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Strategy to Go for Goal in Dyslipidemia with Acute Coronary Syndrome Patients

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Dr. A. Fauzi Yahya, SpJP (K), FIHA, FAsCC. 3rd Pekanbaru Cardiology Update, August 24th 2013. Pangeran Hotel Pekanbaru. Learn more at PerkiPekanbaru.com

Dr. A. Fauzi Yahya, SpJP (K), FIHA, FAsCC. 3rd Pekanbaru Cardiology Update, August 24th 2013. Pangeran Hotel Pekanbaru. Learn more at PerkiPekanbaru.com

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  • 1. Strategy to go for goal in Dyslipidemia with ACS patients A. Fauzi Yahya Department of Cardiology and Vascular Medicine Faculty of Medicine Padjadjaran University/ Hasan Sadikin General Hospital Bandung-Indonesia
  • 2. Why We’ll Never Stop Talking about Dsylipidemia ? Circulation 1993;88:2548-2555
  • 3. Coronary Artery Disease (CAD): Circulation 1993;88:2548-2555
  • 4. Coronary Angiography
  • 5. Braunwald (1996) Risk of death in patients with coronary heart disease is greatest early after an ACS Deaths/100 patients/month Time (months after hospital admission) Acute MI Unstable angina Stable angina 0 5 10 15 20 25 0 1 2 3 4 5 6
  • 6. 6 Men and Women With ACS Are at High Risk of Early Mortality CCU=coronary care unit. Adapted from Perers E et al. Int J Cardiol. 2005;103:120-127. 30-day mortality in men and women with ACS 10.0 6.0 4.0 2.0 0.0 0 5 10 15 20 25 30 Days after admission to CCU Cumulativemortality(%) 8.0 Men (n=1198) Women (n=546)
  • 7. Pra PCI Post PCI
  • 8. 8
  • 9. 4. Plaque rupture, cholesterol content, inflammation (hs-CRP) (statins) 3. Platelet adhesion/ activation/aggregation (aspirin,clopidogrel,ticagrelor, prasugrel GP IIb/IIIa inhibitors) 2. Activation of clotting cascade – thrombin (heparin/LMWH) 1. Downstream from thrombus myocardial ischaemia/necrosis (β-blockers, nitrates etc) Pathophysiology of ACS and potential pharmacological interventions Platelet GP IIb/IIIa receptor Fibrinogen Thrombin Fibrin clot
  • 10. XXII ESC Congress (2000) Statins Revascularisation Combined therapy 0 10 20 30 40 34% 36% 64% 50 60 Swedish registry: Early statin and revascularisation significantly reduces mortality 70 Relative risk reduction in mortality after 1 year
  • 11. Plaque Stabilization/Regression Unstable plaque Fibrous cap Lipid core Stable plaque Lipid core Fibrous cap Inflammatory cells Fewer inflammatory cells Toschi V et al. Circulation. 1997;95:594-599; Libby P. Circulation. 1995;91:2844-2850.
  • 12. 13
  • 13. 14 GRACE: Statin Therapy Improved Clinical Outcomes in ACS 0 2 4 6 8 10 12 14 16 18 In-hospitalevents(%) MI after 24 hours Pulmonary edema Cardiogenic shock Cardiac arrest VT/VF Stroke Death Death, stroke, or in-hospital MI Hospital outcomes of patients with ACS according to statin use On statins and continued Began in hospital No statin use Prior statin discontinued on admission Discontinuation of statin therapy was associated with worse clinical outcomes in GRACE Adapted from Spencer FA et al. Ann Intern Med. 2004;140:857-866. VT=ventricular tachycardia; VF=ventricular fibrillation.
  • 14. 15 NRMI: Statin Use Within 24 Hours of AMI Is Associated With Reduced Early Morbidity and Mortality Adapted from Fonarow GC et al. Am J Cardiol. 2005;96:611-616. *P<.001 vs No/No patients. Yes/yes=patients continued on statin therapy; no/yes=patients newly started on statin therapy; no/ no=patients who did not receive statin therapy before or within the first 24 hours of hospitalization; yes/ no=patients in whom statin therapy was discontinued. Clinical events by statin use 0 5 10 15 20 25 30 Death Heart failure Rupture Shock VT/VF Reinfarct Yes/Yes No/Yes No/No Yes/No Clinicalevents(%) * * * * * * * * * ** * * Statin initiation within 24 hours of hospitalization resulted in a 77% reduction in death compared with no statin use
