Controversial issues in dyslipidemia management

By Ashraf Reda,MD Menoufiya university



ACS



Regression of plaque



Aggressive lipid lowering



Guide lines



Which statin to which pt.?



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 LDL

Mean follow up:24 months

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

1ry end points 26.3% 22.4%

16%RRR (p0.005)

ACS: A to Z trial

 2265 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 Median LDL

Placebo-Simva (20)gr

.

Simva only(40/80) gr.

1 month 8 months 122mg/dl 77mg/dl 68 mg/dl 63mg/dl -------------------------------------------------------------------------------------------------------------- 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

Evidence of an anti-inflammatory effect of statins Patients

(n = 2,924)

with ≥70% stenosis in ≥1 coronary artery average of 2.4 years after discharged on a statin prescription. CRP: <1.2 1.2 to 1.7 >1.7 mg/dl), .

No early statin benefit .

improved survival .

Improved survival .

Survival curves separated after >2 years .

Curve separation:3months .

Curve separation:1week 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 ,

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. II LDL 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 goal But wit persistently high CRP?



ACS



Regression of plaque



Aggressive lipid lowering



Guide lines



Which statin to which pt.?



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 (mm 3 ) (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.

The effect on clinical out come?

REVERSAL: Cholesterol levels and percent change

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

LDL level

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

Final LDL-C, mg/dL Pravastatin, 40 mg (n=249) 110.4

Atorvastatin, 80 mg (n=253) 78.9 % change in LDL-C from baseline -25.2 -46.3

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

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

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

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

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

CRP reductions in REVERSAL

CRP Median % change in CRP Pravastatin, 40 mg (n=249) -5.2 Atorvastatin, 80 mg (n=253) -36.4 p, difference between groups <0.0001

Final LDL-C , mg/dL

110.4(25.2%) 78.9(-46.3%)

Reduction of CRP May be related to the magnitude of LDL reduction Nissen SE et al. JAMA 2004; 291:1071-1080.



ACS



Regression of plaque



Aggressive lipid lowering



Guide lines



Which statin to which pt.?

Lower Cholesterol Levels Associated With Lower CHD Risk

150 125 100 75 50 The Framingham Heart Study 25 0



204 205 234 235 264 265 294



Serum Cholesterol (mg/100 mL) 295

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

Relation of Serum Cholesterol to CHD Mortality

The MRFIT Study 4 3.42

3 2 2.21

1.73

1 1 1.29

n = 356,222 (35-57 yrs)

0 < 182 182-202 203-220 221-244 > 244 Serum Cholesterol (mg/dL)

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

Increased Relative Risk of CHD Associated With Increasing LDL Levels

4.50

ARIC Study Men 2.85

1.80

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

1.15

0.75

2.35 2.85 3.35 3.85 4.35 4.85

91 110 130 149 LDL Cholesterol 168 (mmol/L) 188 (mg/dL)

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



ACS



Regression of plaque



Aggressive lipid lowering



Guide lines



Which statin to which pt.?

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 Sempos CT et al

JAMA Atherosclerosis

1998;140:199-270; 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 Category LDL-C Goal (mg/dL) LDL-C Level for Initiation of TLC (mg/dL) LDL-C Level for Consideration of Drug Therapy (mg/dL) CHD or CHD Risk Equivalents (10-y risk > 20%)

< 100  100  130 (100-129: drug optional)

2 + Risk Factors (10-y risk



20%)

< 130  130 10-y risk 10%-20%:  10-y risk < 10%:  130 160

0-1 Risk Factor

< 160  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

High risk Diabetic Moderate risk 2-3 RFs ----------------------------------------------------------------------------------------------------------- ATPIII Treatment when > 130 Optional 100-129 Trigger is 130 Target<130 ---------------------------------------------------------------------------------------------------------- NCEP update Treatment when >100 Aim: 30-40% reduction Trigger is 100 Target <130 Optional<100 ------------------------------------------------------------------------------------------------------------ Goal still <100, optional goal <70mg/dl Waiting for:

TNT, SEARCH and IDEAL (aggressive lowering in stable Pts)

Lipid profile among patients with ACS in cardiology dep. Menoufiya university

TC < 200mg/dl No % Mean (mg/dl) 25/40 62.5 160.3

Mean BNP 943.2 (N: up to 350)

TC > 200mg/dl 15/40 37.5 238.9

TGs < 200 TGs > 200

Mean BNP 1376

32/40 80 137.2

Mean BNP 988

8/40 20 254

Mean BNP 1599.7

Data from file: Reda et al 2003

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



Regression of plaque



Aggressive lipid lowering



Guide lines



Which statin to which pt.?

