ATP IV: How the New Guidelines Will Affect Your Practicecme.baptisthealth.net/cvdprevention/documents... · · 2013-02-20VYT 02571 CM Ad Bd ATP IV DT3 2/19/2013 3:36 PM 1 ATP IV:

VYT 02571 CM Ad Bd ATP IV DT3 2/19/2013 3:36 PM

1

ATP IV: How the New Guidelines Will Affect Your Practice

Michael Davidson M.D. FACC, Diplomate of the American Board of LipidologyClinical Professor, Director of Preventive Cardiolo gyThe University of ChicagoPritzker School of Medicine

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Two men who died of a MI at age 591960 vs 2008


2

Attributable Declines in CHD Deaths between 1980 and 2000

47%

Net 44%

Therapies Lifestyle/RFs

Attr

ibut

able

red

uctio

n in

CH

D d

eath

s (%

)

Ford et al, N Engl J Med 2007

9%

Unexplained

4

Low HDL-C Target Patient Population

LDL-C HDL-C Triglycerides

ABCG5/8 HFE SORT1 ABCA1 HNF4A PDE3A ACSS2 GALNT2

ABO HMGCR ST3GAL4 ABCA8 IRS1 PGS1 AFF1 GCKR

ANGPTL3 HNF1A TIMD4 ADM KLF14 PLTP ANGPTL3 IRS1

APOA HPR TOP1 ANGPTL4 LACTB PPP1R3B ANKRD55 JMJD1C

APOB IDOL TRIB1 APOA LCAT SBNO1 APOA LIPC

APOE IRF2BP2 APOB LILRA/B SCARB1 APOB LPL

BRAP LDLR APOE LIPC SLC39A8 APOE LRP1

BTNL2 LDLRAP1 ARL15 LIPG STARD3 BTNL2 MLXIPL

CBLN3 LPA C6orf106 LPA TRIB1 CAPN3 MSL2L1

CETP MAFB CETP LPL TRPS1 CETP NAT2

CILP2 MOSC1 CITED2 LRP1 TTC39B CILP2 PINX1

CYP7A1 NPC1L1 CMIP LRP4 UBASH3B COBLL1 PLA2G6

DNAH11 OSBPL7 COBLL1 MACF1 UBE2L3 CTF1 PLTP

FADS PCSK9 DOCK6 MC4R ZNF648 CYP26A1 TIMD4

FRK PLEC1 FADS MLXIPL ZNF664 FADS TRIB1

GPAM PPP1R3B GALNT2 MMAB FRMD5 TYW1B

ZNF664Total Cholesterol

ERGIC3 EVI5 FUT2 RAB3GAP1 RAF1 SPTY2D1

GWAS in > 100,000 individuals: 95 lipid loci

Teslovich, et al Nature 2010


3

2.0

1.0

0.8

0.5 0.5 0.5 0.50.4 0.4

0.3

0

0.5

1

1.5

2

2.5

FH Dominant otosclerosis

Adult PCKD Sickle cell disease

Multiple exostoses

Huntington's disease

Fragile X syndrome

Neuro-fibromatosis

Cystic fibrosis

Duchenne muscular dystrophy

FH: Most Common of Inherited

Disorders

Familial combined hyperlipidemia has a frequency of 1:200 births; however, the genetic cause is unknown . Sickle cell disease varies greatly by ethnicity. P CKD = polycystic kidney disease.Genetic Alliance UK. Available at http://www.geneti calliance.org.uk/education3.htm. Accessed August 25 , 2011. StreetlyA et al. J Clin Pathol . 2010;63:626-629.

7

FH prevalence is 2x the next most common

5x more common

4x more common

Image courtesy of Michael H. Davidson, MD8

TR0013A – 07/11. DRAFT FOR TRAINING PURPOSES ONLY. NOT FOR PROMOTIONAL USE. DO NOT COPY OR DISTRIBUTE

99

Simon Broome Register Diagnostic CriteriaSimon Broome Register criteria for diagnosis of heterozygous familial hypercholesterolemia (HeFH)Criteria

A A plasma cholesterol measurement of either:

• TC>7.5 mmol/L (adult patient) or >6.7 mmol/L (child aged <16 yr)

• Low-density lipoprotein >4.9 mmol/L (adult patient) or >4.0 mmol/L (child aged <16 yr)

B TX in the patient or any of the patient’s first- or second-degree relatives*

C DNA-based evidence in the patient of mutation in LDLR or any other HeFH-related gene

D Family history of myocardial infarction before the age of

• 50 yr, in any first- or second-degree relative*

• 60 yr, in any first-degree relative*

E Family history of plasma TC measurements >7.5 mmol/L in any first- or second-degree relative*

Diagnosis Criteria required

Definite HeFH

Probable HeFH

A + B or C

A + D or A + E

* First-degree relation = parent, offspring or sibling; second-degree relation = grandparent, grandchild, nephew, niece or half-sibling.