  • 15. Very High Risk Subjects
  • 16. *P<.002 vs atorvastatin 20 mg, 40 mg; simvastatin 20 mg, 40 mg, 80 mg; pravastatin 20 mg, 40 mg ** P<.002 vs atorvastatin 40 mg; simvastatin 40 mg, 80 mg; pravastatin 40 mg 1. Jones PH, Davidson MH, Stein EA, et al. Am. J. Cardiology 2003; 93: 152-160. 2. Data on file, DA-CRS-02 AstraZeneca Pharmaceuticals LP, Wilmington, DE. –52.4 * –55.0 ** –51.1 20 40 20 40 80 20 40 80 20 40 –60 –50 –40 –30 –20 –10 0 Rosuvastatin (mg) Pravastatin (mg) Atorvastatin (mg) Simvastatin (mg) MeanPercentChangeFrom BaselineinLDL-C(±SE) -35.0 -29.7 -24.4 -47.8 -42.6 –45.8 -38.8 Percentage Change in LDL-C: Pairwise Comparison of Rosuvastatin 20 mg and 40 mg
  • 17. Lipids Safety Lipids CRP Safety Lipids CRP Safety Patients (n=825) 18–75 years Hospitalised for ACS (STEMI, NSTEMI, UA) within 48hrs of ischaemic symptoms LDL-C >70mg/dL (~1.8 mmol/L) TGs <500 mg/dL (~5.6 mmol/L) Rosuvastatin 40 mg (n=270) Atorvastatin 80 mg (n=278) Rosuvastatin 20 mg (n=277) Visit: Week: 1 4 6 5 12 2 0 3 2 Screening / baseline blood analysis LUNAR Study Design ACS = acute coronary syndrome, STEMI = ST elevation myocardial infarction, NSTEMI = non-ST elevation myocardial infarction, UA = unstable angina, LDL-C = low- density lipoprotein cholesterol, TGs = triglycerides, CRP = C-reactive protein Prospective, multi-centre, randomised, open-label, parallel-group phase IIIb study Symptom Onset Average time from symptom onset to study drug treatment = 3.9 days Pitt B et al. Am J Cardiol 2012; doi:10.1016/j.amjcard.2011.12.015
  • 18. LUNAR Primary Endpoint *p <0.05; **p <0.01 versus atorvastatin 80 mg Time (weeks) 0 2 4 6 8 10 12 Rosuvastatin 20mg Rosuvastatin 40mg Atorvastatin 80 mg 0 -10 -20 -30 -40 -50 -60 * ** * Mean Change in LDL-C from Baseline (%) Pitt B et al. Am J Cardiol 2012; doi:10.1016/j.amjcard.2011.12.015
  • 19. 9.7 11.9 5.6 0 5 10 15 ** Mean change in HDL-C from baseline (%) Rosuvastatin 20 mg Rosuvastatin 40 mg Atorvastatin 80 mg *** LUNAR Secondary Endpoint **p< 0.01, *** p<0.001 versus atorvastatin 80 mg Pitt B et al. Am J Cardiol 2012; doi:10.1016/j.amjcard.2011.12.015
  • 20. LUNAR Secondary Endpoints ** p<0.01, ***p<0.001 versus atorvastatin 80 mg †p< 0.05, †† p<0.01 versus rosuvastatin 20mg -100 -80 -60 -40 -20 0 20 Mean Change in Parameter from Baseline (%) Rosuvastatin 20mg Rosuvastatin 40mg Atorvastatin 80mg *** *** *** ** *** *** † †† Pitt B et al. Am J Cardiol 2012; doi:10.1016/j.amjcard.2011.12.015
  • 21. LUNAR Safety & Tolerability Variable Rosuvastatin 20 mg/day (n=267) Rosuvastatin 40 mg/day (n=263) Atorvastatin 80 mg/day (n=269) Any Serious AE* 28 (10.5%) 23 (8.7%) 38 (14.1%) Serious Cardiovascular AE* 9 (3.4%) 5 (1.9%) 6 (2.2%) Unstable angina 4 (1.5%) 3 (1.1%) 3 (1.1%) Myocardial infarction 5 (1.9%) 2 (0.8%) 2 (0.7%) Cerebrovascular accident 0 0 1 (0.4%) Withdrawal due to AE 10 (3.7%) 16 (6.1%) 25 (9.3%) Musculoskeletal and connective tissue disorders 5 (1.9%) 6 (2.3%) 17 (6.3%) Death* 0 2 (0.8%) 1 (0.4%) AE = adverse event *None of the serious AEs, serious cardiovascular AEs or deaths were considered by the investigators to be related to study treatment Pitt B et al. Am J Cardiol 2012; doi:10.1016/j.amjcard.2011.12.015
  • 22. 24 Conclusion ♦  ACS is common and represents a large burden on clinical, social, and health care systems globally ♦  A significant proportion of the burden is borne in the immediate post-ACS period (<30 days) ♦  Observational evidence suggests pretreatment with statins can impact the ACS burden: ♦ Rosuvastatin has beneficial effect in ACS patient
  • 23. Thank You 25

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