James A. Underberg, MD, MS, FACPM, FACP, FNYAM, FASPC, FNLA Lipidology and Cardiovascular Disease Prevention Clinical Assistant Professor of Medicine NYU Medical School and NYU Center for CV Prevention Director, Bellevue Hospital Lipid Clinic Past President, National Lipid Association New York, NY Twitter: @LipidDoc Jointly provided by and This activity is supported by educational funding provided by Amgen. Elevated LDL-C Cardiovascular Pathobiology
Support for LDL-C Causality in ASCVD Four compelling lines of evidence Experimental models Observational human data Genetic studies Interventional human trials ASCVD = atherosclerotic cardiovascular disease Substantial CVD Risk Remains after ACS 43,810 Patients with ACS in GRACE Registry: 6-month Death Rate 16 Death (%) 12 8 4 STEMI NSTEMI UA 0 0 30 60 90 120 150 180 Days GRACE = global registry of acute coronary events STEMI: ST-segment elevation MI NSTEMI: nonst-segment elevation MI UA: unstable angina Fox KAA et al. BMJ. 2006;333:1091.
Disease Trajectories and CVD Risk Reduction Packard CJ et al. Vasc Pharmacol. 2015;71:37-39. LDL-C Reduction Cardiovascular Benefits
Table 6. Risk-Enhancing Factors for Clinician Patient Risk Discussion Risk Enhancing Factors Family history of premature ASCVD (males, age <55 y; females, age <65 y) Primary hypercholesterolemia (LDL C, 160 189 mg/dl [4.1 4.8 mmol/l); non HDL C 190 219 mg/dl [4.9 5.6 mmol/l])* Metabolic syndrome (increased waist circumference, elevated triglycerides [>175 mg/dl], elevated blood pressure, elevated glucose, and low HDL C [<40 mg/dl in men; <50 in women mg/dl] are factors; tally of 3 makes the diagnosis) Chronic kidney disease (egfr 15 59 ml/min/1.73 m 2 with or without albuminuria; not treated with dialysis or kidney transplantation) Chronic inflammatory conditions such as psoriasis, RA, or HIV/AIDS History of premature menopause (before age 40 y) and history of pregnancyassociated conditions that increase later ASCVD risk such as preeclampsia High risk race/ethnicities (e.g., South Asian ancestry) Table 6 (continued) Risk Enhancing Factors Lipid/biomarkers: Associated with increased ASCVD risk o Persistently* elevated, primary hypertriglyceridemia ( 175 mg/dl); o If measured: Elevated high sensitivity C reactive protein ( 2.0 mg/l) Elevated Lp(a): A relative indication for its measurement is family history of premature ASCVD. An Lp(a) 50 mg/dl or 125 nmol/l constitutes a risk enhancing factor especially at higher levels of Lp(a). Elevated apob 130 mg/dl: A relative indication for its measurement would be triglyceride 200 mg/dl. A level 130 mg/dl corresponds to an LDL C >160 mg/dl and constitutes a riskenhancing factor ABI <0.9
Treatments for Hypercholesterolemia Lifestyle Change Physical activity Medical nutrition therapy Smoking cessation Pharmacologic Therapy Statins Cholesterol absorption inhibitors Bile acid sequestrants Fibrates Omega-3 fish oil PCSK9 inhibitors MTP inhibitors Antisense apo B oligonucleotide Combination therapies Jellinger P et al. Endocr Practice. 2017;23:479-497. Statins The Gold Standard for LDL-C Reduction and ASCVD Prevention
Statins Protect against Recurrence in ASCVD Patients Secondary Prevention Statin Trials: CHD Event Rates -P=placebo; -AT=atorvastatin; -PR=pravastatin O Keefe JH et al. J Am Coll Cardiol. 2004;43:2142-2146. Lower On-treatment LDL-C with Statins Predicts Lower ASCVD Risk LDL-C Levels and Risk of CV Events LDL-C (mg/dl) 175 150 <175 125 <150 100 <125 75 <100 50 <75 <50 0.25 0.5 0.75 1 Adjusted Hazard Ratio 95% Cl Boekholdt SM et al. J Am Coll Cardiol. 2014;64:485-494.