Yuan G, et al. CMAJ. 2006;174:1124–1129.


4

Inherited syndromes of extremes of LDL-C: story of PCSK9

Fre

quen

cy (

%)

LDL-C

Gain of function mutations in PCSK9

Loss of function mutations in PCSK9

80

PCSK9 = proprotein convertase subtilisin/kexin type 9 serine protease.

1. Peterson AS et al. J Lipid Res. 2008;49:1595–1599.2. Cohen J et al. Nat Genet. 2005;37:161–165.

3. Cohen J et al. N Engl J Med. 2006;354:1264–1272.

PCSK9 Loss-of-Function Mutations Resulted

in Low LDL-C Levels and Reduced CHD Rates

� Wild-type PCSK9 degrades LDL receptors.1,2

� Loss-of-function mutations increase hepatic LDL receptor expression, reducing LDL-C levels by 15% to 40%.2,3

� CHD was reduced 47% to 88% in PCSK9 loss-of-function mutation carriers compared with normal individuals.3

12

CH

D, %

Black Subjects

0

8

4

P=0.008

n=85n=3,278

9.7

1.2

Normal subject

Mutation carrier

8

12

White Subjects

4

P=0.003

0n=301n=9,223

11.8

6.3

CH

D, %

The Role of PCSK9 in the Regulation of LDL-Receptor Expression

Reprinted with permission. McKenney JM, et al. J Am Coll Cardiol . 2012 Mar 28. Epub ahead of print


5

Results: Single-dose SQ

Statins reduce all-cause death: Meta-analysis of 14 trials

Cause of death

3.4 0.81

0.910.950.93

Vascular causes:

StrokeOther vascular

Any vascular

Any non-CHD vascular

0.60.61.2

4.7

2.40.20.1

1.13.8

8.5 9.7

4.01.2

0.10.32.4

5.7

1.30.70.6

4.4

Nonvascular causes:Cancer

Respiratory

0.83

1.010.820.89

0.870.95

0.88

Trauma

Other/unknownAny nonvascular

Any death

Events (%)Treatment

(n = 45,054)Control

(n = 45,002) Treatment better

Controlbetter

1.51.00.5

CHD

CTT Collaborators. Lancet . 2005;366:1267-78.

Relative risk

Cholesterol T reatment T rialists’Collaboration

Statin Benefit Independent of Baseline Lipids: Meta-analysis of 14 trials

CTT Collaborators. Lancet . 2005;366:1267-78.CHD death, MI, stroke, coronary revascularization

Groups

Total-C (mg/dL)

LDL-C (mg/dL)

0.79>201–251 13.9 17.4

HDL-C (mg/dL)

14.3 18.2>35–43 0.79

13.4 16.8 0.79≤124

Events (%)Treatment(45,054)

Control(45,002)

1.51.00.5

13.5 0.7616.6≤201

0.80>251 15.2 19.7

18.2 22.7≤35 0.78

11.4 14.2 0.79>43

18.0 0.78>124–177 13.818.8 0.80>177 15.3

14.2 17.6 0.79>135–17415.8 0.8120.4>174

0.7613.4 16.7≤135

0.79

TG (mg/dL)

Overall 17.814.1

Relative risk

Cholesterol T reatment T rialists’ Collaboration

Treatment better

Control better


6

Deficiency of NPC1L1 or Treatment with Ezetimibe Prevents

Atherosclerosis in apo E -/- Mice by Reducing the Cholesterol Content of

Atherogenic Lipoproteins

(modified from M. Huff)

0 1 2 3 4 5 Years of follow-up

0

5

10

15

20

25

Pro

port

ion

suffe

ring

even

t (%

)

