LIPOPROTEIN MANAGEMENT IN ACS
Improving Outcomes in Patients with
Complex Lipid Disorders
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Thank you.
Faculty Disclosures
The faculty reported the following relevant financial relationships that
they or their spouse/partner have with commercial interests:
TO BE FILLED IN BY
PRESENTING PHYSICIAN
• Presenting Physician, MD
Category – Disclosures
Steering Committee & Consultant Disclosures
The Steering Committee and Curriculum Consultants reported the following relevant
financial relationships that they or their spouse/partner have with commercial interests:
• Michael Davidson, MD: Speakers’ Bureau: Abbott, AstraZeneca,
GlaxoSmithKline, Merck; Advisory Board/Consultant: Abbott, Aegerion,
Amgen, AstraZeneca, Atherotech, Daiichi-Sankyo, DTC MD, Esperion,
GlaxoSmithKline, iMD (Intelligent Medical Decisions), Kinemed, LipoScience,
Merck, Novo Nordisk, Roche, Sanofi-Aventis, Synarc, Takeda, Vindico
Medical Education; Grant Research: Abbott, Daiichi-Sankyo,
GlaxoSmithKline, Merck, Roche; Board of Directors/Equity: DTC MD,
Omthera, Professional Evaluation Inc., Sonogene
• Peter P. Toth, MD, PhD: Speaker: Abbott, AstraZeneca, Merck, Takeda,
GlaxoSmithKline, Boehringer-Ingelheim; Consultant: Abbott, AstraZeneca,
Merck, Genentech, Genzyme; Advisory Board: Atherotek
• William E. Boden, MD, FACC, FAHA: Speaker: Gilead, Abbott, SanofiAventis, Kowa
• Michael Miller, MD: Nothing to Disclose
Non-faculty Disclosures
Non-faculty content contributors and/or reviewers reported the
following relevant financial relationships that they or their
spouse/partner have with commercial interests:
• Barry Watkins, PhD; Bradley Pine; Blair St. Amand;
Jay Katz; Dana Simpler, MD:
Nothing to Disclose
Educational Objectives
At the conclusion of this activity, participants should be able to
demonstrate the ability to:
• Examine the need for comprehensive lipid management in
dyslipidemic patients who sustain an ACS
• Compare the relative effectiveness of existing treatments to raise
HDL and reduce CVD risk
• Explain the rationale for developing novel agents to increase HDL
• Provide an overview of clinical trials evaluating efficacy and safety of
emerging therapies to modulate HDL
CASE REPORT
Acute Coronary Syndrome
• A 54-year-old male presents with chest pressureassociated dyspnea and vomiting.
• His father had an MI at age 49, and a second MI one
month after the first event.
• Paternal grandfather had 4 MIs with the first event
occurring in his late 40s.
Lab Data in the ER
• Height: 5’8”
BMI = 24.3 kg/m2
• BP: 104/70 mmHg
HR: 70/min
• Lipid Panel:
― Total cholesterol: 167 mg/dL
― LDL: 95 mg/dL
― HDL: 22 mg/dL
― Triglycerides: 250 mg/dL
― Non-HDL: 127 mg/dL
― FBG: 109 mg/dL
― Cr: 0.8 mg/dL
Coronary Angiogram
Angiogram
Atherosclerosis Is an Inflammatory Response
to Excess Apo-B Lipoproteins (Mostly LDL)
Adapted from: Libby P. Sci Amer. 2002;286:46-55.
CASE REPORT
CV Risk Factors
•
•
•
•
Low HDL-C (22 mg/dL)
High TG (250 mg/dL)
IFG (109 mg/dL)
(+) FH
Framingham Risk Score: 7% (10-yr risk)
Annual CHD Event Rate Based on the
Framingham Risk Score
Braunwald E, JACC 2006;47: 101-103
Wood D et al. Eur Heart J 1998;19: A12-19
Lifetime Risk for CVD Increases With Greater
Risk Factor Burden
Risk Factor Burden at Age 50 (Estimated Risk by Age 95)
Lifetime Risk for CVD, %
80
69
70
60
50
36
40
10
0
50
Women
Men
39
27
30
20
39
46
50
8
5
All Optimal
≥1 Not Optimal
≥1 Elevated
1 Major
≥2 Major
Lifetime burden stratified for risk factor burden years among Framingham Heart Study participants free of CVD at 50 years.