Elevated LDL Causes ASCVD LDL-C lowering Reduces ASCVD Cumulative LDL burden atheroprogression On-treatment LDL-C ASCVD Best evidence is for LDL receptors But likely not exclusive to this mechanism Early treatment to LDL-C is better than late treatment Lowest LDL-C is best Ference BA et al. Eur Heart J. 2017;38:2459-2472. Primary Prevention: Assess ASCVD Risk in Each Age Group Emphasize Adherence to Healthy Lifestyle Age 0-19 y Lifestyle to prevent or reduce ASCVD risk Diagnosis of Familial Hypercholesterolemia statin Age 20-39 y Estimate lifetime risk to encourage lifestyle to reduce ASCVD risk Consider statin is family history premature ASCVD and LDL-C >160 mg/dl (>4.1 mmol/l0 Age 40-75 y and LDL-C 70-<190 mg/dl ( 1.8-<4.9 mmol/l) without diabetes mellitus 10 year ASCVD risk percent begins risk discussion LDL-C 190 mg/dl (24.9 mmol/l) No risk assessment; High-Intensity statin (Class I) Diabetes mellitus and age 40-75 y Moderate-Intensity statin (Class I) Diabetes mellitus and age 40-75 y Risk assessment to consider high-intensity statin (Class IIa) Age >75 y Clinical assessment, Risk reduction
<5% Low Risk 5% - <7.5% Borderline Risk 7.5% - <20% Intermediate Risk 20% High Risk Risk discussion: Emphasize lifestyle to reduce risk factors (Class I) Risk discussion: If risk enhancers present then risk discussion regarding moderateintensity statin therapy (Class IIb) Risk discussion: If risk estimate + risk enhancers favor statin, initiate moderate-intensity statin to reduce LDL- C by 30% - 49% (Class I) Risk discussion: Initiate statin to reduce LDL-C 50% (Class I) If risk decision is uncertain: Consider measuring CAC in selected adults: CAC = zero (lowers risk; consider no statin, unless diabetes, family history of premature CHD, or cigarette smoking are present) CAC = 1.99 favors statin (especially after age 55) CAC = 100+ and/or 75th percentile, initiate statin therapy Secondary Prevention
Table 4. Very High-Risk* of Future ASCVD Events Major ASCVD Events Recent ACS (within the past 12 mo) History of MI (other than recent ACS event listed above) History of ischemic stroke Symptomatic peripheral arterial disease (history of claudication with ABI <0.85, or previous revascularization or amputation) Table 4 (continued) High-Risk Conditions Age 65 y Heterozygous familial hypercholesterolemia History of prior coronary artery bypass surgery or percutaneous coronary intervention outside of the major ASCVD event(s) Diabetes mellitus Hypertension CKD (egfr 15-59 ml/min/1.73 m 2 ) Current smoking Persistently elevated LDL-C (LDL-C 100 mg/dl [ 2.6 mmol/l]) despite maximally tolerated statin therapy and ezetimibe History of congestive HF
Intensive Statin Therapy Reduces MACE PROVE IT - TIMI 22: Study Design 4,162 patients with an Acute Coronary Syndrome <10 days Double-blind Standard Statin Therapy Pravastatin 40 mg ASA + Standard Medical Therapy 2x2 Factorial: Gatifloxacin vs placebo Intensive StatinTherapy Atorvastatin 80 mg Cannon CP et al. N Engl J Med. 2004;350:1495-1504. Duration: Mean 2 year follow-up (>925 events) Primary Endpoint: Death, MI, documented UA requiring hospitalization, revascularization (>30 days after randomization), or stroke Intensive Statin Therapy: PROVE IT-TIMI 22 All-Cause Death or Major CV Events % of Patients with MACE 30 25 20 15 10 5 Intensive Statin Therapy Pravastatin 40mg (26.3%) Standard Statin Therapy Atorvastatin 80mg (22.4%) 16% RR (P=0.005) Cannon CP et al. N Engl J Med. 2004;350:1495-1504. 0 0 3 6 9 12 15 18 21 24 27 30 Months of Follow-up