Risk ratio 0.83 (0.74 – 0.94) Logrank 2P=0.0022

Placebo

Eze/simv

Baigent C for the CHARP Collaborative Group, American Society of Nephrology, 11/20/2010.(accessed via www.sharpinfo.org/ March 27, 2011)

SHARP: Major Atherosclerotic EventsSHARP: Major Atherosclerotic Events

Pro

port

iona

l red

uctio

n in

athe

rosc

lero

tic e

vent

rate

(95

% C

I)

0%

5%

10%

15%

20%

25%

30% Statin vs control(21 trials)

Mean LDL cholesterol differencebetween treatment groups (mg/dL)

More vs Less(5 trials)

SHARP32 mg/dL

0 20 4010 30

SHARP17% risk reduction

Baigent C for the CHARP Collaborative Group, American Society of Nephrology, 11/20/2010.(accessed via www.sharpinfo.org/ March 27, 2011); Lancet. 2010 Nov 13;376(9753):1670-81.

CTT: Effects on Major Atherosclerotic EventsCTT: Effects on Major Atherosclerotic Events


7

Should non-HDL-c supplant LDL-c as the primary goal of therapy?

What Is Non–HDL-C?

HDL LDL IDL VLDLChylomicron

Remnant

apo AI apo B apo B apo B apo B 48

Cholesterol

Triglyceride

BadGood All Atherogenic Lipoproteins

non-HDL

non–HDL-C =total cholesterol − HDL-C

NCEP target level of non–HDL-C is 30 mg/dL greater than the LDL-C goal1

NCEP Expert Panel on Detection, Evaluation, and Tre atment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third Report Executive Summary . 2001; NIH Publication No. 01-3670.

Robinson JG, et al. J Am Coll Cardiol. 2009;53:316-22.

1:1 Ratio RRR for Both Statins and FibratesChange in Non-HDL-C 2× Better Than LDL-C for Predict ing CHD Risk Reduction


8

Among statin-treated patients, non-HDL-C has a stronger association with MACE than LDL-C

22

ADA/ACC 2008 Consensus Statement:Treatment Goals in Patients With Cardiometabolic Risk and Lipoprotein Abnormalities

“In individuals on statin therapy who continue to ha ve low HDL-C or elevated non–HDL-C, especially if apoB levels remain elevate d, combination therapy is recommended. The preferred agent to use in combination with a st atin is nicotinic acid… ”aMajor risk factors beyond dyslipidemia include smok ing, hypertension, and family history of premature CHD.Brunzell JD, et al. Diabetes Care . 2008;31(4):811-822. Copyright © 2008 American Dia betes Association.

Goals

LDL-C Non-HDL-C ApoB

Highest-risk patient• Known CVD• Diabetes plus ≥1 additional major CVD risk factor a

<70 mg/dL <100 mg/dL <80 mg/dL

High-risk patients• No diabetes or known CVD but ≥2 major CVD risk factors a

• Diabetes but no other major CVD risk factors a

<100 mg/dL

<130 mg/dL <90 mg/dL


9

Liver

VLDL

HDL

LDL

TG CECETP

TG

CE

Hypertriglyceridemia

TG

CE

TGTG

TG

TG VLDL

Small, dense LDL

DGAT

Glycerol

Apo A-I

Apo B-100

Miller M, et al. Circulation. 2011;123:2292-2333

LDL

ApoC-III

CETP

ApoC-III

ApoC-III inhibits the conversion of VLDL to LDL and causes small dense LDL and low HDL

Small, dense HDL

ApoC-III

ApoCIII deficiency is associated with longevity in Bronx Aging Trial

26

104 years old

Apo C-III : Circulating levels are associated with increased risk for CHD in prospective studies

Olivieri, J Thromb Haemost 2010 Onat , Diabetic Medicine2009Scheffer , Clinical Chemistry 2008Sacks , Circulation 2000Mendivil, Circulation 2011

Study

Total Apo C-III

Apo C-III in VLDL + LDL

Apo C-III in LDL

Apo C-III in VLDL

Apo C-III in HDL

Olivieri (2010)TARFSHoornHPFS & NHS

CARE

HPFS & NHS

HPFS & NHS

CARE

Population

Patients with CADGeneral populationGeneral populationGeneral population

Patients with MI

General population

General population

Patients with MI

No. of events

6472

231739

418

739

739

418

0.8 1 1.5 2 3 4 6

RR (95% CI) for CHD comparing top vs. bottom thirds of exposure

RR (95% CI)