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



Regression of plaque



Aggressive lipid lowering



Guide lines



Which statin to which pt.?

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

LDL and non HDL cholesterol Patients with triglycerides >200 mg/dL who achieved ATP III LDL cholesterol goal (%) Patients with 0 1 risk factor (n=163) 78 Patients with >2 risk factors (n=340) 71 Patients with CHD or CHD risk equivalents (n=728) 52 Patients with triglycerides >200 mg/dL who achieved ATP III LDL cholesterol and non-HDL goals (%) 64 52 27

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

Lipoprotein subclasses by race and gender Lipoprotein subclass

HDL size (nm) Small HDL (mg/dL) Large HDL (mg/dL) LDL size (nm) Small LDL (mg/dL) Medium LDL (mg/dL) Large LDL (mg/dL) VLDL size (nm) Small VLDL (mg/dL) Medium VLDL (mg/dL) Large VLDL (mg/dL)

Black women (n=40)

9.17

17.3

35.6

21.4

8.5

30.1

85.9

43.6

17.4

26.0

5.98

White women (n=108)

9.05

17.1

35.7

21.2

14.3

35.0

78.1

49.8

16.9

42.3

46.0

Black men (n=29)

8.90

19.3

23.1

21.0

16.2

50.3

56.1

47.4

20.0

35.9

22.5

White men (n=108)

8.67

19.8

18.0

20.5

34.7

41.9

40.1

53.9

18.3

50.5

71.2

p for gender difference

<0.0001

<0.0001

<0.0001

<0.0001

<0.0001

0.0034

<0.0001

0.0019

NS 0.01

0.0006

p for racial difference

0.0004

NS NS 0.002

0.01

NS 0.02

<0.0001

NS 0.0001

<0.0001

What about HDL?

Framingham Study:

Relative Risk for CHD

Impact of High LDL and Low HDL 3,5 3 2,5 2 1,5 1 0,5 0 85 55 25 100 160 LDL mg/dL 220 Kannel WB AJC 1983: 52: 9B -12B

ARBITER-2: Niacin added to statin therapy slows atherosclerotic progression CAD pts with Low HDL And LDL at goal with statin N=167 1 0 , 2 0 0 4 N o v One year: Statin+Niacin Vs Statin + Placebo LDL<89&HDL<45 with statin therapy HDL:39 47(21%) No significant progression in IMT Compared to the placebo group

2004 American Heart Association

(AHA)

Scientific Sessions

, lead investigator

Dr Allen Taylor

Fluvastatin increases HDL cholesterol in type 2 diabetic patients

Variable Fluvastatin Baseline (mg/dL) Month 3 (mg/dL) LDL Triglycerides HDL Apo A-1 Apo B 149 437 41 118 139 95 261 46 124 97 % change -36 -40 12 5 -30 Atorvastatin Variable LDL Triglycerides HDL Baseline (mg/dL) 141 411 41 Month 3 (mg/dL) 84 221 40 % change -40 -46 -2 Apo A-1 Apo B 117 131 114 92 -3 -30

N=50 N=50 Bevilacqua M et al.

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

Percent change in study end points

End point Placebo (n=64) LDL cholesterol (% change)* HDL cholesterol (% change) Triglycerides (% change) Non-HDL cholesterol (% change) ApoB (% change) High-sensitivity CRP (% change) Fibrinogen (% change) 0.2

3.2

-9.2

-0.2

-1.2

9.1

-0.3

-11.3

-6.1

-0.3

Ezetimibe 10 mg (n=187) -13.4

3.9

-11.1

-14.7

-15.2

-28.0

-10.1

Fenofibrate 160 mg (n=189) -5.5

18.8

-43.2

-16.2

Ezetimibe 10 mg + fenofibrate 160 mg (n=185) -20.4

19.0

-44.0

-30.4

-26.1

-27.3

-11.5

*Indicates primary end point

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

CETP inhibitors

Lipid variables CETP mass (% change from baseline) Triglycerides (% change from baseline) Total cholesterol (% change from baseline) ApoA-1 (% change from baseline) ApoB (% change from baseline) Placebo and pravastatin 40 mg (n=52) 2.4