Intensity of Statin Therapies, Based on Clinical Trials High, Moderate, and Low-intensity High-intensity Statin Therapy Moderate-intensity Statin Therapy Low-intensity Statin Therapy Daily dose lowers LDL-C, on average, by approximately 50% Atorvastatin 40*-80* mg Rosuvastatin 20*-40** mg *Statins demonstrated reduction in major CVD events **FDA-approved doses not tested in clinical trials Daily dose lowers LDL-C, on average, by approximately 30% to <50% Atorvastatin 10* (20**) mg Rosuvastatin (5**) 10* mg Simvastatin 20*-40* mg Pravastatin 40* (80**) mg Lovastatin 40* mg Fluvastatin XL 80** mg Fluvastatin 40 mg BID* Pitavastatin 2-4** mg Daily dose lowers LDL-C, on average, by approximately <30% Simvastatin 10** mg Pravastatin 10*-20* mg Lovastatin 20* mg Fluvastatin 20**-40** mg Pitavastatin 1** mg Stone NJ et al. Circulation. 2014;129(25 Suppl 2):S1-45. Goff DC et al. Circulation. 2014;129(25 Suppl 2):S49-73. Add-on Therapies to Statins To Enhance LDL-C Reduction and Lower CVD Risk
Efficacy of Statin Treatment to Lower LDL-C Only about 1/3 of High-risk Patients Achieve LDL-C Goal 80 70 All Patients High-Risk 1 o Prevention Secondary Prevention 71 Patients Achieving LDL-C Goal (%) 60 50 40 30 20 10 51 22 30 13 31 Electronic Medical Records (2003-2010) 0 High-Risk Patients CHD Patients At High-Risk 1 o Prev Goal (<100 mg/dl) At High-Risk LDL-C Goal (<70 mg/dl) CHD Patients At 2 o Prev at LDL-C Goal Goal (<100 mg/dl) (<70 mg/dl) Jones PH et al. J Am Heart Assoc. 2012;1:e001800. Residual CHD Risk Despite Statin Monotherapy
Considerable ASCVD Risk Remains Despite Even Intensive Statin Monotherapy Statin-based LDL-C lowering to reduce CAD risk 2-10 Relative Risk Reduction (%) 0-10 -20-30 -40-50 -60-70 -80-90 -100 4S CARE WOSCOPS LIPID AFCAPS HPS CARDS ASCOT 24% 24% 24% 29% 34% 37% 37% 36% R E S I D U A L R I S K JUPITER 44% Statins reduce CAD/CVD risk by ~24%-44% but 56% to 76% residual risk remains 1-10 1. Adapted from Rader DJ et al. http://www.medscape.org/viewarticle/569095. 2. Shepherd J et al. N Engl J Med. 1995;333:1301-1307. 3. Scandinavian Simvastatin Survival Study Group. Lancet. 1994;344:1383-1389. 4. Ballantyne CM. Am J Cardiol. 1998;82:3Q-12Q. 5. Sacks FM et al. N Engl J Med. 1996;335:1001-1009. 6. Downs JR et al. JAMA. 1998;279:1615-1622. 7. LIPID Study Group. N Engl J Med. 1998;339:1349-1357. 8. Brown BG. Eur Heart J Suppl. 2005;7:F34-F40. 9. Grundy SM et al. Circulation. 2004;110:227-239. 10. Ridker PM et al. N Engl J Med. 2008;359:2195-2207. Non-statin Add-on LDL-lowering Therapies Ezetimibe
Ezetimibe: IMPROVE IT Trial Design Patients stabilized post-acs 10 days LDL-C 125 mg/dl (or 100 mg/dl if prior statin) Double-blind n ~ 18,000 ASA + Standard Medical Therapy Simvastatin 40 mg* Ezetimibe / Simvastatin 10/40 mg* *up-titrated to 80 mg if LDL-C >79 mg/dl Follow-up visit day 30, every 4 months Duration: Minimum 2.5 year follow-up (5250 events) Primary Endpoint: CV death, MI, Hospitalization for UA, Revascularization (>30 days after randomization), or Stroke Study drug is administered once daily in the evening. Cannon CP et al. Am Heart J. 2008;156:826-832. IMPROVE-IT Trial LDL-C and Other Lipid Effects with Ezetimibe 1 Yr Mean LDL-C TC TG HDL hscrp Simva 69.9 145.1 137.1 48.1 3.8 EZ/Simva 53.2 125.8 120.4 48.7 3.3 Δ in mg/dl -16.7-19.3-16.7 +0.6-0.5 Median Time avg 69.5 vs. 53.7 mg/dl Cannon CP et al. Am Heart J. 2008;156:826-832.