3.22 (1.27, 8.15)2.82 (1.31, 6.08)1.70 (1.02, 2.85)1.36 (0.97, 1.90)

1.88 (1.30, 2.72)

1.70 (1.20, 2.40)

1.24 (0.91, 1.69)

1.21 (0.85, 1.73)


10

28*Source: McPherson, R. Remnant Cholesterol. JACC http://dx.doi.org/10.1016/j.jacc.2012.11.009

Remnant Cholesterol and Atherosclerosis

29*Source: Jorgensen et al. Genetically elevated non- fasting triglycerides. European Heart

What is the Clinical Utility of Inflammatory Markers and Advanced Lipoprotein Testing?


11

Summary Recommendations

Abbreviations: Apo = apolipoprotein, CHD = coronary heart disease, hs-CRP = high-sensitivity C-reactive protein, HDL = high-density lipoprotein, LpPLA2 = lipoprotein-associated phospholipase A2, LDL = low-density lipoprotein, LDL-P = LDL particle number, Lp(a) = lipoprotein (a)

Initial Clinical AssessmentApoB LDL-P Lp(a) HDL or LDL

Subfractionshs-CRP LpPLA2

Low Risk Not Recommended

Not Recommended

Not Recommended

Not Recommended

Consider for Selected Patients

Not Recommended

Intermediate Risk Reasonable for Many Patients

Reasonable for Many Patients


Not Recommended

Recommended for Routine

Measurement


CHD Equivalent Consider for Selected Patients



Not Recommended



Family History Reasonable for Many Patients



Not Recommended



Recurrent Event Reasonable for Many Patients



Not Recommended



Intra-abdominal (Visceral) Fat is a Metabolically Active Organ Infiltrated by Inflammatory Cells

Adapted from Tilg H and Moschen AR Nat Rev Immunol 2006; 6: 772-3 and Wellen KE and Hotamisligil GS J Clin Invest 200 3; 112: 1785-8

FFA: free fatty acidsIL-1ββββ: interleukin-1 ββββIL-6: interleukin-6JNK: jun N-terminal kinase

MCP-1: monocyte chemotactic protein-1NF-κκκκB: nuclear factor- κκκκBTNF-αααα: tumor necrosis factor- ααααVEGF: vascular endothelial growth factor

Preadipocyte

Adipocyte

Weight gain

TNF-α

MCP-1

Endothelialcell

Macrophagerecruitment

Macrophage

FFA

Physical stress/oxidativedamage to endothelium?

LeptinVEGF

Angiogenesis

Macrophagerecruitment

MCP-1

Il-6IL-1βTNF-α

JNKNF-кB

Insulinresistance

Weight gain

Who are the Patients with Higher C-Reactive Protein (CRP) Levels in PROVE-IT after 4 Months of Statin Therapy?

80 90 100 110 120 130 140

NCEP-ATP III cutpoint formetabolic syndrome

0.9

0.8

0.7

0.6

0.5

0.4

0.3

Month 4Log (CRP)

50 100 150 200 250 300 350


1.0

0.8

0.6

0.4

0.2

0.0

Month 4Log (CRP)

20 30 40 50 60 70


in men

1.4

1.2

1.0

0.8

0.4

0.2

Month 4Log (CRP)

0.6

NCEP-ATP III cutpoint for metabolic syn-drome in women

60 65 70 75 80 90


1.4

1.2

1.0

0.8

0.4

0.2

Month 4Log (CRP)

0.6

85100 110 120 130


0.8

0.6

0.4

0.2

Month 4Log (CRP)

14020 25 30 35

WHO cutpointfor obesity

1.0

0.6

0.4

0.0

Month 4Log (CRP)

40

WHO cutpointfor overweight

0.2

0.8

1.2

Glucose (mg/dl) Triglycerides (mg/dl) HDL (mg/dl)

Body mass index (kg/m 2) Systolic blood pressure (mmHg)

Diastolic blood pressure (mmHg)

Month 4 Glucose Month 4 Triglycerides Month 4 HDL

Body mass index Month 4 Systolic blood pressure

Month 4 Diastolic blood pressure

Adapted from Ray KK et al. J Am Coll Cardiol 2005; 46: 1417-24


12

Meta-analysis: CRP response to weight loss

Baseline weight & CRPCRP response to weight loss

Surgical trials=squares Lifestyle intervention tri als=circlesSelvin et al. Arch Intern Med 2007; 167: 31-39