-1.8

0.6

0.4

0.5

JTT-705 300 mg and pravastatin 40 mg (n=47) 64.1

1.7

3.4

10.7

-0.4

JTT-705 600 mg and pravastatin 40 mg (n=53) 102.6

p vs baseline <0.001

-8.2

2.5

13.6

-4.2

<0.05

<0.01

<0.001

NS

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

Side effects

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

No of deaths: Death and cancer incidence in the original treatment groups ( median total follow-up time of 10.4 years) Simva 414 Placebo 468 Coronary mortality 238 300 Cancer death 85 100 Incident cancer 227 248 RR 0.85 ,95% CI 0.74-0.97, p=0.02

0.76 [0.64-0.90], p=0.0018 0.81 [0.60-1.08], p=0.14 0.88 [0.73-1.05], p=0.15

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

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.

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 conventional aggregometry, rapid analyzers, and flow cytometry 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 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,

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.

Abdallah Abou Hashem Abdallah Moustafa Abdel Moneim Ibrahim Adel Allam Adel El Banna Adel El Etreby Ahmed Abdel Moneim Ahmed Nassar Ahmed Shafie Amar Aliaa Abdel Fattah Aly Ramzy Amany Serag Amr Serag Amr Zaki Ashraf Ragab Ashraf Reda Ayman Abu El Magd Galal El Saied Hala Mahfouz Hany Ragui Helmi Bakr Hesham El Ashmawy Hesham Hassan Hossam Kandil Ibtehag Hamdy Ihab Abdel Fattah Ihab Attia Ikram Sadek Kawkab Khedr Khairy Abd El Dayem Khaled Sorour Mahmoud Hassanein May Salama Medhat El Ashmawy Mohamed Ashraf

Conference Guest Faculty

(Chairpersons & Speakers are ordered alphabetically)

Zagazig Menoufiya Cairo Al Azhar NHI Ain Shams Banha Ain Shams Zagazig Cairo Ain Shams Menoufiya Tanta Alexandria Cairo Menoufiya Al Azhar Cairo Menoufiya NHI Mansoura Alexandria Menoufiya Cairo Alexandria Menoufiya Ain Shams Tanta Alexandria Ain Shams Cairo Alexandria Tanta Tanta Cairo

Mohamed Awad Taher Mohamed El Noomany Mohamed El Seteiha Mohamed Gamal Mohamed Hamed Badr Mohamed Sobhy Mohamed Wafaii Mohsen Ibrahim Mokhtar Gomaa Moustafa El Sayed Moustafa Nawar Nabil El Kafrawy Nasser Rasmy Nesim Shaaban Omar Awwad Ossama Abd El Aziz Ossama Sanad Ramez Guindy Ramzi El Mawardi Rania Gaber Saeid El Malah Saied Khaled Saied Shalaby Sameh Zaghloul Samir Abdel Kader Samir Rafla Sherif El Beltagui Sherif El Tobgi Sherif Mokhtar Taher El Kadi Tarek Helmy Tarek Zaki Wagdy Ayad Wagdy Galal Ain Shams Menoufiya Tanta Assiut Tanta Alexandria Zagazik Cairo Al Azhar Al Azhar Alexandria Menoufiya Cairo Tanta Ain Shams Tanta Banha Ain Shams Ain Shams Tanta Menoufiya Ain Shams Menoufiya Cairo Assiut Alexandria Alexandria Cairo Cairo NHI Cairo Ain Shams Alexandria Ain Shams

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

Lipidology

Plenary- 1 16:30

-

18:30

Chairperson(s)

Mahmoud Hassanein, Alex 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- 1 19:00

-

20:00

Case Presentation & Panel Discussion

19:00-19:30

Case1: Aorto osteal restenotic lesion: Management of unexpected procedural complications

Mohamed Ashraf

Panelist(s):

Ihab Abdel Fattah, Menoufiya Amr Zaki, Alexandria Cairo Mohamed Sobhy, Alexandria Tarek Zaki, Ain Shams

19:30 - 20:00

Case 2: Coronary intervention in a diabetic patients

Hossam Kandil Cairo

Panelist(s):