IMPROVE IT Trial: Ezetimibe + Simvastatin Lowers ASCVD More than Simvastatin Alone ~10% relative risk after 1 st year Primary endpoint: cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary revascularization Cannon CP et al. N Engl J Med. 2015;372:2387-2397. Non-statin Add-on LDL-lowering Therapies PCSK9 Inhibitors
Rationale Behind PSCK9 as a Therapeutic Target Rationale Behind PSCK9 as a Therapeutic Target PCSK9 # of LDL Receptors LDL-C PCSK9 # of LDL Receptors LDL-C
Physiology of PCSK9 Proprotein Convertase Subtilisin/Kexin Type 9 PCSK9 retains LDL-R in endosome LDL-R destruction LDL removal plasma LDL-C Sever P, Mackay J. Br J Cardiol. 2014;21:91-93. Giugliano RP et al. Lancet. 2012;380:2007-2017. Sabatine MS et al. N Engl J Med. 2015;372:1500-1509. PCSK9 Mutations and Effect on LDL Metabolism Gain of Function LDL-R levels LDL clearance Loss of Function LDL-R levels LDL clearance LDL High risk for ASCHD) LDL Protection from atherosclerosis and CHD LDL = low-density lipoprotein Adapted from Catapano AL, Papadopoulos N. Atherosclerosis. 2013;228:18-28. Soufi M et al. Gene. 2013;521:200-203.
PCSK9 Loss-of-Function Mutations Resulted in Lower LDL-C Levels and Reduced CHD Rates Wild-type PCSK9 degrades LDL receptors 1,2 1%-3% of population have a loss-offunction (LOF) mutation LOF mutations increase hepatic LDL receptor expression, reducing LDL-C levels by 15%-40% 2,3 CHD incidence was reduced 47%- 88% in PCSK9 loss-of-function mutation carriers compared with normal individuals 3 CHD (%) 12 10 8 6 4 2 0 Black Subjects P=0.008 9.7 1.2 n=3,278 n=85 White Subjects 11.8 P=0.008 6.3 n=9,223 n=301 Normal Subject Mutation Carrier 1. Peterson AS et al. J Lipid Res. 2008;49:1595-1599. 2. Cohen J et al. Nature Genetics. 2005;37:161-165. 3. Cohen JC et al. N Engl J Med. 2006;354:1264-1272. PCSK9 Inhibition Enhanced LDL-C Reduction and Reduced CVD Risk
LDL-C Lowering Efficacy Dose-Response of Alirocumab and Evolocumab* ALIROCUMAB mab added to stable atorva dose of 10-40 mg QD with LDL-C 100 mg/dl n=183, Duration = 12 wks % Change LDL-C EVOLOCUMAB mab added to stable statin and LDL-C > ~85 mg/dl n=631, Duration = 12 wks % Change LDL-C 50 mg Q2W -35% 70 mg Q2W -42% 100 mg Q2W -59% 105 mg Q2W -60% 150 mg Q2W -67% 140 mg Q2W -66% 300 mg Q4W -43% 280 mg Q4W -42% 350 mg Q4W -50% 420 mg Q4W -50% *Added to Stable Statin Therapy - Week 12 Giugliano et al. Lancet. 2012;380:2007-2017. McKenney et al. J Am Coll Cardiol. 2012;59:2344-2353. Clinical Outcomes of PCSK9 Inhibitors Meta-Analysis of 35 Randomized Clinical Trials End Point Fixed-effects Odds Ratio (95% CI) P Myocardial Infarction 0.72 (0.64-0.81) <0.001 Stroke 0.8l (0.68-0.97) 0.02 Coronary Revascularization 0.79 (0.72-0.86) <0.001 All Cause Mortality* 1.00 (0.88-1.14) 0.999 Cardiovascular Mortality 1.01 (0.85-1.19) 0.936 Neurocognitive Adverse Events 1.12 (0.94-1.33) 0.218 *: A significant association was shown between LDL-C and benefit in all-cause mortality Karatasakis A et al. J Am Heart Assoc. 2017;6:e006910.
Clinical Data on Alirocumab Alirocumab: ODYSSEY Outcomes Evaluation of Alirocumab After ACS Schwartz GG. Am Heart J. 2014;168:682-689.
ODYSSEY Outcomes Design: Alirocumab Dose Adjustments to Stay within LDL-C Target Range Undesirably high baseline range 0 15 25 50 70 LDL-C (mg/dl) Schwartz GG et al. Am Heart J. 2014;168:682-689.e1. ODYSSEY Outcomes Design: Alirocumab Dose Adjustments to Stay within LDL-C Target Range We attempted to maximize the number of patients in the target range and minimize the number below target by blindly titrating alirocumab (75 or 150 mg SC Q2W) or blindly switching to placebo. 0 Below target Acceptable range 15 25 Target range Alirocumab 50 70 LDL-C (mg/dl) Undesirably high baseline range Approximately 75% of months of active treatment were at the 75 mg dose Schwartz GG et al. Am Heart J. 2014;168:682-689.e1. Steg G. Presented at: American College of Cardiology; March 2018.
