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Controversial issues in

dyslipidemia
management
By
Ashraf Reda,MD
Menoufiya university

http://www.cardiolipid.com/cardiolipid%20files/ppt/Dyslipidemia%202004.ppt
qACS
q
qRegression of plaque
q
qAggressive lipid lowering
q
qGuide lines
q
qWhich statin to which pt.?
qACS
q
qRegression of plaque
q
qAggressive lipid lowering
q
qGuide lines
q
qWhich statin to which pt.?
ACS:PROVE-IT TIMI 22
4162 Pts With ACS

40mg Pravastatin 80mg Atorvastatin

Mean follow up:24 months


LDL 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
q2265 Pts with ACS receiving 40 mg/d of simvastatin for 1 month
followed by 80 mg/d thereafter

q2232 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.


Median LDL
1 month 122mg/dl 68 mg/dl
8 months 77mg/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?
qACS
q
qRegression of plaque
q
qAggressive lipid lowering
q
qGuide lines
q
qWhich statin to which pt.?
qDecrease the progression
q
qPrevent progression
q
qRegression
q
q0r is it the plaque stabilization?
Main 1ry and 2ry end-point results of
REVERSAL
End points Pravastatin, 40 mg Atorvastatin, p, difference
(n=249) 80 mg between
(n=253) groups

Median % change in 2.7 -0.4 0.02


atheroma volume (95% (0.2-4.7) (-2.4-1.5)
CI)

Median change in total 4.4 -0.9 0.02


atheroma volume (mm3) (0.1-6.0) (-3.5-1.6)
(95% CI)

-----------------------------------------------------------------------------------------------------
Median % change in 1.6 0.2 0.0002
atheroma volume (95% (1.2-2.2) (-0.3-0.5)
CI)
-----------------------------------------------------------------------------------------------------
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 Pravastatin, 40 mg Atorvastatin, 80


(n=249) mg (n=253)
Final LDL-C, mg/dL 110.4 78.9
------------------------------------------------------------------------------------------

% change in LDL-C -25.2 -46.3


---------------------------------------------------------------------------------------
from baseline

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 luminal volume increase


from 3.3+/-0.1.4 to was less accentuated
2.9+/-1.4 cm3 at 6 months (from 12.0+/-3.9 to
(P<0.02) 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 Pravastatin, 40 mg Atorvastatin, p, difference


(n=249) 80 mg between
(n=253) groups

Median % -5.2 -36.4 <0.0001


change in CRP

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.


qACS
q
qRegression of plaque
q
qAggressive lipid lowering
q
qGuide lines
q
qWhich statin to which pt.?
Lower Cholesterol Levels Associated
With Lower CHD Risk
CHD Incidence per 1000 150 The Framingham Heart Study

125

100

75

50

25

0
 205- 235- 265-  295
204 234 264 294
Serum Cholesterol (mg/100 mL)

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


Relation of Serum Cholesterol to
CHD Mortality
The MRFIT Study
4
Mortality Relative Risk

3 3.42

2
2.21

1.73
1 1.29 n = 356,222
1 (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
ARIC Study
4.50 Men
Relative Risk of CHD

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

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


qACS
q
qRegression of plaque
q
qAggressive lipid lowering
q
qGuide lines
q
qWhich 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 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
LDL-C Level for
LDL-C Level for Consideration of
LDL-C Goal Initiation of TLC Drug Therapy
Risk Category (mg/dL) (mg/dL) (mg/dL)

CHD or CHD
Risk Equivalents < 100  100 ≥ 130
(10-y risk > 20%) (100-129: drug optional)

2 + Risk Factors < 130  130 10-y risk 10%-20%:  130


(10-y risk  20%) 10-y risk < 10%:  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
------------------------------------------------------------------------------------------------------------
Treatment when > 130 Trigger is 130
ATPIII Target<130
Optional 100-129

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

Trigger is 100 Target <130


NCEP update Treatment when >100 Optional<100
Aim: 30-40% reduction

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

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
No % Mean (mg/dl)
TC < 200mg/dl 25/40 62.5 160.3
Mean BNP 943.2 (N: up to 350)

TC > 200mg/dl 15/40 37.5 238.9


Mean BNP 1376
TGs < 200 32/40 80 137.2
Mean BNP 988
TGs > 200 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.
qACS
q
qRegression of plaque
q
qAggressive lipid lowering
q
qGuide lines
q
qWhich statin to which pt.?
Should our targets differ?

qACS:

qChronic stable CAD

qHigh LDL

qLow HDL
q
qRACE
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)
qACS
q
qRegression of plaque
q
qAggressive lipid lowering
q
qGuide lines
q
qWhich statin to which pt.?
Thank
you
Percent of patients who achieved
their LDL and non-HDL cholesterol
goals
LDL and non- Patients with 0- Patients with Patients with CHD
HDL cholesterol 1 risk factor >2 risk factors or CHD risk
equivalents
(n=163) (n=340)
(n=728)