Adel El Banna, Ain Shams Mohamed El Seteiha, Tanta Sherif El Tobgi, Cairo Nabil El Kafrawy, Menoufiya

Plenary- 2 20:00- 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 Etriby Ain Shams

21:00-21:25

Reduction of infract size after AMI: PCI or Lytics

Abdallah Moustafa Menoufiya

Flash- 1 21:30 - 23:00

Chairperson(s)

Abdallah Abou Hashem, Zagazig Hala Mahfouz, Menoufiya Kawkab Khedr, Alexandria May Salama, Tanta Adel Allam, Al Azhar Immaging ECG: Case Presentation

21:30-21:45

Case1: Tissue Doppler imaging: IHD or cardiomyopathy ?

Mohamed El Noomany

21:45-22:00

Case 2: Carotid A-V fistula

Menoufiya Rania Gaber Tanta

22:00-22:15

Case 3: Myocardial aneurysms

22:15 –22:30

Sameh Zaghloul Cairo

Case4: Unusual myocardial infiltration

Abdallah Abou Hashem

22:30 – 22:45

Case 5: ECG commentary

Zagazig Samir Rafla

22:45 – 23:00

Alexandria

Case 6 : Perfusion imaging in ACS

Aliaa Abdel Fattah Cairo

Friday, 19/Nov/2004 Action- 2 16:00 - 16:30

Case Presentation & Panel Discussion

16:00-16:30

Case1: Interventional vs. medical therapy for arteritis

Galal El Saied Cairo

Panelist(s)

Khaled Sorour, Cairo Medhat El Ashmawy, Tanta Saeid El Malah, Menoufiya Gaafer Ragab, Cairo

16:30-17:00

Case 2: Decision making in prosthetic valve endocarditis with renal failure

Panelist(s)

Amany Serag Menoufiya Amr Serag, Menoufiya Ibtehag Hamdy, Alexandria Nasser Rasmy, Cairo Ossama Sanad, Banha

17:00-17:30

Case 3

:

Drug Elluting Stent: pitfalls of the technique

Sherif El Beltagui Alexandria

Panelist(s)

Aly Ramzy, Ain Shams Hany Ragui, NHI Hesham El Ashmawy, Alex Wagdy Galal, Ain Shams

Flash- 2 17:30 – 18:00

Chairperson(s)

Ahmed Shafie Amar, Zagazig Nessim Shaaban, Tanta Taher El Kadi Tarek Helmy, Cairo Surgery PCI: Case Presentations

17:30-17:45

Case I: Volume reduction surgery in heart failure

Adel El Banna NHI

17:45-18:00

Case II: Mulivessel PCI

Hesham Hassan Menoufiya

Plenary -3 18:00 - 19:00

Chairperson(s)

Ashraf Reda, Menoufiya Mohamed Sobhy, Alexandria Peripheral Vascular Disease

18:00-18:20

Molecular bases

Abdel Moneim Ibrahim Cairo

18:30-18:50

Current therapy and recent trends in the medical

Mohamed Awad Taher

therapy PVD

Ain Shams

19:00 – 19:30 TEA TIME

Plenary- 4 19:30 - 21:00

Chairperson(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 risk

Saied Khaled Ain Shams

Plenary- 5 21:00 - 23:00

Chairperson(s)

Mohamed Gamal, Assiut Moustafa El Sayed, Al Azhar Saied Shalaby, Menoufiya Sherif Mokhtar, Cairo Controversial Issues

21:00-21:25

Diabetes with multivessal disease: PCI or CABG

Mohamed Sobhy Alexandria

21:30-21:55

Therapeutic strategies for ACS: cooling off or aggressive

Ahmed Abdel Moneim Banha

22:00-22:25

Would oral sirolimous replace drug eluting stents ?

Ayman Abu El Magd Al Azhar

22:30-22:55

Metabolic approache in the management of IHD

Adel El Etriby Ain Shams

23: 00 Gala Dinner ( Sponsored by Novartis )

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 Percent change in HDL cholesterol Percentage of patients reaching their NCEP goal for LDL cholesterol Percentage of CHD/CHD risk equivalent patients who reached <70 mg/dL -45.3

4.3

81.1

NA -53.4

7.9

89.7

NA EZ/S=Ezetimibe/simvastatin

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

Comparing hyperlipidemia control with daily versus twice-weekly simvastatin.

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.

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 ,