ODYSSEY Outcomes: Alirocumab Lowers LDL-C Mean LDL-C (mg/dl) 105 90 75 60 45 30 15 93.3 37.6 55.7 mg/dl 62.7% 96.4 42.3 54.1 mg/dl 61.0% Placebo Alirocumab 101.4 48.1 mg/dl 53.3 54.7% 0 0 4 8 12 16 20 24 28 32 36 40 44 48 Months Since Randomization Excludes LDL-C values after premature treatment discontinuation or blinded switch to placebo Approximately 75% of months of active treatment were at the 75 mg dose Steg G. Presented at: American College of Cardiology; March 2018. Alirocumab: ODYSSEY Outcomes Alirocumab MACE by 15% ARR* 1.6% 4-Point MACE = CHD death, Non-fatal MI, Ischemic stroke Unstable angina requiring hospitalization Steg G. Presented at: American College of Cardiology; March 2018. *Based on cumulative incidence.
Alirocumab: ODYSSEY Outcomes Alirocumab MACE by 15%, same as Evolocumab ARR* 1.6% 4-Point MACE = 4-Point MACE = CHD CHD death, death, Non-fatal non-fatal MI, MI, Ischemic ischemic stroke Unstable unstable angina requiring hospitalization Steg G. Presented at: American College of Cardiology; March 2018. *Based on cumulative incidence. Alirocumab: ODYSSEY Outcomes Alirocumab Reduces MACE Steg G. Presented at: American College of Cardiology; March 2018. Late-Breaker Presentation.
Alirocumab Effects on Main Secondary Efficacy Endpoints: Hierarchical Testing in ODYSSEY Outcomes *Nominal P-value Steg G. Presented at: American College of Cardiology; March 2018. Late-Breaker Presentation. Alirocumab: ODYSSEY Outcomes Alirocumab May Reduce Total Mortality* *Nominal P-value Based on cumulative incidence ARR 0.6% Steg G. Presented at: American College of Cardiology; March 2018. Late-Breaker Presentation.
Alirocumab: ODYSSEY Outcomes Post Hoc Analysis: All-cause Death by Pre-specified Baseline LDL-C Subgroups Steg G. Presented at: American College of Cardiology; March 2018. Late-Breaker Presentation. Clinical Data on Evolocumab
Evolocumab: FOURIER LDL Cholesterol Sabatine MS et al. Am Heart J. 2016;173:94-101. Evolocumab: FOURIER Primary Efficacy Endpoint ARR 2.0% Sabatine MS et al. Am Heart J. 2016;173:94-101.
Evolocumab: FOURIER Key Secondary Endpoint Sabatine MS et al. Am Heart J. 2016;173:94-101. Evolocumab: FOURIER Landmark Analysis Sabatine MS et al. Am Heart J. 2016;173:94-101.
Lowest LDL-C is Best for ASCVD Prevention Evolocumab (FOURIER) Key 2 o Endpoint (CV Death, MI, or Stroke) LDL-C (mg/dl) Adj HR (95% CI) <20 0.69 (0.56-0.85) 20-50 0.75 (0.64-0.86) 50-70 0.87 (0.73-1.04) 70-100 0.90 (0.78-1.04) > 100 referent P = 0.0001 Giugliano RP et al. Lancet. 2017;390:1962-1971. 20 40 60 80 100 120 140 160 180 20 40 LDL-C 60 (mg/dl) 80 at 4 weeks 100 120 140 Evolocumab Appears Effective (CVD) and Safe (SAE, D/C) to LDL-C <10 mg/dl* CARDIOVASCULAR EFFICACY 15 HR 0.69 (0.49-0.97) P=0.03 11.9 100 mg/dl <10 mg/dl SAFETY 30 25 HR 0.94 (0.74-1.20) P=0.61 23.3 22.8 100 mg/dl <10 mg/dl Percent 10 5 7.3 HR 0.59 (0.37-0.92) P=0.02 7.8 4.4 Percent 20 15 10 5 HR 1.08 (0.63-1.85) P=0.78 3.4 3.4 0 CVD, MI, Stroke, UA, Cor Revasc CVD, MI, Stroke *Exploratory Analysis of FOURIER n = 504: Median [IQR] LDL-C: 7 [5-9] mg/dl Giugliano RP. Presented at: ESC Congress 2017, Barcelona; 8/28/2017. 0 Serious adverse event AE -> drug discontinued An Academic Research Organization of Brigham and Women s Hospital and Harvard Medical School
Ebbinghaus: Evolocumab Evaluation of Cognition with Aggressive LDL-C Lowering CANTAB Tests Adj P trend Executive function 0.11 Working memory 0.61 Episodic memory 0.61 Reaction Time 0.47 Global Everyday Score Cognition Self Survey 0.30 Adj P trend Memory 0.11 Executive function 0.12 Planning 0.27 Organization 0.98 Divided attention 0.038 Total Score 0.017 Even slightly better scores at lower achieved LDL-C Giugliano RP et al. N Engl J Med. 2017;377:633-643. New Guidance for PCSK9 Inhibitors and Ezetimibe In Light of Cardiovascular Outcomes Data
Severe Hypercholesterolemia (LDL-C 190 mg/dl [ 4.9 mmol/l]) Recommendations for Primary Severe Hypercholesterolemia (LDL-C 190 mg/dl [ 4.9 mmol/l]) COR LOE Recommendations In patients 20 to 75 years of age with an LDL-C level of 190 I B-R mg/dl ( 4.9 mmol/l) or higher, maximally tolerated statin therapy is recommended. IIa B-R In patients 20 to 75 years of age with an LDL-C level of 190 mg/dl ( 4.9 mmol/l) or higher who achieve less than a 50% reduction in LDL-C while receiving maximally tolerated statin therapy and/or have an LDL-C level of 100 mg/dl ( 2.6 mmol/l) or higher, ezetimibe therapy is reasonable. Severe Hypercholesterolemia (LDL-C 190 mg/dl [ 4.9 mmol/l]) Recommendations for Primary Severe Hypercholesterolemia (LDL-C 190 mg/dl [ 4.9 mmol/l]) COR LOE Recommendations IIb B-R In patients 20 to 75 years of age with a baseline LDL-C level 190 mg/dl ( 4.9 mmol/l), who achieve less than a 50% reduction in LDL-C levels and have fasting triglycerides 300 mg/dl ( 3.4 mmol/l). while taking maximally tolerated statin and ezetimibe therapy, the addition of a bile acid sequestrant may be considered. IIb B-R In patients 30 to 75 years of age with heterozygous FH and with an LDL-C level of 100 mg/dl ( 2.6 mmol/l) or higher while taking maximally tolerated statin and ezetimibe therapy, the addition of a PCSK9 inhibitor may be considered.
Severe Hypercholesterolemia (LDL-C 190 mg/dl [ 4.9 mmol/l]) Recommendations for Primary Severe Hypercholesterolemia (LDL-C 190 mg/dl [ 4.9 mmol/l]) COR LOE Recommendations IIb C-LD In patients 40 to 75 years of age with a baseline LDL-C level of 220 mg/dl ( 5.7 mmol/l) or higher and who achieve an on-treatment LDL-C level of 130 mg/dl ( 3.4 mmol/l) or higher while receiving maximally tolerated statin and ezetimibe therapy, the addition of a PCSK9 inhibitor may be considered. Value Statement: Uncertain Value (B-NR) Among patients with FH without evidence of clinical ASCVD taking maximally tolerated statin and ezetimibe therapy, PCSK9 inhibitors provide uncertain value at 2018 U.S. list prices. Approval/Reimbursement Barriers Faced by Patients % of Attempts to Get a PCSK9 Inhibitor Prescription that are Successful 100.0% 80.0% ASCVD (n=298) FH (n=284) Responses, % 60.0% 40.0% 64% of respondents with ASCVD patients and 57% of respondents with FH patients were unable to get 3 out of every 4 PCSK9 inhibitor prescriptions approved, despite multiple appeals 20.0% 0.0% Cohen JD et al. J Clin Lipidol. 2017;11:891-900. None 1-25% 26-50% 51-75% More Than 75% Successful approvals, %
Defining a Reimbursement Roadmap To Address Cumbersome Approval/Reimbursement Process More consistent criteria by payers and checklists, algorithms, apps, sharing of best practices which: Improve patient selection Help to assure that required documentation is submitted Reduce wasted time Avoid frustration by healthcare providers and patients in the approval/denial process Educational Resources from the National Lipid Association Visit the resource table in the foyer to pick up a copy of the NLA s Recommendations for Patient-Centered Management of Dyslipidemia, part I and part II, Pocket Guides. Want more? Visit Lipid.org to gain access to free online activities, educational flyers for your office, and more.
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