Treatment of Atherosclerosis in 2007
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1 Treatment of Atherosclerosis in 2007 Szilard Voros, M.D. Medical Director Cardiovascular MR and CT Piedmont Hospital, Piedmont Hospital
2 Our Paradigm Genotype Phenotype Environment Atherosclerotic Disease Progression Atherosclerosis Clinic Non-Invasive Imaging Lab, Piedmont Hospital Invasive Imaging and Therapeutic Lab
3 Introduction My Perspective, Piedmont Hospital
4 Introduction My Perspective A. C. E. G. B. D. F. H., Piedmont Hospital Superko, Voros. In PK Shah 2006.
5 New Paradigm Dual Inhibition of esterol Metabolism Dual inhibition of cholesterol metabolism is becoming first-line therapy in the treatment of dyslipidemias, Piedmont Hospital
6 New Paradigm Dual Inhibition of esterol Metabolism Dual inhibition of cholesterol metabolism is becoming first-line therapy in the treatment of dyslipidemias 1. LDL Argument 1. To reach LDL<70, dual inhibition is needed for LDL > Biological Argument 1. esterol in plaque comes from two sources 2. Treatment of one pathway upregulates the other 3. Dual-inhibition is synergistic for inflammation, Piedmont Hospital
7 Biological Arguments The Disease: Atherosclerosis LDL, Piedmont Hospital
8 Biological Arguments The Disease: Atherosclerosis, Piedmont Hospital
9 Biological Arguments The Disease: Atherosclerosis, Piedmont Hospital
10 Biological Arguments The Disease: Atherosclerosis, Piedmont Hospital
11 Biological Arguments Role of esterol in CAD CAD mortality rate per 1000 over 10 y MR-FIT (N=316,099) Serum cholesterol (mg/dl), Piedmont Hospital Neaton et al. Arch Intern Med 1992;152:56.
12 Biological Arguments Role of esterol in CAD, Piedmont Hospital JAMA 1984;251:
13 Biological Arguments Role of esterol in CAD, Piedmont Hospital rticles/nobel_prize/cholesterol_ldl.j pg
14 Biological Arguments Role of esterol in CAD ApoB ApoB Particles Particles ApoA Particles, Piedmont Hospital
15 Biological Arguments Atherosclerosis Progression and Regression Apo-B lipoproteins VLDL, LDL, Lp(a), IDL Progression LDL Non-HDL CRP, IL6, CD-40 MPO, MMP Stabilization Apo-A lipoproteins HDL Regression HDL, Piedmont Hospital
16 Biological Arguments Atherosclerosis Progression: ApoB, Piedmont Hospital von Ballmoos et al. ATVB 2006;26:
17 New Paradigm Dual Inhibition of esterol Metabolism Dual inhibition of cholesterol metabolism is becoming first-line therapy in the treatment of dyslipidemias 1. LDL Argument 1. To reach LDL<70, dual inhibition is needed for LDL > Biological Argument 1. esterol in plaque comes from two sources 2. Treatment of one pathway upregulates the other 3. Dual-inhibition is synergistic for inflammation, Piedmont Hospital
18 Diet 300mg Intestine 1100mg Biological Arguments 1. esterol in Plaque from Two Sources Absorption Inhibitors LDL, VLDL Chylomicron HDL Liver (10%) 800mg Statins Tissues (90%), Piedmont Hospital
19 Biological Arguments 1. esterol in Plaque from Two Sources Intestinal Absorption 300 mg Chylomicrons ApoB48 Atherogenic Particles Hepatic Synthesis 800 mg VLDL, LDL ApoB100, Piedmont Hospital
