Cascade Screening for FH: the U.S. experience

Similar documents
Focus on FH (Familial Hypercholesterolemia) Joshua W. Knowles, MD PhD for PCNA May, 2013

Inhibition of PCSK9: The Birth of a New Therapy

Role of Genetic Counseling in FH: What Referring Physicians Need to Know. Amy C. Sturm, MS, CGC September 21, 2013

Familial hypercholesterolaemia

Identification and management of familial hypercholesterolaemia (FH) - An overview

4/14/2018 DYSLIPIDEMIA CASES. Mary Malloy, MD. I have nothing to disclose

1. Which one of the following patients does not need to be screened for hyperlipidemia:

Defining and Controlling Severe Familial Hypercholesterolemia

Case Discussions: Treatment Strategies for High Risk Populations. Most Common Reasons for Referral to the Baylor Lipid Clinic

Katsuyuki Nakajima, PhD. Member of JCCLS International Committee

Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan. 4

Low-density lipoproteins cause atherosclerotic cardiovascular disease (ASCVD) 1. Evidence from genetic, epidemiologic and clinical studies

REPATHA (PCSK9 INHIBITORS)

Familial Hypercholesterolemia What a cardiologist should know

Cost effectiveness of cascade testing for FH:

Approach to Dyslipidemia among diabetic patients

Proprotein Convertase Subtilisin/Kexin type 9(PCSK9) Inhibitors Prior Authorization with Quantity Limit Program Summary

Genetic Dyslipidemia and Cardiovascular Diseases

2017 Update in Internal Medicine: Clinical Dyslipidemia Update

Alirocumab Treatment Effect Did Not Differ Between Patients With and Without Low HDL-C or High Triglyceride Levels in Phase 3 trials

Cholesterol Reduction Therapy in 2018 A Perspective Role Of Statins, Ezetimibe and PCSK9-Inhibitors

Distinguishing FH from non-fh: Right therapy, right patient, right time. Joshua W. Knowles, MD, PhD Stanford and the FH Foundation

How would you manage Ms. Gold

Comprehensive Treatment for Dyslipidemias. Eric L. Pacini, MD Oregon Cardiology 2012 Cardiovascular Symposium

Appendix E Health Economic modelling

PCSK9 Inhibitors and Modulators

ATP III (Adult Treatment Panel III) CLASSIFICATION C IN ADULTS

STATIN UTILIZATION MANAGEMENT CRITERIA

LIPID CLUB Rome, 2014

Pharmacy Management Drug Policy

Guidelines for the Diagnosis and Management of Familial Hypercholesterolaemia

Best Lipid Treatments

DIAGNOSIS AND TREATMENT OF FH CHILDREN. O. GUARDAMAGNA Dipartimento di Scienze della Sanità Pubblica e Pediatriche UNIVERSITA DI TORINO

Cholesterol; what are the future lipid targets?

Conceptual Approach to CAD Risk. Disclosures. Integrating Imaging and Biomarkers for Optimal CVD Risk Assessment and Management 2/10/2014.

ADMINISTRATIVE POLICY AND PROCEDURE

LIPOPROTEINE ATEROGENE E ANTI-ATEROGENE ATEROGENE

LDL Apheresis: Familial Hypercholesterolemia

Familial hypercholesterolaemia in children and adolescents

Pathophysiology of Lipid Disorders

LIPOPROTIEN APHERESIS. Bruce Sachais, MD, PhD Executive Medical Director New York Blood Center

Preclinical Detection of CAD: Is it worth the effort? Michael H. Crawford, MD

Appendix F Simon Broome Diagnostic criteria for index individuals and relatives

Inflammation and and Heart Heart Disease in Women Inflammation and Heart Disease

Familial Hypercholeterolaemia

Dyslipidemia in the light of Current Guidelines - Do we change our Practice?

Low-density lipoprotein as the key factor in atherogenesis too high, too long, or both

Contemporary management of Dyslipidemia

Defining Severe Familial Hypercholesterolemia. Raul D. Santos MD, PhD Brazil

Making War on Cholesterol with New Weapons: How Low Can We/Should We Go? Shaun Goodman

Latest Guidelines for Lipid Management

PCSK9 Inhibition: From Genetics to Patients

Clinical Policy: Evolocumab (Repatha) Reference Number: ERX.SPMN.184 Effective Date: 01/2017

Genetic and biochemical characteristics of patients with hyperlipidemia who require LDL apheresis

THE CLINICAL BIOCHEMISTRY OF LIPID DISORDERS

Lipid Management: A Case-Based Approach. Overview. Simple Lipid Therapy Approach. Patients have lipid disorders of:

WORKSHOP 1. Management of Patients with Familial Hypercholesterolemia

ATP IV: Predicting Guideline Updates

Lipids, Lipoproteins and Cardiovascular Risk: Getting the Most out of New and Old Biomarkers. New and Old Biomarkers. Disclosures

Guidelines for Management of Dyslipidemia and Prevention of Cardiovascular Disease

Clinical Policy: Evolocumab (Repatha) Reference Number: ERX.SPA.169 Effective Date:

Drug Prior Authorization Guideline PCSK9 Inhibitors -

See Important Reminder at the end of this policy for important regulatory and legal information.

HYPERLIPIDEMIA IN THE OLDER POPULATION NICOLE SLATER, PHARMD, BCACP AUBURN UNIVERSITY, HARRISON SCHOOL OF PHARMACY JULY 16, 2016

Review of guidelines for management of dyslipidemia in diabetic patients

Cardiovascular Disease Prevention: Current Knowledge, Future Directions

Managing Dyslipidemia in Disclosures. Learning Objectives 03/05/2018. Speaker Disclosures

Drug Class Monograph

Novel PCSK9 Outcomes. in Perspective: Lessons from FOURIER & ODYSSEY LDL-C. ASCVD Risk. Suboptimal Statin Therapy

Dan Koller, Ph.D. Medical and Molecular Genetics

Familial Hypercholesterolemia: Improving Detection and Management

Section Editor Mason W Freeman, MD

JUPITER NEJM Poll. Panel Discussion: Literature that Should Have an Impact on our Practice: The JUPITER Study

Need Help.. 4. Resources Abbreviations used in the FH Registry Eligibility Criteria for Inclusion in the FH Registry..

Drug Class Prior Authorization Criteria PCSK9 Inhibitors

DYSLIPIDEMIA. Michael Brändle, Stefan Bilz

CVD Risk Assessment. Michal Vrablík Charles University, Prague Czech Republic

Juxtapid (lomitapide)

Presenter Disclosure Information

Hyperlipidemia. Prepared by : Muhannad Mohammed Supervisor professor : Dr. Ahmed Yahya Dallalbashi

ROUNDTABLE DISCUSSION: IMPLICATIONS OF ADULT TREATMENT PANEL (ATP) III GUIDELINES AND EMERGENT RESEARCH FOR CLINICAL PRACTICE

Cardiometabolics in Children or Lipidology for Kids. Stanley J Goldberg MD Diplomate: American Board of Clinical Lipidology Tucson, Az

The Metabolic Syndrome: Is It A Valid Concept? YES

Non-fasting Lipid Profile Getting to the Heart of the Matter! Medimail Dec 2017

PCSK9 and its Role in LDL Receptor Regulation Muscat, Oman - 9 February 2019

Update On Diabetic Dyslipidemia: Who Should Be Treated With A Fibrate After ACCORD-LIPID?

Treating Hyperlipidemias in Adults. Lisa R. Tannock MD Division of Endocrinology and Molecular Medicine, University of Kentucky Lexington KY VAMC

Cardiovascular Complications of Diabetes

The JUPITER trial: What does it tell us? Alice Y.Y. Cheng, MD, FRCPC January 24, 2009

Lipoprotein (a) Disclosures 2/20/2013. Lipoprotein (a): Should We Measure? Should We Treat? Health Diagnostic Laboratory, Inc. No other disclosures

Dyslipidemia: Lots of Good Evidence, Less Good Interpretation.