Patients with 78 71 52
triglycerides >200
mg/dL who
achieved ATP III
LDL cholesterol
goal (%)

Patients with 64 52 27
triglycerides >200
mg/dL who
achieved ATP III
LDL cholesterol
and non-HDL
goals (%)

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 Black women White women Black men White men p for gender p for racial
subclass (n=40) (n=108) (n=29) (n=108) difference 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 30.1 35.0 50.3 41.9 0.0034 NS
(mg/dL)
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 26.0 42.3 35.9 50.5 0.01 0.0001
(mg/dL)
Large VLDL (mg/dL) 5.98 46.0 22.5 71.2 0.0006 <0.0001
What about HDL?
Framingham Study:
Relative Risk for CHD
Impact of High LDL and Low HDL
3,5
3
2,5 85 55 25
Relative Risk

2
1,5
1
0,5
0
100 160 220
LDL mg/dL
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 N=167
o
v
1
One year: Statin+Niacin Vs Statin + Placebo
0,
LDL<89&HDL<45 with statin therapy
2
0
0 HDL:39 47(21%)
4

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 diabeticFluvastatin
patients
Variable Baseline Month 3 (mg/dL) % change
LDL (mg/dL)
149 95 -36
Triglycerides 437 261 -40
HDL 41 46 12
N=50
Apo A-1 118 124 5
Apo B 139 97 -30

Atorvastatin
Variable Baseline (mg/dL) Month 3 (mg/dL) % change
LDL 141 84 -40
Triglycerides 411 221 -46
HDL 41 40 -2 N=50
Apo A-1 117 114 -3
Apo B 131 92 -30

Bevilacqua M et al. Drugs Affecting Lipid Metabolism 2004 meeting; October 24-27,
2004; Venice, Italy; Abstract 184.
VYVA: Primary and secondary
end points at six weeks
End points Atorvastatin 10 EZ/Simva 10/10 Atorvastatin 20 EZ/Simva
mg (n=235) mg (n=230) mg (n=230) 10/20 mg
(n=233)
Percent change in LDL -36.1 -47.1 -43.7 -50.6

Percent change in HDL 6.9 7.7 5.1 7.2


Percentage of patients 69.4 86.1 80.9 87.6
reaching their NCEP goal
for LDL

Percentage of CHD/CHD 6 20 17 39
risk equivalent patients
who reached <70 mg/dL

EZ/S=Ezetimibe/simvastatin

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 Atorvastatin 40 EZ/Simva Atorvastatin 80 EZ/Simva
mg (n=232) 10/40 mg mg (n=230) 10/80 mg
(n=236) (n=224)

Percent change in LDL -48.3 -57.4 -52.9 -58.6

Percent change in HDL 3.8 9.0 1.4 7.5

Percentage of patients 85.3 93.5 89.1 91.5


reaching their NCEP goal for
LDL

Percentage of CHD/CHD risk 23 57 36 64


equivalent patients who
reached <70 mg/dL

EZ/S=Ezetimibe/simvastatin

Ballantyne C. Drugs Affecting Lipid Metabolism 2004 meeting;


October 24-27, 2004; Venice, Italy.
Percent change in study end
points
End point Placebo Ezetimibe 10 Fenofibrate 160 Ezetimibe 10 mg +
(n=64) mg (n=187) mg (n=189) fenofibrate 160 mg
(n=185)
LDL cholesterol 0.2 -13.4 -5.5 -20.4
(% change)*
HDL cholesterol 3.2 3.9 18.8 19.0
(% change)
Triglycerides -9.2 -11.1 -43.2 -44.0
(% change)
Non-HDL cholesterol -0.2 -14.7 -16.2 -30.4
(% change)

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


High-sensitivity CRP (% 9.1 -6.1 -28.0 -27.3
change)
Fibrinogen -0.3 -0.3 -10.1 -11.5
(% change)

*Indicates primary end point


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

Lipid variables Placebo and JTT-705 300 mg and JTT-705 600 mg and p vs
pravastatin 40 mg pravastatin 40 mg pravastatin 40 mg baseline
(n=52) (n=47) (n=53)
CETP mass 2.4 64.1 102.6 <0.001
(% change from
baseline)
Triglycerides -1.8 1.7 -8.2 <0.05
(% change from
baseline)
Total cholesterol (% 0.6 3.4 2.5 <0.01
change from baseline)

ApoA-1 0.4 10.7 13.6 <0.001


(% change from
baseline)
ApoB (% change from 0.5 -0.4 -4.2 NS
baseline)

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).

Death and cancer incidence in the original treatment groups


( median total follow-up time of 10.4 years)

Simva Placebo

No of deaths: RR 0.85 ,95% CI 0.74-0.97,


414 468 p=0.02

Coronary mortality 238 300 0.76 [0.64-0.90],


p=0.0018

0.81 [0.60-1.08],
Cancer death 85 100 p=0.14

Incident cancer 227 248 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

qStatins in general, and atorvastatin in particular, do not affect


the ability of clopidogrel to inhibit platelet function.

qstatins 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

qACS: Abrupt discontinuation increase the risk


q
qChronic 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 Zagazig
Abdallah Moustafa Menoufiya
Abdel Moneim Ibrahim Cairo
Adel Allam Al Azhar
Adel El Banna NHI
Adel El Etreby Ain Shams
Ahmed Abdel Moneim Banha
Ahmed Nassar Ain Shams
Ahmed Shafie Amar Zagazig
Aliaa Abdel Fattah Cairo
Aly Ramzy Ain Shams
Amany Serag Menoufiya
Amr Serag Tanta
Amr Zaki Alexandria
Ashraf Ragab Cairo
Ashraf Reda Menoufiya
Ayman Abu El Magd Al Azhar
Galal El Saied Cairo
Hala Mahfouz Menoufiya
Hany Ragui NHI
Helmi Bakr Mansoura
Hesham El Ashmawy Alexandria
Hesham Hassan Menoufiya
Hossam Kandil Cairo
Ibtehag Hamdy Alexandria
Ihab Abdel Fattah Menoufiya
Ihab Attia Ain Shams
Ikram Sadek Tanta
Kawkab Khedr Alexandria
Khairy Abd El Dayem Ain Shams
Khaled Sorour Cairo
Mahmoud Hassanein Alexandria
May Salama Tanta
Medhat El Ashmawy Tanta
Mohamed Ashraf Cairo
Mohamed Awad Taher Ain Shams
Mohamed El Noomany Menoufiya
Mohamed El Seteiha Tanta
Mohamed Gamal Assiut
Mohamed Hamed Badr Tanta
Mohamed Sobhy Alexandria
Mohamed Wafaii Zagazik
Mohsen Ibrahim Cairo
Mokhtar Gomaa Al Azhar
Moustafa El Sayed Al Azhar
Moustafa Nawar Alexandria
Nabil El Kafrawy Menoufiya
Nasser Rasmy Cairo
Nesim Shaaban Tanta
Omar Awwad Ain Shams
Ossama Abd El Aziz Tanta
Ossama Sanad Banha
Ramez Guindy Ain Shams
Ramzi El Mawardi Ain Shams
Rania Gaber Tanta
Saeid El Malah Menoufiya
Saied Khaled Ain Shams
Saied Shalaby Menoufiya
Sameh Zaghloul Cairo
Samir Abdel Kader Assiut
Samir Rafla Alexandria
Sherif El Beltagui Alexandria
Sherif El Tobgi Cairo
Sherif Mokhtar Cairo
Taher El Kadi NHI
Tarek Helmy Cairo
Tarek Zaki Ain Shams
Wagdy Ayad Alexandria
Wagdy Galal 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 Chairperson(s) Mahmoud Hassanein, Alex


16:30-18:30 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- 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 Cairo
Panelist(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 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 EtribyAin 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 Menoufiya
21:45-22:00 Case 2: Carotid A-V fistula
Rania Gaber Tanta
22:00-22:15 Case 3: Myocardial aneurysms
Sameh Zaghloul Cairo
22:15 –22:30 Case4: Unusual myocardial infiltration
Abdallah Abou Hashem Zagazig
22:30 – 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/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
Amany Serag Menoufiya
Panelist(s) 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
therapy PVD
Mohamed Awad Taher 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 MawardiAin 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 )
A to Z: Changes in LDL
cholesterol

Gr ou p Baseline LDL 4 months 24 months


cholesterol (mg/dL) (mg/dL)
(mg/dL)

Placebo/
simvastatin 20 mg 111 124 81

Simvastatin 40 mg/
simvastatin 80 mg 112 62 66

De Lemos J et al. European Society of Cardiology Congress


2004; August 28-September 1, 2004; Munich, Germany.
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 81.1 89.7


goal for LDL cholesterol

Percentage of CHD/CHD risk equivalent NA NA


patients who reached <70 mg/dL

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.

qThe 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.

qEstimated 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
LDL cholesterol potentiates the proatherogenic activity
of C-reactive protein

high levels of LDL and CRP resulted in a potent attenuation


of endothelium-dependent vasodilation

Dr Erik S Stroes ,2004 Drugs Affecting Lipid Metabolism


Two-year statin therapy does not alter the progression of IMT
in type 2 diabetic patients
Mean common carotid IMT of the 182 patients who completed the

study
Patients Baseline 2-year Mean 95% CI p
IMT (mm) IMT (mm) change
(mm)
Placebo 0.780 0.774 -0.006 -0.022 to 0.50
(n=79) 0.011
Statin 0.763 0.765 0.002 -0.011 to 0.78
(n=103) 0.015

Beishuizen ED. Drugs Affecting Lipid Metabolism 2004


meeting; October 24-27, 2004; Venice, Italy

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