Optimal risk factors defined as total cholesterol <180 mg/dL, BP <120/<80 mmHg, nonsmoker, and nondiabetic.
Nonoptimal risk factors are defined as total cholesterol 180–199 mg/dL, systolic BP 120–139 mmHg, diastolic BP 80–89 mmHg, nonsmoker, and nondiabetic.
Elevated risk factors are defined as total cholesterol 200–239 mg/dL, systolic BP 140–159 mmHg, diastolic BP 90–99 mmHg, nonsmoker, and nondiabetic.
Major risk factors are defined as total cholesterol ≥240 mg/dL, systolic BP ≥160 mmHg, diastolic BP ≥100 mmHg, smoker, and diabetic.
CVD = cardiovascular disease; BP = blood pressure.
Lloyd-Jones DM et al. Circulation. 2006;113:791-798.
Attributable Declines in CHD Deaths
Attributable reduction in CHD deaths (%)
Between 1980 and 2000
Net 44%
↑TG,↓HDL
Target
Population
47%
Therapies
Ford ES et al. N Engl J Med. 2007;356:2389-2398.
Lifestyle/RFs
Unexplained
CAD Hospitalization and Temporal Trends
In Lipid Levels from 2000-2006 (Mean)
Sachdeva A et al. Am Heart J. 2009;157:111-117.e2.
Tim Russert
Residual CVD Risk
• April 2008
– Known CAD (preclinical) on a statin
– LDL-C 67mg/dl, Triglycerides 300mg/dl,
HDL 32mg/dl
– Performed well on stress test
• June 2008
– AMI at work
– Attempts to resuscitate fail
• Could this have been avoided?
Grady D. A Search for Answers in Russert’s Death. The New York Times. June 17, 2008.
Johnson A. NBC’s Tim Russert Dies of a Heart Attack at 58. NBC News and msnbc.com. June 14, 2008.
Residual CVD Risk in Statin vs Placebo Trials
CHD Events Occur in Patients Treated with Statins
Patients Experiencing
Major CHD Events, %
40
30
20
28.0
Placebo
Statin
19.4
15.9
12.3
13.2
10
0
N
 LDL
4S1
LIPID2
CARE3
11.8
8.7
HPS4
4S
LIPID
CARE
HPS
4444
-35%
9014
-25%
4159
-28%
20 536
-29%
Secondary
14S
Group. Lancet. 1994;344:1383-1389.
Study Group. N Engl J Med. 1998;339:1349-1357.
3Sacks FM, et al. N Engl J Med. 1996;335:1001-1009.
2LIPID
10.2
7.9
10.9
WOSCOPS5
WOS
6595
-26%
High Risk
6.8
5.5
AFCAPS/
AFCAPS
/
TexCAPS6
TexCAPS
6605
-25%
Primary
4HPS
Collaborative Group. Lancet. 2002;360:7-22.
J, et al. N Engl J Med. 1995;333:1301-1307.
6 Downs JR, et al. JAMA. 1998;279:1615-1622.
5Shepherd
Residual CVD Risk Is Particularly High in
Patients with Diabetes Treated with Statins
Meta-Analysis of CHD Patients in 14 Statin Trialsa
Major Vascular Event Rateb, %
40
30
34.9
29.6
24.8
19.4
20
Residual
Risk
Residual
Risk
10
0
a
Placebo
Treatmentc
CVD Risk Higher Than Patients
With No Diabetes on Placebo
Diabetes
Diabetes
4.3-year mean follow-up of 18 686 patients
with diabetes; n = 71 370 patients with no diabetes
bNonfatal
cEvent
MI, CHD death, stroke, or coronary revascularization
rate per 1 mmol/L (39 mg/dL) reduction in LDL-C
No Diabetes
No Diabetes
CTT Collaborators. Lancet. 2008;371:117-125.
Circulating Lipoproteins Play a
Major Role in Atherosclerosis
LDL
HDL
ApoBa
ApoAI
ApoB-containing lipoproteins1
ApoAI-containing lipoproteins1
 Non-HDL (atherogenic)
 HDL (antiatherogenic)
–
–
–
–
–
LDL
IDL
VLDL /VLDL remnants
Chylomicron remnants
Lp(a)
– α-HDL
– Pre-β HDL
aApoB
is a component of all lipoprotein particles currently considered atherogenic. 2
Apo = apolipoprotein; IDL = intermediate-density lipoprotein; VLDL = very low-density lipoprotein; Lp(a) = lipoprotein (a).
1. Olofsson SO et al. Vasc Health Risk Manag. 2007;3:491-502.
2. Grundy SM. Circulation. 2002;106:2526-2529.
3. Kunitake ST et al. J Lipid Res. 1992;33:1807-1816.
Images available at: http://www.mc.vanderbilt.edu/lens/article/?id=186&pg=999. Accessed January 2010. Adapted with permission.
Cardiovascular Risk Increases with Increased
Plasma Apo B Lipoproteins
Rationale for therapeutic lowering of Apo B lipoproteins: decrease the
probability of inflammatory response to retention
Apo B lipoprotein
particles
Blood
Monocytes bind to
adhesion molecules
Smooth muscle
Inflammatory
response
Modification
Macrophage
Foam cell
Tabas I et al. Circulation. 2007;116(16):1832-1844. Williams KJ et al. Arterioscler Thromb Vasc Biol. 1995;15(5):551-561.
Williams KJ et al. Arterioscler Thromb Vasc Biol. 2005;25(8):1536-1540. Hoshiga M et al. Circ Res. 1995;77(6):1129-1135.
Merrilees MJ et al. J Vasc Res. 1993;30(5):293-302. Nakata A et al. Circulation.1996;94(11):2778-2786.
Steinberg D et al. N Engl J Med. 1989;320(14):915-924.
Residual CVD Risk in Patients Treated With
Intensive Statin Therapy
40
Statistically significant, but clinically inadequate CVD reduction1
Patients Experiencing
Major CVD Events, %
30
26.3
Standard statin therapy
Intensive high-dose statin therapy
22.4
20
13.7
12.0
10.9
10
0
n
LDL-C,a
mg/dL
1Superko
2
PROVEIT-TIMI
IT-TIMI 22
PROVE
22
4162
95
62
HR. Br J Cardiol. 2006;13:131-136.
2Cannon CP et al. N Engl J Med. 2004;350:1495-1504.
3Pedersen TR et al. JAMA. 2005;294:2437-2445.
4LaRosa JC et al. N Engl J Med. 2005;352:1425-1435.
IDEAL3
8.7
TNT4
IDEAL
8888
104
81
TNT
10 001
101
77
aMean
or median LDL-C after treatment
Residual CVD Risk: Framingham Heart Study
Low HDL-C Predicts CHD Independent of LDL-C
HDL-C is inversely
correlated with CAD
risk
Correlation is
independent of LDL-C
CAD Risk
After 4 Yearsa
3
2
1
25
45
65
0
85
100
a
Men aged 50–70
Castelli W. Can J Cardiol. 1988;4(suppl A):5a-10a.
160
220
LDL-C, mg/dL
HDL-C
mg/dL
Normal Values for Plasma HDL-C*
CHD Risk According to HDL-C Levels
The Framingham Heart Study
4.0
CHD risk ratio
4.0
3.0
2.0
2.0
1.0
1.0
0
25 45 65
HDL-C (mg/dL)
Kannel WB. Am J Cardiol 1983;52:9B–12B.
Copyright ©1983, with permission from Excerpta Medica Inc.
National Health and Nutrition Examination Survey III
Distribution of Low HDL-C Bottom Tertile of Population
16
% of the Population
14

< 40/50 mg/dL
men/women are
the bottom tertile of
population

<20 mg/dL
occurs in 1/200
men & 1/400
women

<10 mg/dL occurs
in ~ 1/20,000
Men
12
Women
10
8
6
4
2
0
5-9
10-14
15-19
20-24
25-29
HDL-C (mg/dL)
Miller M & Zahn M. Curr Opin Cardiol 2004;19:380-384
30-34
35-39
Gene Ontology Analysis of HDL Proteins
PLTP
CETP
LCAT ApoC-I
ApoC-II
ApoM
ApoC-III
ApoF
ApoC-IV
ApoE
Lipid Metabolism
ApoD
SAA4
SAA2
ApoA-II
Clusterin
ApoA-IV
ApoH PON1
Complement
Regulation
SAA1
ApoA-I
AHSG
HRP
SERA1
AMP
KNG1
Acute Phase Response
C3
C4A
C4B
C9
Courtesy of J Heinecke.
SERF1
Proteinase
Inhibitor
PON3
ApoL-1
SERF2
AGT
VTN
ORM2
TTR
ITIH4 RBP4 TF
FGA
HPX
The Role of HDL Proteins in Reverse
Cholesterol Transport
© 2006 American Society for Clinical Investigation.
Potential Antiatherogenic Actions of HDL
Vasodilatory
Activity
Antithrombotic
Activity
Anti-infectious
Activity
Reverse
Cholesterol
Transport
Cellular
Cholesterol
Efflux
Anti-inflammatory
Activity
Antiapoptotic
Activity
Endothelial
Repair
Chapman MJ et al. Curr Med Res Opin. 2004;20:1253-1268.
Assmann G et al. Annu Rev Med. 2003;53:321-341.
Antioxidative
Activity
Apo A-I
Apo A-II
Residual CVD Risk: TNT Study
HDL-C Predictive of Risk Even at LDL-C < 70 mg/dL
10
Hazard ratio (95% CI) versus Q1
Q2
0.85 (0.57 - 1.25)
Q3
0.57 (0.36 - 0.88)
Q4
0.55 (0.35 - 0.86)
Q5
0.61 (0.38 - 0.97)
9
8
7
6
5
4
3
2
1
0
Q1
(<37)
Q2
(37 to <42)
Q3
(42 to <47)
Q4
(47 to <55)
Quintile of HDL Cholesterol Level (mg/dl)
Barter P et al. N Engl J Med. 2007;357:1301-1310.
Q5
(≥55)
Each 1 mg/dL
increase in HDL-C
decreases the risk
of major CV
events by
approximately
1.1%, in models
created both at
baseline and at 3
months.
Effects of Lifestyle Modifications on
HDL-C Levels
• Weight Reduction
− For every 3 kg (7 lb) of weight loss, HDL-C levels increase
1 mg/dL
• Smoking Cessation
− HDL-C levels in smokers are 7%-20% lower than those in
nonsmokers
− HDL-C levels return to normal within 30-60 days after smoking
cessation
• Exercise
− Aerobic exercise (e.g. running) increases HDL-C in
dose-dependent manner
Rössner S et al. Atherosclerosis. 1987;64:125-130.
Wood PD et al. N Engl J Med. 1988;319:1173-1179.
Cullen P et al. Eur Heart J. 1998;19:1632-1641.
Kokkinos PF et al. Arch Intern Med. 1995;155:415-420.
Effects of Drugs on HDL-C Levels
Nicotinic acid
Fibrates
Estrogens
Statins
α-blockers
Alcohol
↑
↑
↑
↑
↑
↑
15%–35%
10%–15%
10%–15%
5%–10%
10%–20%
10%
Belalcazar LM, Ballantyne CM. Prog Cardiovasc Dis. 1998;41:151-174.
Angiographic Effects of Lipid Drug Classes
Meta-Analysis, 12 Trials
Change from Baseline in Mean Proximal %
Stenosis
Δ%s = 3.0 – 0.076 (%ΔHDL-C) + 0.06 (%ΔLDL-C) R2 = 0.96; P<.004
4
HATS* Placebo
Placebo (6)
Fibrates (1)
Statins (6)
3
Statin+Resin (1)
Niacin Combos (4)
S+N=simvastatin + niacin
2
1
Progression
0
HATS* S+N
Regression
-1
-2
ASTEROID
0
25
50
75
% HDL-C
Minus
% LDL-C
%ΔHDL-C
Minus%
Δ LDL-CininRxRx(%)
(%)Placebo-Adjusted
Placebo-adjusted
HATS (HDL - Atherosclerosis Treatment Study) data not shown in original study.
Brown BG et al. Curr Opin Lipidol. 2006;17:631-636.
S+N=simvastatin + niacin
Should High-density Lipoprotein Be a
Target of Therapy ?
ATP III and HDL-C
“A specific HDL cholesterol goal level to reach with
HDL raising therapy is not identified”
AIM-HIGH
• On-treatment lipids
– 3300 men and women with vascular disease and
HDL ≤40 [50-F], TG 150-400 and LDL-C ≤160
• Therapy
– simvastatin vs simva+niaspan
• 1° Endpoints
– CHD Death, MI, CVA, high-risk ACS hospitalization
AIM-HIGH Terminated by Data Safety Monitoring Board
32-month Follow-up
• On-treatment lipids
– HDL ↑ 20% / TG ↓ 25%
– Baseline LDL: 71 mg/dL
• 1° Endpoints: Negative
– 28 strokes (1.6%) on extended release niacin (ERN)
– 12 strokes (0.7%) in control group.
– 9 of 28 strokes in ERN discontinued drug at least 2 months
and up to 4 yrs before CVA
Press conference transcript; May 26, 2011. Available at: www.nhlbi.nih.gov/new/remark/aim-high-transcript.htm.
Bays H, McKenney J, Davidson M. Exp. Rev. Cardio. Therapy 2005
Role of CETP Inhibition in Atherosclerosis
LDL-R
LDL
VLDL
CE
CETP
Foam
cells
TG
ABC-A1
RCT
Bile
LIVER
HDL
Atherosclerosis
LDL
ABC-G1
PLASMA
Free
cholesterol
PERIPHERAL TISSUE
• Human CETP deficiency is usually associated with marked ↑ in HDL-C
• CETP activity is inversely correlated with plasma HDL-C
• Decreasing CETP activity has consistently inhibited atherosclerosis in animal models
Barter PJ et al. Arterioscler Thromb Vasc Biol. 2003;23:160-167.
Contacos C et al. Atherosclerosis. 1998;141:87-98.
Guerin M et al. Arterioscler Thromb Vasc Biol. 2008;28:148-154.
CETP Inhibitors and Modulators
CETP
http://www.ama-assn.org/ama1/pub/upload/mm/365/dalcetrapib.doc; http://www.ama-assn.org/ama1/pub/upload/mm/365/torcetrapib.doc;
http://www.ama-assn.org/ama1/pub/upload/mm/365/anacetrapib.pdf; Barter et al. N Engl J Med. 2007;357:2109-2122;
Qiu et al. Nat Struct Mol Biol. 2007;14:106-112.
Torcetrapib
“Beneficial” Effects on Lipoproteins, but Increased Cardiovascular
and Non-Cardiovascular Morbidity and Mortality
+49%
+55%
+42%
HDL-C
LDL-C
+1% +1%
-1%
Placebo
60 mg
-18%
-20%
90 mg
120 mg
Is the toxicity of torcetrapib related to the mechanism or the molecule?
Barter PJ et al. N Engl J Med. 2007;357:2109-2122.
Torcetrapib
Patients Without Event (%)
“Beneficial” Effects on Lipoproteins, but Increased Cardiovascular
and Non-Cardiovascular Morbidity and Mortality (cont)
100
Atorvastatin only
98
96
94
92
Torcetrapib plus atorvastatin
90
0
0
90 180 270 360 450 540 630 720 810
Days After Randomization
Is the toxicity of torcetrapib related to the mechanism or the molecule?
Barter PJ et al. N Engl J Med. 2007;357:2109-2122.
Off-target Pharmacological Effects of Torcetrapib
• In patients receiving torcetrapib in the ILLUMINATE trial there was a
significant:1
– Increase in blood pressure:
–
–
–
–

5.4 mmHg in SBP in the torcetrapib arm

>15 mmHg in SBP at 12 months in 9.4% of the atorvastatin-only group and 19.5% of
the torcetrapib group (P<0.001)
Decrease in serum potassium
Increase in serum bicarbonate
Increase in serum sodium
Increase in serum aldosterone
• The adverse outcomes in the ILLUMINATE trial may have been the
consequence of off-target actions of torcetrapib and not related to CETP
inhibition1,2
1. Barter PJ et al. N Engl J Med. 2007;357:2109-2122.
2. Rosenson RS. Curr Athero Rep. 2008;10:227-229.
Analysis of the Off-target Characteristics of the
CETP Inhibitors
1. Barter et al. N Engl J Med. 2007;357:2109-2122.
3. Stein et al. Am J Cardiol. 2009;104:82-91.
5. Stroes et al. Br J Pharmacol. 2009;158:1763-1770.
2. Masson D. Curr Opin Invest Drugs. 2009;10:980-987.
4. Forrest et al. Br J Pharmacol. 2008;154:1465-1473.
6. Clerc et al. J Hypertens. 2010: in press.
Effects of Anacetrapib on LDL-C and HDL-C
LDL-C
100
120
100
-39.8% (p<0.001)
HDL-C (mg/dL) (SE)
LDL-C (mg/dL) (SE)
80
60
40
20
0
HDL-C
Anacetrapib
Placebo
80
60
40
20
BaselineWk 6Wk 12Wk 18Wk 24Wk 30
Wk 46
Wk 62
Wk 76
Anacetrapib n = 804 771 716 687 646
604
568
540
Placebo n = 803 759 741 743 735
711
691
666
Study Week
Cannon CP et al. N Engl J Med. 2010;363:2406-2415.
+138.1% (p<0.001)
0
Anacetrapib
Placebo
BaselineWk 6Wk 12Wk 18Wk 24Wk 30
Wk 46
Wk 62
Wk 76
Anacetrapib n = 776 757 718 687 647
607
572
543
Placebo n = 766 761 741 744 736
711
691
666
Study Week
Comparison of the Effect of CETP Agents on
HDL-C·AUC and Fecal Radioactivity
1000
HDL-C•AUC
*P < 0.01
#P < 0.01
*
Fecal [3H] total sterols
*
#
20
15
*
#
10
500
5
0
0
Control
Dalcetrapib
Niesor EJ et al. J Lipid Res. 2010;51:3443-3454.
Torcetrapib
Anacetrapib
Fecal [3H] Total Sterols
(% of Injection)
HDL-C·AUC (mg/dL/day)
1500
Dalcetrapib and Torcetrapib Differ in Mechanism
by Which They Decrease CETP Activity
dal
HDL
• Dalcetrapib binds to CETP,
inducing a conformational change
to CETP that hinders its further
association to HDL1
• Dalcetrapib binds to CETP only2
CETP
tor or ana
HDL
• Torcetrapib or anacetrapib binding
to CETP results in a high affinity
complex of CETP inhibitor, HDL,
and CETP2,3
NB: The clinical relevance of these differences is unknown; these compounds have not been
studied in head-to-head clinical trials. Therefore, no conclusion should be drawn based on these
comparisons. Clinical development of torcetrapib was halted due to off-target adverse effects.
1Okamoto
H et al. Nature. 2000;406:203-207.
3Clark RW et al. J Lipid Res. 2006;47:537-552.
2Niesor
EJ et al. Atherosclerosis. 2008;199:231.
Dalcetrapib Phase IIb Trial
HDL-C Increase at Week 12
Change From Baseline (%)
40
35
*P < 0.0001 vs placebo
*
*
30
25
20
*
15
10
5
0
placebo
n = 73
dalcetrapib
300 mg
n = 75
NOTE: Dalcetrapib 600 mg is the dose used in phase III
Stein EA. Am J Cardiol. 2009;104:82-91.
dalcetrapib
600 mg
n = 67
dalcetrapib
900 mg
n = 72
Dalcetrapib Phase IIb Trial
Summary Safety Profile
Pravastatin +
placebo
Pravastatin +
dalcetrapib
300 mg
Pravastatin +
dalcetrapib
600 mg
Pravastatin +
dalcetrapib
900 mg
74
76
68
74
39 (53%)
36 (47%)
38 (56%)
40 (54%)
Cardiac AEs
1 (1%)
4 (5%)
3 (4%)
3 (4%)
Vascular AEs
1 (1%)
2 (3%)
0
0
22 (30%)
17 (22%)
15 (22%)
21 (28%)
Withdrawals due to
AEs
2 (3%)
2 (3%)
2 (3%)
3 (4%)
SAEs
1 (1%)
1 (1%)
1 (1%)
1 (1%)
Deaths
0
0
0
0
n
Any AE
Treatment-related AEs
NOTE: Dalcetrapib 600 mg is the dose used in phase III
Stein EA. Am J Cardiol. 2009;104:82-91.
Conclusions
• Residual CV risk remains problematic despite statinmediated LDL reduction
• HDL-C is an independent risk factor for CHD and metaanalyses and multivariate regression support the hypothesis
that raising HDL-C reduces risk for CVD
• A variety of approaches to HDL therapy are being tested
prospectively in randomized trials
• CETP inhibitors are among the most important novel
therapies for serum HDL modulation
LIPOPROTEIN MANAGEMENT IN ACS
Improving Outcomes in Patients with
Complex Lipid Disorders
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