Corporate Medical Policy

Study of serum Lipid Profile patterns of Indian population in young Ischaemic Heart Disease

Risk Factors for Heart Disease

Efficacy, Safety and Tolerability of 150 mg Q2W Dose of the PCSK9 mab REGN727/SAR236553: Data from Three Phase 2 Studies

Hypertriglyceridemia. Ara Metjian, M.D. Resident s Report 20 December 2002

Results of ODYSSEY OUTCOMES Trial

4 th and Goal To Go How Low Should We Go? :

*Carbohydrate & Lipid Metabolism Research Unit, Faculty of Health Sciences, University of Witwatersrand, Johannesburg, South Africa

Lipoprotein Particle Profile

Transcription:

Cascade Screening for FH: the U.S. experience Paul N. Hopkins, MD, MSPH Professor of Internal Medicine Cardiovascular Genetics University of Utah

Disclosures Consultant Genzyme, Amgen, Regeneron Research funding Regeneron, Merck

A striking family history Roger R. Williams, MD Aug 11, 1944 Sep 2, 1998 Roger was shocked as a teenager when his neighbor died from from MI on the golf course at age 42. And more shocked to learn the family had expected it! Several generations of males in this family had died from MIs before meeting their grandchildren.

Initial efforts in Utah Characterization of Coronary Prone Pedigrees Roger R. Williams, MD, principal investigator NIH grant 1977 1992 Goal: to understand the genetics and epidemiology of different types of early familial coronary disease...

Syndromes in 97 Utah Multiplex Families (2+ cases with early CAD and risk factor) Hypertension 24% FDH (MetS) 12% Diabetes 8% Homocysteine 12% Cigarette Smoking 37% High Lp(a) 23% FCHL 12 60% High TG Only 14% High TG, Low HDL 7% All Low HDL 23% Type III 3% High LDL Not FH 5% FH 4% Williams RR, et al. Arch Intern Med 1990; 150:582 and unpublished

Familial dyslipidemias in premature CHD kindreds (n = 102) No identifiable familial abnormality 43% L(a) excess 18.6% Familial dyslipidemia 14.7% Familial apo A-1 deficiency 1.0% Familial high TG 1.0% FH 3.0% Familial hyperapobeta 5.0% Familial hypoalpha 4.0% FCHL 13.7% Genest JJ, et al. Circulation 1992; 85:2025

Familial Syndromes of Early CAD in Seattle, Boston, and Utah Seattle (N = 366) Boston (N = 102) Utah (N = 97) No diagnosis 60% 35% 25% Familial combined hyperlipidemia 13% 18% 36% Familial hypertriglyceridemia 6% 18% 21% Isolated low HDL 4% 15% all low HDL 35% 20% Elevated Lp(a) 19% 23% Familial hypercholesterolemia 4% 3% 4% Type III hyperlipoproteinemia 2 3% 0% 3% Hypertension 24% Diabetes 8% Smoking 37% Goldstein JL, et al. J Clin Invest 1973; 52:1544 Genest JJ Circulation 1992 Williams RR Arch Int Med 1990

MEDPED A humanitarian project to find and help persons with familial hypercholesterolemia

Brief Historical Review of MEDPED MEDPED was officially started at the University of Utah by Roger Williams in 1989 First 5 years funding from the CDC established MEDPED methods refined ascertainment methods since then

Major findings from CDC study Documented Need for More Effective Diagnosis and Treatment of Familial Hypercholesterolemia According to Data from 502 Heterozygotes in Utah 101 FH probands with 502 identified relatives 50% had been told they had very high cholesterol 31% of those had been told they had FH 42% taking a cholesterol lowering medication 23% had total C or LDL C below the 90 th percentile Cascade screening most cost effective way to find new probands Williams RR, Am J Cardiol 1993; 72:18D

0.01 0.01 Non-FH FH Probability 0.01 0.00 0.00 0.00 0.00 0.00 False negatives 80% probability of FH False positives 0 50 100 150 200 250 300 350 400 450 500 LDL cholesterol (mg/dl) 1993 LDL cholesterol levels mean SD FH 289 63.0 (OLD) Non-FH 130 31.4 (OLD) First degree relatives Hopkins PN. Clin Lipidol 2010; 5:339

1993 MEDPED Criteria for Diagnosing Heterozygous FH in U.S. Population Cut points chosen for 80% probability that an individual is affected. ADDITIONAL CRITERIA were applied to Dx a newly identified family. Shown are total C (LDL C) in mg/dl Degree of Relation to Closest FH Age First Second Third General 100% <20 220 (155) 230 (165) 240 (170) 270 (200) (240) 20-29 240 (170) 250 (180) 260 (185) 290 (220) (260) 30-39 270 (190) 280 (200) 290 (210) 340 (240) (280) 40+ 290 (205) 300 (215) 310 (225) 360 (260) (300) Williams RR, et al. Am J Cardiol 1993; 72:171

General philosophy of MEDPED diagnostic approach FH is a dominantly (or co dominant) transmitted disease. To provide a clinically definite diagnosis of FH, there should be evidence of dominant transmission in the family. LDL C levels in family members besides proband were used to diagnose FH using additional criteria or rules. NOTE: other diagnostic approaches do not explicitly utilize actual LDL levels in the family for diagnosis.

Examples of additional criteria to diagnose new FH probands/families For DEFINITE HETEROZYGOTE diagnosis by gene testing (rare) For CLINICALLY DEFINITE HETEROZYGOTE Tendon xanthoma present and LDL C meets at least first degree relative criteria. Isolated pediatric case (<20 years old) with LDL cholesterol 240 mg/dl (>99.9 percentile). Two first degree relatives meet general population criteria for LDL cholesterol. ETC!! (including rules for probable, etc. WHO Consultation on FH http://libdoc.who.int/hq/1998/who_hgn_fh_cons_98.7.pdf

Industry funding begins in 1994 5 centers added Cincinnati (Stein) Baltimore (Kwiterovich/Kafonek) Boston (Lees) Portland (Illingworth) San Francisco (Kane/Malloy)

U.S. MEDPED Registry Growth Number of Cases Found 9000 8000 7000 6000 5000 4000 3000 2000 1000 0 Utah USA + Utah 1989 1991 1993 1995 1997 1999 2001 Year

MEDPED Case Finding (FH Only) by Center Coord. Center Utah Cincinnati Portland San Francisco Lipid Clinics Baltimore Cambridge relatives probands 0 1000 2000 3000 4000 Number registered

Total C Levels in the Treatment Support Program Total cholesterol (mg/dl) 400 380 360 340 320 300 280 260 240 220 200 <1993 (14) 1993 (21) 1994 (43) 1995 (75) Baseline Final (by 2000) 1996 (176) 1997 (56) Year (number) Stephenson SH, et al. J Clin Lipidol 2009; 3:94

Multiple lipid phenotypes in a Utah FH kindred with a novel LDLR mutation (D92K) Affected Chol Trig HDL LDL Age 64 Ages 24 50 302 106 47 237 443 278 40 286 222 94 50 159 Ages 4 21 294 370 45 168 223 164 48 153 226 240 34 143 200 316 36 101 259 160 37 195 131 59 45 74 292 193 40 204 200 103 57 127 268 149 48 185 298 240 50 185 324 95 54 257 326 98 58 232 252 103 64 157 228 222 107 44 139 184 119 44 121 213 172 45 129 248 183 41 164 223 109 42 170 166 66 56 101 204 55 48 148 Wu LL, et al. J Hum Genet 2000; 45:154

Utah FH Pedigree

What are some of the challenges of FH screening? Identifying FH patients DNA (gold standard only if found) versus clinical? Who pays for DNA diagnosis? How can clinical Dx be made available to anyone? There is urgency to finding FH Previously, the Dx usually came after MI Earlier, aggressive Rx better outcomes Universal screening of teenagers cost effective for CAD prevention

Additional challenges in the U.S. No current data on: How many FH are currently diagnosed What percent are treated (any Rx) How well FH are treated (current LDL C) CURRENT CAD RISKS OR OUTCOMES

Rethinking practical aspects of MEDPED Prior approach to diagnosis was labor intensive and relatively costly. telephone contacting and data collection diagnosis by MEDPED physician Diagnostic rules for initial FH pedigree or proband diagnosis lacked theoretical rigor, generalizability, or specific probabilities. MEDPED cutpoints had low sensitivity generally. Both general population and FH total C and LDL C mean ±SD needed updating.