R=0.76 R=0.85

JUPITERJUPITERJUPITERJUPITERPrimary Trial EndpointPrimary Trial EndpointPrimary Trial EndpointPrimary Trial Endpoint : : : : MI, Stroke, UA/Revascularization, CV DeathMI, Stroke, UA/Revascularization, CV DeathMI, Stroke, UA/Revascularization, CV DeathMI, Stroke, UA/Revascularization, CV Death

Placebo Placebo Placebo Placebo 251 / 8901251 / 8901251 / 8901251 / 8901

Rosuvastatin Rosuvastatin Rosuvastatin Rosuvastatin 142 / 8901142 / 8901142 / 8901142 / 8901

HR 0.56, 95% CI 0.46HR 0.56, 95% CI 0.46HR 0.56, 95% CI 0.46HR 0.56, 95% CI 0.46----0.690.690.690.69P < 0.00001P < 0.00001P < 0.00001P < 0.00001

Number Needed to Treat (NNTNumber Needed to Treat (NNTNumber Needed to Treat (NNTNumber Needed to Treat (NNT5555) = 25) = 25) = 25) = 25

---- 44 %44 %44 %44 %

0 1 2 3 4

0.00

0.02

0.04

0.06

0.08

Cum

ulat

ive

Inci

denc

e

Number at Risk Follow-up (years)

RosuvastatinPlacebo

8,901 8,631 8,412 6,540 3,893 1,958 1,353 983 544 1578,901 8,621 8,353 6,508 3,872 1,963 1,333 955 534 174

NEJM 2008;359:2195-2207

Source: FDA.gov


13

Lifetime Risk of CVD Events at Age 50 by Risk Factor Strata

Lloyd-Jones DM, et al. Circulation . 2006;113:791-798. ��

Combination therapy with a statin: is it beneficial in patients with mixed dyslipidemia

17.32%

10.11%

0

5

10

15

20

Pro

port

ion

with

CV

eve

nt

With atherogenic dyslipidemia*(n=456)

Without atherogenic dyslipidemia(n=2,284)

Patients on simvastatin alone

1. ACCORD Lipid results reinforce the residual risk hypothesis

� Despite achieving a mean LDL-C of 80 mg/dL, patients in the atherogenic dyslipidemia* subgroup had a 70% higher rate of major CV events compared to those without atherogenic dyslipidemia

*TG ≥204 mg/dL and HDL-C ≤34 mg/dL

ACCORD Study Group. N Engl J Med March 14, 2010. Epub.

+70% + 70%

AC48


14

The CV benefits of triglyceride lowering in patient s with hypertriglyceridemia (TG > 200mg/dl) is supported by seven consecutive trials

40

Trial (drug)Primary endpoint:

entire cohort (p-value)

Lipid subgroup criterion

Primary endpoint

subgroup (p-value)

HHS (gemfibrozil)

-34% (0.02)TG > 200 mg/dL

LDL-C/HDL-C > 5.0Post-hoc

-71% (<0.005)

BIP (bezafibrate)

-7.3 (0.24) TG ≥ 200 mg/dLPost-hoc

-39.5% (0.02)

VA-HIT(gemfibrozil)

-22% (0.006) TG ≥ 150 mg/dLPost-hoc

-27% (0.01)

FIELD(fenofibrate)

-11% (0.16)TG ≥ 204 mg/dL

HDL-C < 42 mg/dLPost-hoc

-27% (0.005)

ACCORD(fenofibrate)

-8% (0.32)TG ≥ 204 mg/dL

HDL-C ≤ 34 mg/dLPrespecified -

31% (.06)

JELIS(ethyl-EPA)

-19% (0.011)TG > 150 mg/dL

HDL-C < 40 mg/dLPost-hoc

-53% (.043)

AIM-HIGH(niacin)

1% (0.79)HR=1.02

TG > 200 mg/dLHDL-C < 32 mg/dL

Post-hoc-37% (.017)

But…minimal (5%) Net TG lowering effect

5210 3 4Years

Cum

ulat

ive

Inci

denc

e of

M

ajor

Cor

onar

y E

vent

s (%

)

