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
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%)---------------------------------------------------------------------------------------------------------------
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[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
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
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 (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
Nissen SE et al. JAMA 2004; 291:1071-1080.
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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
Nissen SE et al. JAMA 2004; 291:1071-1080.
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
Regression of plaque
Aggressive lipid lowering
Guide lines
Which statin to which pt.?
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
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 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
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.?
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.