Diagnostic approach using complex segregation analysis and likelihood theory..., Indices comprising all combinations of genotypes. Each combination defines a string. Likelihood products for probability of given set of genotypes. Separated into founders (prior probabilities) and offspring (transmission probabilities). Penetrance function(s). Probability of an observed phenotype given the genotype. MEDPED patent pending

Diagnostic approach using complex segregation analysis and likelihood theory..., M F C 0 0 0 0 0 1 0 1 0 0 1 1 1 0 0 1 0 1 1 1 0 1 1 1 MEDPED patent pending

Diagnostic approach using complex segregation analysis and likelihood theory..., M F C 0 0 0 0 0 1 0 1 0 0 1 1 1 0 0 1 0 1 1 1 0 1 1 1 0.998 or 0.002 Mendelian transmission probabilities MEDPED patent pending

Diagnostic approach using complex segregation analysis and likelihood theory..., M F C 0 0 0 0 0 1 0 1 0 0 1 1 1 0 0 1 0 1 1 1 0 1 1 1 0.998 or 0.002 Mendelian transmission probabilities updated means, SD penetrance functions MEDPED patent pending

Diagnostic approach using complex segregation analysis and likelihood theory Actual family with LDL C values known M F C 0 0 0 0 1 1 MI death age 39, smoked prior LDL C 216 age 24 age 11 LDL C 198 (treated) 2 most informative product strings (0.998)(0.998)(1.0)(2.34E 06)(3.04E 05) (0.998)(0.002)(0.5)(7.19E 03)(4.25E 03) = 99.3% child has FH MEDPED patent pending

What if? Clinical situation: FH Dx % we only knew daughter s LDL C 58.9% her untreated LDL C was 220 98.6% we only knew dad had MI age 39 93.3% the dad had a tendon xanthoma (almost regardless of dad s LDL C) 99.8% MEDPED patent pending

Accurate Dx of FH using this method will depend on good underlying data Prior probability of FH in founders Limited US data may need to be re assessed LDL C mean ±SD for FH and non FH general population LDL C has dropped old mean for FH was too high (ascertainment bias) CAD risk in FH and non FH some reasonable estimates exist Xanthoma by age in FH (available) almost unheard of in non FH MEDPED patent pending

Cumulative Probability of Fatal and Non Fatal CAD in 116 FH Pedigrees Cumulative Probability of Clinical CAD 0.60 0.50 0.40 0.30 0.20 Non FH Men FH Men 0.60 0.50 0.40 0.30 0.20 Non FH Women FH Women 0.10 0.10 0.00 0.00 Age Age Stone NJ, et al Circulation 1974; 49:476

Cumulative Probability of Non Fatal CAD in Utah FH vs a Random U.S. Population Cumulative Probability of Clinical CAD 0.30 0.25 0.20 0.15 0.10 0.05 Non FH Men FH Men 0.05 0.04 0.03 0.02 0.01 Non FH Women FH Women 0.00 0.00 Age Age Hopkins PN. Clin Lipidol 2010; 5:339

Cumulative probability of CAD 1 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0 FH men FH women non FH men non FH women 20 30 40 50 60 70 80 90 Age (years

Cumulative probability of CAD 0.25 0.20 0.15 0.10 0.05 FH men FH women non FH men non FH women 0.00 20 25 30 35 40 45 Age (years

Prevalence (%) in 346 Utah FH Heterozygotes 60 50 40 30 20 10 Xanthoma Full Arcus 0 <30 30-39 40-49 50-59 60+ Age (years) Hopkins PN. Current Treatment Options in Cardiovascular Medicine 2002; 4:121

60 Tendon xanthoma prevalence by age in Utah FH 50 Prevalence of xanthoma 40 30 20 10 0 y = 0.8205x 1.8113 R² = 0.9936 prevalence of xanthoma expected to be 0 at age 2.2 0 10 20 30 40 50 60 70 Age (years)

Conclusions By 2004, about 8,000 FH had been diagnosed in the MEDPED registry about 1.3% of US FH We have a long way to go! New automated approach will help!