, elevated fasting insulin values and elevated apo B identified a group of individuals who has a 20-fold increased risk for CV events. In 2012, Robinson et al published results of a Bayesian random-effects meta-analysis of RCTs to compare the effectiveness of lowering apo B versus LDL-C and non-HDL- C for reducing CVD, CHD and stroke risk. The analysis consisted of more than 131,000 patients from 25 RCTs including 12 trials on statins, 5 on niacins, 4 on fibrates, 1 on simvastatin plus ezetimibe, 1 on aggressive versus standard LDL and on blood pressure targets, and 1 on ileal bypass surgery. In the analysis of all trials, each apo B decrease of 10 mg/dL resulted in a 6% decrease in major CVD risk and a 9% decrease in CHD risk prediction, but stroke risk was not decreased. Decreased apo B levels were not superior to decreased non-HDL- levels in decreasing CVD and CHD risk prediction. When non-HDL-C plus LDL-C decrease were added to apo B decrease, CVD risk prediction improved slightly (BF=1.13) but not CHD risk prediction. Stroke risk prediction worsened. In summary, any apo B decrease did not consistently add information to LDL, non-HDL or LDL/non-HDL decreases to improve CVD risk prediction when analyzed across lipid-modifying treatment of any types. In another 2012 publication, Sniderman et al reported more than 9300 acute MI patients and found apo B to be more accurate than non-HDL-C as a marker for CV risk. The Emerging Risk Factors Collaboration examined a variety of traditional and a nontraditional lipid markers for risk prediction. For apo B, evidence from 26 studies on over 139,000 subjects reported that apo B was an independent risk factor for CV events, but on reclassification analysis, when apo B and apo AI were substituted for traditional lipids, there was no improvement in risk prediction. Despite numerous large prospective cohort studies and nested case-control studies suggesting that apo B is a better predictor of CV risk than LDL-C, some meta-analyses have concluded that apo B is not a better predictor of CV risk than HDL or non-HDL combined with LDL. Furthermore, there is uncertainty around the degree of improvement in risk prediction, and whether the magnitude of improvement is clinically significant. Furthermore, apo B is not included in the most commonly used risk models such as the Framingham and the Prospective CV Munster Study (PROCAM) score model. The commenter cites no published literature to conclude that the use of apo B levels will improve outcomes in routine clinical care. No studies have demonstrated improved health outcomes by using apo B in place of LDL-C for either risk assessment and/or treatment response. Neither the Framingham prediction model, widely used for risk assessment, nor the widely used ATP III guidelines provide the tools necessary for clinicians to incorporate apo B measurements into routine assessment and management of hyperlipidemic patients, thus creating difficulties in interpreting and applying apo B and/or apo B/apo AI measurement to routine clinical care. Robinson JG, Wang S, Jacobson TA. Meta-analysis of comparison of effectiveness of lowering apolipoprotein B versus low-density lipoprotein cholesterol and nonhigh-density lipoprotein cholesterol for cardiovascular risk reduction in randomized trials. Am J Cardiol. Nov 15 2012;110(10):1468-1476. PMID 22906895. Sniderman AD, Islam S, Yusuf S, et al. Discordance analysis of apolipoprotein B and non-high density lipoprotein cholesterol as markers of cardiovascular risk in the INTERHEART study. Atherosclerosis. Dec 2012;225(2):444-449. PMID 23068583.
7 LDL-P The commenter notes that the amount of cholesterol carried on each apoB molecule can vary considerably and is believed this heterogeneity of cholesterol content creates the discordance amongst related measures of risk. They note that apoB particles can contain a normal mass of cholesterol, or be depleted or enriched with cholesterol. The commenter cites Tabas et al 2007 that the number of particles (LDL-P) or apoB in the plasma is the driving force of cholesterol and particles into the subendothelial space commencing atherogenesis. They specify that the Women’s Health Study (WHS), the Multi-Ethnic Study of Atherosclerosis (MESA), the Malmo Diet and Cancer Study (MALMO) and the Jupiter study have shown that LDL-P adds incremental value to finding CV risk in patients. So, the question is whether apoB or LDL-P is a better predictor of risk, although both are highly correlated, or are they complementary? Cole et al (2013) reported that apoB and LDL-P are nearly equivalent to asses CVD risk, but noted that both are clearly superior to LDL-C. The commenter notes that the emerging body of evidence seems remarkably consistent that the measure of particle concentrations, originally by apoB and now by LDL-P constitutes a better way to assess CV compared with LDL-C. The policy states: “LDL particle number (NMR LDL-P), rather than LDL size or subclass, has been shown to be significantly associated with CV risk independent of traditional lipid and established risk factors. The American Association of Clinical Endocrinologists (AACE), the National Lipid Association (NLA), the American Diabetes Association (ADA) in conjunction with the American College of Cardiology (ACC), and the American Association of Clinical Chemistry (AACC) have developed consensus position statement on lipoprotein particle management in individuals at risk for CVD. Due to the prevalence of discordantly elevated LDL-P despite achieving low LDL-C and non-HDL-C values, each endorses use of LDL particle number to evaluate LDL response and aid decision making regarding potential adjustment of therapy. The 2013 AACE Comprehensive Diabetes Management Algorithm, as well as the 2015 joint AACE/American College of Endocrinology Clinical Practice Guidelines for Comprehensive Diabetes Mellitus Care, advocate specific LDL particle number goals for statin treated diabetic patients at high CV risk.” The policy does not deny testing for LDL-P when ordered appropriately and documented in the medical record.
8 Vitamin D The commenters disagree with the draft policy statement that vitamin D supplementation had no effect on CV disease risk. They note that low vitamin D levels correlate with markers of inflammation, oxidative cell damage, and cell adhesion, all of which promote atherosclerosis. They note that men with low levels are at > twice the risk of heart attack, noting the HR for CV death was 2.22 for vitamin D deficient men. The commenters noted that ~20% of patients suffer from joint pain with statin therapy, and that 95% of vitamin D deficient patients can tolerate statins if vitamin D levels are increased yielding a decrease in LDL by 50-70%. Groups at risk for developing adverse CV events include older adults and individuals with obesity and a sedentary lifestyle who have poor dietary habits. These same individuals are likely at risk for vitamin D deficiency because their sedentary life style includes limited sun exposure and poor dietary habits that may result in decreased intake of vitamin D. Determining a casual effect between vitamin D deficiency and CV events would require large prospective trials designed to demonstrate that correcting vitamin D deficiency reduces adverse CV events. Drs. Andersons and Muhlestein note in chapter 28 in the Handbook of Vitamin D in Human Health: Prevention, treatment and toxicity (edited by RR Watson, 2013) that “not all recent evidence has been supportive of CV disease association or the benefits of vitamin D supplementation.” They cite a systematic review of 13 observational studies that the associations between vitamin D status and cardiometabolic outcomes were heterogeneous, while another review included 51 trials reported that the evidence that vitamin D status and vitamin D supplementation could be used to reduce CV risk and mortality was inconclusive. In the Women’s Health Initiative, low dose vitamin D plus calcium supplements did not improve CV outcomes in post-menopausal women.
9 Apo E Genotype The commenters state that a Medicare contractor denied coverage for Apo E genotyping last year. They state that clinicians believe this test is essential for prescribing the right therapy for each patient. They state that E2E2 hyper-producers of cholesterol tend to respond better to statins than drugs that effect cholesterol absorption. They also note that individuals with E2:E4 and E3:E4 have a strong predisposition toward cholesterol hyper-absorption and usually respond to diet and medications that effect cholesterol absorption. They note that homozygous E4 have a marked increased risk for CHD, have a strong predisposition toward cholesterol hyper-absorption and usually respond very well to diet and medication that effect cholesterol absorption, but require a more aggressive approach to CHD risk modification. Dysbetalipoproteinemia or hyperlipoproteinemia type III is a rare genetic disorder with an estimated incidence in the US population of 1 in 5,000-10,000 people. Symptoms of hyperlipoproteinemia type III do not appear unless a secondary genetic or environmental factor increases lipid levels – diabetes, obesity or hypothyroidism. However, the most consistent finding of this disease is the development of xanthomas, and signs and/or symptoms of CHD. The majority of cases occur during early adulthood, although cases have been reported in children and in the elderly. The diagnosis of dysbetalipoproteinemia is based upon a thorough clinical evaluation including identification of xantomata, detailed patient history, diagnostic laboratory workup demonstrating elevated cholesterol and triglyceride levels, elevated VLDL and VLDL to plasma triglyceride ratio. Apo E phenotyping by a variety of methods including isoelectric focusing is a quick, reliable and available procedure for identifying the alleles. Apo E genotyping by PCR methods provide confirmatory testing. Homozygous E2E2, and E4E4 individuals, as well as heterozygous E2:E4 or E3:E4 individuals, all respond to diet and lifestyle changes that treat the triggering cause (diabetes, obesity, insulin resistance, etc). In the rare event that a definitive diagnosis is unable to be obtained, a denied claim for Apo E can be appealed with documentation of medical necessity.
10 Testimonials Approximately 70 signed testimonial form letters were received from NC and CA. This contractor views multiple signed form letters as a single comment. Each complained that the policy was too restrictive. No scientific literature was provided.
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