3

0

1

2

4 Control (statin)EPA (statin+Epadel)

–19% (p=0.011)

JELIS Study: Ethyl-EPA reduced CV Events

Yokoyama M, et al. Lancet. 2007;370:215


15

Years of Follow-up

Pro

port

ion

with

eve

nts

0.0

0.05

0.10

0.15

0.20

0.25

0.30

0 1 2 3 4 5 6 7

n-3 fatty acids

Placebo

# at Risk 1 2 3 4 5 6 7

n-3

P

6281 6161 6034 5882 5706 5503 3896 879

6255 6143 6017 5848 5685 5492 3893 837

Primary Outcome: CV Death

HR 0.98; 95% CI, 0.87-1.10;P=0.72

The Omega-3 and CVD Roller CoasterRizos et al. Meta-Analysis of Omega-3 Supplementation Studies

(including open label trials)

Rizos E et al. JAMA 2012;308:1024-1032.(Sept 11)

Critical level set at p=0.006 to control for multiple comparisons

Too conservative for a safe agent?

Relationship Between EPA+DHA Levels and CV Risk

High Red Blood Cell Content of Omega-3 is Associated with Reduced CV Risk

Albert CM et al. N Engl J Med 2002:346:1113-1118.

1.0%

0.5%

0.2%0.1%

0.0%

0.3%

0.6%

0.9%

1.2%

3.3 4.3 5.0 6.5

Mean RBC EPA+DHA by Quartile (%)

Odds Ratio

45

Source: Physician’s Health Study


16

9.5 13.0

32.2 36.6 41.4 38.9

93.0

34.0

143.0

43.4

125.7

174.7

199.7

172.0

0

50

100

150

200

250

4g 4g Olive Oil 2g 3g 4g JELIS

Free fatty acid formulation with enhanced bioavailability achieves EPA levels reached in JELIS trial in a Western Population

CONFIDENTIAL © 2012 Omthera Pharmaceuticals, Inc. All Rights Reserved.

ug/m

L

(1)

(1) Incremental TG reduction of 6% compared to statin alone

46

0.98(0.70-1.36)

0.95(0.76-1.36)

0.80(0.64-0.99)

1.0

0.0

0.2

0.4

0.6

0.8

1.0

< 87 87-99 100-149 > 150Relationship between on-treatment EPA concentration and adjusted risk of major coronary events

Plasma EPA Concentration (ug/mL)

Baseline EOT

EPA Levels vs. Epadel Levels in JELIS

Lovaza Epanova Epanova Epanova (Epadel)

ECLIPSE II Study EVOLVE Study

Lovaza’s ethyl ester formulation resulted in

muted increases in EPA

Japanese samples exhibited significantly

greater baseline EPA levels

Epanova

Conclusions: What can we expect from ATP IV

• Identify patients at risk for CHD events (secondary prevention and other other high risk patients) and initiate statin therapy and titrate to the highest tolerated dose

• Achievement of LDL-C and Non-HDL-C should be the pr imary goal of lipid therapy and the lower the better

• Lifetime low LDL levels are associated with a marke d reduction of CVD events

• In the US population with a growing prevalence of m etabolic syndrome and obesity, non-HDL/ApoB is more predicti ve of CVD than LDL-C

• In patients at high risk (CVD, diabetes, elevated C RP), LDL reduction with statins has proven outcome benefits regardless of baseline LDL-C levels

• In patients with mixed dyslipidemia at the LDL-c go al on statin therapy but with elevated triglycerides and low HDL -c, lifestyle changes need to be implemented with consideration f or initiation of combination therapy to further reduce residual r isk.

FUTURE INTERVENTIONAL LIPIDOLOGISTFUTURE INTERVENTIONAL LIPIDOLOGIST

WWW.LIPID.ORGWWW.LIPID.ORGFor Board CertificationFor Board Certification


17

Superior doctors prevent the disease.Mediocre doctors treat the disease before evident.Inferior doctors treat the full blown disease.

— Huang Dee: Nai-Ching (2600 BC; first Chinese medical text).

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ATP IV: How the New Guidelines Will Affect Your Practicecme.baptisthealth.net/cvdprevention/documents... · · 2013-02-20VYT 02571 CM Ad Bd ATP IV DT3 2/19/2013 3:36 PM 1 ATP IV: