controversial issues in dyslipidemia management

Controversial issues in dyslipidemia management

ByAshraf Reda,MD

Menoufiya university

http://www.cardiolipid.com/cardiolipid%20files/ppt/Dyslipidemia%202004.ppt

ACS

Regression of plaque

Aggressive lipid lowering

Guide lines

Which statin to which pt.?

ACS:PROVE-IT TIMI 22

4162 Pts With ACS

40mg Pravastatin 80mg Atorvastatin

Mean follow up:24 months

95 mg/dl (2.46 mmol/l) 62 mg/dl (1.6 mmol/l)LDL

26.3% 22.4%1ry end points

16%RRR (p0.005)

ACS: A to Z trial2265 Pts with ACS receiving 40 mg/d of simvastatin for 1 month

followed by 80 mg/d thereafter

2232 Pts with ACS patients receiving placebo for 4 months

followed by 20 mg/d of simvastatin

6-24 months follow up

Placebo-Simva (20)gr. Simva only(40/80) gr.

122mg/dl 77mg/dl

68 mg/dl63mg/dl

Median LDL1 month8 months

1ry EPs 343(16.7%) 309(14.4%)---------------------------------------------------------------------------------------------------------------

------------------------------------------------------------------------------

[HR], 0.89; 95%

[CI] 0.76-1.04; P =.14).

CVD 109(5.4%) 83(4.1%) HR, 0.75; 95% CI, 0.57

-1.00; P =.05) Myopathy occurred in 9 patients (0.4%) receiving simvastatin 80 mg/d, in no patients receiving lower doses of simvastatin

, and in 1 patient receiving placebo (P =.02).

Is It due to

Difference in LDL reduction or

Different in anti inflammatory effect

?

Statin effect and baseline CRP

Joseph B. Muhlestein, a,b,* , Jeffrey L. Anderson, a,b, Benjamin D. Horne, a, John F. Carlquist, a,b, Tami L. Bair, a, T.Jared Bunch, a, Robert R. Pearson,

Patients (n = 2,924) with ≥70% stenosis in ≥1 coronary artery

average of 2.4 years after discharged on a statin prescription.

<1.2 1.2 to 1.7 >1.7 mg/dl), CRP:

.No early statin benefit

.Survival curves separated

after >2 years

.improved survival

.Curve separation:3months

.Improved survival

.Curve separation:1week

Evidence of an anti-inflammatory effect of statins

mailto:[email protected]

Treating to dual targets

Investigators also further stratified patients based on levels of CRP and LDL cholesterol:

LDL cholesterol >70 mg/dL and CRP >2.0 mg/L. LDL cholesterol >70 mg/dL and CRP <2.0 mg/L. IILDL cholesterol <70 mg/dL and CRP >2.0 mg/L. LDL cholesterol <70 mg/dL and CRP <2.0 mg/L.

"Even with the most aggressive statin that we have used to date, 56% of patients still did not make it to the dual target,"

What can we do to patient with LDL reaching the goalBut wit persistently high CRP?

ACS



Guide lines


Decrease the progression

Prevent progression

Regression

0r is it the plaque stabilization?

Main 1ry and 2ry end-point results of REVERSAL

End points Pravastatin, 40 mg (n=249)

Atorvastatin,80 mg

(n=253)

p, difference between groups

Median % change in atheroma volume (95% CI)

2.7(0.2-4.7)

-0.4(-2.4-1.5)

0.02

Median change in total atheroma volume (mm3) (95% CI)

4.4(0.1-6.0)

-0.9(-3.5-1.6)

0.02

Median % change in atheroma volume (95% CI)

1.6(1.2-2.2)

0.2(-0.3-0.5)

0.0002

Nissen SE et al. JAMA 2004; 291:1071-1080.

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The effect on clinical out come?

REVERSAL: Cholesterol levels and percent

change

LDL level Pravastatin, 40 mg (n=249)

Atorvastatin, 80 mg (n=253)

Final LDL-C, mg/dL

110.4 78.9

% change in LDL-C from baseline

-25.2 -46.3


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Symptomatic CAD Pts with LDL: 125-210mg/dl

Simvastatin and plaque regression after 6 months of MRI-monitored therapy.

Circulation. 2004 Oct 19;110(16):2336-41.

Lima JA, Desai MY, Steen H, Warren WP, Gautam S, Lai S.

27 patients (treated with simvastatin 20 to 80 mg daily)

(MRI) for aortic atherosclerotic plaque (AP) before and after 6 months of therapy

AP volume was reduced from 3.3+/-0.1.4 to 2.9+/-1.4 cm3 at 6 months (P<0.02)

luminal volume increase was less accentuated (from 12.0+/-3.9 to 12.2+/-3.7 cm3, P<0.06).

LDL cholesterol decreased by 23% (from 125+/-32 to 97+/-27 mg/dL, P<0.05) in 6 months.

?LDL or CRP

CRP reductions in REVERSAL

CRP Pravastatin, 40 mg

(n=249)

Atorvastatin,80 mg

(n=253)

p, difference between groups

Median %

change in CRP -5.2 -36.4 <0.0001


Reduction of CRP May be related to the magnitude of LDL reduction

Final LDL-C, mg/dL 110.4(25.2%) 78.9(-46.3%)

ACS



Guide lines


Lower Cholesterol Levels Associated With Lower CHD Risk

0

25

50

75

100

125

150

204 205-234

235-264

265-294

295

Castelli WP. Am J Med. 1984;76:4-12.

CH

D I

ncid

en

ce p

er

1000

Serum Cholesterol (mg/100 mL)

The Framingham Heart Study

Relation of Serum Cholesterol to CHD Mortality

The MRFIT Study

11.29

1.73

2.21

3.42

0

1

2

3

4

< 182 182-202 203-220 221-244 > 244

Mort

ality

Rela

tive R

isk

Serum Cholesterol (mg/dL)

n = 356,222(35-57 yrs)

Stamler J, et al. JAMA. 1986;256:2823-2828.

4.50

2.85

1.80

1.15

0.75

2.35 2.85 3.35 3.85 4.35 4.85

LDL Cholesterol

ARIC StudyMen

Rela

tive R

isk o

f C

HD

Adjusted for age and race 12-year follow-up n = 5432

Adapted from Sharrett AR, et al. Circulation. 2001;104:1108-1113.

Increased Relative Risk of CHD Associated With Increasing LDL Levels

(mmol/L)

91 110 130 149 168 188 (mg/dL)

ACS



Guide lines


New Features of ATP III

⇒ Modifications of Lipid Targets:

• MAIN TARGET: LDL <100 mg/dL

• HDL <40 mg/dL considered low (instead of 35 mg/dL)

• Triglycerides >200 mg/dL considered to be high

⇒ Focus on Multiple Risk Factors:

• Diabetes (without CHD) raised to the level of CHD equivalent

⇒ Support for Implementation:

• Recommends complete lipoprotein profile (TC, LDL, HDL & TG) as preferred initial test

NCEP-ATP III = National Cholesterol Education Program-Adult Treatment Panel III

Expert Panel JAMA 2001;285(19):2486-2497; Wood D et al Atherosclerosis 1998;140:199-270; Sempos CT et al JAMA 1993;269(23):3009-3014; Pearson TA et al Arch Intern Med 2000;160:459-467

LDL Cholesterol Goals for Therapeutic Lifestyle Changes (TLC) and Drug Therapy According to NCEP ATP III

Risk CategoryLDL-C Goal

(mg/dL)

LDL-C Level forInitiation of TLC

(mg/dL)

LDL-C Level forConsideration of

Drug Therapy(mg/dL)

CHD or CHD Risk Equivalents(10-y risk > 20%)

2 + Risk Factors(10-y risk 20%)

0-1 Risk Factor

< 100

< 130

< 160

100

130

160

³ 130(100-129: drug optional)

10-y risk 10%-20%: 13010-y risk < 10%: 160

190(160-189: LDL-C-lowering

drug optional)

NCEP, Adult Treatment Panel III. JAMA. 2001;285:2486-2497.

Previous guidelines set the upper limit of normal according to the risk:

160, 130, 100

But

They didn’t tell us how low should we go?

Changes in the guide lines LDL 100 is not enough

ATPIII

NCEP update

High risk

Treatment when > 130Optional 100-129

Treatment when >100Aim: 30-40% reduction

Diabetic

Trigger is 130

Trigger is 100

Moderate risk2-3 RFs

Target<130

Target <130Optional<100

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Goal still <100, optional goal <70mg/dlWaiting for: TNT, SEARCH and IDEAL (aggressive lowering in stable Pts)

Lipid profile among patients with ACS incardiology dep. Menoufiya university

TC < 200mg/dl 25/40 62.5 160.3

No % Mean (mg/dl)

Mean BNP 943.2 (N: up to 350)

TC > 200mg/dl 15/40 37.5 238.9

Mean BNP 1376

Data from file: Reda et al 2003

TGs < 200 32/40 80 137.2

Mean BNP 988

TGs > 200 8/40 20 254Mean BNP 1599.7

Waiting for the big trials

Treating to New Targets (TNT) trial (Atorva80 Vs Atorva 10)

+ 10000 CHD patients and should be completed in December 2004. In this trial, patients are treated to different goals to compare the conventional NCEP guideline of an LDL cholesterol goal of less than 100 mg/dL with a more aggressive LDL cholesterol goal of less than 75 mg/dL.

The Study of the Effectiveness of Additional Reduction in Cholesterol and Homocysteine with Simvastatin and Folic Acid/Vitamin B12

(SEARCH) (Simva 20 Vs Simva 80)

Compares the intensity of lipid lowering, rather than specific goals, in 12000 subjects who have had a prior MI.

The Incremental Decrease in Endpoints through Aggressive Lipid

Lowering (IDEAL) trial (Atorva 80 Vs Simva 20 or Simva 40)

7600-patient, investigating whether additional clinical benefits can be achieved by greater percentage reductions in LDL-cholesterol levels in patients with existing CHD.

ACS



Guide lines


Should our targets differ?

ACS:

Chronic stable CAD

High LDL

Low HDL

RACE

Pravastatin: Primary prevention (WOSCOPE) Secondary prevention (CARE, LIPID) Combination therapy

Fluvastatin: PCI&ACS (LIPS) Diabetes & low HDL High Apo-B & small LDL Combination therapy

Simvastatin High risk & Diabetes (HPS) Secondary prevention (4S) ACS (A to Z)

Atorvastatin: ACS (MIRACLE, PROVEIT) Hypertension Decrease CRP (PROVE-IT, REVERSAL) Diabetes (CARDS)

ACS



Guide lines


Davidson MH, et al. Drugs Affecting Lipid Metabolism 2004 meeting; Oct 24-27, 2004; Venice, Italy; Abstract 204.

Percent of patients who achieved their LDL and non-HDL cholesterol goals

LDL and non-HDL cholesterol

Patients with 0-1 risk factor (n=163)

Patients with >2 risk factors (n=340)

Patients with CHD or CHD risk equivalents (n=728)

Patients with triglycerides >200 mg/dL who achieved ATP III LDL cholesterol goal (%)

78 71 52

Patients with triglycerides >200 mg/dL who achieved ATP III LDL cholesterol and non-HDL goals (%)

64 52 27

Lipoprotein subclasses by race and gender

Lipoprotein subclass

Black women (n=40)

White women (n=108)

Black men (n=29)

White men (n=108)

p for gender difference

p for racial difference

HDL size (nm) 9.17 9.05 8.90 8.67 <0.0001 0.0004

Small HDL (mg/dL)

17.3 17.1 19.3 19.8 <0.0001 NS

Large HDL (mg/dL)

35.6 35.7 23.1 18.0 <0.0001 NS

LDL size (nm) 21.4 21.2 21.0 20.5 <0.0001 0.002

Small LDL (mg/dL)

8.5 14.3 16.2 34.7 <0.0001 0.01

Medium LDL (mg/dL)

30.1 35.0 50.3 41.9 0.0034 NS

Large LDL (mg/dL)

85.9 78.1 56.1 40.1 <0.0001 0.02

VLDL size (nm) 43.6 49.8 47.4 53.9 0.0019 <0.0001

Small VLDL (mg/dL)

17.4 16.9 20.0 18.3 NS NS

Medium VLDL (mg/dL)

26.0 42.3 35.9 50.5 0.01 0.0001

Large VLDL (mg/dL)

5.98 46.0 22.5 71.2 0.0006 <0.0001

What about HDL?

00,5

11,5

22,5

33,5

100 160 220

LDL mg/dL

Re

lati

ve

Ris

k 85 55 25

Kannel WB AJC 1983: 52: 9B -12B

Impact of High LDL and Low HDL

Framingham Study:Relative Risk for CHD

ARBITER-2: Niacin added to statin therapy slows atherosclerotic progression

Nov 10, 2004

CAD pts with Low HDLAnd LDL at goal with statin

N=167

One year: Statin+Niacin Vs Statin + PlaceboLDL<89&HDL<45 with statin therapy

2004 American Heart Association (AHA) Scientific Sessions, lead investigator Dr Allen Taylor

HDL:39 47(21%)

No significant progression in IMTCompared to the placebo group

Fluvastatin increases HDL cholesterol in type 2 diabetic patients

Variable Baseline (mg/dL)

Month 3 (mg/dL)

% change

LDL 149 95 -36

Triglycerides 437 261 -40

HDL 41 46 12

Apo A-1 118 124 5

Apo B 139 97 -30

Bevilacqua M et al. Drugs Affecting Lipid Metabolism 2004 meeting; October 24-27, 2004; Venice, Italy; Abstract 184.

N=50

Variable Baseline (mg/dL)

Month 3 (mg/dL)

% change

LDL 141 84 -40

Triglycerides 411 221 -46

HDL 41 40 -2

Apo A-1 117 114 -3

Apo B 131 92 -30

Atorvastatin

N=50

Fluvastatin

Farnier M et al. Drugs Affecting Lipid Metabolism 2004 meeting; October 24-27, 2004; Venice, Italy.

Percent change in study end points

End point Placebo (n=64)

Ezetimibe 10 mg (n=187)

Fenofibrate 160 mg (n=189)

Ezetimibe 10 mg + fenofibrate 160 mg (n=185)

LDL cholesterol(% change)*

0.2 -13.4 -5.5 -20.4

HDL cholesterol(% change)

3.2 3.9 18.8 19.0

Triglycerides(% change)

-9.2 -11.1 -43.2 -44.0

Non-HDL cholesterol(% change)

-0.2 -14.7 -16.2 -30.4

ApoB (% change) -1.2 -11.3 -15.2 -26.1

High-sensitivity CRP (% change)

9.1 -6.1 -28.0 -27.3

Fibrinogen(% change)

-0.3 -0.3 -10.1 -11.5

*Indicates primary end point

Kuivenhoven JA. Drugs Affecting Lipid Metabolism 2004 meeting; October 24-27, 2004; Venice, Italy.

CETP inhibitors

Lipid variables Placebo and pravastatin

40 mg (n=52)

JTT-705 300 mg and pravastatin 40 mg (n=47)

JTT-705 600 mg and pravastatin 40 mg (n=53)

p vs baseline

CETP mass(% change from baseline)

2.4 64.1 102.6 <0.001

Triglycerides(% change from baseline)

-1.8 1.7 -8.2 <0.05

Total cholesterol (% change from baseline)

0.6 3.4 2.5 <0.01

ApoA-1(% change from baseline)

0.4 10.7 13.6 <0.001

ApoB (% change from baseline)

0.5 -0.4 -4.2 NS

Side effects

Mortality and incidence of cancer during 10-year follow-up of the Scandinavian Simvastatin Survival Study (4S).

Strandberg TE, Pyorala K, Cook TJ, Wilhelmsen L, Faergeman O, Thorgeirsson G, Pedersen TR, Kjekshus J; 4S Group.

Death and cancer incidence in the original treatment groups

( median total follow-up time of 10.4 years)

No of deaths:

Simva Placebo

414 468RR 0.85 ,95% CI 0.74-0.97,

p=0.02

Coronary mortality 238 300 0.76 [0.64-0.90], p=0.0018

Cancer death 85 1000.81 [0.60-1.08],

p=0.14

Incident cancer 227 248 0.88 [0.73-1.05], p=0.15

Genetic risk factors for statin myopathy found; coenzyme Q10, carnitine supplements might help

the American College of Rheumatology 2004

Absence of interaction between atorvastatin or other statins and clopidogrel: results from the interaction study.

Arch Intern Med. 2004 Oct 11;164(18):2051-7

Serebruany VL, Midei MG, Malinin AI, Oshrine BR, Lowry DR, Sane DC, Tanguay JF, Steinhubl SR, Berger PB,

conventional aggregometry, rapid analyzers, and flow cytometry

All patients (n = 75) received 325 mg of aspirin daily for at least

1 week and 300 mg of clopidogrel immediately prior to stent implantation

atorvastatin (n = 25), any other statin (n = 25), or no statin (n = 25)

for at least 30 days prior to stenting

comparison of platelet biomarkers 4 and 24

Statins in general, and atorvastatin in particular, do not affect the ability of clopidogrel to inhibit platelet function.

statins may inhibit platelets directly via yet unknown mechanism(s)possibly related to the regulation of the PAR-1 thrombin receptors

Stopping statins in the short-term is okay for stable patients Oct 13, 2004

ACS: Abrupt discontinuation increase the risk

Chronic stable condition: Up to 6 weeks my not be risky

Dr Mary P McGowan (New England Heart Institute, Manchester, NH) and colleagues from the Treating to New Target (TNT)

Scientific Board Directors

Prof. Dr. Ikram Sadek.

Prof. Dr. Abdel Fattah Ferer.

Prof. Dr. Samir Abdel Kader.

Prof. Dr. Helmy Bakr.

Prof. Dr. Saeid Shalaby.

Prof. Dr. Ahmed Abdel Moneim.

Prof. Dr. Abdulla Moustafa.

Prof. Dr. Osama Sanad.

Conference Guest Faculty (Chairpersons & Speakers are ordered alphabetically)Abdallah Abou Hashem ZagazigAbdallah Moustafa MenoufiyaAbdel Moneim Ibrahim CairoAdel Allam Al AzharAdel El Banna NHIAdel El Etreby Ain ShamsAhmed Abdel Moneim BanhaAhmed Nassar Ain ShamsAhmed Shafie Amar ZagazigAliaa Abdel Fattah CairoAly Ramzy Ain ShamsAmany Serag MenoufiyaAmr Serag TantaAmr Zaki AlexandriaAshraf Ragab CairoAshraf Reda MenoufiyaAyman Abu El Magd Al AzharGalal El Saied CairoHala Mahfouz MenoufiyaHany Ragui NHIHelmi Bakr MansouraHesham El Ashmawy AlexandriaHesham Hassan MenoufiyaHossam Kandil CairoIbtehag Hamdy AlexandriaIhab Abdel Fattah MenoufiyaIhab Attia Ain ShamsIkram Sadek TantaKawkab Khedr AlexandriaKhairy Abd El Dayem Ain ShamsKhaled Sorour CairoMahmoud Hassanein AlexandriaMay Salama TantaMedhat El Ashmawy TantaMohamed Ashraf Cairo

Mohamed Awad Taher Ain ShamsMohamed El Noomany MenoufiyaMohamed El Seteiha TantaMohamed Gamal AssiutMohamed Hamed Badr TantaMohamed Sobhy AlexandriaMohamed Wafaii ZagazikMohsen Ibrahim CairoMokhtar Gomaa Al AzharMoustafa El Sayed Al AzharMoustafa Nawar AlexandriaNabil El Kafrawy MenoufiyaNasser Rasmy CairoNesim Shaaban TantaOmar Awwad Ain ShamsOssama Abd El Aziz TantaOssama Sanad BanhaRamez Guindy Ain ShamsRamzi El Mawardi Ain ShamsRania Gaber TantaSaeid El Malah MenoufiyaSaied Khaled Ain ShamsSaied Shalaby MenoufiyaSameh Zaghloul CairoSamir Abdel Kader AssiutSamir Rafla AlexandriaSherif El Beltagui AlexandriaSherif El Tobgi CairoSherif Mokhtar CairoTaher El Kadi NHITarek Helmy CairoTarek Zaki Ain ShamsWagdy Ayad AlexandriaWagdy Galal Ain Shams

Cairo: 13Ain shams: 12Menoufiya: 10Alex: 10Tanta: 9Alazhar: 4Zagazig: 3NHI: 3Banha: 2Assuite: 2Mansoura: 1Military: 1

Lipidology

Plenary- 1 Chairperson(s) Mahmoud Hassanein, Alex16:30-18:30 Ossama Abd El Aziz, Tanta

Samir Abdel Kader, Assiut Wagdy Ayad, Alex

16:30-16:55 Statin and ACS: When?, how and for whom ? Mohamed Wafaii Zagazig

17:00-17:25 The pleotropic effects of statin: Do they really matter? Omar Awad Ain Shams

17:30-17:55 Controversial issues in Dyslipidemia Ashraf Reda Menoufiya

18:00-18:25 HDL: The Forgotten target Ihab Attia Ain Shams

Action- 119:00 - 20:00

Case Presentation & Panel Discussion19:00-19:30 Case1: Aorto osteal restenotic lesion:

Management of unexpected procedural complicationsMohamed Ashraf CairoPanelist(s): Ihab Abdel Fattah, Menoufiya

Amr Zaki, Alexandria Mohamed Sobhy, Alexandria

Tarek Zaki, Ain Shams

19:30 - 20:00 Case 2: Coronary intervention in a diabetic patientsHossam Kandil

CairoPanelist(s): Adel El Banna, Ain Shams

Mohamed El Seteiha, Tanta Sherif El Tobgi, Cairo Nabil El Kafrawy, Menoufiya

Plenary- 220:00- 21:30 Chairperson(s) Ahmed Nassar, Ain Shams

Helmi Bakr, Mansoura Ikram Sadek, Tanta Moustafa Nawar, Alexandria

Thrombosis and anti thrombotics

20:00-20:25 PCI & LMWH: From A to Z to synergy Ramez Guindy Ain Shams

20:30-20:55 Clopidogrel: 1 month, 9 months or 12 months ? Adel El EtribyAin Shams

21:00-21:25 Reduction of infract size after AMI: PCI or Lytics Abdallah Moustafa Menoufiya

Flash- 121:30 - 23:00

Chairperson(s) Abdallah Abou Hashem, ZagazigHala Mahfouz, MenoufiyaKawkab Khedr, Alexandria

May Salama, Tanta Adel Allam, Al Azhar

Immaging ECG: Case Presentation21:30-21:45 Case1: Tissue Doppler imaging: IHD or cardiomyopathy ?

Mohamed El Noomany Menoufiya21:45-22:00 Case 2: Carotid A-V fistula

Rania Gaber Tanta22:00-22:15 Case 3: Myocardial aneurysms

Sameh Zaghloul Cairo22:15 –22:30 Case4: Unusual myocardial infiltration

Abdallah Abou Hashem Zagazig22:30 – 22:45 Case 5: ECG commentary

Samir Rafla Alexandria 22:45 – 23:00 Case 6 : Perfusion imaging in ACS

Aliaa Abdel Fattah Cairo

Friday, 19/Nov/2004Action- 216:00 - 16:30

Case Presentation & Panel Discussion16:00-16:30 Case1: Interventional vs. medical therapy for arteritis

Galal El Saied CairoPanelist(s) Khaled Sorour, Cairo

Medhat El Ashmawy, TantaSaeid El Malah, Menoufiya

Gaafer Ragab, Cairo16:30-17:00 Case 2: Decision making in prosthetic valve endocarditis

with renal failureAmany Serag Menoufiya

Panelist(s) Amr Serag, Menoufiya Ibtehag Hamdy, AlexandriaNasser Rasmy, CairoOssama Sanad, Banha

17:00-17:30 Case 3: Drug Elluting Stent: pitfalls of the techniqueSherif El Beltagui Alexandria

Panelist(s) Aly Ramzy, Ain ShamsHany Ragui, NHIHesham El Ashmawy, AlexWagdy Galal, Ain Shams

Flash- 217:30 – 18:00 Chairperson(s) Ahmed Shafie Amar, Zagazig

Nessim Shaaban, TantaTaher El Kadi

Tarek Helmy, CairoSurgery PCI: Case Presentations17:30-17:45 Case I: Volume reduction surgery in heart failure

Adel El Banna NHI17:45-18:00 Case II: Mulivessel PCI

Hesham Hassan Menoufiya

Plenary -318:00 - 19:00

Chairperson(s) Ashraf Reda, MenoufiyaMohamed Sobhy, Alexandria

Peripheral Vascular Disease18:00-18:20 Molecular bases

Abdel Moneim Ibrahim Cairo18:30-18:50 Current therapy and recent trends in the medical

therapy PVDMohamed Awad Taher Ain Shams

19:00 – 19:30 TEA TIME

Plenary- 419:30 - 21:00Chairperson(s) Khairy Abd El Dayem, Ain Shams

Mohamed Hamed Badr, Tanta Mokhtar Gomaa, Al Azhar

Hypertension & Risk Reduction

19:30-19:55 Therapeutic strategies in hypertension control: Minimal or optimal?

Mohsen Ibrahim Cairo

20:00-20:25 ARB’s and the value of life: A, B, or C.Ramzi El Mawardi Ain Shams

20:30-20:55 ACEI and reduction of CV riskSaied Khaled Ain Shams

Plenary- 521:00 - 23:00Chairperson(s) Mohamed Gamal, Assiut

Moustafa El Sayed, Al AzharSaied Shalaby, MenoufiyaSherif Mokhtar, Cairo

Controversial Issues

21:00-21:25 Diabetes with multivessal disease: PCI or CABGMohamed Sobhy

Alexandria21:30-21:55 Therapeutic strategies for ACS: cooling off or

aggressiveAhmed Abdel Moneim Banha

22:00-22:25 Would oral sirolimous replace drug eluting stents ?Ayman Abu El Magd Al

Azhar22:30-22:55 Metabolic approache in the management of IHD

Adel El EtribyAin Shams

23: 00 Gala Dinner ( Sponsored by Novartis )

Ballantyne C. Drugs Affecting Lipid Metabolism 2004 meeting; October 24-27, 2004; Venice, Italy.

VYVA: Primary and secondary end points at six weeks

End points All atorvastatin (n=927)

All EZ/S (n=923)

Percent change in LDL cholesterol -45.3 -53.4

Percent change in HDL cholesterol 4.3 7.9

Percentage of patients reaching their NCEP goal for LDL cholesterol

81.1 89.7

Percentage of CHD/CHD risk equivalent patients who reached <70 mg/dL

NA NA

EZ/S=Ezetimibe/simvastatin

Comparing hyperlipidemia control with

daily versus twice-weekly simvastatin.

Ann Pharmacother. 2004 Nov;38(11):1789-93.

Mangin EF, Robles GI, Jones WN, Ford MA, Thomson SP. University of Arizona Center for Health Outcomes & Pharmaco-Economic Research,

nonrandomized, open-label, proof-of-concept study

simvastatin 10 or 20 mg daily 40 or 80 mg twice weekly, respectively, for 12 weeks.

The twice-weekly regimen safely maintained most of the patients at their LDL-C goal level, and over half the patients found this regimen to be the same or easier to follow than a daily regimen. Large outcome studies evaluating this approach are needed.

Estimated cost-savings at our institution associated with this regimen would be $32 000 per 1000 patients per year.

controversial issues in dyslipidemia management

Documents

acs patients

mgdl cvd

q qguide lines q qwhich

ldl cholesterol

mgd of simvastatin

statin effect

ldl reduction

median ldl