20 Biological Arguments 1. esterol in Plaque from Two Sources, Piedmont Hospital Proctor et al. ATVB 2003;23:1595.
21 Biological Arguments 1. esterol in Plaque from Two Sources, Piedmont Hospital Voros et al
22 Biological Arguments 1. esterol in Plaque from Two Sources, Piedmont Hospital Voros et al
23 Biological Arguments 1. esterol in Plaque from Two Sources, Piedmont Hospital Le Couteur et al. Lancet 2002; 359:
24 Biological Arguments Reverse esterol Transport Intestines Chylomicron ApoB48 Liver LDL-R VLDL IDL LDL ApoB100 ApoB100 ApoB100 Reverse esterol Transport Direct HDL LDL-R Tissues SR-B1 Reverse esterol Transport Indirect ABC Transporters ApoA, Piedmont Hospital
25 Intestinal Cell Chylomicrons Chylomicron remnants TG ApoB Gene Liver TG LPL ApoE CETP LCAT CE CE TG TG HDL ApoB Gene ApoE ApoE ApoE ApoE ApoE VLDL VLDL-Remnants LDL, Piedmont Hospital
26 Biological Arguments 1. esterol in Plaque from Two Sources, Piedmont Hospital Miettinen et al. JACC 2005;45:
27 Biological Arguments 1. esterol in Plaque from Two Sources Patients with CAD by invasive X-ray 1.00angiography (Chylomicron, remnants and 0.0 some VLDL) CAD by Angio p<0.05 have higher ApoB48/ApoB100 ratio in the Sf>60 4-hour post-prandial 0.5samples Control ApoB48/B Q1 Q2 Q3 Q4 Adjusted OR for CAD by Quartile, Piedmont Hospital Simons LA et al. Atherosclerosis 1987;65:
28 40% 30% 20% 10% 0% Biological Arguments 1. esterol in Plaque from Two Sources Quartiles of cholesterol absorption Placebo Simvastatin 4S population, Piedmont Hospital Turley et al. Clin Card 2004;27(Suppl. III):16-21.
29 Biological Arguments 1. esterol in Plaque from Two Sources Intestinal Absorption 300 mg Chylomicrons ApoB48 Atherogenic Particles Hepatic Synthesis 800 mg BAS VLDL, LDL Fibers ApoB100, Piedmont Hospital
30 Biological Arguments 1. esterol in Plaque from Two Sources Intestinal Absorption 300 mg Chylomicrons ApoB48 Atherogenic Particles Hepatic Synthesis 800 mg Ezetimibe (Zetia) VLDL, LDL ApoB100, Piedmont Hospital
31 Biological Arguments 1. esterol in Plaque from Two Sources Intestinal Absorption 300 mg Statins Chylomicrons ApoB48 Atherogenic Particles Hepatic Synthesis 800 mg VLDL, LDL ApoB100, Piedmont Hospital
32 Biological Arguments 1. esterol in Plaque from Two Sources Intestinal Absorption 300 mg DUAL INHIBITION Chylomicrons ApoB48 Atherogenic Particles Hepatic Synthesis 800 mg VLDL, LDL ApoB100, Piedmont Hospital
33 Biological Arguments Ezetimibe (Monotherapy) % Change in Lipids in 12 Weeks* 10% 5% 0% -5% -10% -15% -20% LDL 1:1 ApoB TC HDL TG Particle numbers 0.4% -17% -1.4% % 0.6% -12% -1.6% 1% 5.7% -6% BAS increase TG *Seen at 2 weeks and maintained at 12 weeks Placebo Ezetimibe, Piedmont Hospital Dujovne et al. Am J Cardiol 2002;90:
34 % Change in LDL-esterol from Statin Baseline 0% -5% -10% -15% -20% -25% -30% Biological Arguments Ezetimibe (Add-On Therapy) -3.7% p< % Placebo, Piedmont Hospital Ezetimibe Gagne et al. Am J Cardiol 2002;90:
35 New Paradigm Dual Inhibition of esterol Metabolism Dual inhibition of cholesterol metabolism is becoming first-line therapy in the treatment of dyslipidemias 1. LDL Argument 1. To reach LDL<70, dual inhibition is needed for LDL > Biological Argument 1. esterol in plaque comes from two sources 2. Treatment of one pathway upregulates the other 3. Dual-inhibition is synergistic for inflammation, Piedmont Hospital
36 Biological Argument 2. Inhibiting One Pathway Upregulates Other 60% 50% 40% 30% 20% 10% 0% 49.8% 54% reduction 22.7% % increase Placebo Ezetimibe Placebo Ezetimibe Absorption esterol Synthesis, Piedmont Hospital Circulation 2002;106:
37 Biological Argument 2. Inhibiting One Pathway Upregulates Other 200% 150% 100% 50% 0% -50% -100% -42.0% 187.0% Synthesis Absorption Long-term atorvastatin treatment in T2DM, Piedmont Hospital Miettinen et al. Eur J Clin Invest 2003;33:
38 Mean change in ratio* at 12 weeks Biological Argument 2. Inhibiting One Pathway Upregulates Other Placebo (n=62) 3 4 Statin mg (n=232) Ezetimibe 10 mg + statin mg (n=229) Total cholesterol esterol production esterol absorption, Piedmont Hospital Assmann G et al. ACC, New Orleans, Louisiana, USA, March 7 10, 2004.
39 Biological Argument 2. Inhibiting One Pathway Upregulates Other Sitosterol Concentration Serum Tissue 290 No Statin Statin, Piedmont Hospital Miettinen et al. JACC 2005;45:
40 New Paradigm Dual Inhibition of esterol Metabolism Dual inhibition of cholesterol metabolism is becoming first-line therapy in the treatment of dyslipidemias 1. LDL Argument 1. To reach LDL<70, dual inhibition is needed for LDL > Biological Argument 1. esterol in plaque comes from two sources 2. Treatment of one pathway upregulates the other 3. Dual-inhibition is synergistic for inflammation, Piedmont Hospital
41 Biological Argument 3. Dual-Inhibition: Synergy for Inflammation 10% 0% -10% -20% -30% -40% Placebo 11.5% Simva alone -1.2% -18.2% -34.8% EZ alone Simva+EZ -5% Simva 10-15% -25% -35% -45% -27% Simva 20-12% % EZ -31% Simva 40-24% -40% Simva 80-28% -36% Statin alone, Piedmont Hospital Sager et al. AJC 2003;92:
42 New Paradigm Dual Inhibition of esterol Metabolism Dual inhibition of cholesterol metabolism is becoming first-line therapy in the treatment of dyslipidemias, Piedmont Hospital
43 5% -15% -35% -55% -75% Dual Inhibition Simvastatin+Ezetimibe (VYTORIN): LDL Starting dose 10_20 10_40 10_ % 1528 patients Double blind, RCT 12 weeks Optional starting -55.0% LDL Reduction -60.0%, Piedmont Hospital Bayes et al. ACC 2004.
44 Dual Inhibition VYTORIN Versus Atorvastatin (VYVA) LDL 5% -15% -35% -55% -75% 10/10 vs 10 10/20 vs 20 10/40 vs 40 10/80 vs % -36% ~2000 patients Double blind, RCT 6 weeks ~ half were high risk (10-year risk>20%) -44% -50.6% Vytorin -48% % -57.4% -58.6% Atorvastatin, Piedmont Hospital Ballantyne CM et al. Am Heart J 2005:149:
45 Dual Inhibition VYTORIN Versus Atorvastatin (VYVA) HDL 15% 10% 5% 0% -5% ~2000 patients Double blind, RCT 6 weeks ~ half were high risk (10-year risk>20%) 7.7% 6.9% 7.2% 5.1% 9.0% 3.8% 7.6% 7.9% 1.4% 4.30% 10/10 vs 10 10/20 vs 20 10/40 vs 40 10/80 vs 80 Pooled Vytorin Linear (Atorvastatin) Atorvastatin Linear (Vytorin), Piedmont Hospital Ballantyne CM et al. Am Heart J 2005:149:
46 Dual Inhibition VYTORIN Versus Atorvastatin (VYVA) CRP 0% -10% -20% -30% 10/10 vs 10 10/20 vs 20 10/40 vs 40 10/80 vs 80 Pooled -17% -21.1% -21.4%-22% -29.5%-29% -26.9% % -24.8% % ~2000 patients Double blind, RCT 6 weeks ~ half were high risk (10-year risk>20%) -40% Vytorin, Piedmont Hospital Atorvastatin Ballantyne CM et al. Am Heart J 2005:149:
47 Dual Inhibition VYTORIN Versus Atorvastatin in T2DM LDL 1229 patients Double blind, RCT 6 weeks All with T2DM NEW! 5% -15% -35% -55% -75% -38% p<0.05 Vytorin 10/20 Vytorin 10/40-45% -54% p< % -58% p<0.05 Atorvastatin 10 Atorvastatint 20 Atorvastatin 40 Vytorin, Piedmont Hospital Goldberg et al. ADA; June 2006.
48 NEW! Goal Attainment Dual Inhibition VYTORIN Versus Atorvastatin in T2DM 100% 80% 60% 40% 20% 0% 22% p< % 60% p< % Vytorin 10/20 Vytorin 10/40 p< % Atorvastatin 10 Atorvastatint 20 Atorvastatin 40 Vytorin, Piedmont Hospital Goldberg et al. ADA; June 2006.
49 Dual Inhibition NEW! HDL Raise 10% 8% 6% 4% 2% 0% VYTORIN Versus Atorvastatin in T2DM p<0.05 p<0.05 p<0.05 8% 6% 4.3% 4.5% 2.3% Vytorin 10/20 Vytorin 10/40 Atorvastatin 10 Atorvastatint 20 Atorvastatin 40 Vytorin, Piedmont Hospital Goldberg et al. ADA; June 2006.
50 Dual Inhibition VYTORIN Versus Atorvastatin in T2DM CRP Change 1229 patients Double blind, RCT 6 weeks All with T2DM NEW! -5% Vytorin 10/20 Vytorin 10/40-15% -25% -35% -13.7%-13.8% p< % -28.6% -33% p<0.05 p<0.05 Atorvastatin 10 Atorvastatint 20 Atorvastatin 40 Vytorin, Piedmont Hospital Goldberg et al. ADA; June 2006.
51 LDL 5% -15% -35% -55% -75% Dual Inhibition VYTORIN Versus Rosuvastatin 10/20 vs 10 10/40 vs 20 10/80 vs % -46% -55.0% -52% -61.0% -57% ~2855 patients Double blind, RCT Vytorin Rosuva 6 weeks, Piedmont Hospital ISA Meeting; Rome, June 2006.
52 New Paradigm Dual Inhibition of esterol Metabolism Dual inhibition of cholesterol metabolism is becoming first- line therapy in the treatment of dyslipidemias 1. LDL Argument 1. To reach LDL<70, dual inhibition is needed for LDL > Biological Argument 1. esterol in plaque comes from two sources 2. Treatment of one pathway upregulates the other 3. Dual-inhibition is synergistic for inflammation 3.?Outcomes Argument?, Piedmont Hospital
53 Dual Inhibition Outcomes Studies 1. SEAS: Aortic stenosis (n=1400) 2. SHARP: Renal dz (n=9000) 3. ENHANCE: FH (n=725) 4. Im-PROVE IT (n~10,000) 1. Simvastatin Vytorin 10/40, Piedmont Hospital
54 Apo-B lipoproteins VLDL, LDL, Lp(a), IDL Progression LDL Non-HDL REVERSAL HALTING CRP, IL6, CD-40 MPO, MMP Stabilization QUENCHING Conclusions Present and Future Apo-A lipoproteins HDL Regression HDL ApoAI Milano MELTING, Piedmont Hospital
55 Conclusions, Piedmont Hospital Proctor et al. ATVB 2003;23:1595.
56 NPC1L1 ApoB48 ApoB48 ApoB100 LDL-R LDL-R ApoB100 ApoB100 VLDL LDL, Piedmont Hospital
57 Atherosclerosis Ezetimibe and Lipoproteins NPC1L1 LDL-R ApoB48 ApoB48 ApoB100 LDL-R LDL-R LDL-R LDL-R ApoB100 VLDL, Piedmont Hospital Increased FCR ApoB100 LDL LDL ApoB 18%
58 NPC1L1 ApoB48 ApoB48 ApoB100 Statin LDL-R LDL-R ApoB100 VLDL, Piedmont Hospital ApoB100 LDL LDL 40% ApoB 25%
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